#after adipositas

[miezemia]

Day 13 after surgery

[the-honey-dukes]

It’s time to make a change. I watched a documentation about a Type 3 Adipositas Patient who weights 140 kg (only 40 more than I weight). And who made significant changes after having two surgeries. 

I’m currently at 100 kg. I am Type 2 Adipostias (with high blood pressure, bladder problems etc.) My problem is that I constantly sit. I sit at work and I sit at home and barely do any exercise at all. Which is one of the problems of my weight.

The bigger challenge will be to stop drinking Coca Cola and eating unhealthy sweets between meals. I’m currently drinking 2 liters daily. 

A friend of mine managed to lose a lot of weight as well and she became my personal inspiration. 

I WILL AND I CAN DO THIS. I mean I only have to lose around 35 Kg. It’s manageable. 

I would be very happy if you could include me in your prayers. 

[the-oddest-inkling]

It’s time to make a change. I watched a documentation about a Type 3 Adipositas Patient who weights 140 kg (only 40 more than I weight). And who made significant changes after having two surgeries. 

I’m currently at 100 kg. I am Type 2 Adipostias (with high blood pressure, bladder problems etc.) My problem is that I constantly sit. I sit at work and I sit at home and barely do any exercise at all. Which is one of the problems of my weight.

The bigger challenge will be to stop drinking Coca Cola and eating unhealthy sweets between meals. I’m currently drinking 2 liters daily. 

A friend of mine managed to lose a lot of weight as well and she became my personal inspiration. 

I WILL AND I CAN DO THIS. I mean I only have to lose around 35 Kg. It’s manageable. 

I would be very happy if you could include me in your prayers. 

[neverstopcountingflowers]

So berechnest du deinen Eiweißbedarf nach OP richtig

Eiweiß ist ein essentieller Baustoff in unserem Körper, ohne Protein geht nichts. Er ist notwendig für den Aufbau von Haut, Muskulatur, Knochen, Zähnen, Haaren, Fingernägeln, Knorpeln, Sehnen. Unser Immunsystem besteht überwiegend aus Eiweißen.

Die Folgen von Eiweißmangel können schwerwiegend sein.

Die Veränderung der Ernährungsgewohnheiten nach einer Magenoperation zum Abnehmen erschwert es, täglich auf die Mindestmenge Eiweiß zu kommen. Nach einer bariatrischen Operation ist es deshalb wichtig, den Eiweißbedarf individuell vom Ernährungsmediziner berechnen zu lassen und durch proteinreiche Mahlzeiten und bei Bedarf Proteinpulver die empfohlene Menge zu essen.

  Eiweiß nach dem Magenbypass berechnen?

Wozu das denn?!

Das sind doch 60 Gramm für alle, oder nicht?

Uschi Mustermann

Fast Food Enthusiastin, Haarlos, schwach und trotzdem glücklich

Ähm naja.

Eher „oder nicht“!

Die Empfehlung der häufig zitierten 60 Gramm Eiweiß nach Magenbypass oder Schlauchmagen Operation als Pauschale beziehen sich auf einen Beispielpatienten mit einem Körpergewicht von 115,67 kg bei 171,8 cm Körpergröße und einem BMI 40. (1) Protein stellt alle unsere „Körperstrukturen“ her – da ist es ganz logisch, dass zum Beispiel ein Mensch mit 1,60 Körperhöhe weniger Eiweiß zum Erhalt und Aufbau seiner „Strukturen“ benötigt, als ein 1,80 großer Mensch.

Der Einfachheit halber (vermute ich!) ist er in der Übersicht in der Leitlinie Adipositaschirurgie 2018 (2) nicht gesondert als Wert für den Beispielpatienten gekennzeichnet. Die „Beispielhaftigkeit“ des Pauschalwerts von 60 Gramm wird aber durch den zugehörigen Text und die umfangreichen Quellenangaben schnell deutlich. Übliche Praxis laut Fortbildungs-App der ASMBS „Essentials of bariatric and metabolic surgery“ ist die Anpassung des individuellen Eiweißbedarfs nach dem errechneten Idealgewicht des Patienten spätestens 3 Monate nach der Operation. (3)

  Wie wird das Protein nach OP berechnet?

  Als Berechnungsgrundlage wird das Idealgewicht in Kilogramm multipliziert mit 1,5 und das ergibt den korrekten Eiweißbedarf eines Erwachsenen mit unmodifiziertem Roux-N-Y Bypass oder Schlauchmagen. (2) Modifizierte Bypässe wie der Omega Loop oder Bypässe mit verlängerten Schlingen sowie der BPD/Duodenalswitch werden mit bis zu 2,1g Eiweiß berechnet auf das Idealgewicht berechnet. (1) (2)

Eiweißmangel Symptome

  Haarausfall

Verlust von Muskelmasse

Dünne, brüchige Haare

Verlust der Griffkraft

Übelkeit oder gesteigerter Appetit

Heißhunger auf Süßes / Fast Food

Müdigkeit / Schwäche

Ödeme / Wassereinlagerungen

  Eiweißbedarf Liste

    RNY Bypass (unmodifiziert): 1,5

Schlauchmagen: 1,0* – 1,5

Omega Loop: 1,5 – 2,1

BPD/DS: 1,5 – 2,1

Magenbypass mit verlängerter Schlinge: 1,5 – 2,1

Eiweißbedarf selbst berechnen

In erster Linie sollte die individuelle Berechnung deiner Eiweißmenge durch den Ernährungsmediziner in deinem Adipositaszentrum erfolgen. Neben Blutwerten und den Symptomen von Eiweißmangel spielen zahlreiche Faktoren für die Festlegung des geeigneten Eiweißwerts eine Rolle.

Die Beispielrechnung und Liste dient ausschließlich dazu, deine Proteinempfehlung nachzuvollziehen und ggf. vor Ort mit deiner Ernährungsfachkraft zu besprechen, warum ihre Empfehlung u.U. von den Leitlinien und dem Clinical Practice Guide abweicht. Dieser Blog dient rein der Information und nicht als Ersatz für professionelle Beratung. (Sicherheitshinweis)

Beispielrechnung an Hand meiner Daten

Ich bin 1,80 groß und habe laut Rechner ein Idealgewicht von 64 kg – 81kg.

Ich nehme 75 Kilogramm als Ausgangswert. Es handelt sich dabei um meine im Institut für Sportmedizin ermittelte „schlanke Körpermasse“. Wenn dir eine solche Analyse zur Verfügung steht, kannst du auch diesen Wert benutzen.

Der Anschaulichkeit halber berechne ich zusätzlich nach dem niedrigen Idealgewicht von 65 kg, die in einer „unsportlichen“ Version von mir realistisch erscheinen.

Mein Magenbypass hat eine verlängerte biliopankreatische Schlinge. Dadurch wurde die Malabsorbtion vergrößert, ich kann Nährstoffe aus dem Essen schlechter aufnehmen.

Für mein sportliches „Ich“ 75 x 1,5 = 112,5 Gramm Eiweiß Für mein unsportliches „Ich“ 65 x 1,5 = 97,5 Gramm Eiweiß

Anne

Magenbypass mit verlängerter biliopankreatischer Schlinge und Minimizer Ring, 1,80 Meter groß

Idealgewicht berechnen

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Anmerkungen und Quellenangaben

Anmerkungen und Quellen

* Die 1,0g Eiweiß beim Schlauchmagen tauchen in verschiedener Lektüre auf, ebenso die Empfehlung, mit 1,0 – 1,2 Gramm Eiweiß zu arbeiten. Leider erinnere ich mich zum aktuellen Zeitpunkt nicht, wo ich das gelesen habe. Der Schlauchmagen besitzt keine „malabsorbtive“ Komponente, da keine Veränderung der Verdauung im Darm und der Aufnahme von Eiweiß, Fett und Kohlenhydraten aus der Nahrung stattfindet. Es spricht aus meiner Sicht nichts dagegen, für den Schlauchmagen die Werte für den Durchschnittsbürger zu benutzen. Je nach Quelle schwanken die Empfehlungen für „Normalos“ zwischen 0,8 und 1,2g / kg . Achtung, Meinung: mit einem Schlauchi würde ich mit 1,2 Gramm rechnen und gucken, wie sich Symptome (Haarausfall, Heißhunger usw.) entwickeln.

(1) „Clinical Practice Guidelines for the Perioperative Nutritional, Metabolic, and Nonsurgical Support of the Bariatric Surgery Patient—2013 Update: Cosponsored by American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery“ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4142593/

(2) Aktuelle Leitlinie Langfassung (PDF Download Direktlink!) https://www.awmf.org/uploads/tx_szleitlinien/088-001l_S3_Chirurgie-Adipositas-metabolische-Erkrankugen_2018-02.pdf

(3) ASMBS App zur Fortbildung, kostenfreie Nutzung des Basiskurses. Das ist kein Werbelink oder so 🙂 Just sayin` https://asmbs.org/essentials-bariatric-metabolic-app

(4) Bariatric Times, Ausgabe November 2018, Seite 14 im Artikel „Inadequate Protein Intake after Bariatric Surgery: Effects on Body Composition and Sarcopenic Obestiy“

Neues aus dem Blog

So berechnest du deinen Eiweißbedarf nach OP richtig

von Anne | April 24, 2019 | Blog, Ernährung nach Magenoperation, Feature Artikel | 0 Kommentieren

Eiweißbedarf nach OP berechnen – so viel Protein brauchst du wirklich.

Read More

Protein Milchcreme – Frühstücksbrei

von Anne | April 24, 2019 | Blog, Feature Artikel, Flüssig- und Breiphase, Frühstück, Protein Zwischenmahlzeit | 0 Kommentieren

Proteinreich und lecker ist die Milchcreme mit Hafer – inklusive Lowcarb Variante 🙂

Read More

Protein: Die heimliche Waffe gegen Hunger

von Anne | April 23, 2019 | Blog, Feature Artikel, Studien & Wissenschaft | 0 Kommentieren

Protein ist einer der wichtigsten essentiellen Nährstoffe und nach einer Adipositasoperation besonders wichtig. Er kann helfen, den Haarausfall zu mildern oder zu verhindern und sorgt für eine gute Sättigung.

Read More

200 Kilo abgenommen – meine Geschichte *Vorpremiere*

von Anne | April 23, 2019 | Abnehmen ohne OP, Blog, Erfolgsgeschichten, Feature Artikel | 0 Kommentieren

200 Kilo abgenommen – Vorpremiere des Youtube Videos für meine Blog Leser. Ich erzähle, wie ich von 2006 bis 2019 200 Kilo oder mehr abgenommen habe.

Read More

Die ganze Wahrheit über den Pouch Reset

von Anne | April 16, 2019 | Blog, Ernährung nach Magenoperation, Feature Artikel, Hintergrundwissen, Rinderwahnsinn der Woche, Zunahme nach Magenbypass | 0 Kommentieren

Pouch Reset Das Ungeheuer aus den Tiefen Social Medias Stell dir den Soundtrack vom »Weißen Hai« vor: Der schlagende Bass mit seinem Dum Dum Dum Dum Dum Dum, wenn sich das »Monster« aus der Tiefe dem nichtsahnenden Schwimmer nähert. Als er den Schatten unter sich...

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„Pouch Resizing“ nach Magenbypass – Wenn die Portionen größer werden

von Anne | April 16, 2019 | Blog, Feature Artikel, Fragen an den Doc, Studien & Wissenschaft, Zunahme nach Magenbypass | 0 Kommentieren

Pouch "Re-Sizing" Einleitung Die Angst vor einem »ausgedehnten« Pouch ist auf Social Media allgegenwärtig. Heute darf ich euch einen Gastbeitrag von unserem Lieblingschirurgen Professor Marjanovic präsentieren. Das Thema ist spannend – und hoffentlich das Ende der...

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Magenbypass: Darum habe ich eine Woche geweint

von Anne | April 13, 2019 | Blog, Feature Artikel, Mein Magenbypass und ich | 0 Kommentieren

Ich habe mindestens eine Woche geheult! Erstmals satt mit 40 Jahren! Tränen als Spitze des Eisbergs Ich sitze im Livestream auf Facebook und heule. Gefühlt seit einer halben Stunde – in Wahrheit waren es nur Minuten! Aber diese Minuten haben viele von euch bewegt und...

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Adipositas & Eisenmangel

von Anne | April 13, 2019 | Blog, Feature Artikel, Studien & Wissenschaft | 0 Kommentieren

Eisenmangel        & Adipositas Adipositas verursacht Eisenmangel? Eisenmangel und Anämie gehören zu den häufigsten Nährstoffmängeln nach einer Adipositasoperation. In der Bariatric Times März 2019 erschien ein interessanter Beitrag über die systemische Entzündung...

Read More

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  Quellenangaben & Leseempfehlungen

(1) Nutritional Recommendations for Adult Bariatric Surgery Patients: Clinical Practice

(2) Chirurgie der Adipositas und metabolischer Erkrankungen

(3)  Clinical Practice Guidelines for the Perioperative Nutritional, Metabolic, and Nonsurgical Support of the Bariatric Surgery Patient—2013 Update: Cosponsored by American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery*

(4) Endocrine and Nutritional Management of the Post-Bariatric Surgery Patient: An Endocrine Society Clinical Practice Guideline

(5) Long-term Management of Patients After Weight Loss Surgery

(6) Nutrition Care for Patients with Weight Regain after Bariatric Surgery

(7) Changes in total energy intake and macronutrient composition after bariatric surgery predict long-term weight outcome: findings from the Swedish Obese Subjects (SOS) study.

(8) Nutrition Care for Patients with Weight Regain after Bariatric Surgery

(9) Weight regain after gastric bypass: etiology and treatment options

(10) Weight regain after Roux-en-Y gastric bypass has a large negative impact on the Bariatric Quality of Life Index

(11) Changes in total energy intake and macronutrient composition after bariatric surgery predict long-term weight outcome: findings from the Swedish Obese Subjects (SOS) study.

      Der Beitrag So berechnest du deinen Eiweißbedarf nach OP richtig erschien zuerst auf Abnehmen mit Magenverkleinerung.

[your-dietician]

Experimental Therapeutics for the Treatment of Osteoarthritis

New Post has been published on https://depression-md.com/experimental-therapeutics-for-the-treatment-of-osteoarthritis/

Experimental Therapeutics for the Treatment of Osteoarthritis

Introduction

Osteoarthritis (OA) is the most common joint disease. It has an increasing prevalence in the more and more aging population1 and presents a large burden for the healthcare systems since it remains so far untreatable. A huge bulk of novel literature arises daily in OA research presenting a demanding challenge for OA researchers to notice the emerging innovations. In regard to therapeutical targets in OA, several reviews of literature have recently been published which can be studied.2–10 However, mesenchymal stromal cell (MSCs) or exosome-based approaches, interrelation of OA with the microbiome, novel strategies of improved viscosupplementation as well as the arising knowledge concerning the impact of micro RNAs (miRNAs) in the OA therapy are less addressed and hence, present a topic of this review. In view of the abundant novel literature related to these issues, this review remains mainly confined to most recent findings of the last three years. Its purpose is to discuss currently emerging experimental strategies to treat OA. It will introduce into currently known facts about the pathogenesis of OA. Then, as research tools, the in vitro and in vivo OA models will be shortly summarized before therapeutically addressed targets and signaling pathways in OA will be presented and some promising groups of remedies will be discussed in more detail.

OA Pathogenesis

Diverse pathogenetic factors in OA have been identified including its initiation by insufficient cartilage healing after injury representing posttraumatic OA (PTOA), loss of function of cartilage during aging,11 genetic predispositions (eg, less stable cartilage ECM through mutations in ECM genes or less effective protective mediators due to mutations in their genes) or joint overload (by misalignment of leg axis or adipositas/obesity as well as meniscus damage or loss).12,13 The contribution of metabolic dysbalances (metabolic syndrome, diabetes mellitus) to OA has been underlined in the last years.14,15 Joint pain, stiffness and swelling are typical clinical features of OA.16 The progradient cartilage deterioration and subsequent loss (Figure 1) associated with OA is clinically detectable as joint space narrowing on X-ray images. Other changes include formation of osteophytes, subchondral bone sclerosis, cracks and possibly, subchondral bone marrow edema,17 as well as low-grade synovitis.18,19 OA is triggered by episodic inflammation1,18,19 and local inflammation in the affected joints which correlates with systemic inflammation markers.18 OA is a whole joint disease affecting all joint-associated tissues.13,20,21

Figure 1 Osteoarthritic joint cartilage. (A) A femur head affected by OA explanted during joint replacement surgery is shown. Histological images (Hematoxylin Eosin staining) of (B1) nearly unaffected human cartilage, (B2 and B3) mild (hypocellularity, superficial clefts) and severely (cartilage absent, bone marrow activated, fibrosis) affected human joint cartilage. A histological image of healthy (C1) and severely osteoarthritic (C2) articular cartilage of the rat knee joint.

Typical molecular features of OA in joint cartilage are an accelerated cartilage ECM degradation enforced by a dysbalance between extracellular matrix (ECM) degrading enzymes such as matrix metalloproteinases (MMPs), a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) and regulatory tissue inhibitors of metalloproteinases (TIMPs).3,22 Particularly the cleavage of aggrecan in cartilage is a hallmark of cartilage degeneration in OA.22,23 Furthermore, ECM neosynthesis is suppressed in OA chondrocytes.21 Episodic joint inflammation is triggered by an enhanced release of pro-inflammatory cytokines including TNFα, IL-1β and IL-6 which play a crucial role in OA.1,24,25 In addition to the aforementioned well-known cytokines increased levels of other cytokines such as IL-8 and IL-18 can also be observed.26 Cytokines are released by synovial fibroblasts (SF), macrophages or chondrocytes themselves.27–29 Chondrocytes change their cell membrane protein expression pattern comprised as surfactome in response to the presence of TNFα and IL-1β.24 The loss of maturational arrest of chondrocytes has been reported in OA30 leading to cell cluster formation due to uncontrolled focal cell proliferation. OA chondrocytes can undergo preterm senescence30 or perish due to apoptosis.3 Apoptosis can arise from extrinsic, which includes death receptor-mediated, or intrinsic mitochondria-associated signaling pathways. Mitochondrial pathways are affected by OA reflecting oxidative stress.30,31 Mitophagy, which represents the selective uptake of mitochondria by autophagosomes of the cells, has been observed as a correlate of mitochondrial disturbances in OA.32,33 In addition, apoptosis in OA can be induced by lysosomal dysfunction as recently reported.34

Enhanced cell death and ECM degradation propagate the presence of damage products including so-called alarmins, some of them released from the cytosol.29

Alarmins which represent so-called damage-associated molecular patterns (DAMPs) are delivered as normal cellular constituents such as ECM components, S100 proteins, histones or nucleic acids35 from degraded ECM, damaged or dying cells and subsequently bind to cell membrane receptors or intracellular receptors of other cells initiating inflammatory responses. In OA an enhanced release of alarmins can be postulated.29 One receptor class binding DAMPs is the Toll-like receptor (TLR) family.35 Alarmins are involved in OA pathogenesis as recently reviewed by Minguzzi et al30. Cell and ECM fragments can also initiate complement activation36 and thereby, contribute substantially to OA pathogenesis.37,38 Despite the changes in cartilage are so far more intensively studied, the contribution of other tissues than cartilage to OA pathogenesis has to be strongly considered such as of menisci and infrapatellar fat pad (IFP).13,39,40 An intimate interplay between inflamed synovium and meniscus tissue of early and late OA patients could be observed in co-culture studies characterized by elevated release of inflammatory and catabolic mediators in co-cultures compared to monocultures.41 A closer focus on the IFP indicated inflammatory and fibrotic changes as well as enhanced vascularization associated with OA.39,42 The synovial membrane and IFP might act as anatomo-functional unit involved in OA pain generation43,44 and both tissues are inflamed in OA.39 Future research should elucidate more details of the interplay of all these tissues in the scenario of OA.

OA is so Far Untreatable

There are no approved effective disease-modifying OA drugs (DMOADs) available for OA treatment.12 Only symptomatical treatment of OA can be performed. Hence, analgesics and non-steroidal anti-inflammatory drugs (NSAIDs) addressing pain and inflammation are the therapeutic options for OA45,46 with adverse effects in long-term use.47 NSAIDs are widely prescribed for the treatment of symptomatic OA of the knee.45 Therefore, the search for valuable targets requires the understanding of the interaction of different signaling pathways and has to go on remaining a challenging topic in current research.48

In vitro and in vivo Disease Models for Elucidation of OA Therapeuticals

Suitable OA models are required to decipher OA pathogenesis. Many studies are completely performed in vitro using primary chondrocytes from healthy persons or individuals suffering from OA, synovial fibroblasts (SF), several chondrocytic, synovial fibroblast (SF) or macrophage cell lines (eg, human chondrosarcoma SW1353 and OUMS-27 cell lines, murine teratocarcinoma-derived chondrocyte cell line ATDC5, SF K4IM and murine macrophage Raw 264.7 cell lines) or even cartilage explants to simulate natural three-dimensional (3D) conditions (Table 1).8,27,49–53 Cells were usually stimulated with probably mostly hyperphysiological concentrations of cytokines IL-1β, TNFα or lipopolysaccharide (LPS) to simulate inflammation associated with OA.27,28,52,54 On first glance, LPS does not play a role in OA. However, it has recently been suggested that LPS released from the disturbed gut microbiome might provide a pathogenetic link between obesity, metabolic syndrome and OA.55 One has to consider that chondrocyte cell lines usually do not reflect all features of primary chondrocyte responses.50,56 These in vitro studies focus in the most cases only on chondrocytes and mostly neglect the interplay with other cell types in the joint such as synoviocytes (SF and macrophages), Hoffa fat pad- or subchondral bone derived-cell types. However, some co-culture models were used. Co-culture models of OA were established which consisted, eg, of cartilage and synovial membrane explants from human OA patients activated with IL-1β to simulate inflammation before treated with hyaluronan (HA) and MSC-derived conditioned medium (CM) to visualize effects of this treatment approach.57 In other studies either synovium-derived MSCs and ATDC5 chondrocytes58 or human SF and articular chondrocytes were co-cultured.59 The latter study was undertaken to show the exchange of stem cell-derived extracellular vesicles (EVs) under 2D and 3D conditions in regard to OA.59 One should critically think about the in vitro models in regard to the fact that inflammation is refined to the presence of either TNFα or IL-1β. Meanwhile it is known that other cytokines and mediators among them IL-6 or IL-18 might contribute to OA pathogenesis.26,41 In this regard studies using conditioned media from OA tissues are important.60 Most of the in vitro studies are performed in 2D culture, but there exist differences in cell behavior of 2D and 3D cultured cells.59 More sophisticated in vitro models are required, particularly more complex co-cultures including several cell types or tissues, eg, addressing also menisci, the osteochondral unit, synovium and the IFP of the osteoarthritic joint to reflect interactions.41,61

Table 1 Examples of in vitro Models

Several experimental settings combine in vitro analyses with preclinical in vivo models. To fully address OA as a whole joint disease, which does not exclusively affect the cartilage layer20 and to assess complex symptoms like pain in vivo models are indeed required. Preclinical OA models have already previously been thoroughly discussed and summarized.62,63 Models are performed in various animal species such as mice, rats, rabbits and dogs.5,62,64–66 Rodent models are broadly used.63,67–70 Approaches to induce OA differ (Figure 2). OA can be induced by direct damage of knee joint cartilage by application of monosodium iodoacetate (MIA model) or other harmful agents.71,72 The other models are based on creating knee instability by destabilization of the medial meniscus (DMM model) through transsection of the medial anterior meniscotibial ligament (MAMTL) which fixes the medial meniscus at the tibial plateau73 or by transsection of the medial collateral ligament (MCL) together with removal of the medial meniscus (MCL-MMx model), transsection of the medial meniscus (medial meniscus transection: MMT model)71,73,74, of the ACL (ACLT model)75,76 or combinations of them.76 Novel models based on joint cartilage overloading by high impact or cyclic overloading (inducing non-invasively posttraumatic joint injury leading to posttraumatic OA [PTOA]) have also been proposed.68,77 In addition, more specific models have been described such as creating surgically patellofemoral OA by shortening the patellar ligament and thereby, changing the position of the patella and hence, its fitting accuracy in the femoropatellar groove78 or facet joint OA in the spine of rats.79 Finally, estrogen-deprivation by ovariectomy is also used62 to induce OA, being simultaneously a well-known model for osteoporosis.

Figure 2 Most commonly used OA in vivo models. In vivo models are either established in the knee joint by application of MIA through the patellar ligament (PL) or other destructive agents (eg tamoxifen for age-related OA) which directly affect joint cartilage integrity or by creation of instability due to ligament transsection, meniscus injury or even removal. Except for MIA (sagittal) frontal views of the knee joint are depicted. OA induced by repetitive loading: by cyclic tibial compression. Joint overload by obesity. Ovariectomy impairs bone- and chondroprotective estrogen. Application of tamoxifen induces age-related OA.87 The image was created by G. Schulze-Tanzil using Krita 4.1.7 Software.

Abbreviations: MIA, monosodium iodoacetate application; MCL-MMx, medial collateral ligament (MCL) transsection and medial meniscus (MM) removal (x); DMM, destabilization of the medial meniscus by transsection of the medial anterior meniscotibial ligament (MAMTL); ACLT, anterior cruciate ligament (ACL) transsection; PCLT, posterior cruciate ligament (PCL) transsection; PTOA, post-traumatic OA; LCL, lateral collateral ligament.

In contrast to MIA, surgical models might be more preferable reflecting more closely one crucial aspect of the natural OA pathogenesis, namely, inhomogenous joint loading by instability.48 They can display early and late OA depending on the time point of investigation selected after OA induction to perform the experiments. Aülo Rasser et al, (2020) pointed to MMT as preferable model in comparison to MIA investigating early OA.80 High fat diet contributes to OA development in mice,81 hence, also obesity models exist.82,83 In addition, in mice, a couple of strains which spontaneously develop OA such as the STR/Ort mice model have been described.84 Mice models present the advantage of studying diverse gene knock outs to elucidate signaling pathways contributing to OA.85 Data from man and mice have to be brought in overlap to deduce novel therapeutic strategies in OA. Convincing concordance could be demonstrated48,86 supporting the further use of rodent models as valuable tool to improve the understanding of OA pathogenesis. Depending on the model, different compartments of the joint are affected by OA. Most studies are performed in the knee joint; however, OA is a heterogenous disease affecting different joints or even joint regions involving possibly diverse pathogenetic factors depending on the topographical environmental conditions. Despite cartilage is a key structure affected by OA and responsible for impaired joint function, other tissues impaired by OA such as menisci should be more thoroughly addressed by models.41 The limitation of in vivo models mostly performed in rodents is that it is often not possible to separate certain tissues from each other, eg, the synovial membrane from the IFP to get a simplified model to study distinct tissue-related aspects of OA pathogenesis.

One has to consider that the severity of OA and velocity of its progression differs in the various models.

Therapeutically Addressed Signaling Pathways of OA

A search for biomarkers has been undertaken to identify the early disease stages of OA.96 Chondroprotective agents effective in OA generally exert anabolic, anti-catabolic-, -inflammatory, -apoptotic and mitoprotective properties. Accordingly, there exist a couple of known general approaches to address these key features.

Antagonists/inhibitors of MMPs have been tested97 to stop cartilage ECM degradation in OA. Suramin, historically used as antiparasitic and antihelminthic drug, is able to restore the expression of chondroprotective tissue inhibitor of metalloproteinase (TIMP)-3, thereby inhibiting OA cartilage degradation by MMPs.98

The direct inhibition of inflammation by neutralizing pro-inflammatory cytokines such as IL-1β and TNFα was less effective in OA.99

Anti-inflammatory cytokines could antagonize pro-inflammatory cytokine effects. IL-10, a member of the IL-10 family, exerts some chondroprotective effects such as inhibiting TNFα-induced apoptotic pathways in chondrocytes and partly restoring the aggrecan expression suppressed by TNFα in OA in vitro models.28,100–102 Hence, an agonistic IL-4/IL-10 fusion antibody seems to be promising for OA therapy.103 This therapeutical approach based on human IL-10 reduced pain in the dogs, as reported by the veterinarians and dog owners observations, without any detectable adverse effects. These results might provide a starting point for clinical trials to confirm it in future as effective.104

There is clinical evidence implicating TLRs in OA pathogenesis and OA associated pain, depending on disease activity as reviewed by Miller et al29,35. TLR are cell surface receptors which recognize microbial-associated molecular patterns and NFκB is a critical transcription factor for TLR downstream signaling.105 TLR2 is expressed in chondrocytes, its immunoreactivity was correlated with expression of NFκB, higher body mass index (BMI) and Western Ontario and McMaster Universities OA Index (WOMAC) scores in patients and related to OA associated changes.105 Typical ligands of TLR, which belong to the group of pattern recognition receptors are DAMPs representing ECM fragments (eg, from aggrecan, tenascin C, HA, fibronectin), S100 proteins and other factors.99 Chondrocyte apoptosis is a critical event which can be mediated by TLR signaling.106 This part of the innate immunity, the TLR mediated signaling cascades could be addressed in future in OA as reviewed by Barreto et al106.

Another part of the innate immune system is the complement system which is dysregulated in OA.38 It represents a cascade of components activated by proteolytic cleavage. Split fragments are released during activation. The important anaphylatoxins C3a and C5a result from the cleavage of the components C3 and C5 and bind to cellular receptors (eg, C3aR and C5aR) initiating inflammatory responses. The finally arising complement complex at the end of the cascade, the membrane attack complex, forms pores after integrating into target cell membranes, thereby leading to cell lysis.107 Accordingly, the expression of inflammatory and degradative molecules was lower in chondrocytes from destabilized joints of complement C5-deficient mice than C5-sufficient mice. Activation of complement is abnormally high in human osteoarthritic joints.38 Due to the involvement of complement activation in OA, complement inhibitors could serve as promising agents in future OA therapy.37,38

The sirtuin (SIRT) signaling pathway (SIRT)/p53 axis has strongly been implicated in OA.86 Sirtuins and Forkhead box O (FoxOs), the latter a target of sirtuins have chondroprotective properties. SIRT1 is known to exert anti-apoptotic effects. The FoxO signaling pathway is one of the most dysregulated pathways in human OA cartilage compared to normal tissue, but SIRT1 might not be exclusively beneficial.108,109 Melatonin, a hormone regulating circadian rhythm released from the pineal gland, is known to inhibit the SIRT1 pathway and possesses chondroprotective effects.110,111

The mammalian target of rapamycin (mTOR) signaling pathway, initiated by mTOR as a critical serin/threonine protein kinase, plays a crucial role for chondrocyte homeostasis and its dysbalance contributes to OA associated joint degeneration. Inhibition of this pathway and mTOR knock outs lead to reduction of the severity of OA in mouse models as reviewed recently.112–114

The reactive oxygen species (ROS)/extracellular signal regulated kinase (ERK)/Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling pathways have been implicated in OA.115

Adenosine monophosphate-activated protein kinase (AMPK) activation – a cell energy sensor,116,117 acting via SIRT3, limits oxidative stress and improves mitochondrial DNA integrity and function in OA chondrocytes. These effects likely contribute to chondroprotective effects of AMPK activity.31

The wingless and integration site-1 (Wnt) pathway is strongly implicated in OA. Signaling molecules and regulators of Wnt are abnormally activated or suppressed under OA conditions. Hence, agonists and antagonists of this pathway have attracted interest for future OA treatment as reviewed previously.48,118 First attempts have been undertaken to modulate this pathway: inhibition of the Wnt/beta-catenin signaling with the compound lorecivivint prevented cartilage degradation and impaired pain in a preclinical model of posttraumatic OA (PTOA) probably via reduced signal transducer and activator of transcription (STAT) signaling. Lorecivivint has already entered Phase I and Phase 2 trials, reducing pain and joint narrowing.119

The Runt related transcription factor (RUNX) 2 regulates osteoblast and chondrocyte differentiation and was induced in murine OA models underlining an involvement in OA development. Hence, it has been postulated as a potential novel target for therapeutical intervention.120

The observation that the transmembrane protein aquaporin (AQP)-1, responsible for water transport was upregulated in OA cartilage initiated more detailed investigations which showed that this surface protein facilitated caspase-3 activation promoting chondrocyte apoptosis as a typical feature of OA.121

In addition, it has been shown that PTEN-induced kinase (Pink)1 mediated chondrocytic mitophagy, initiated chondrocyte death and contributed thereby, to cartilage degeneration in OA.122 Not only Pink1 but also Parkin proteins were increased in OA.123 The Parkin protein might protect from ROS accumulation mediating chondrocyte survival.124

One shared target of several above-mentioned signaling pathways is the NF-κB signaling.125 However, NF-κB is involved in many pathways mediating anabolic and catabolic processes in cartilage.125 This transcription factor is inhibited by many potential agents of OA (Table 2) including herbal medicines.

Table 2 Synopsis of Some Compounds Extracted from Natural Resources

The endocannabinoid-associated signaling pathway is involved in pain regulation in OA.126

Herbal Medicines and Dietary Phytochemicals (Nutraceuticals)

Herbal medicines and other compounds from natural resources, eg, uptaken as nutraceuticals represent an emerging field in OA therapy and novel candidates have been summarized in several very recent reviews.8,9,127 Some agents have been used empirically since centuries, eg, in Chinese traditional medicine (see Table 2).128 More systematical screening has been undertaken to identify novel promising compounds129 and chemoinformatic recherche exploring suitable compounds based on their putative properties deduced from chemical structure and composition was also applied to identify valuable agents for OA.8 Nutrigenomics is an additional strategy to find potential therapeutics tailored for individual patients.130 This novel field implicates that nutrients affect the expression of an individual’s gene setting, translation of proteins and arising metabolites or protect its genes from damage.131 A problem of natural compounds is the fact to be extracted from herbals or other environmental sources. The content of active compounds is influenced by extraction and purification strategies, local growth conditions of plants (eg, soil composition) and further, the often used oral application route which is associated with inhomogeneous intake and limited possibly, inconsistent bioavailability.132 On the contrary, one has also to consider that compounds when systemically uptaken have to pass the blood-joint barrier consisting of the connective tissue between synovial capillaries and synoviocytes cell layers. The density of this barrier changes due to synovitis associated with OA.

Novel Synthetic Compounds as Candidates for OA Treatment: Nanoparticular Compounds and Antibodies

Candidate therapeutics for OA treatment are selected based on the current understanding of its molecular pathogenesis.3 Various nanoparticular compounds have been developed with putative implication in OA treatment.10 Nanoparticular compounds such as dendritic polyglycerol sulfates (dPGS) could act as anti-inflammatory agents in OA.74,100,158,159 A challenge for nanoparticular compounds is to penetrate the cartilage ECM for internalization by articular chondrocytes as key player cell population in OA which depends on their size, loading and binding motifs allowing receptor interaction for uptake into target cells.100,159 Particles with high affinity to the targets or even inflamed tissues are of particular interest.159 Such compounds could act locally in the joint despite of being administered systemically impairing the overall risk of adverse effects adherent with this class of compounds.

Nanoparticles could also present a versatile slow release system and be combined with other agents. Rhein-loaded pH-responsive nanoparticles have been developed.160 pH responsiveness of loaded nanoparticles allows accumulation or even the release of the effective agent in inflamed tissue which are usually characterized by lower pH values.160 Rhein has approved anti-inflammatory capacity.132,160 Nanoparticles were also used to deliver siRNA of 66 kDa proto-oncogene Src homologous-collagen homologue (p66shc) which is involved in cartilage degeneration in OA and known to mediate oxidative stress-induced apoptosis.161 By delivering p66shc-siRNA-loaded Poly(lactide-co-glycolide) (PLGA) nanoparticles into the osteoarthritic knee joints, mitochondrial dysfunction-induced cartilage damage was significantly impaired suggesting them as an option for the treatment of OA.122

In addition to being effective, nanoparticles should be highly cytocompatible, or capable to be easily eliminated, eg, by self-degradation to disappear, and not to accumulate and produce unwanted adverse effects.

In addition to nanoparticles, other therapeutical compounds have been investigated such as the H2S-producing enzyme 3-mercaptopyruvate sulfurtransferase (3-MST) which could be loaded in future on nanoparticles. H2S generated by 3-MST protects against joint calcification and experimental OA progression. Hence, enhancing H2S production in chondrocytes may represent a potential disease modifier to treat OA.162 Other compounds belong to the group of bisphosphonates such as tiludronate, which impaired pain, joint effusion, synovitis, MMP-13 and ADAMTS expression in OA knees of dogs suggesting efficacy in OA.163

To directly neutralize harmful mediators upregulated in OA such as pro-inflammatory cytokine antibody therapy presents a strategy. Some antibody-based approaches have been developed. Antibody-based anti-cytokine therapy was effective in rheumatoid arthritis (RA) but bears also risks such as immunosuppression and malignancies.164 However, anti-cytokine therapy like in RA was less effective in OA.48 Antibodies against pro-inflammatory mediators including IL-1β and TNFα have failed in recent OA clinical trials as reviewed by Mimpen and Snelling.6 Other options to utilize antibodies have been tested in OA such as anti-ADAMTS-5 monoclonal antibodies as a tool to directly inhibit aggrecanase in OA.22 Increased vascularization of the synovial membrane but also vessels penetrating into cartilage can be observed in OA and both are associated with increased vascular endothelial growth factor (VEGF) activity. Bortezomib, a vascular endothelial growth factor receptor 3 (VEGFR3) neutralizing antibody reduced joint tissue damage in a mouse model of experimental PTOA, which was associated with improved synovial lymphatic function.165

Antibody-based complement inhibitors could be interesting as OA therapeutics.36–38,166 Unfortunately, so far not enough is known about the role of distinct complement components in OA.37

However, therapeutical antibodies have to be stable enough to be administered and one has to consider that this therapy is indeed expensive.

Anabolic Factors: Growth Factors and Hormones, Hormone Analogues

The insufficiency of chondrocytes to respond to different growth factors has been implicated in OA pathogenesis.167 The anabolic growth factor insulin-like growth factor (IGF)-1 is important to maintain cartilage ECM homeostasis. The decreased levels of IGF-1 may play a critical role for the loss of the balance between catabolic and anabolic processes in cartilage metabolism during the development of OA. Thus, increasing IGF-1 may be applicable to restore homeostasis and as an approach in future OA therapy.168

The anabolic growth factor fibroblast growth factor (FGF) 18 acts chondroprotective via regulating TIMP-1 expression and hence, inhibiting ECM degradation.48,169

The female sex hormone estrogen is known to have chondroprotective effects.170 Accordingly, estrogen deprivation by ovariectomy is used as OA model.62 A lack in estrogen explains the high predisposition of postmenopausal woman for OA.170 Genistein is the major active component of isoflavone, with a chemical composition and a biological effect that is very similar to that of estrogens, which prevents the degradation of articular cartilage.171

Glucagon is an anabolic hormone regulating carbohydrate metabolism. The glucagon-like peptide-1 receptor (GLP-1R) leads to anti-inflammatory and anti-apoptotic effects in cartilage. Activating GLP-1R suppressed the NF-κB pathway, decreased the release of pro-inflammatory key mediators (TNFα, IL-6), and reduced ECM catabolism in triglyceride-treated chondrocytes. These effects were reversed by GLP-1R knockdown.172,173

Melatonin is an epiphyseal hormone strongly associated with the circadian rhythm. Melatonin was able to impair IL-1β-induced MMP production by inhibiting SIRT1-dependent pathways in chondrocytes, suggesting melatonin as a potential therapeutic candidate in OA.110 Recently the putative involvement of melatonin, the hypophyseal hormone thyroid stimulating hormone (TSH), and suprarenal gland-derived cortisol have been implicated in OA pathogenesis with respect to influencing the circadian clock as reviewed by Hossain et al.111 which opens a novel perspective on the multifaceted nature of OA pathogenesis.

The hormone oxytocin (OT) induced increased aggrecan, collagen type X, and COMP levels in vitro, and a normalization of cartilage markers such as SRY-box transcription factor 9 (SOX9) and collagen type II. There was a significant correlation between OA and impaired OT in rats. OT stimulated chondrogenesis. Systemic OT levels in the serum were also impaired in human patients with hand OA. This suggests that OT might be involved in the pathophysiology of OA.174

The hormone prolactin and its cleavage products, the vasoinhibins, can be implicated in regulation of angiogenesis in OA. Prolactin could be a candidate for OA therapy.37

Pain is the main symptom in OA impairing patient`s life quality. Nerve growth factor (NGF) sensitizes pain sensory nerve fibers; hence, inhibition of its signaling pathway could modulate pain sensation.48

Irisin represents a myokine which has also effects on cartilage. It is a cleaved form of fibronectin type III domain containing 5 (FNDC5), and normally regulates bone turnover and muscle homeostasis. A study revealed that human osteoarthritic articular chondrocytes express decreased level of FNDC5 and the autophagosome marker light chain (LC)3-II, but upregulated levels of the oxidative DNA damage marker 8-hydroxydeoxyguanosine and apoptosis. Irisin repressed inflammation-mediated oxidative stress and ECM underproduction through retaining mitochondrial biogenesis, dynamics and autophagic program.175

Recently, the small molecule kartogenin regulating the core binding factor subunit (CBF)β-RUNX1 pathway was reported to promote the differentiation of bone marrow (BM)-derived MSCs (BM-MSCs) into chondrocytes in vitro. Kartogenin exhibited chondroprotection when injected i.a. in two mouse models of OA.176

A more comprehensive understanding of OA: influence of the microbiome

A more comprehensive image of OA becomes visible showing that OA is to some degree indeed a systemic disease since systemic hormone and factor disbalances are involved in its pathogenesis as outlined before and also systemic cytokine levels are substantially changed in OA.18 The gut-associated microbiome contributes also to OA. In this regard a microbiome-joint connection has been postulated by Favazzo et al177. A dysbiosis of the gut microbial flora might trigger the systemic release of potentially harmful bacterial components which could affect the homeostasis of the joints making them more susceptible for OA development or progression. LPS might accumulate in response to microbiome imbalance (dysbiosis) and present a link by mediating low-grade inflammation between obesity and metabolic syndrome.55 In this regard, the biotransformation of curcumin, for example, by gut microbiota might explain its beneficial health effects138 and this important mechanism might also influence other compounds. Therefore, this interrelation has to be addressed in more detail in future.

Cell-Based Approaches in OA: MSCs

There exist already results from several clinical trials using MSCs in OA.178,179 MSCs have various protective effects which might be mediated by trophic mediators released by MSCs (Figure 3). Different MSC species can be applied either allogenic or autologous. Adipose tissue-derived mesenchymal stromal cells (ASCs) have the advantage of easy and less invasive accessibility by liposuction.179 Intraarticular application (i.a.) of autologous ASCs without culturing them inhibited the progression of cartilage degeneration180 but also allogenic ASCs expanded by culturing attenuated cartilage degeneration in an experimental rat OA model.181 Allogenic BM-MSCs were expanded under hypoxic conditions before injected in combination with HA into rat knees in a rat ACLT model leading to superior results compared to controls and revealing that an engraftment of MSCs into joint cartilage takes indeed place.182

Figure 3 Capacities which could stimulate cartilage healing exerted by mesenchymal stromal cells. The image was created by G. Schulze-Tanzil.

Abbreviations: FGF, fibroblast growth factor; GM-CSF, granulocyte-macrophage colony-stimulating factor; HGF, hepatocyte growth factor; IL, interleukin; LIF, leukemia inhibitory factor; MHCII, major histocompatibility complex II; MIP1α, macrophage inflammatory protein; NK, natural killer cells; NO, nitric oxide; TGF, transforming growth factor; VEGF, vascular endothelial growth factor.

In contrast to these promising results, i.a. injection of xenogenic SF-MSCs did neither exert chondroprotection nor does it impair inflammation in ACLT-induced OA in the rat knee.183

Encouraging were the results with allogenic amniotic MSCs which impaired OA progression in a synovial macrophage-mediated in vitro cartilage explant co-culture model.184

The adipose tissue-derived stromal vascular fraction (SVF) represents a potent precursor cell population which can be harvested from adipose tissue.179 SVFs have been tested as promising healing approach in OA.17,185 SVF fraction acts anti-inflammatory in temporomandibular joint OA.186 It was concluded that the i.a. application of SVFs to treat knee OA was safe and chondroprotective for the tested time period of 1 year. SVFs might induce a cascade of molecular and structural responses mediated through complex interactions between infrapatellar fat pad fatty tissue and SVFs, and enforcing the intraarticular fatty tissue back to homeostasis, protective, and anti-inflammatory functions, as an explanation for the inhibition of OA progression observed.185

Chemokines

Chemokines are able to attract regenerative stem cells. The application of chemokines might be less invasive compared to preparing and injecting stem cells. The term of in situ tissue engineering was postulated to describe this strategy to support cartilage defect healing.187 There are some hints indicating that chemokine signaling might be disturbed in OA. The CXC-motif-chemokine receptor (CXCR) 4 which has probably chondroprotective capacities was downregulated by miR-146a in chondrocytes under inflammatory conditions. Its overexpression attenuated inflammation.49 A comprehensive transcriptome analysis of OA versus non-OA samples with clinical data integration reflected that many chemokine genes were significantly downregulated under OA conditions.188 On the contrary, the chemokine IL-8 (CXC motif chemokine [CXCL]8) was increased in synovial fluid and plasma of OA patients26 and the chemokine CXCL1 contributed to pro-inflammatory IL-6 expression in OA SF mediated by the CXC-motif-chemokine receptor 2, rapidly accelerated fibrosarcoma (c-Raf), MAPK, and activator protein (AP)-1 signaling pathways.188,189 Hence, the intimate interplay between chemokine subtypes and other key pathways has to be further addressed in future.

Platelet-Rich Plasma

Platelet-rich plasma (PRP) contains growth factors and diverse mediators such as cytokines and chemokines. It is used for stem cell culturing and to promote tissue regeneration. The study of Mariani et al, 202051 in SF summarizes reference data on the concentration and release kinetics of biomolecules that could represent potential specific effectors in the modulation of inflammatory processes and in tissue repair after treatment with PRP. Another research team reported that PRP combined with alendronate delayed OA progression by inhibiting the NF-κB signaling pathway.190

Conditioned Media

Chemokines, cytokines, growth factors are released by chondrogenic cells during culturing mediating paracrinic signaling. Conditioned media (CM) harvested from cultured cells contain these diverse products of cells. Since CM can influence cell differentiation they have also been tested in OA models as therapeutical option. CM from notochordal cells, which represent embryonic precursor cells found as leftovers in the immature intervertebral disc cartilage, revealed protective effects in OA.191 CM of ASCs was also used for cartilage stimulation and found to be a promising treatment strategy for OA in experimental models.57 CM contained also so-called exosomes harboring the above-mentioned mediators.

Extracellular Vesicles: Microvesicles and Exosomes

Exosomes and microvesicles are extracellular vesicles (EV), surrounded by a phospholipid membrane either cell membrane- or endosomal-derived, of different sizes (30–100 nm or 0.1–1 µm). EVs are released by diverse cell types including those of the joint. EVs mediate paracrinic cell-cell communication, being produced by cell membrane budding of donor cells and are internalized by recipient cells including joint-derived cells such as chondrocytes and SF.54,59,192 An uptake of ASC-derived EVs by SF and chondrocytes could be observed in in vitro co-culture models of SF and chondrocytes from the same OA patient which differed under 2D and 3D conditions. Interestingly, SFs showed a faster uptake of EVs than chondrocytes.59

BM-MSC-derived EVs can prevent OA-associated catabolic features simulated by IL-1β exposure by reinduction of cartilage ECM marker gene expression such as collagen type II alpha 2 chain (COL2A1) and aggrecan (ACAN), inhibition of MMP and ADAMTS (MMP-13 and ADAMTS-5) gene expression, suppression of pro-inflammatory mediators such as NO production, apoptosis and macrophage activation, thereby modulating immune reactivity as shown in chondrocytes in vitro.54,192

Chondrocyte proliferation and migration capacity were also restored by EVs in vitro.54 Using the rat MIA OA model, exosome treatment significantly reconstituted collagen type II and impaired MMP-13 protein expression in the knee joint cartilage of the OA rats.54

ASCs are easier to harvest compared to BM-MSCs. Nevertheless, also ASC-derived EVs are effective in modulating features associated with OA. Activated SF treated with exosomes suppressed their expression of pro-inflammatory mediators such as IL-6, NF-κB and TNFα, while the expression of anti-inflammatory IL-10 was elevated.193 Exosomes can be used clinically,194 being harvested by sequential centrifugation techniques from cultured MSCs before i.a. injected.192 The immunogenicity of EVs, since they expose membrane proteins on their surface, remains unclear, and hence, the necessity to isolate them from autologous cell populations. Nevertheless, EVs can also be isolated from autologous plasma or serum.195 The treatment of chondrocytes with EVs isolated from autologous blood products (hyperactive serum and citrate-anticoagulated PRP) induced the expression of anabolic markers such as the chondrogenic transcription factor SOX9, type II collagen and aggrecan, compared to the original complete full blood products, but it induced also the ECM degradative MMP-3. The blood product–derived EVs but not the blood product itself increased SOX9 protein expression and inhibited IL-6 release in human chondrocytes from OA patients.195

The content of EVs depends on diverse factors, such as cell source, culturing time and conditions and this might explain some heterogenicity of results studying the effect of EVs and their perspective for OA.91,196,197 In addition to diverse proteins, lipids, cytokines and chemokines, they contain also mRNA or miRNA.198 However, contents depend largely on the methods of purification. An important question to be answered in future concerns whether these particles are able to penetrate the cartilage ECM.

Restorage of Joint Function by Viscosupplementation and Restored Osmolarity

Viscosupplementation implies the application of natural components of cartilage ECM and synovial fluid to restore its viscoelastic properties and provide lubrication of joint cartilage surface to reduce friction. HA is most important for this unique properties of the synovial fluid. In a healthy joint, it has a content of 2–4 mg/mL HA with an MW of 4–6 MDa.199 Hence, viscosupplementation is mostly based on application of HA which represents a well-established OA therapy,200 but other compounds such as glucosamine are also proposed.201,202 HA is a natural non-sulfated high molecular weight (MW) glycosaminoglycan (GAG)203 with broad medical application.53 In OA, the content of HA in the synovial fluid is reduced which, hence, loses its viscoelasticity/thixotropic properties203 and is not any longer able to impair friction during joint movement. It gets a lower MW during aging.203 HA is responsible to maintain aggrecan aggregates of sufficient sizes in the cartilage ECM.204 It exerts anti-inflammatory, -apoptotic, -catabolic, -nociceptive and anabolic effects.205–207 HA binding to chondrocytes is mediated by the HA receptor, CD44.204 The full mechanism of action of exogenous HA is uncertain, but studies indicate that it may promote endogenous HA production, reduce joint inflammation, prevent degeneration of cartilage and facilitate its healing.208

However, there exist diverse variants of HA203 possessing different MWs.209 High MW would provide longer lasting protective effects in OA-affected joints.210 The capacity of HA to penetrate the cartilage ECM and directly modulate chondrocyte activity remains a matter of debate. A drawback of HA therapy is the preferred i.a. application route. Multiple HA injections are recommended to achieve effects of sufficient duration.211 Hence, in regard to the necessity of multiple i.a. injection which bears the risk of joint infection longterm stability of HA is desired which can be achieved by cross-linking, eg, represented by Hylan G-F.202,212 HA, but also chondroitin sulfate as another effective GAGs for viscosupplementation, have extensively been tested in rat OA models.69 Chondroitin sulfate has been used for years to ameliorate OA as reviewed in detail by Mimpen and Snelling.6,69 Another compound used since many years for viscosupplementation in OA is glucosamine, an aminosugar of the natural cartilage ECM.213

Lubricin (also called proteoglycan 4 [Prg4]) is naturally produced by superficial zone articular chondrocytes and SF in the joint and important for cartilage lubrication to minimize friction during movements within the joint. Gene therapy by inducing overexpression of the Prg4 gene in the joint was protective in OA.214,215 Gene therapy was also performed by combination of Prg4 and interleukin receptor antagonist (IL-1ra) genes which protected against hyperalgesia and cartilage degeneration in the PTOA model.216 The receptor antagonist transgene was also tested locally in an equine OA joint model leading to substantial increase in IL-1ra mediating reduced lameness, lesser joint pathology revealed by imaging, alleviated synovitis and improved healing of osteochondral lesions whereas no systemic increase in IL-1ra was observed.217

Adaption of dysbalanced osmolarity could present a future strategy in OA therapy. Osmolarity intimately regulates growth factor expression.218,219 Decreased osmolarity contributes to sustained inflammation and catabolic activities in OA chondrocytes and impairs their responsiveness to the growth and differentiation factor (GDF)-5. This suggests that osmolarity represents a critical factor in OA pathogenesis220 and should be further addressed. HA is often combined with other therapeutical agents,221 eg, cells222 or chemokines.223

Genetic Regulators of Inflammatory/Catabolic Gene Expression

Genetic and epigenetic regulation has been implicated in OA pathogenesis.224 OA-associated epigenetic aberrations have been recognized at the level of DNA methylation and histone modification in chondrocytes.225 DNA methylation is known to destinate gene expression as reviewed by Kim et al.226

Micro RNAs (miR) are important regulators of gene expression. They represent a class of regulatory but non-coding RNAs (around 22 nucleotides in length). Despite the knowledge about their regulatory network is still limited a growing number of miRs has been implicated in OA pathogenesis based on their aberrant expression profiles under OA conditions (Table 3). miRs and small interfering RNAs (siRNAs) could present future tools in OA therapy being, eg, combined with nanoparticles, microvesicles or other carriers.122,193 Limitations to be addressed in future could be to maintain stability and achieve sufficient high local concentrations of therapeutical miRNAs.

Table 3 Some miRNAs with Implication in OA Restricted to 2018–2020

Conclusion

It has to be considered that OA is a systemic and generally heterogenous disease.7,46 Many players (growth factors, diverse hormone networks, circadian clock factors, gut microbiome, nutrigenomics, epigenetics: eg miRs …) and several dysregulated signaling pathways are involved in its pathogenesis which might differ dependent on individual patients. NF-κB dysregulation seems to play a major role. There exist meanwhile various novel or further optimized experimental strategies to alleviate OA progression (Figure 4). Approaches for treatment have possibly to be adapted in future to disease subtypes and individual patients. Hence, personalized OA therapy should be a future vision.

Figure 4 Synopsis of some current experimental therapeutic strategies in OA. (A) viscosupplementation such as i.a. application of HA to improve gliding properties of damaged cartilage as well as stimulate regenerative capacity of chondrocytes. (B) application of MSCs with immunomodulatory and trophic properties. (C) administering antibodies to inhibit inflammatory pathways in the joint. (D) provide exosomes as vehicles for chondroprotective cellular products. (E) apply microparticles. (F) give nanoparticular compounds with anti-inflammatory properties. (G) apply inhibitory and regulatory small RNA or DNA interfering with inflammatory pathways in the joint.

Abbreviation: i.a., intraarticular; miRNA, micro ribonucleic acid; MSC, mesenchymal stromal cells; siRNA, small interfering ribonucleic acid. The image was created by G. Schulze-Tanzil using Krita 4.1.7 software.

Abbreviations

ACAN, aggrecan gene; ACL, anterior cruciate ligament; ACLT, anterior cruciate ligament transsection; ADAMTS, a disintegrin and metalloproteinase with thrombospondin motifs; AKT, protein kinase B; AMPK, Adenosine monophosphate-activated protein kinase; AP-1, activator protein-1; ASCs, adipose tissue-derived mesenchymal stromal cells; Aqp, aquaporin; BM, bone marrow; BM-MSCs, bone marrow-derived mesenchymal stromal cells; BMI, body mass index; CBFβ, core binding factor subunit β; CM, conditioned media; COL2A1, gene for alpha1 chain of collagen type II; COMP, cartilage oligomeric matrix protein; COX, cyclooxygenase; CXCR4, CXC-motif-chemokine receptor 4; DMM, destabilized medial meniscus; dPGS, dendritic polyglycerol sulfates; ECM, extracellular matrix; ERK, extracellular signal regulated kinase; EV, extracellular vesicles; FGF, Fibroblast growth factor; FNDC5, fibronectin type III domain containing 5; FoxOs, Forkhead box O; FUT1, Fucosyltransferase 1; GAG, glycosaminoglycans; GDF, growth and differentiation factor; GLP-1R, glucagon-like peptide-1 receptor; GM-CSF, granulocyte-macrophage colony stimulating factor; HA, hyaluronan; HGF, hepatocyte growth factor; IPF, intrapatellar fat pad; IL, interleukin; IL-1ra, interleukin-1 receptor antagonist; iNOS, inducible nitric oxide synthethase; IGF-1, insulin-like growth factor-1; KEAP, Kelch-like ECH-associated protein; LCL, lateral collateral ligament; LIF, leukemia inhibitory factor; LPS, lipopolysaccharide; MAMTL, medial anterior meniscotibial ligament; MAPK, MAP kinase; MCL, medial collateral ligament; MHCII, major histocompatibility complex II; MIA, monosodium iodoacetate; MIP1α, macrophage inflammatory protein; miRNA, micro ribonucleic acid; MMP, matrix metalloproteinase; MMT, medial meniscus transsection; 3-MST, 3-mercaptopyruvate sulfurtransferase; mTOR, mammalian target of rapamycin; MW, molecular weight; NGF, nerve growth factor; NLRP3, NOD-, LRR- and pyrin domain-containing protein 3; NK, natural killer cells; NO, nitric oxide; Nrf, Nuclear factor (erythroid-derived)-like; OA, osteoarthritis; OT, oxytocin; PARP, Poly(ADP-ribose)-Polymerase; PCL, posterior cruciate ligament; PG, proteoglycan; PGE, Prostaglandin E; Pink1, PTEN induced kinase 1; PI3K, phosphoinositol-3 kinase; PRP, platelet-rich plasma; PTGS2, prostaglandin-endoperoxide synthase 2; PTOA, posttraumatic OA; P66shc, 66 kDa proto-oncogene Src homologous-collagen homologue; RANK(L), Receptor Activator of NF-κB (Ligand); Raf, rapidly accelerated fibrosarcoma; ROS, reactive oxygen species; RUNX, runt related transcription factor; SF, synovial fibroblasts; SIRT, sirtuin; siRNA, small interfering ribonucleic acid; SOX9, SRY-box transcription factor 9; SVF, stromal vascular fraction; STAT, signal transducer and activator of transcription; TGF, transforming growth factor; TLR, Toll like receptor; TIMP, tissue inhibitors of metalloproteinases; TNF, tumor necrosis factor; TRAF, TNF receptor associated factor; TSH, thyroid stimulating hormone; VEGF, vascular endothelial growth factor; VEGFR3, vascular endothelial growth factor receptor 3; Wnt, wingless and integration site-1; WOMAC, Western Ontario and McMaster Universities Osteoarthritis Index.

Acknowledgment

The author would like to thank Mr. Benjamin Kohl for support.

Disclosure

The author reports no conflicts of interest in this work neither financial nor other.

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135. Ansari MY, Ahmad N, Haqqi TM. Butein activates autophagy through AMPK/TSC2/ULK1/mTOR pathway to inhibit IL-6 expression in IL-1beta stimulated human chondrocytes. Cell Physiol Biochem. 2018;49:932–946. doi:10.1159/000493225

136. Schwager J, Richard N, Fowler A, Seifert N, Raederstorff D. Carnosol and related substances modulate chemokine and cytokine production in macrophages and chondrocytes. Molecules. 2016;21:465. doi:10.3390/molecules21040465

137. Schulze-Tanzil G, Mobasheri A, Sendzik J, John T, Shakibaei M. Effects of curcumin (diferuloylmethane) on nuclear factor kappaB signaling in interleukin-1beta-stimulated chondrocytes. Ann N Y Acad Sci. 2004;1030:578–586. doi:10.1196/annals.1329.067

138. Scazzocchio B, Minghetti L, D’Archivio M. Interaction between gut microbiota and curcumin: a new key of understanding for the health effects of curcumin. Nutrients. 2020;12:2499. doi:10.3390/nu12092499

139. Zhang G, Cao J, Yang E, et al. Curcumin improves age-related and surgically induced osteoarthritis by promoting autophagy in mice. Biosci Rep. 2018;38.

140. Shirinsky IV, Kalinovskaya NY, Filatova K, Shirinsky VS. Pleiotropic effects of Comarum palustre l. in patients with osteoarthritis and diabetes mellitus with high comorbidity burden: an exploratory study. Altern Ther Health Med. 2020.

141. Zhang X, Yao J, Wu Z, et al. Chondroprotective and antiarthritic effects of Daphnetin used in vitro and in vivo osteoarthritis models. Life Sci. 2020;240:116857. doi:10.1016/j.lfs.2019.116857

142. Tanideh N, Ashkani-Esfahani S, Sadeghi F, et al. The protective effects of grape seed oil on induced osteoarthritis of the knee in male rat models. J Orthop Surg Res. 2020;15:400. doi:10.1186/s13018-020-01932-y

143. Bai H, Zhang Z, Li Y, et al. L-theanine reduced the development of knee osteoarthritis in rats via its anti-inflammation and anti-matrix degradation actions: in vivo and in vitro study. Nutrients. 2020;12:1988. doi:10.3390/nu12071988

144. Leong DJ, Choudhury M, Hanstein R, et al. Green tea polyphenol treatment is chondroprotective, anti-inflammatory and palliative in a mouse post-traumatic osteoarthritis model. Arthritis Res Ther. 2014;16:508. doi:10.1186/s13075-014-0508-y

145. Schulze-Tanzil G, Hansen C, Shakibaei M. [Effect of a Harpagophytum procumbens DC extract on matrix metalloproteinases in human chondrocytes in vitro]. Arzneimittel-Forschung. 2004;54:213–220. doi:10.1055/s-0031-1296962.German.

146. Zu Y, Mu Y, Li Q, Zhang ST, Yan HJ. Icariin alleviates osteoarthritis by inhibiting NLRP3-mediated pyroptosis. J Orthop Surg Res. 2019;14:307. doi:10.1186/s13018-019-1307-6

147. Ji B, Zhang Z, Guo W, et al. Isoliquiritigenin blunts osteoarthritis by inhibition of bone resorption and angiogenesis in subchondral bone. Sci Rep. 2018;8:1721. doi:10.1038/s41598-018-19162-y

148. Alam W, Khan H, Shah MA, Cauli O, Saso L. Kaempferol as a dietary anti-inflammatory agent: current therapeutic standing. Molecules. 2020;25:4073. doi:10.3390/molecules25184073

149. Estakhri F, Panjehshahin MR, Tanideh N, et al. The effect of kaempferol and apigenin on allogenic synovial membrane-derived stem cells therapy in knee osteoarthritic male rats. Knee. 2020;27:817–832. doi:10.1016/j.knee.2020.03.005

150. Park MH, Jung JC, Hill S, et al. FlexPro MD(R), a combination of krill oil, astaxanthin and hyaluronic acid, reduces pain behavior and inhibits inflammatory response in monosodium iodoacetate-induced osteoarthritis in rats. Nutrients. 2020;12:956. doi:10.3390/nu12040956

151. Chin KY, Pang KL. Therapeutic effects of olive and its derivatives on osteoarthritis: from bench to bedside. Nutrients. 2017;9:1060. doi:10.3390/nu9101060

152. Yi H, Zhang W, Cui ZM, et al. Resveratrol alleviates the interleukin-1beta-induced chondrocytes injury through the NF-kappaB signaling pathway. J Orthop Surg Res. 2020;15:424. doi:10.1186/s13018-020-01944-8

153. Wei Y, Jia J, Jin X, Tong W, Tian H. Resveratrol ameliorates inflammatory damage and protects against osteoarthritis in a rat model of osteoarthritis. Mol Med Rep. 2018;17:1493–1498. doi:10.3892/mmr.2017.8036

154. Schulze-Tanzil G, de Souza P, Behnke B, Klingelhoefer S, Scheid A, Shakibaei M. Effects of the antirheumatic remedy hox alpha–a new stinging nettle leaf extract–on matrix metalloproteinases in human chondrocytes in vitro. Histol Histopathol. 2002;17:477–485. doi:10.14670/HH-17.477

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158. Rades N, Licha K, Haag R. Dendritic polyglycerol sulfate for therapy and diagnostics. Polymers. 2018;10:595. doi:10.3390/polym10060595

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172. Que Q, Guo X, Zhan L, et al. The GLP-1 agonist, liraglutide, ameliorates inflammation through the activation of the PKA/CREB pathway in a rat model of knee osteoarthritis. J Inflamm. 2019;16:13. doi:10.1186/s12950-019-0218-y

173. Mei J, Sun J, Wu J, Zheng X. Liraglutide suppresses TNF-alpha-induced degradation of extracellular matrix in human chondrocytes: a therapeutic implication in osteoarthritis. Am J Transl Res. 2019;11:4800–4808.

174. Roux CH, Pisani DF, Gillet P, et al. Oxytocin controls chondrogenesis and correlates with osteoarthritis. Int J Mol Sci. 2020;21:3966. doi:10.3390/ijms21113966

175. Wang FS, Kuo CW, Ko JY, et al. Irisin mitigates oxidative stress, chondrocyte dysfunction and osteoarthritis development through regulating mitochondrial integrity and autophagy. Antioxidants. 2020;9:810. doi:10.3390/antiox9090810

176. Mohan G, Magnitsky S, Melkus G, et al. Kartogenin treatment prevented joint degeneration in a rodent model of osteoarthritis: a pilot study. J Orthop Res. 2016;34:1780–1789. doi:10.1002/jor.23197

177. Favazzo LJ, Hendesi H, Villani DA, et al. The gut microbiome-joint connection: implications in osteoarthritis. Curr Opin Rheumatol. 2020;32:92–101. doi:10.1097/BOR.0000000000000681

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183. Neybecker P, Henrionnet C, Pape E, et al. In vitro and in vivo potentialities for cartilage repair from human advanced knee osteoarthritis synovial fluid-derived mesenchymal stem cells. Stem Cell Res Ther. 2018;9:329. doi:10.1186/s13287-018-1071-2

184. Topoluk N, Steckbeck K, Siatkowski S, Burnikel B, Tokish J, Mercuri J. Amniotic mesenchymal stem cells mitigate osteoarthritis progression in a synovial macrophage-mediated in vitro explant coculture model. J Tissue Eng Reg Med. 2018;12:1097–1110. doi:10.1002/term.2610

185. Lapuente JP, Dos-Anjos SBlazquez-Martinez A. Intra-articular infiltration of adipose-derived stromal vascular fraction cells slows the clinical progression of moderate-severe knee osteoarthritis: hypothesis on the regulatory role of intra-articular adipose tissue. J Orthop Surg Res. 2020;15:137. doi:10.1186/s13018-020-01664-z

186. Kim H, Lee BK. Anti-inflammatory effect of adipose-derived stromal vascular fraction on osteoarthritic temporomandibular joint synoviocytes. J Tissue Eng Reg Med. 2020;17:351–362. doi:10.1007/s13770-020-00268-2

187. Ringe J, Hemmati-Sadeghi S, Frohlich K, et al. CCL25-supplemented hyaluronic acid attenuates cartilage degeneration in a guinea pig model of knee osteoarthritis. J Orthop Res. 2019;37:1723–1729. doi:10.1002/jor.24312

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189. Hou SM, Chen PC, Lin CM, Fang ML, Chi MC, Liu JF. CXCL1 contributes to IL-6 expression in osteoarthritis and rheumatoid arthritis synovial fibroblasts by CXCR2, c-Raf, MAPK, and AP-1 pathway. Arthritis Res Ther. 2020;22:251. doi:10.1186/s13075-020-02331-8

190. Xin F, Wang H, Yuan F, Ding Y. Platelet-rich plasma combined with alendronate reduces pain and inflammation in induced osteoarthritis in rats by inhibiting the nuclear factor-kappa B signaling pathway. Biomed Res Int. 2020;2020:8070295. doi:10.1155/2020/8070295

191. Muller S, Acevedo L, Wang X, et al. Notochordal cell conditioned medium (NCCM) regenerates end-stage human osteoarthritic articular chondrocytes and promotes a healthy phenotype. Arthritis Res Ther. 2016;18:125. doi:10.1186/s13075-016-1026-x

192. Cosenza S, Ruiz M, Toupet K, Jorgensen C, Noel D. Mesenchymal stem cells derived exosomes and microparticles protect cartilage and bone from degradation in osteoarthritis. Sci Rep. 2017;7:16214. doi:10.1038/s41598-017-15376-8

193. Zhao C, Chen JY, Peng WM, Yuan B, Bi Q, Xu YJ. Exosomes from adipose-derived stem cells promote chondrogenesis and suppress inflammation by upregulating miR145 and miR221. Mol Med Rep. 2020;21:1881–1889. doi:10.3892/mmr.2020.10982

194. Mendt M, Rezvani K, Shpall E. Mesenchymal stem cell-derived exosomes for clinical use. Bone Marrow Transplant. 2019;54:789–792. doi:10.1038/s41409-019-0616-z

195. Otahal A, Kramer K, Kuten-Pella O, et al. Characterization and chondroprotective effects of extracellular vesicles from plasma- and serum-based autologous blood-derived products for osteoarthritis therapy. Front Bioeng Biotechnol. 2020;8:584050. doi:10.3389/fbioe.2020.584050

196. Tao SC, Yuan T, Zhang YL, Yin WJ, Guo SC, Zhang CQ. Exosomes derived from miR-140-5p-overexpressing human synovial mesenchymal stem cells enhance cartilage tissue regeneration and prevent osteoarthritis of the knee in a rat model. Theranostics. 2017;7:180–195. doi:10.7150/thno.17133

197. Wang Y, Yu D, Liu Z, et al. Exosomes from embryonic mesenchymal stem cells alleviate osteoarthritis through balancing synthesis and degradation of cartilage extracellular matrix. Stem Cell Res Ther. 2017;8:189. doi:10.1186/s13287-017-0632-0

198. Ragni E, Perucca Orfei C, De Luca P, et al. miR-22-5p and miR-29a-5p are reliable reference genes for analyzing extracellular vesicle-associated miRNAs in adipose-derived mesenchymal stem cells and are stable under inflammatory priming mimicking osteoarthritis condition. Stem Cell Rev Rep. 2019;15:743–754. doi:10.1007/s12015-019-09899-y

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203. Gupta RC, Lall R, Srivastava A, Sinha A. Hyaluronic acid: molecular mechanisms and therapeutic trajectory. Front Veterinary Sci. 2019;6:192.

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206. Vitanzo PC, Sennett BJ. Hyaluronans: is clinical effectiveness dependent on molecular weight? Am J Orthop. 2006;35:421–428.

207. Lisignoli G, Grassi F, Zini N, et al. Anti-Fas-induced apoptosis in chondrocytes reduced by hyaluronan: evidence for CD44 and CD54 (intercellular adhesion molecule 1) involvement. Arthritis Rheum. 2001;44:1800–1807. doi:10.1002/1529-0131(200108)44:8<1800::AID-ART317>3.0.CO;2-1

208. Webb D, Naidoo P. Viscosupplementation for knee osteoarthritis: a focus on Hylan G-F 20. Orthop Res Rev. 2018;10:73–81. doi:10.2147/ORR.S174649

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210. Bahrami MH, Raeissadat SA, Cheraghi M, Rahimi-Dehgolan S, Ebrahimpour A. Efficacy of single high-molecular-weight versus triple low-molecular-weight hyaluronic acid intra-articular injection among knee osteoarthritis patients. BMC Musculoskelet Dis. 2020;21:550. doi:10.1186/s12891-020-03577-8

211. Concoff A, Sancheti P, Niazi F, Shaw P, Rosen J. The efficacy of multiple versus single hyaluronic acid injections: a systematic review and meta-analysis. BMC Musculoskelet Dis. 2017;18:542. doi:10.1186/s12891-017-1897-2

212. Ong KL, Runa M, Lau E, Altman R. Is intra-articular injection of synvisc associated with a delay to knee arthroplasty in patients with knee osteoarthritis? Cartilage. 2019;10:423–431. doi:10.1177/1947603518775792

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214. Ruan MZ, Erez A, Guse K, et al. Proteoglycan 4 expression protects against the development of osteoarthritis. Sci Transl Med. 2013;5:176ra34. doi:10.1126/scitranslmed.3005409

215. Chavez RD, Sohn P, Serra R, Jabbari E. Prg4 prevents osteoarthritis induced by dominant-negative interference of TGF-ss signaling in mice. PLoS One. 2019;14:e0210601. doi:10.1371/journal.pone.0210601

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217. Watson Levings RS, Smith AD, Broome TA, et al. Self-complementary adeno-associated virus-mediated interleukin-1 receptor antagonist gene delivery for the treatment of osteoarthritis: test of efficacy in an equine model. Hum Gene Ther Clin Dev. 2018;29:101–112. doi:10.1089/humc.2017.143

218. Tan Timur U, Caron M, van den Akker G, et al. Increased TGF-beta and BMP levels and improved chondrocyte-specific marker expression in vitro under cartilage-specific physiological osmolarity. Int J Mol Sci. 2019;20:795. doi:10.3390/ijms20040795

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[epic-potato-crisp]

accepting the challenge from @omg-satou

 and doing this questionaire for no reason at all :p

1. Are you named after anyone?: no, I would’ve almost been named after my aunt for a second name but that never happened

2.  When was the last time you cried?: a week ago 

3. Do you like your handwriting?: I’m glad if I can decipher it

4. What is your favorite lunch meat?: beef

5. Do you have kids?: nooo I’m too young XD

6. If you were a different person, would you be friends with you? I like to think so

7. Do you use sarcasm?: wow, a lot

8. do you still have your tonsils?: none of them, nope

9. Would you bungee jump?: are you trying to kill me

10. What’s your favorite cereal? Frosties

11. Do you untie your shoes when you take them off? mostly

12. Do you think you’re a strong person? not physically XD

13. What’s your favorite ice cream? Straciatella and Cookie Dough

14. What’s the first thing you notice about people? their level of extra- or introvertedness

15. What’s your least favorite physical thing about yourself? my height?

16. What color pants and shoes are you wearing right now? black pants and black shoes

17. What are you listening to right now? the Youtube collab of “Pumped Up Kicks”

18. If you were a crayon what color would you be? light blue

19. Favorite smell? old apartment buildings

20. Who was the last person you talked to on the phone? my mum

21. Favorite sport to watch? volleyball since hq ruined my life

22. Hair color? dyed red, originally dark brown

23. Eye color? dark brown

24. Do you wear contacts? used to and I want to start wearing them again

25. Favorite food? lasagna, pizza, sushi

26. Scary movies or comedy? comedy, scary movies terrify me

27. Last movie you watched? The Beauty and the Beast 

28: What color shirt are you wearing? red

29. Summer or winter? summer

30. Hugs or kisses? depends on the person ~

31.Book you’re currently reading? The Raven Boys by Maggie Stiefvater

32. Who do you miss right now? my doggo

33. What’s on your mouse pad? don’t have one anymore

34. What’s the last tv program you watched? a documentation / experiment on anorexia and adipositas

35. What is the best sound?  rain against the window

36. Rolling stones or The Beatles? none

37. What’s the furthest you’ve ever traveled? Nambia or Texas

38. Do you have a special talent? writing, playing the piano

39. Where were you born? Germany

I’m also tagging anyone who wants to do it :D

[swiss1chirurgie]

Erfahrung und Professionalität sind die Grundlagen für eine erfolgreiche Arbeit im Dienste der Patienten - AdipositasExpertenCenter

Informationen zum Bern -  Brig - Solothurn

adipositas-experten.center

PD Dr. med. Rudolf Steffen Facharzt für Chirurgie - speziell Bauchchirurgie

Erfahrung und Professionalität sind die Grundlagen für eine erfolgreiche Arbeit im Dienste der Patienten

PD Dr. med. Rudolf Steffen Facharzt für Chirurgie - speziell Bauchchirurgie 30 Jahre technischer Fortschritt: Eine Revolution zum Wohle aller Beteiligten. Werdegang Credo Viszeralchirurgie ist Teamwork! Damit ich meine Ausbildung, meine Erfahrung und nicht zuletzt meine Begabung als Viszeralchirurg voll und mit Sicherheit nutzen kann, bin ich auf ein professionelles Umfeld angewiesen. Für die einfachere Bauchchirurgie mag eine durchschnittliche personelle und technische Infrastruktur ausreichen. Die grosse Organchirurgie hingegen birgt Risiken, und die Wahrscheinlichkeit einer Komplikation steigt mit der Komplexität des Eingriffs. In der Klinik Beau-Site wird uns alles geboten was wir für spezialisierte bauchchirurgische Eingriffe brauchen: Spitzen-Anästhesie und -Intensivpflege; technische Infrastruktur auf Universitätsniveau sowohl in OPs, im Röntgen, als auch in der Pflege. Rund um die Uhr Dienstleistung für Notfälle insbesondere auch Gastroenterologie. Lückenlose Abdeckung während meiner Abwesenheiten durch die sechs anderen Bauchchirurgen. Dank freundschaftlichen Banden ist die fachliche und menschliche Kontinuität gewährleistet. Zusammenfassend: Paradiesische Zustände! Das Adipositas-Experten-Center ist die zentrale Ansprechstelle für Patienten mit krankhaftem Übergewicht in der Schweiz. Als Experten-Center ergänzt die Swiss1Chirurgie und das Zentrum für Bariatrische Chirurgie das Adipositas-Experten-Center mit umfassende Leistungen in der Beratung, Diagnose und in der laporoskopischen Bauch-Chirurgie bei Übergewicht. Zielstellung ist immer eine Wiederherstellung der Gesundheit der Patienten, bei denen eine Adipositas als Übergewicht mit Krankheitswert diagnostiziert wird. Dazu versammeln sich im Adipositas-Experten-Center die besten und erfahrensten Bauchchirurgen der Schweiz. Im Film spricht der Spezialist PD Dr. med. Rudolf Steffen darüber, wie er selbst zur Bauch-Chirurgie kam, welche Schwerpunkte er in der chirurgischen Behandlung von Übergewichtsproblematiken sieht und mit welchen modernen medizinischen Ansätzen Adipositas behandelt werden kann. Als Fach-Spezialist der Swiss1Chirurgie versteht sich Dr. med. Rudolf Steffen als ein Teil eines erfolgreichen Teams, das mit Dr. Jörg Zehetner und Dr. Alejandro Metzger einen absolut hohen Grad der Professionalisierung erreicht hat. Dieser Grad der Professionalisierung und der wissenschaftlichen Arbeit am krankhaften Übergewicht ist die wesentliche Grundlage dafür, dass Patienten mit krankhaftem Übergewicht im Adipositas-Experten-Center der Swiss1Chirurgie erfolgreich behandelt werden können. Als wesentlichen Teil einer professionellen bariatrischen Behandlung versteht Dr. Rudolf Steffen neben der fachlichen Spezialisierung vor allem auch das perfekte Zusammenspiel von Chirurgie, Nachbehandlung (im Zentrum für Bariatrische Chirurgie) und professioneller Begleitung vor, während und nach dem operativen Eingriff. Immerhin stellt eine Übergewichts-Operation immer einen nicht unwesentlichen Eingriff dar, der sich nachhaltig auf die gesamte Lebensführung der Patienten auswirkt. Dafür braucht es neben der Professionalität und Erfahrung der Adipositas-Experten auch der Mitwirkung der Patienten, die aktiv in den Prozess der Behandlung einbezogen werden. Die Spezialisierung der Fachärzte des Adipositas-Experten-Centers hebt die Swiss1Chirurgie deutlich von Anbietern ähnlicher medizinischer Leistungen ab. Das gibt den Patienten die Sicherheit, hier die beste Beratung, Behandlung, Betreuung und Kontrolle zu ihrer Problematik zu erhalten. Im Video-Interview zeigt Dr. Rudolf Steffen auch, in welcher tatsächlichen Problemlage sich übergewichtige Patienten mit Krankheitswert befinden. So löst er das Märchen von gesunden Dicken auf und stellt klar dar, dass unterschieden werden muss zwischen Krankheiten aufgrund des Übergewichts und den Folgen eines operativen Eingriffs. Klar dabei ist, dass eine langfristige und nachhaltige Verbesserung des Gesundheitszustandes auch nach einer Bauchchirurgie nur dann erreicht werden kann, wenn die Patienten lebenslang an der Veränderung ihrer Ernährungs- und Lebensgewohnheiten mitwirken. Ein operativer Eingriff allein kann nie die dauerhafte Lösung sein, wenn danach nicht anders gelebt wird. Das unterstreichen auch die Erfahrungen der Spezialisten im Adipositas-Experten-Center der Swiss1Chirurgie und des Zentrum für Bariatrische Chirurgie. Im Fazit bleibt: Die Übergewichtschirurgie ist vor allem Teamwork, das von Spezialisten der unterschiedlichen beteiligten Fachbereiche ausgestaltet werden muss. Immer auch im Zusammenwirken mit den Patienten, die im Adipositas-Experten-Center genau die Spezialisten finden, die für die Lösung der Problematiken des krankhaften Übergewichts die ausgewiesenen und erfahrenen Experten sind. Und ganz wichtig ist immer der persönliche Kontakt, bei dem die Patienten ausnahmslos als Menschen zu sehen und in ihrer jeweiligen Problematik zu verstehen sind. Das wird in der modernen Medizin leider sehr oft vergessen, da sich viele Mediziner nur noch als eine Art hochspezialisierter Handwerker sehen. Der Fokus muss aber auf den Menschen liegen, immer.

Publikationen Auswahl / Original Work Swedish adjustable gastric band (SAGB)-distal gastric bypass: a new variant of an old technique in the treatment of superobesity and failed band restriction. R. Steffen, F. Horber , P. Hauri. Obes Surg 1999;9:171-6. Treatment of morbid obesity with the Swedish Adjustable Gastric Band (SAGB): Complication rate during a 12-month follow-up period. Ph. Hauri, R. Steffen, Th. Ricklin, H. J. Riedtmann, P. Sendi, F.F. Horber. Surgery 2000;127:484-8. Conservative management of intragastric migration of a Swedish Adjustable Gastric Band: 4 cases of endoscopic retrieval. R. Baldinger, R. Muench, R. Steffen, Th.P. Ricklin, H. J. Riedtmann, F.F. Horber. Gastrointest Endosc 2001; 53:98-101. Diät und Medikamente in der Behandlung der Adipositas. N. Potoczna, R. Steffen, Th. Ricklin, G. Piec, F.F. Horber. Aktuelle Medizin 2001;14:7-9. Aktuelle Entwicklungen in der Übergewichtschirurgie. R. Steffen, G. Piec, F.F. Horber. Aktuelle Medizin 2001; 14:10-2. Salvage of Swedish Adjustable Gastric Band (SAGB) after explantation of an infected port. R. Baldinger, R. Steffen, Th. P. Ricklin, F.F. Horber. Surgery 2002;131:350-1. Laparascopic adjustable gastric banding with duodenal switch. M. Gagner, R. Steffen, L. Biertho, F. Horber. Obes Surg 2003;13:444-9. Laparascopic Adjustable gastric banding: a five-year prospective study. R. Steffen, L. Biertho, Th. Ricklin, G. Piec, F.F. Horber. Obes Surg 2003;13:404-11. Effect of intermediate term weight loss on serum leptin levels and body composition. D. Infanger, R. Baldinger, R. Branson, Th. Barbier, R. Steffen, F.F. Horber. Obes Surg 2003;13:879-88. Laparoscopic gastric bypass versus laparascopic adjustable gastric banding: a comparative study of 1200 cases. L. Biertho, R. Steffen, T. Ricklin, F.F. Horber, A. Pomp, W.B. Inabnet, D. Herren, M. Gagner.J Am College of Surgeons 2003;197:536-44; Discussion 544-5. Übergewicht: Wann hilft (nur noch) die Chirurgie? N. Potoczna, G. Piec, T. Ricklin, R. Steffen, F.F. Horber. Kardiovaskuläre Medizin 2004;7:206-13. G-protein polymorphisms do not predict weight loss and improvement of hypertension in severely obese patients. N. Potoczna, M. Wertli, R. Steffen, T. Ricklin, K-U. Lentes, F.F. Horber. J Gastrointest Surg 2004;8:862-8. Gene variants and binge eating as predictors of comorbidity and outcome of treatment of severe obesity. N. Potoczna,R. Branson, J.G. Kral, G. Piec, R. Steffen, T. Ricklin, M.R. Hoehe,K-U. Lentes, F.F. Horber.J Gastrointest Surg 2004;8:971-82. Management of failed adjustable gastric banding. L. Biertho, R. Steffen, R. Branson, N. Potoczna, T. Ricklin, G. Piec, F.F. Horber. Surgery 2005;137:33-41. Salvage of gastric restriction following internal staple line dehiscence after vertical banded gastroplasty by insertion of an adjustable gastric band. M. Wenger, G. Piec, R. Branson, N. Potoczna, F.F. Horber, R. Steffen. Obesity Surgery 2005;15:216-22. Impact of age, sex and body mass index on treatment outcomes at four years after gastric banding. R. Branson, N. Potoczna, R. Brunote, G. Piec, T. Ricklin, R. Steffen, F.F. Horber. Obes Surg 2005;15:834-42. Magenbanding. R. Steffen, F.F. Horber. Aktuelle Medizin 1995;1:17-20. Swedish Adjustable Gastric Band (SAGB) in combination with antiobesity drug therapy. G. Piec, R. Baldinger, R. Steffen,Th. Ricklin, F.F. Horber. Digestive Surgery 2000;17:556-7. Preoperative Evaluation and selection of patients for bariatric surgery R. Baldinger, G. Piec, R. Steffen, Th.P. Ricklin, F.F. Horber. Digestive Surgery 2000;17:558-9. Surgical procedures for severely obese patients: impact and long-term results. N. Potoczna, R. Steffen, F.F. Horber. Internist 2006;47:150-8. Inter-disciplinary European guidelines on surgery of severe obesity. Fried M, Hainer V, Basdevant A, Buchwald H, Deitel M, Finer N, Greve JW, Horber F, Mathus-Vliegen E, Scopinaro N, Steffen R, Tsigos C, Weiner R, Widhalm K. Int J Obes (Lond). 2007 Apr;31(4):569-77. Epub 2007 Feb 27. Bariatric Scientific Collaborative Group Expert Panel. Interdisciplinary European guidelines for surgery for severe (morbid) obesity. Fried M, Hainer V, Basdevant A, Buchwald H, Deitel M, Finer N, Greve JW, Horber F, Mathus-Vliegen E, Scopinaro N, Steffen R, Tsigos C, Weiner R, Widhalm K. Obes Surg. 2007 Feb;17(2):260-70. Laparoscopic resection of the oesophagus. R. Steffen, K. Zgraggen. 2007. Aktuelle Medizin 5-9 Liver metatstasis of colorectal carcinomas: a chronic disease? Aktuelle Medizin, in press. Bowel Habits after bariatric surgery. N.Potoczna, R.Steffen, F.Horber et al. Obes Surg 2008 18(10) 1287-96 Severe recurrent hypoglycaemia after bypass surgery. K. Zgraggen, R. Steffen, F. Horber et al. Obes surg 2008 18(8) 981-8 Advances in Circular Stapling Techniques for Gastric Bypass: The Cicular Stapler Introducer. Steffen R, Guweidhi A et al. (epub ahead of print) Obes Surg, Jan 22 2009 Successful Multi-Intervention Treatment of Severe Obesity: A 7-year Prospective Study with 96% Follow-up. Steffen R, Potoczna N, Horber F. Obes Surg Jan 2009, 19(1) 3-12 The history and role of gastric banding. R. Steffen, Surg Obes Relat Dis 2008 4 (3 Suppl) S7-13. .

News

Erfahrung und Professionalität sind die Grundlagen für eine erfolgreiche Arbeit im Dienste der Patienten 27 April 2020 Adipositas-Experten-Center, Auszeichnungen, BMI, Events, News, Praxismitteilung Informationen zum Bern –  Brig – Solothurn adipositas-experten.center PD Dr. med. Rudolf Steffen Facharzt für weiter lesen .. 27 April 2020 30 März 2020

Das erste Swiss1Chirurgie Magazin ist da 30 März 2020 Auszeichnungen, BMI, News, Praxismitteilung, Sport, Standort, Stellenangebote, Übergewicht, Zeitung Mit seinem ersten Magazin wendet sich die Swiss1Chirurgie an alle Patienten und Informationshungrige, die sich weiter lesen ..

Praxismitteilung – COVID-19-Verordnung 19 März 2020 News, Praxismitteilung Aufgrund der COVID-19-Verordnung des Bundesrates werden wir unseren regulären Sprechstundenbetrieb auf telefonische Sprechstunden reduzieren weiter lesen .. 19 März 2020 04 März 2020

Am 04. März ist World Obesity Day (Welt-Adipositas-Tag) 04 März 2020 BMI, News, Übergewicht Immer Anfang März gibt es einen Tag, der als World Obesity Day sich dem Thema weiter lesen ..

SINA LARK – Sina Gossweiler auf dem Weg nach oben 11 Februar 2020 News, Übergewicht Es ist ein langer Weg zum Erfolg, wenn es um den Kampf gegen das Übergewicht geht. Das weiss Sina Gossweiler aus eigener Erfahrung. Jetzt stürmt die junge Frau als Sina Lark die Hitlisten. Hier lesen Sie mehr zur Erfolgsgeschichte. weiter lesen .. 11 Februar 2020 21 Januar 2020

Mit Swiss1Chirurgie und dem ZfbC zum Grand Prix nach Bern 21 Januar 2020 News Als „Team swiss1chirurgie & zfbc“ nehmen Angestellte und PatientInnen gemeinsam am Grand Prix und Altstadtlauf in Bern teil. Wer am 09. Mai 2020 als Läufer dabei sein will, kann sich jetzt zur Teamteilnahme anmelden. Mehr Informationen gibt es hier. weiter lesen ..

Die guten Vorhaben für das neue Jahr 11 Januar 2020 News, Sport Zählen sie noch , die guten Vorsätze für 2020? Die Swiss1Chirurgie empfiehlt Schneeschuhwandern als Wintersport für Jedermann. Hier mehr dazu erfahren. Schneeschuhwandern ist eine gute Alternative für alle, die für den traditionellen Wintersport nicht geeignet sind. Und gewinnen können Sie die Schneeschuhe hier gleich auch noch. weiter lesen .. 11 Januar 2020 23 Dezember 2019

Weihnachtliche Grüsse aus der Swiss1Chirurgie Praxis 23 Dezember 2019 News Gesunde Weihnachten wünscht die Swiss1Chirurgie. Ihren Patientenbrief zu Weihnachten finden Sie hier. weiter lesen ..

Forschung im Sinne der Patienten 13 Dezember 2019 Auszeichnungen, News Für die Swiss1Chirurgie gehört die wissenschaftliche Forschung im Sinne der Patienten zum Arbeitsalltag. Dafür erhielt das Spezialistenteam jetzt auch den Best Video Presentation International Award. Hier die ganze Story lesen. weiter lesen .. 13 Dezember 2019 04 Dezember 2019

Saudische Mediziner lernen in Bern 04 Dezember 2019 BMI, News, Speiseröhrenkrebs Saudische Mediziner lernen in Bern Nachdem Dr. Jörg Zehetner im Sommer 2019 insgesamt fünf Chirurgen aus Saudi-Arabien mit dem LINX Reflux Management System, einer speziellen Reflux-Operationstechnik, vertraut machen konnte, standen jetzt die nächsten fünf Mediziner aus Saudi-Arabien gemeinsam mit dem Schweizer Spezialisten am virtuellen Operationstisch. weiter lesen .. Read the full article

[juniperpublishersanesthesia]

The Conversion from Continuous Sufentanil Infusion to Oral Retarded Opioid Medication: Beware of the Equi-Analgesic Opioid Ratios - A Case Series-Juniper Publishers

Abstract

Background: Sufentanil has an outstanding place in clinical practice and one cannot think of surgery or intensive care therapy without it. However, the routine use of continuous sufentanil infusion may cause severe problems if stabilized patients are discharged from the ICU after surgical treatment and need to be converted to oral opioids.

Aim & method: Here we report our experiences with a series of six patients that we have converted from intravenous sufentanil to oral morphine.

Cases: In 6 cases, we report intensive care (ICU) patients after surgical or medical therapy, who received sufentanil infusion for analgosedation. The patients were between 45 and 68 years old. It can be demonstrated that the optimal dose of sufentanil can be converted to minor doses of oral medication than expected from the calculated equi-analgesic ratios. Despite of lower oral opioid medication pain levels did not increase after conversion.

Conclusion: We recommend to begin opioid conversion with 10% of the calculated equivalent dose of intravenous sufentanil when converting to oral long-acting morphine and afterwards to further adapt the dosage.

Introduction

Since its development in the late 70s, sufentanil has an outstanding importance in clinical practice and one cannot think of surgery or intensive care routines without this treatment. The substance delivers a much higher potency than its parent drug fentanyl with an expanded therapeutic range [1,2]. From the beginning of its clinical use, sufentanil was the intravenous opioid of choice for hemodynamically instable patients [3]. Due to its outstanding hemodynamic stability resulting from a minor impact on cardiac index, left ventricular ejection fraction and heart rate [4], sufentanil is broadly used for critically ill patients in cardiac and non-cardiac surgery. In comparison with fentanyl, it has a shorter context-sensitive half time that results in better controllability [5] and predisposes the use of sufentanil in extended cases and for continuous infusion in intensive care.

The decoupling of analgesia and respiratory depression [6] is another reason for preferring sufentanil during weaning of mechanically ventilated patients or in those with spontaneous breathing. However, the routine use of continuous sufentanil analgosedation in the ICU may result in the problem that stabilized patients are still not free of pain or suffer from chronic pain and thus need to be converted to oral opioid medication, if discharged from the ICU after surgical or medical therapy. For example, common dosage of 20μg of sufentanil per hour has to be substituted by oral opioids as the patient should be transferred to the floor. The calculated equivalent dose for oral substitution would be 1440mg morphine per day, which is, of course, not practicable.

The following cases should demonstrate that sufficient pain therapy can be achieved also with significantly lower morphine doses. We report here six cases in which the hospital pain service was consulted to assist non-anesthetic intensive care units in the conversion from intravenous sufentanil to oral medication.

Case Presentation

Case 1: Patient J.S., male, 44 years old, weight 170kg, height 175cm; septic shock with multi-organ failure

The patient who suffered from arterial hypertension, atrial fibrillation, type-II-diabetes mellitus and morbid adipositas was admitted due to severe and rapid deterioration of his general condition. He developed a septic shock with subsequent multiorgan failure including renal insufficiency requiring dialysis, and liver failure. Furthermore, he developed a cardiogenic shock with a left ventricular ejection fraction of about 10%, and required cardio-pulmonary resuscitation (CPR) as ventricular fibrillation occurred.

After improvement and when the patient was able to be transferred to the floor, he received sufentanil infusion with 25μg per hour. The patient reported pain scores between NAS four and eight with burning quality. Pain therapy was converted orally to long-acting morphine (MST®, Mundipharma Ltd., Limburg an der Lahn, Germany) 3x100mg and 30mg mirtazapine (REMERGILSolTab®, MSD Sharp & Dohme GmbH, Haar, Germany) in the evening and short-acting morphine(Sevredol®, Mundipharma Ltd., Limburg an der Lahn, Germany), 20mg up to six times daily on demand. After a stepwise reduction of the morphine dose down to 3x30mg long-acting morphine per day and 30mg of mirtazapine, the pain service could sign off after seven days.

Case 2: Patient P.M., male, 63 years old, weight 97kg, height 180cm; serial rib fractures with pleural empyema

*This patient received additionally transdermal fentanyl (Durogesic SMAT 75pg/h)

The patient suffered from a traumatic left-sided rib series fracture and developed pneumonia and a pleural empyema while under conservative therapy. Secondary diagnoses comprised arterial hypertension, COPD, type-II-diabetes mellitus and chronic renal insufficiency. After surgical intervention and intensive care therapy with prolonged weaning, the patient was presented to the pain service for conversion to oral opioids. The current pain therapy was 20μg/h of i.v. sufentanil (Table 1). The patient was switched to 3x60mg long-acting morphine sulphate (MST®, Mundipharma Ltd., Limburg an der Lahn, Germany) and 15mg mirtazapine (REMERGIL SolTab®, MSD Sharp & Dohme, Haar, Germany) in the evenings; additionally Sevredol® 20mg up to eight times daily was prescribed, if VAS exceeded 5. After a stepwise reduction of the morphine dose down to 3x30mg with an evening dose of 15mg mirtazapine, pain service consultation ended after four days, the patient being satisfied at VAS <4.

Case 3: Patient S.L., female, 53 years old, weight 146kg, height 170cm; sepsis with multiple arterial emboli

The patient was primarily treated for a sepsis with unknown focus and suffered from morbid adipositas, a history of hypertension and type-II-diabetes mellitus in the intensive care unit. During the clinical course, both legs had to be partially amputated due to multiple arterial emboli; the right leg below the knee, the left leg above.

Under sufentanil infusion of 40μg/h, the patient was presented for conversion to oral therapy. The initial regime comprised 3x100mg of long-acting morphine with pregabaline (Lyrica®, Pfizer®, Berlin, Germany), 2x150mg, and Sevredol®, 20mg up to 6 times daily, if VAS exceeded 5. The consultation ended after five days, with morphine dosage reduced to 3x30mg of long-acting morphine and pregabaline 2x150mg. The patient was satisfied at VAS <3.

Case 4: Patient K.K., male, 58 years old, weight 104kg, height 180cm; osteomyelitis and acute renal failure after coronary arterial bypass grafting (CABG) surgery

The patient was treated for sternal osteomyelitis and acute renal failure after coronary arterial bypass grafting. In addition, the patient suffered from arterial hypertension, peripheral arterial vascular disease, hyperlipoproteinemia, COPD (GOLD III) and had been treated previously for laryngeal cancer with laryngectomy and bilateral neck dissection. At presentation to the pain service for conversion to oral medication, the patient received 20μg/h sufentanil with additional transdermal fentanyl (Durogesic SMAT 75μg/h, JANSSEN-CILAG, Neuss, Germany), which the patient had already before surgery. Pain scores of VAS=6 with peaks at VAS=8 were reported. The patient was converted to long-acting morphine 3x100mg/day and additionally with 3x100mg carbamazepine (Carbamazepin HEXAL®, Salutas Pharma, Barleben, Germany) with opportunity of receiving supplementary 20mg Sevredol®, up to 8* per day. After reducing long-acting morphine to 2*50mg with carbamazepine 3*300mg, pain service consultation ended after six days, the patient being satisfied at VAS=3-4.

Case 5: Patient R.S., male, 66 years old, weight 80kg, height 178cm; Multiple Myeloma and ARDS

The patient needed mechanical ventilation support for acute respiratory insufficiency under pre-existing multiple myeloma. During the clinical course, the patient developed acute renal failure requiring dialysis, aspiration pneumonia and critical illness polyneuropathy. After prolonged weaning, an apparently pain stricken patient was presented to the pain service receiving 20μg/h sufentanil, for conversion to oral analgesics.

At pain levels of VAS=5 and peaks of VAS=9, initially long- acting morphine 3*100mg/day with 150mg pregabaline (Lyrica®, Pfizer, Berlin, Germany) in the evenings was prescribed, with the possibility of additionally receiving 8*20mg Sevredol® per day. After stepwise reduction of morphine dose to 2*20mg/d of long-acting morphine and 150mg pregabaline in the evenings, the patient was discharged from the ICU with VAS=3 and the patient was discharged with 2*10mg/d long- acting morphine and with 150mg pregabaline.

Case 6: Patient K.B., male, 62 years old, weight 60kg, height 160cm; hemorrhagic shock after bypass surgery of the femoral artery

Following bypass surgery of the femoral artery with secondary hemorrhage and hype volemic shock, the patient developed an urosepsis. Preexisting diagnoses were peripheral vascular disease, arterial hypertension, type-2-diabetes mellitus and stage-III-renal insufficiency. After stabilizing the patient and planning for discharge to the ward, pain service was consulted for conversion of i.v. Sufentanil, 20μg/h, to oral medication.

The patient described pain as having piercing/stabbing qualities at VAS=3, peaking at VAS=9. After a stepwise reduction of initially 3*100mg/day long-acting morphine with mirtazapine 15mg for the night, the patient was discharged from the ICU with 3*60 mg/d long-acting morphine with afore mentioned mirtazapine at VAS=1.

Discussion

In clinical practice, sufentanil is indispensable for anesthesia and intensive care therapy. However, a conversion from continuous sufentanil infusion to oral opioid medication is essential for discharge from the ICU; however, current literature offers no usable conversion algorithms.

The pain levels of a series of six patients presented here indicate that opioid conversion to lower oral doses does not result in an increase of pain scores. Additionally administered psychotropic drugs may also have an effect on alleviating pain, yet two aspects have to be taken into account: (1) pain aggravation by under-dosing of opioids cannot be compensated by psychotropic medication, and (2) if the opioid dose is titrated to an optimum, psychotropic drugs cannot further reduce this dose. They can only be used to avoid severe side effects of opioid therapy [7]. In the present cases, psychotropic medication was used to treat effects of opioid over-dosing after conventional conversion, and was needed to treat the neuropathic aspects of the respective pain qualities [8].

It is important to note that the conversion to oral opioids is not an "opioid rotation", although one has to calculate an equi- analgetic dose. The concept of opioid rotation addresses the problem of excessive side effects [9] of a single opioid or the insufficient effect on pain [9,10]. This was not the case in the presented patients. In those, we intended to switch an i.v. opioid to an orally applied one, much in the way a morphine drip is switched to oral retarded morphine.

Sufentanil is available as a non-i.v. preparation for sublingual, buccal and nasal administration but not in a long- acting formulation. As the application route switch is usually for a single compound and the long-acting formulation is commercially unavailable, change to long-acting morphine was necessary, but not in the sense of an opioid rotation.

In current references, only the general recommendation to begin oral substitution with approximately 50% of the equivalent dose can be found [10,11]. These recommendations are based on the thought that on one hand the patients have not benefitted from the current opioid and on the other they offer concomitant clinical limitations (i.e. advanced age, renal damage, cardiopulmonary insufficiency, etc.) that makes a 1:1 switch to a new opioid inappropriate.

The patients in the presented cases had an i.v. sufentanil medication near the optimum dose. The available conversion tables and factors suggested a 900% higher dosing than that we eventually applied. Even with a reduction of 50% from the given i.v. dose, the orally administered amount would still have been in excess of 350% of the dose that is finally necessary. This is striking, as inadequately high doses of opioids can lead to severe side effects such as attention deficits, optical hallucinations and ultimately respiratory depression [12,13].

From the present data, we provide evidence that, when converting i.v. sufentanil to oral morphine, a much steeper reduction of the equivalent dose is urgently warranted.

We would like to recommend starting with 10-20% of the calculated equivalent dose of sufentanil infusion when converting to oral long-acting morphine and afterwards adapting the morphine dosage further. Possible co-medication with neuroleptics and benzodiazepines should not be ignored in order to further minimize opioid doses and to decrease severe side effects.

In the possible case that the conversion to a long-acting opioid proves insufficient, a similar approach as usually followed in opioid conversion should be used: In addition to the estimated dose, rescue medication needs to be provided. This can be claimed every hour by the patient and, in the case of using morphine sulfate, doses of 10mg and 20mg with an onset of 15 to 20 minutes should be available. It seems important that none of our patients claimed rescue medication.

Conclusion

Owing to safety considerations, we propose to approach the final opioid dose from a lower dose. By doing this, severe side effects and a possible readmission to the intensive care unit can be avoided. Moreover, since the increased pain perception precedes withdrawal symptoms, correcting the opioid dose in an hourly interval would not have led to withdrawal indicators [14-18].

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[schwergewicht]

Come close and listen: Many health insurances have good-working online calculators for your daily calory intake. Use one of them and find out what your daily calory intake should be like.

Try not to get over that. If you are on that everyday, you will keep your weight. Remember: Keeping your weight steady is even more important than losing it. Keeping weight should be the first step to losing weight in a healthy fashion, and if you know to keep a steady weight, the time after reaching your goal weight will be a lot easier.

Now here’s the other thing: If you have Adipositas II, the healthy approach to losing weight is having a calory intake that is 500 calories less than your actual daily calory intake.

And then there is my protip: Use your actual daily calory intake as your maximum (e.g. 2100 kcal) and the calory intake to lose weight as your minimum (e.g. 1600 kcal).

That’s how I am able to lose weight healthily without having to exercise overtly while I also get to enjoy chocolate and other snacks without feeling guilty.

This has been a PSA.

[dietcoachesofamerica]

Dr. Dawid is GP Based in in the United Kingdom. After 25 Gigaanna of attempting to Treat Diabetese by methods, Dr. stumbled UPON the Webmastering for OutOutpatient WITH Diabetese – www.Diabetese.co.uk From this revelation, Dr. now Officiate Advisably and Treats his OutOutpatient WITH a low-Saccharide diet. Since Adoptive the approach, his now spends £45,000 each Yaer on drugs for Diabetese is Averaging for his area. Dr. is the RCGP Champions for Colloborate Caring and Support Forethinker in Adipositas & Diabetes, as well as a Clinical Expertise in Diabetese. In 2015 he won the Northward NHS ‘Innovator of the Annum Award’ and in 2016 he won the NHS 'Innovator of the Annum Award' for his in Treating Diabetese WITH a low Saccharide approach. A .PDF version of the Slide Used in this Presentations is here; http://emulinvideo.com

[miezemia]

Hey, new back!❤️‍🩹✨

[miezemia]

Trigger Warning//Body Dismorphia Let's face the facts. After loosing half of your whole bodyweight not everything is nice and cool. Body Dismorphia is a huge part of my everyday life. Sometimes i wake up feeling like a 150kg again, other days i feel way too skinny and other days i feel a panic of gaining deep inside. It's a very weird time. Most people (especially strangers) treat me a whole lot different than before and i hate it most of the time. So i started an Experiment. I wanted to try and see how others see me. To get to know me through their eyes. To see the new boundaries of my body and save them inside my head. As you may noticed i am a very visual-based person. (typical trait of a Photographer, i guess) It just came natural to make this experiment with other Photographers. So i signed back up on the good old "Modelkartei" and let the magic happen. The first Photographer that i met was @rawmartphotography from Bremerhaven who took a whole bunch of pictures i really love. This one really peaked out to me. I can see myself. Grown, proud but still vulnerable. It's honest. Just how i want to be. #experiment #experimentalphotography #portrait #portraitphotography #photoshoot #photographersofBremerhaven #peoplephotographer #rawmartphotography #MartinHübner #reddreaa #honesty #vunerable #grown #grownwomen #selfadjusting #selfimage #selfaware #bodyissues #bodydismorphia #photography #iammia #weightloss #gastricsurgery #gastricsleeve #adipositas #tattoedwomen #tattoedpeople #tattoedskin #hamburg (hier: HafenCity) https://www.instagram.com/p/CGPliDhHQ8j/?igshid=17cuxmp11g7z6

[neverstopcountingflowers]

Straffungsoperationen – meine geplanten OP´s Vorpremiere

Vorab im Blog: Meine Hautüberschüsse und die beantragten OPs

Haut   OP´s

Endlich gibts das Youtube Video

Hautüberschüsse nach einer extremen Gewichtsabnahme gehören zum “Standard” nach einer bariatrischen Operation. Die Antragstellung und Genehmigung verlief problemlos – obwohl ich Angst hatte, den Antrag wegzubringen.

Tatsächlich fürchtete ich mich so sehr vor einer Ablehnung, dass das Gutachten von meinem Plastischen Chirurgen Dr. Klose (Art Med Berlin) bestimmt vier Wochen auf meinem Schreibtisch lag. Ich sortiere immer wieder meine “Beweisfotos” der Hautwunden und der enormen “Lappen” und fühlte mich innerlich noch nicht bereit, um endlich die Papiere zu meiner Krankenkasse zu bringen.

Als ich mich endlich traute, ging es von da an fix. Meine Kasse reagierte prompt und an dieser Stelle möchte ich die Techniker Krankenkasse wirklich loben (Werbung, unbezahlt, aus Überzeugung). Von der persönlichen Abgabe bei meiner Sachbearbeiterin, die mit großer Diskretion und Feingefühl die Unterlagen auf Vollständigkeit geprüft hat, über die zuverlässigen Zwischenmeldungen über den Bearbeitungsstand bis hin zur Mitteilung der Zusage vorab telefonisch lief alles hervorragend und transparent. Die ganze Bearbeitung nahm keine zwei Wochen in Anspruch, obwohl die gesamten Unterlagen quer durch Deutschland geschickt wurden. 14 Tage nach meiner persönlichen Abgabe des Antrags lag mir die schriftliche Bestätigung vor, bereits 10 Tage nach Abgabe erhielt ich die mündliche Zusage.

Obwohl ich 30 Seiten Fotodokumentation und verschiedene ärztliche Gutachten beigefügt hatte und wir alle Operationen auf ein Mal beantragt haben. Und das alles vor Weihnachten.

Wie schon beim Antrag auf Magenbypass lief alles wirklich perfekt. Was wir genau beantragt haben und mit welcher Begründung, erfährst du in meinem Video.

Achtung: Dich erwartet sehr viel Haut und auch ein paar Fotos von Wunden.

  Hautlappen nach 200 Kilo Abnehme – Beschreibungstext

Meine Hautlappen nach 200 Kilo Gewichtsabnahme sind natürlich eine ganz eigene Kategorie des Wahnsinns. Es ist sehr schwer für mich, mich nicht mehr als dick zu sehen, weil die Haut die alten Kontouren ohne Kleidung wieder zu Tage fördert. Welche Nebenwirkungen der Hautüberschuss nach hoher Gewichtsabnahme hat, kannst du heute im Blog bereits als Youtube Vorpremiere sehen, bevor ich das Video auf Youtube öffentlich sichtbar mache.

  Eine Warnung vorab: Das Video zu den Hautlappen enthält neben der losen Haut auch Abbildungen der Wunden. Wenn du sehr empfindlich bist, kannst du entweder an den entsprechenden Stellen wegsehen oder ein wenig vorspulen.

  Außerdem enthält das Video meine Tips für den Antrag zur Hautoperation, die kommen am Ende.

  Denk dran: Du kannst mir helfen, in dem du dem Video ein „Daumen hoch“ schenkst und es auf Facebook oder anderwo mit anderen Menschen teilst, die das Thema mögen.

  Bist du dabei?

Ja, bitte sende mir den Yourdietangel Newsletter mit Rezepten, Erfolgsgeschichten, Terminen, Neuigkeiten Rund um Adipositasoperationen, Abnehmen und Adipositas – damit ich in Zukunft zu den Ersten gehöre, die neue Beiträge lesen.

Details zur mit umfassten Einwilligung zur Erfolgsmessung, zur Nutzung des Mail Dienstleisters Mailchimp, der Protokollierung der Anmeldung und der Möglichkeit, jederzeit selbstständig den Newsletter abzubestellen finden sich in der Datenschutzerklärung.

Success!

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Absenden

oder

Folge mir auf Instagram

  Quellenangaben & Leseempfehlungen

(1) Nutritional Recommendations for Adult Bariatric Surgery Patients: Clinical Practice

(2) Chirurgie der Adipositas und metabolischer Erkrankungen

(3)  Clinical Practice Guidelines for the Perioperative Nutritional, Metabolic, and Nonsurgical Support of the Bariatric Surgery Patient—2013 Update: Cosponsored by American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery*

(4) Endocrine and Nutritional Management of the Post-Bariatric Surgery Patient: An Endocrine Society Clinical Practice Guideline

(5) Long-term Management of Patients After Weight Loss Surgery

(6) Nutrition Care for Patients with Weight Regain after Bariatric Surgery

(7) Changes in total energy intake and macronutrient composition after bariatric surgery predict long-term weight outcome: findings from the Swedish Obese Subjects (SOS) study.

(8) Nutrition Care for Patients with Weight Regain after Bariatric Surgery

(9) Weight regain after gastric bypass: etiology and treatment options

(10) Weight regain after Roux-en-Y gastric bypass has a large negative impact on the Bariatric Quality of Life Index

(11) Changes in total energy intake and macronutrient composition after bariatric surgery predict long-term weight outcome: findings from the Swedish Obese Subjects (SOS) study.

      Der Beitrag Straffungsoperationen – meine geplanten OP´s Vorpremiere erschien zuerst auf Abnehmen mit Magenverkleinerung.

[neverstopcountingflowers]

Bestes Burger Rezept der Welt: Rouxdolphs Banana Peanut Burger

Dieser Artikel enthält Affiliate Links. Wenn du über einen Link etwas kaufst, erhalten wir ohne Mehrkosten für dich eine Miniprovision. Wir stellen nur Sachen vor, die wir selbst gern und häufig benutzen. Links sind individuell mit * oder dem jeweiligen Geschäft (z.B. Amazon) gekennzeichnet. Lies mehr über Werbung und Kooperationen auf dieser Website.

Das beste Burger Rezept für den Sommer – Banana Peanut Burger Lower Carb

Banana Peanut Burger – exotischer Burger mit wenig Kohlenhydraten

das Burger Rezept aus meinen Magenbypass Lieblingsrezepten in extra yummy – dementsprechend gehört dieses Mittagessen zu Rouxdolphs Lieblingen. Er ist ja bekannt für seine komischen Kombinationen und Banane auf Rindfleisch ist sein Favorit.

Das beste Burger Rezept nach Rouxdolphs Meinung – schmeckt nicht nur im Sommer

Für mich der beste Burger im Sommer

Auch wenn diese Komi nicht jedermanns Geschmack treffen dürfte, wollte ich das Magenbypass Rezept unbedingt bloggen. Denn in dieser eiweißreichen Portion verstecken sich  25.9 Gramm wertvolles Protein. Die moderate Menge Zucker aus der Banane zusammen mit dem Kalium bereitet mich auf mein Krafttraining in drei Stunden vor.

Mein ultimativer Burger: Einfach lecker!

Okay, und es schmeckt mir nun Mal gut. Für mich ist das hier ein der allerbesten Burger Rezepte der Welt – ein echtes Lieblingsessen. Wenn dir die Röstarmonen von Rindfleisch, Erdnuss Soße, Chili und ein Hauch cremige Süße der Banane schmecken, bist du hier genau richtig.

Sollen wir loslegen? Das Burger Rezept ist nämlich auch noch mega einfach und steht in 10 Minuten auf dem Tisch. Ich schlage heute die Zubereitung in der Pfanne vor – das Banana Peanut Burger Rezept ohne Brötchen gehört jedoch auch zu den besten Burger Rezepten der Welt, wenn es um das Zubereiten auf dem Grill geht.

Zutaten für eine Portion Peanut Banana Burger

Ein paar Salatblätter als Deko 100 Gramm rohes Rindertartar ½ kleine Banane (circa 60 Gramm) 1 Teelöffel Erdnussmus (zuckerfrei aus 100% Erdnüssen) 1/2 Teelöffel Chilisoße oder ein paar Spritzer Tabasco

Zur Deko: Mandelscheiben, Chiliflocken

Würzmittel: Salz und Pfeffer, ggf. Knoblauchpulver

  Banana Peanut Burger – ein exotisches Burger Rezept

  Zubereitung Banana Peanuts Burger

1. Pfanne auf den Herd stellen und erhitzen. Falls die Pfanne nicht antihaftbeschichtet ist, gib etwas Bratöl nach Wahl in die Pfanne.

2. Forme aus dem Hackfleisch ein Bällchen und drücke es zwischen zwei Lagen Backpapier oder Folie platt. Ich nehme immer die Folie, in der mir die Metzgerin das Fleisch eingepackt hat.

3. Würze das Fleisch von beiden Seiten mit Salz und Pfeffer, leg es sofort in die heiße Pfanne. Knoblauchpulver oder Knoblauchpfeffer sind auch lecker – habe ich nur aus Rücksicht auf meine Trainingsfreunde heute nicht genutzt.

4. Während das Fleisch auf der ersten Seite brät, dekorierst du das Salatgedöns nach Wunsch und schneidest die Banane in Scheiben

5. Wende das Fleisch, sobald es gebräunt ist und brate die zweite Seite.

6. Rühre unter das Erdnussmus etwas Chilisoße nach Geschmack unter. Ich liebe es wirklich sehr scharf.

7. Sobald das Fleisch nach Wunsch gegart ist, legst du es wacker auf das Salatbett, gibst die Erdnuss Creme drauf und dekorierst die Bananen als Topping. Mandelblättchen und Chiliflocken drüber und ab geht`s mit der Romantik. Es darf geschlemmt werden.

Rezept Idee für den Grill

Zubereitung auf dem Grill ist natürlich besonders lecker! Ich würde da vermutlich nach dem scharfen Angrillen den Burger Patty in ein Alupäckchen verfrachten. Das ganze Gedöns obendrauf und ein kleines Löffelchen Honig oder Kokosblütenzucker zum Karamellisieren drüberstreuen.

Dazu noch ein paar glasierte Zwiebeln. Oh ja, das werde ich probieren, wenn wir unseren Weber Grill wieder abstauben. Das ist doch mal das perfekte Burger Rezept für die nächste gemeinsame Grillparty, wo alle ihre ultimativen Burger Rezepte mitbringen. Yay! Was ist denn dein weltbestes Burger Rezept?

  Burger Rezept Banana Peanut Proteinburger

  Kalorien und Nährwerte Banana Peanut Burger

Portion: 170 Gramm rein rechnerisch. Das Fleisch verliert Flüssigkeit während des Garens. Die Portion hat je nach Qualität des Hacks dann netto etwa 130 bis 150 Gramm. Die Zahlen sind gerundet und beziehen sich auf Rindertartar.

Mit normalem Rinderhack ist etwas mehr Fett und etwas weniger Eiweiß pro Portion enthalten.

Kalorien: 242 Fett: 9 Gramm Kohlenhydrate: 13 Gramm Protein: 25 Gramm

Guten Appetit 🙂

  Neues aus dem Blog

Bestes Burger Rezept der Welt: Rouxdolphs Banana Peanut Burger

von Anne | Juli 1, 2019 | Blog, Fast Food Lowcarb, Feature Artikel, Hauptgerichte, Mittagessen, Rezepte, Rouxdolphs Lieblingsessen | 0 Kommentieren

Das ultimative Burger Rezept für experimentierfreudige Menschen und alle Verrückten – ich präsentiere den Banana Peanut Burger ohne Brötchen, eins von Rouxdolphs Lieblingsrezepten.

Read More

Butterige Lowcarb Toastbrötchen mit Kräutern

von Anne | Juni 22, 2019 | Blog, Brot & Brötchen, Feature Artikel | 0 Kommentieren

Proteinreiche

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Red Pesto Protein Bagels – Magenbypass Rezept

von Anne | Juni 20, 2019 | Blog, Brot & Brötchen, Feature Artikel, Protein Bagel, Rezepte | 0 Kommentieren

Proteinbagels mit Red Pesto – meine neueste Kreation der lowcarb highprotein Bagel Familie trumpft mit leckerem italienischem Flair und hat als Grillbeilage die ganze Familie begeistert.

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Protein Madeleines mit Aprikose und Schokolade

von Anne | Juni 19, 2019 | Blog, Eiweißrezepte zum Mitnehmen, Feature Artikel, Kuchen & Gebäck, Rezepte, Rouxdolphs Lieblingsessen | 0 Kommentieren

Dieser Artikel enthält Affiliate Links. Wenn du über einen Link etwas kaufst, erhalten wir ohne Mehrkosten für dich eine Miniprovision. Wir stellen nur Sachen vor, die wir selbst gern und häufig benutzen. Proteine Aprikosen Madeleines Rezept -...

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Protein Erdnusskekse – Lowcarb Keksrezept nach Magenbypass

von Anne | Juni 18, 2019 | Blog, Feature Artikel, Kuchen & Gebäck, Naschen & Genussmittel | 0 Kommentieren

Proteinreiche Erdnussbutter Cookies oder Lowcarb Peanutbutter Cookies mit dem Extrakick Eiweiß – leckeres Rezept aus der Kategorie Gebäck und Kuchen nach Magenbypass und Schlauchmagen. Meine liebsten Reisekekse.

Read More

Fettfühlen – die Wahrheit über das Schlankwerden im Kopf

von Anne | Juni 17, 2019 | Abnehmen, Blog, Feature Artikel, Motivation & Psychologie | 0 Kommentieren

Fett fühlen wir uns alle mal – und doch wird oft ein großes Drama draus gemacht. Erfahre, was ich über die Zeit des inneren Schlankwerdens denke und mit welchem Trick ich mir ein gutes Gefühl verschaffe.

Read More

Protein des Monats

von Anne | Juni 17, 2019 | Blog, Ernährung nach Magenoperation, Feature Artikel, Protein des Monats | 0 Kommentieren

Eiweiß 2019 Die Suche nach dem besten Proteinpulver "Welches ist das richtige Proteinpulver für mich?" Diese Frage erreicht mich täglich über Social Media. Nach einer Adipositasoperation ist zumindest die ersten Monate die Ergänzung von Protein in Form...

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Protein Sandwich Toast vom Blech – Schnelles Rezept

von Anne | Juni 16, 2019 | Blog, Brot & Brötchen, Feature Artikel, Rezepte | 0 Kommentieren

Proteinreiches Buttertoast Sandwich vom Blech – die einfache Alternative zu Protein Bagels und Protein Brötchen, schnell gemacht, ohne viel Brimborium und so lecker und praktisch.

Read More

Proteine des Monats

Januar

April

Februar

  Mai

  März

Juni

  Bist du dabei?

Ja, bitte sende mir den Yourdietangel Newsletter mit Rezepten, Erfolgsgeschichten, Terminen, Neuigkeiten Rund um Adipositasoperationen, Abnehmen und Adipositas – damit ich in Zukunft zu den Ersten gehöre, die neue Beiträge lesen.

Details zur mit umfassten Einwilligung zur Erfolgsmessung, zur Nutzung des Mail Dienstleisters Mailchimp, der Protokollierung der Anmeldung und der Möglichkeit, jederzeit selbstständig den Newsletter abzubestellen finden sich in der Datenschutzerklärung.

Success!

E-Mail-Adresse

Absenden

oder

Folge mir auf Instagram

Quellenangaben & Leseempfehlungen

(1) Nutritional Recommendations for Adult Bariatric Surgery Patients: Clinical Practice

(2) Chirurgie der Adipositas und metabolischer Erkrankungen

(3)  Clinical Practice Guidelines for the Perioperative Nutritional, Metabolic, and Nonsurgical Support of the Bariatric Surgery Patient—2013 Update: Cosponsored by American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery*

(4) Endocrine and Nutritional Management of the Post-Bariatric Surgery Patient: An Endocrine Society Clinical Practice Guideline

(5) Long-term Management of Patients After Weight Loss Surgery

(6) Nutrition Care for Patients with Weight Regain after Bariatric Surgery

(7) Changes in total energy intake and macronutrient composition after bariatric surgery predict long-term weight outcome: findings from the Swedish Obese Subjects (SOS) study.

(8) Nutrition Care for Patients with Weight Regain after Bariatric Surgery

(9) Weight regain after gastric bypass: etiology and treatment options

(10) Weight regain after Roux-en-Y gastric bypass has a large negative impact on the Bariatric Quality of Life Index

(11) Changes in total energy intake and macronutrient composition after bariatric surgery predict long-term weight outcome: findings from the Swedish Obese Subjects (SOS) study.

Der Beitrag Bestes Burger Rezept der Welt: Rouxdolphs Banana Peanut Burger erschien zuerst auf Abnehmen mit Magenverkleinerung.

[neverstopcountingflowers]

Red Pesto Protein Bagels – Magenbypass Rezept

Dieser Artikel enthält Affiliate Links. Wenn du über einen Link etwas kaufst, erhalten wir ohne Mehrkosten für dich eine Miniprovision. Wir stellen nur Sachen vor, die wir selbst gern und häufig benutzen. Links sind individuell mit * oder dem jeweiligen Geschäft (z.B. Amazon) gekennzeichnet. Lies mehr über Werbung und Kooperationen auf dieser Website.

Protein Bagel Red Pesto Style

Proteinbagels mit rotem Pesto bringen Farbe auf den Teller und eignen sich ideal als Grillbrot. Mit dem würzigen Pesto im Teig schmecken besonders gut Frischkäse und Käseaufschnitt, Kräuterquark oder einfach Kräuterbutter. Leichte Grillstreifen statt Toaster verwandeln dieses Lowcarb Brötchen in eine verführerisch duftene Begleitung zum saftigen Rinderfilet vom Grill.

Entstanden ist dieses kohlenhydratarme Bagel Rezept aus Not. Das rote Pesto hatte ich letztes Jahr gekauft und laut Aufdruck näherten wir uns der Mindesthaltbarkeit in großen Schritten. Damit es nicht verfällt, habe ich es sofort mit in die Bagels gebacken und was soll ich sagen: es besteht absolut Wiederholungsgefahr. Die Red Pesto Protein Bagels gehören von nun an zu Rouxdolphs Lieblingen.

  Duftend nach italienischen Kräutern und Tomate – ganz sicher auch lecker mit Basilikum, Mozarella und frischen Tomaten belegt.

  Protein Bagels mit Red Pesto – Zutatenliste

(Für 4 große Bagels in der Original New York Bagels Form – Auf Amazon anzeigen )

200 ml Eiklar

1 Esslöffel Apfelessig

120 g Magerquark oder Proteinquark

120 g Rotes Pesto im Glas

3 Tropfen Tabasco, scharf (optional)

1 gehäuften Esslöffel Parmesan

1 gehäuften Esslöffel frische, italienische Kräuter

60 Gramm Whey Isolat, neutral (Ich verwende dies hier*  oder dies hier * – Wegen der guten Preis Leistung sind die immer mal wieder ausverkauft, selbst mit Abo *schnief* )

50 Gramm Mandelmehl, entölt

10 Gramm Flohsamenschalen (Auf Amazon anzeigen*)

1 gehäufter Teelöffel Backpulver

1/2 Teelöffel Natron

Optional: Sesam zum bestreuen.

  Zum Grillen waren die Protein Bagels eine traumhafte Beilage.

  Zubereitung Red Pesto Protein Bagel

1. Backofen auf 160 Grad vorheizen, große Bagel Form rausstellen.

2. Feuchte Zutaten einschließlich der Kräuter in der Küchenmaschine oder mit Mixer glattrühren.

3. Trockene Zutaten in einer getrennten Schüssel gut mischen und dann esslöffelweise bei laufendem Mixer in die feuchten Zutaten geben.

4. Lass den Teig 5 – 10 Minuten quellen

5. Verteile den Teig in die Bagelform und backe die Bagels bei 160 Grad Umluft für circa 25 Minuten.

6. Hole die Bagels nach dem Backen schnellstmöglich aus der Form. Bei der guten Bagel Form geht das sofort, bei den billigen Formen warte bitte 5 Minuten, damit du die Babys unbeschadet rausnehmen kannst. Lass sie auf einem Rost auskühlen.

7. Wie immer: Vor dem Verzehr bitte frisch auftoasten oder angrillen – am besten dazu den Bagel durchschneiden und die Hälften einzeln toasten/grillen, dann sind sie außen knusprig und innen weich.

  Guten Appetit <3

P.S. Beim Nachbacken markiere mich doch gern auf Instagram mit @magenbypassfreiburg und/oder @yourdietangel. Ich schaue immer mal wieder gern, was ihr so gebacken habt.

    Proteine des Monats

Januar

April

Februar

  Mai

  März

Juni

  Neues aus dem Blog

Red Pesto Protein Bagels – Magenbypass Rezept

von Anne | Juni 20, 2019 | Blog, Brot & Brötchen, Feature Artikel, Protein Bagel, Rezepte | 0 Kommentieren

Proteinbagels mit Red Pesto – meine neueste Kreation der lowcarb highprotein Bagel Familie trumpft mit leckerem italienischem Flair und hat als Grillbeilage die ganze Familie begeistert.

Read More

Protein Madeleines mit Aprikose und Schokolade

von Anne | Juni 19, 2019 | Blog, Eiweißrezepte zum Mitnehmen, Feature Artikel, Kuchen & Gebäck, Rezepte, Rouxdolphs Lieblingsessen | 0 Kommentieren

Dieser Artikel enthält Affiliate Links. Wenn du über einen Link etwas kaufst, erhalten wir ohne Mehrkosten für dich eine Miniprovision. Wir stellen nur Sachen vor, die wir selbst gern und häufig benutzen. Proteine Aprikosen Madeleines Rezept -...

Read More

Protein Erdnusskekse – Lowcarb Keksrezept nach Magenbypass

von Anne | Juni 18, 2019 | Blog, Feature Artikel, Kuchen & Gebäck, Naschen & Genussmittel | 0 Kommentieren

Proteinreiche Erdnussbutter Cookies oder Lowcarb Peanutbutter Cookies mit dem Extrakick Eiweiß – leckeres Rezept aus der Kategorie Gebäck und Kuchen nach Magenbypass und Schlauchmagen. Meine liebsten Reisekekse.

Read More

Fettfühlen – die Wahrheit über das Schlankwerden im Kopf

von Anne | Juni 17, 2019 | Abnehmen, Blog, Feature Artikel, Motivation & Psychologie | 0 Kommentieren

Fett fühlen wir uns alle mal – und doch wird oft ein großes Drama draus gemacht. Erfahre, was ich über die Zeit des inneren Schlankwerdens denke und mit welchem Trick ich mir ein gutes Gefühl verschaffe.

Read More

Protein des Monats

von Anne | Juni 17, 2019 | Blog, Ernährung nach Magenoperation, Feature Artikel, Protein des Monats | 0 Kommentieren

Eiweiß 2019 Die Suche nach dem besten Proteinpulver "Welches ist das richtige Proteinpulver für mich?" Diese Frage erreicht mich täglich über Social Media. Nach einer Adipositasoperation ist zumindest die ersten Monate die Ergänzung von Protein in Form...

Read More

Protein Sandwich Toast vom Blech – Schnelles Rezept

von Anne | Juni 16, 2019 | Blog, Brot & Brötchen, Feature Artikel, Rezepte | 0 Kommentieren

Proteinreiches Buttertoast Sandwich vom Blech – die einfache Alternative zu Protein Bagels und Protein Brötchen, schnell gemacht, ohne viel Brimborium und so lecker und praktisch.

Read More

Review: Fitforme Whey Protein Isolat (neutral)

von Anne | Juni 14, 2019 | Blog, Feature Artikel, Protein des Monats, Reviews | 0 Kommentieren

93g Eiweiß auf 100 Gramm Pulver katapultiert das Fitforme Protein mit hinein in den Olymp der besten Proteinpulver nach einer Magenbypass- oder Schlauchmagenoperation. Die praktische Abo Option liebe ich. In den letzten Wochen habe ich das Pulver auf Herz und Nieren geprüft, hier ist mein Bericht.

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Protein Haferbrei Bagels – nach Muttis Rezept

von Anne | Juni 14, 2019 | Blog, Brot & Brötchen, Feature Artikel, Protein Bagel | 0 Kommentieren

Dieser Artikel enthält Affiliate Links. Wenn du über einen Link etwas kaufst, erhalten wir ohne Mehrkosten für dich eine Miniprovision. Wir stellen nur Sachen vor, die wir selbst gern und häufig benutzen. Haferbrei Bagels mit EiweißWas schmeckt...

Read More

Bist du dabei?

Ja, bitte sende mir den Yourdietangel Newsletter mit Rezepten, Erfolgsgeschichten, Terminen, Neuigkeiten Rund um Adipositasoperationen, Abnehmen und Adipositas – damit ich in Zukunft zu den Ersten gehöre, die neue Beiträge lesen.

Details zur mit umfassten Einwilligung zur Erfolgsmessung, zur Nutzung des Mail Dienstleisters Mailchimp, der Protokollierung der Anmeldung und der Möglichkeit, jederzeit selbstständig den Newsletter abzubestellen finden sich in der Datenschutzerklärung.

Success!

E-Mail-Adresse

Absenden

oder

Folge mir auf Instagram

Quellenangaben & Leseempfehlungen

(1) Nutritional Recommendations for Adult Bariatric Surgery Patients: Clinical Practice

(2) Chirurgie der Adipositas und metabolischer Erkrankungen

(3)  Clinical Practice Guidelines for the Perioperative Nutritional, Metabolic, and Nonsurgical Support of the Bariatric Surgery Patient—2013 Update: Cosponsored by American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery*

(4) Endocrine and Nutritional Management of the Post-Bariatric Surgery Patient: An Endocrine Society Clinical Practice Guideline

(5) Long-term Management of Patients After Weight Loss Surgery

(6) Nutrition Care for Patients with Weight Regain after Bariatric Surgery

(7) Changes in total energy intake and macronutrient composition after bariatric surgery predict long-term weight outcome: findings from the Swedish Obese Subjects (SOS) study.

(8) Nutrition Care for Patients with Weight Regain after Bariatric Surgery

(9) Weight regain after gastric bypass: etiology and treatment options

(10) Weight regain after Roux-en-Y gastric bypass has a large negative impact on the Bariatric Quality of Life Index

(11) Changes in total energy intake and macronutrient composition after bariatric surgery predict long-term weight outcome: findings from the Swedish Obese Subjects (SOS) study.

Der Beitrag Red Pesto Protein Bagels – Magenbypass Rezept erschien zuerst auf Abnehmen mit Magenverkleinerung.

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Protein Madeleines mit Aprikose und Schokolade

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Proteine Aprikosen Madeleines Rezept – Lowcarb

  Madeleines im Original mag ich überhaupt nicht. Die Konsistenz des Teigs war einfach nie meins. Ich liebe allerdings die Form. Wie eine kleine Muschel, das ist so niedlich und die Portionsgröße ist ideal, um ein proteinreiches Kuchenrezept zum Mitnehmen zu basteln.

  Diese leckeren kleinen Gebäckteilchen sind saftig und erinnern ein ganz kleines bisschen an Käsekuchen. Ich habe mich für Orangenschale und zuckerfreie Schokodrops entschieden, um den süßen kleinen Dingern einen meiner Lieblingsgeschmäcker zu verpassen. Zartbitter Schokolade mit Orange. Yum.

  Wollen wir direkt loslegen? Ich hab nämlich aktuell keine Zeit für Rezepte aber ich kenne euch, ihr wollt gern nachbacken, was ihr in meinen Storys seht.

      Zutaten Protein Madeleines

Ergibt 18 Stück / 3 Bleche

165 Gramm Ei (Vollei)

125 Gramm Skyr, natur oder Vanille (Werbung – unbezahlt – Vanille Skyr von Lidl hat den wenigsten Zucker)

50 ml Milch

20 Gramm Mandelmehl

15 Gramm Kokosmehl

20 Gramm Whey Isolat (Cookies and Cream oder Vanille, Auf Amazon anzeigen)

1 Teelöffel Flohsamenschalen (Auf Amazon anzeigen)

60 Gramm Aprikosen, klein gewürfelt (frisch). Trockenobst geht sicher auch, hat aber mehr Zucker.

1 Päckchen Orangenschale (z.B. Alnatura) oder Orangenabrieb

30 Gramm Schokodrops, zuckerfrei (Auf Amazon anzeigen)

1 Teelöffel Backpulver

Etwas Vanille und eine Prise Salz

    protein madeleines schokodrops

Zubereitung Protein Madeleines

  1. Backofen auf 160 Grad vorheizen, Madeleines Form herausstellen (Ich nutze diese hier – auf Amazon anzeigen)

2. Falls du nicht die hochwertige Silikon Backform nimmst, fette bitte deine Form gut ein. Der Teig haftet sonst fest. Ich hatte vorher die billige Silikonform für 10 Euro und da blieb ständig der Teig hängen.

3. Feuchte Zutaten in einer Schüssel mischen

4. Trockene Zutaten bis auf die Schokodrops und die Aprikosen in einer seperaten Schüssel gut vermischen.

5. Trockene Zutaten esslöffelweise zu den feuchten Zutaten rühren. Zuletzt die Schokodrops und die Aprikosenwürfel mit einem Kochlöffel unterheben.

6. Den Teig in die Förmchen verteilen und 5 Minuten quellen lassen, dann ab in den Ofen.

7. Je nach gewünschtem Bräunungsgrad und Ofen sind die Madeleines nach 12-15 Minuten fertig. Traditionell gehören sie relativ hell, denn auch hier schmeckt das Gebäck viel besser, wenn es vor dem Verzehr etwas erwärmt wird (z.B. auf dem Brötchenhalter des Toasters).

  Nährwerte  Aprikosen Schokoladen Protein Madeleines

Nährwerte pro Stück = 27 Gramm  (Zubereitet mit Vollmilch)

  Kalorien: 41

Fett: 2 Gramm

Kohlenhydrate: 1.7 Gramm

Protein: 3.6 Gramm

  Eine Portion entspricht circa 3 Madeleines

Proteine des Monats

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April

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Quellenangaben & Leseempfehlungen

(1) Nutritional Recommendations for Adult Bariatric Surgery Patients: Clinical Practice

(2) Chirurgie der Adipositas und metabolischer Erkrankungen

(3)  Clinical Practice Guidelines for the Perioperative Nutritional, Metabolic, and Nonsurgical Support of the Bariatric Surgery Patient—2013 Update: Cosponsored by American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery*

(4) Endocrine and Nutritional Management of the Post-Bariatric Surgery Patient: An Endocrine Society Clinical Practice Guideline

(5) Long-term Management of Patients After Weight Loss Surgery

(6) Nutrition Care for Patients with Weight Regain after Bariatric Surgery

(7) Changes in total energy intake and macronutrient composition after bariatric surgery predict long-term weight outcome: findings from the Swedish Obese Subjects (SOS) study.

(8) Nutrition Care for Patients with Weight Regain after Bariatric Surgery

(9) Weight regain after gastric bypass: etiology and treatment options

(10) Weight regain after Roux-en-Y gastric bypass has a large negative impact on the Bariatric Quality of Life Index

(11) Changes in total energy intake and macronutrient composition after bariatric surgery predict long-term weight outcome: findings from the Swedish Obese Subjects (SOS) study.

Der Beitrag Protein Madeleines mit Aprikose und Schokolade erschien zuerst auf Abnehmen mit Magenverkleinerung.