#hyper IgM syndrome

[centralbiohubgermany]

Zika Virus- causes, symptoms and prevention

What Exactly is Zika?

Zika virus disease is a mosquito-borne infectious disease highly prevalent in tropical and subtropical countries. It transmits through the bite of Aedes mosquitos (Ae. aegypti and Ae. albopictus). It can also transmit through the exchange of body fluids during sexual intercourse, blood transfusion, organ transplant and from the infected mother to the newborn. Usually, Zika virus infection is mild and self-limiting. However, in serious cases, it can lead to neurological disorders, congenital defects and Guillain-Barre syndrome (GBS).

What are the symptoms of Zika?

In general, the signs and symptoms of a Zika virus infection are mild and self-limiting. Although most patients remain asymptomatic throughout the early disease phase, usually, the patient develops a high-grade fever, fatigue, headaches, musculoskeletal pain, muscle pain, conjunctivitis, and maculopapular rashes in the later stages.

Pregnant women experience severe negative effects due to the teratogenicity of the Zika virus, which can result in congenital CNS abnormalities, including miccrocephaly, fetal death, and adverse pregnancy outcomes.

Prevention of Zika:

Complete avoidance of mosquito bites is the cornerstone to staying away from Zika virus infection. There is currently no authorized prophylactic vaccine for Zika virus infection. The following are effective methods to prevent Zika virus infection:

●       Avoid visiting Zika-affected areas.

●       Avoid having sexual contact with Zika patients.

●       If you have Zika, you should avoid getting pregnant.

●       Use insect repellents.

●       Wear long-sleeved shirts and pants to avoid mosquito bites.

●       To prevent mosquitoes from entering the house, use air conditioning and avoid opening doors and windows.

●       Sleep with mosquito nets.

●       Avoid standing water, which can be a breeding ground for mosquitoes.

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[mcatmemoranda]

Going through questions:

Chédiak–Higashi syndrome[1] (CHS) is a rare autosomal recessive disorder that arises from a mutation of a lysosomal trafficking regulator protein,[2] which leads to a decrease in phagocytosis. The decrease in phagocytosis results in recurrent pyogenic infections, albinism, and peripheral neuropathy.

Defect in neutrophil phagosome-lysosome fusion. Pyogenic bacteria = staph, strep, pneumococcus.

Cytotoxic (CD8+) T cells have a PD-1 receptor. Tumor cells can express programmed death ligand-1 (PD-L1), which binds to the PD-1 receptors on cytotoxic T cells. PD-L1 binding to the PD-1 receptor prevents cytotoxic T cells from doing their apoptotic function. This is how cancer cells evade destruction by cytotoxic T cells. The binding of PD-L1 to PD-1 receptor causes T cell exhaustion (inability of the T cell to induce apoptosis). Monoclonal antibodies against PD-1 or PD-L1 prevent PD-L1 interaction with PD-1 receptor, so cancer cells can't evade cytotoxic T cell destruction. Pembrolizumab, nivolizumab = PD-1 antibodies. Atezolizumab = PD-L1 antibody.

T lymphocytes release interferon gamma, which activates macrophages to express MHC-> Th1 differentiation. Viral and bacterial infection result in interferon gamma release from T lymphocytes and NK cells. Interferon Gamma Release Assay (IGRA) tests for latent TB; measures amount of interferon gamma released by T lymphs in response to M. tuberculosis antigens; measures cell-mediated immunity.

Mast cells release tryptase. Tryptase is released by mast cells in anaphylactic reactions. Serum tryptase level is used to diagnose anaphylaxis after the pt is stabilized.

The FceRI IgE on mast cells and basophils bind to the Fc portion of circulating IgE antibodies. Antigen binds to multiple IgEs, which causes aggregation of the FceRI receptors (the IgEs on basophils and mast cells)-> degranulation of histamine and tryptase from basophils and mast cells. Ok so this is more complex than I remember learning. I thought it was the IgEs that aggregate. It's specifically the FceRIs (high affinity IgEs) that aggregate. FceRI receptor on mast cells bind to the circulating IgEs. The the FceRIs aggregate via the antigen and that causes degranulation. Aggregation of the FceRIs activates a tyrosine kinase, which then causes degranulation.

Question 14 of my first immunology quiz has an explanation I want to draw a table from

Etanercept is a TNF-alpha inhibitor it links the Fc portion of human IgG1 to soluble TNF alpha receptors, functioning as a fusion protein. It functions as a decoy receptor, which binds all TNF alpha to keep it from binding to TNF alpha receptors. It treats rheumatoid arthritis when MTX fails to work.

Question 13 also has a figure I want to copy.

Azathioprine and mycophenolate inhibit nucleotide synthesis. This prevents B cells and T cells from proliferating. These are immunosuppresants. Azathioprine-> 6 mercaptopurine-> 6 Thioguanine active metabolites; the Thioguauanine metabolites inhibit purine synthesis. If you can't replicate your DNA/RNA, you can't reproduce, so azathioprine prevents B and T cells from proliferating. Activated T lymphs make IL-2, so less IL-2 will be made as well. Immunoglobulins come from plasma cells, which form from B cells. So azathioprine also reduces immunoglobulins (because azathioprine prevents the T cells from proliferating and you need T cells to activate B cells with the costimulatory response).

I got a question right because I remembered from watching an OnlineMedEd video yesterday that MHC Class I receptor is edited in the endoplasmic reticulum. Part of MHC Class I receptor is beta 2 microglobulin. Cells that are infected break up the pathogen in their cytoplasm and then send pieces of the pathogen (antigens) into the endoplasmic reticulum via the TAP receptor. Inside the ER, antigen is added to MHC Class I, then the MHC Class I-Antigen complex is sent to the cell membrane. TAP = Transporter Associated with Antigen Processing. Mutations in the TAP1 gene, which codes for TAP, lead to inability to bring antigen into the ER. So the pt gets granulomatous skin ulcers and respiratory infections even though lymphocyte and immunoglobulin levels are normal.

Pneumococcal conjugate vaccine (PCV13) induces a more robust immune response than the pneumococcal polysaccharide vaccine (PPSV23) because the conjugate vaccine causes B and T cell recruitment-> memory. The polysaccharide vaccine (PPSV23) doesn't create memory cells. PCV13 has a conjugated protein whereas PPSV23 doesn't. Pneumovax = PPSV23; Prevnar = PCV13.

In the blood vessels, bradykinin relaxes smooth muscle, causing vasodilation. But in smooth muscle that is not in the vasculature, bradykinin actually causes contraction of that non-vascular smooth muscle. So, bradykinin dilates blood vessels but constricts smooth muscle that is not in the blood vessels. That’s why it causes cough–it causes constriction of smooth muscle in the bronchi. Since bradykinin is degraded by ACE, when you inhibit ACE with ACEIs such as lisinopril, you stop breakdown of bradykinin–> increased vasodilation and bronchoconstriction. That’s why ACEIs can cause angioedema and cough.

Bradykinin vasodilates-> angioedema (fluid leaves blood vessels).

Hereditary angioedema is AD; can also be due to ACEIs. In hereditary angioedema, pts lack C1 esterase inhibitor, which is normally involved in break down of bradykinin. So no C1 esterase inhibitor-> increased bradykinin-> angioedema. Dx hereditary angioedema with low serum C1 esterase inhibitor and C4 levels. C1 esterase inhibitor suppresses C1-> no classic complement pathway. Kininogen is converted to bradykinin by kallikrein. C1 esterase inhibitor inhibits kallikrein-> decreased bradykinin. So of course without C1 esterase inhibitor, you have increased kallikrein-> more bradykinin.

In germinal centers in lymph nodes, B cells undergo somatic hypermutation, which is what allows the B cells that can respond to a particular antigen to proliferate. Somatic hypermutation = immunoglobulin mutation.

Serum sickness = type III hypersensitivity reaction (antigen-antibody complexes in tissues); occurs 1 to 2 weeks after being exposed to non-human proteins. Pts present with vasculitis, arthralgia, fever, rash, low C3 and C4. Histologically, you see fibrinoid necrosis and infiltrating neutrophils. Low complement occurs because complement-fixing IgM and IgG are in the immune complexes.

Hyper IgM syndrome = X-linked recessive deficiency of CD40L (CD40 Ligand located in T cells and necessary to interact with CD40R on B cells); causes recurrent pulmonary and sinus infections, GI infection, infection with opportunistic bugs (e.g., cryptosporidium), failure to thrive. Pts have lots of IgM, but little IgG, IgA, and IgE. B cells have trouble class switching (because the CD40L-CD40R interaction is necessary to create the costimulatory signal that causes B cell class switching and proliferation). Class switching occurs when heavy chain constant region genes are spliced out so the B cell can create the isotype of immunoglobulin it needs to make. That doesn't happen in Hyper-IgM syndrome because the CD40R-CD40L initeraction necessary to cause that can't happen when there's deficient DC40L. CD40 deficiency is autosomal recessive form of this disease. If B cells don't class switch, they stay as IgM-secreting cells.

Severe Combined Immunodeficiency (SCID) = autosomal recessive adenosine deaminase (ADA) deficiency. Adenosine deaminase deficiency leads to accumulation of adenosine in T cells and B cells (lymphocytes)-> cellular and humoral immunodeficiency. Tx: gene therapy; hematopoietic stem cell transplant. X-linked SCID is more commone than ADA deficiency. No lymphocytes-> bacterial, viral, and fungal infections.

Henoch-Schonlein Purpura (HSP) = small vessel leukocytoclastic angiitis + deposition of IgA-C3 complexes in skin and GI tract. It's a hypersensitivity reaction related to recent infection. Pts have a purpuric rash, arthralgia, abdominal pain. Can lead to acute glomerulonephritis. Occurs in kids.

[doctorfoxtor]

I've genuinely been saying TIL way, WAY too often lately

100 days of productivity

Day 11

CVS/RS

HOCM: although beta-blockers/non-DHP Ca blockers are first line drugs to prevent or control symptoms, ACEis/ARBs MUST be started in all patients as there is evidence that they arrest the septal hypertrophy (or can even reverse it!) (angiotensin II and aldosterone are said to accelerate the hypertrophy; so are beta-1 agonists but with poorer evidence)

other than antiRAAS drugs and nitrate-hydralazine, ivabradine also has a mortality-reducing effect in CHF, specifically in patients with sustained HR > 70 bpm despite maximum beta blockade

atorvastatin fucks with digoxin, but ONLY atorvastatin fucksn't with warfarin

although verapamil is a contraindication to adenosine due to the risk of precipitating heart block, beta blockers are not

reversed split S2 in LBBB (P2 followed by A2)

Endo/Repro

haemochromatosis: pituitary dysfunction and hypogonadism are *not reversible*; hormone replacement is the mainstay of therapy

isolated FSH deficiency → ↓androgen binding proteins → oligospermia

toxic adenoma: 300-500 megabecquerels of radioiodine is 1st line; surgical excision is *second line* (radioiodine is preferentially taken up by adenomatous tissue bc it takes up iodine at a fast rate, and ↓TSH means the rest of the gland takes up much less iodine)

checkpoint inhibitors in oncology lead to persistent immune activation, but this may lead to loss of self tolerance especially against endocrine organs; this may lead to thyroiditis, adrenalitis, hypophysitis, endocrine pancreatitis etc; it is important to screen for the maintenance of the hormonal axes in patients on such drugs (eg, nivolumab, ipilimumab)

Rheum/Derm

increased BMI (without diabetes) is actually generally *protective* against osteoporosis d/t ↑oestrone (adipose oestrogen)

ANAs are mostly IgG; much less common are IgA and IgM ANAs

osteomyelitis: plain films are for screening, MRI is definitive

tennis-racquet Brisbeck granules on biopsy of a bone lesion → Langerhans cell histiocytosis

presence of pruritus is circumstantial evidence for bullous pemphigoid over pemhigus vulgaris

osteoporosis risk is high with steroid equivalent to prednisolone 7.5 mg/day over 3 months (or more); if it is anticipated that a patient might need such a long dose of steroids, start prophylaxis *immediately* with vitamin D + calcium + alendronate

Renal/Biochem/Toxo

natriuresis/hyponatraemia despite volume loss = suspect RAAS deficiency (eg, primary adrenal insufficiency)! SIADH does NOT explain profound hyponatraemia when volume depletion is evident, as aldosteronergic drive is usually sufficient to keep sodium levels as high as possible

FB GoT All Hyper about Liddle syndrome: Furosemide toxicity mimicks Bartter syndrome, Gitelman syndrome mimicks Thiazide toxicity and HyperAldosteronism mimicks Liddle syndrome

platinum compounds → hypomagnesaemia

GIT

pigment laden macrophages on colon biopsy = melanosis coli → stimulant laxative abuse

CNS/Ophthal/ENT

absent ankle jerk + positive Babinski: 3 major differentials: syrinx, motor neuron disease or subacute combined degeneration (SCD can have either exaggerated, decreased or absent reflexes)

sacral sparing = maintenance of sensation/power in central cord syndrome (eg, intramedullary metastatic tumour and syringes) and incomplete spinal cord injury due to peripheral arrangement of sacral spinothalamic fibres (test with lack of saddle anaesthesia; reduction deep touch sensation is sensitive for severity of cord injury)

orbital apex syndrome → optic neuropathy, 6th nerve palsy, proptosis, chemosis/injection, miosis, ptosis

Kearns-Sayer syndrome: MERT: Mitochondrial inheritance, External ophthalmoplegia, Retinitis pigmentosa, Teenage onset (<20 yrs)

Refsum disease: CANID: Cerebellar ataxia, Anosmia, Neuropathy, Icthyosis, Deafness

when deprescribing benzos, switch to equivalent dose of diazepam and reduce by 1/8ths every 2 weeks (typically 2 mg per 2 weeks); reinstate previous dose if patient withdraws, then after another 2 weeks try to reduce the dose again

[healthcare-market]

Primary Immunodeficiency Market is Booming Worldwide Scrutinized in New Research

Primary Immunodeficiency Market: Introduction

Transparency Market Research has published a new report titled, ‘Global Primary Immunodeficiency Market ’. According to the report, the global primary immunodeficiency market was valued at US$ 5.7 Bn in 2019 and is projected to expand at a CAGR of ~6% from 2020 to 2028. The primary immunodeficiency disorders (PIDs) are clinically heterogeneous disorders, the majority of which arise from genetic defects in immunologically relevant genes. Primary immune deficiencies are present in a heterogeneous manner, and a high index of suspicion is required to diagnose primary immune deficiencies. Any patient with a suspected or proven primary immunodeficiency disorder (PID) should be referred to the care of a clinical immunologist. Immune dysregulation phenotypes of PID are commonplace and include multiorgan autoimmunity, malignancy (particularly hematological), and autoinflammatory pathology such as periodic fever syndromes.

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In terms of type, the global primary immunodeficiency market has been segmented into antibody deficiency, cellular deficiency, and innate immune. Antibody deficiency has been categorized into agammaglobulinaemia, common variable immune deficiency, selective IgA deficiency, IgG subclass deficiency, and others. Cellular deficiency has been classified into Ataxia Telangiectasia, hyper IgM syndromes, Wiskott-Aldrich syndrome, DiGeorge syndrome, and others. Innate immune has been split into complement deficiencies, hyper IgE syndrome, and others. The antibody deficiency segment captured the largest market share in 2019. The segment is expected to expand at the highest CAGR during the forecast period, owing to rise in need and demand for diagnosis by patients.

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Based on treatment type, the global primary immunodeficiency market has been divided into immunoglobuline replacement therapy, antibiotic therapy, stem cell and gene therapy, and others (vaccines, nutritional supplements, and others). The immunoglobuline replacement therapy segment captured the largest market share in 2019. The segment is expected to expand at the highest CAGR during the forecast period due to increase in need and demand for diagnosis by patients.

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Primary Immunodeficiency Market: Prominent Regions

North America held a major share of the global primary immunodeficiency market in 2019. Highly structured healthcare industry, presence of key players, and growth strategies of these players are the major factors driving the market in the region. Rise in awareness about benefits of procedures and increase in healthcare expenditure also contribute to the growth of the market in North America. Asia Pacific held the second largest share of the global primary immunodeficiency market in 2019. Growth of the primary immunodeficiency market in the region can be attributed to rise in prevalence of chronic diseases and well-developed health care sector in the region. The market in Asia Pacific is expected to grow at a rapid pace during the forecast period. Increase in the number of people with cardiovascular diseases, product approvals, and rise in awareness about cardiovascular diseases which ultimately lead to regular checkup and diagnosis, are factors anticipated to fuel the growth of the primary immunodeficiency market in the region.

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Primary Immunodeficiency Market: Key Players

Key players are expanding their footprint to strengthen their position in the global primary immunodeficiency market. Gradual increase in incidence of primary immunodeficiency diseases globally offers lucrative opportunities to key players to increase their share in the primary immunodeficiency market. Hence, manufacturers are engaging in new product development, collaborations, and distribution to gain market share. Leading players operating in the global primary immunodeficiency market include Shire plc, CSL Behring, Kedrion Biopharma Inc, Grifols, S.A., Octapharma, China Biologic Products Holdings, Inc., Biotest AG, Sanquin, and LFB SA.

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[biomedres]

Journals on Biomedical Engineering - BJSTR Journal

Plantibodies: A New Approach for Immunomodulation in Human Health by Anurag Malik in Biomedical Journal of Scientific & Technical Research https://biomedres.us/fulltexts/BJSTR.MS.ID.002061.php Antibodies or immunoglobulins are the vital component of adaptive immune system in mammals. These are mainly present in the body fluid and constitute an assembly of glycoproteins released by B-cells. B-cells constitute the humoral type of adaptive immune system. They are highly specific their mode of action. First they recognize their target specifically, binds to the antigen/toxin of pathogen and produce and elicit the immune response. These features permit immunoglobulins to be employed in diverse range of applications such as diagnosis, prevention and treatment [1]. Production of defective antibody response results in increased vulnerability to pyogenic infections due to impairment in B-cell function, e.g. in hyper-IgM syndrome as a result of improper signaling between B and T cells and in X-linked agammaglobulinemia. To overcome these defects, constant region of a human immunoglobulin is modified by transgenic approach to create recombinant antibody [2]. With this advancement, a new expectation of a reliable, inexpensive cure for diseases like, diabetes and cancer was awakening; but the major drawback was its cost ineffectiveness.  Hence, production of cost-effective and scalable platforms that is safe for therapeutics is urgently required [3]. Transgenics is one of the most potential applications in therapeutics for the preparation of various biological substances such as antibodies, proteins and vaccines. They can be produced from plants by transforming antibody-coding genes from humans to plants as ‘transgene’. Plants acts as suitable host for production of antibodies referred as “plantibodies”. Fore more articles on Journals on Biomedical Engineering please click here bjstr Follow on Twitter : https://twitter.com/Biomedres01 Follow on Blogger : https://biomedres01.blogspot.com/ Like Our Pins On : https://www.pinterest.com/biomedres/

[siva3155]

300+ TOP DISEASE ASSOCIATED with IMMUNE SYSTEM Objective Questions and Answers

DISEASE ASSOCIATED with IMMUNE SYSTEM Multiple Choice Questions :-

1. The HIV virus infects primarily A. brain cells B. cells in the immune system C. red blood cells D. liver cells Answer: B 2. Chronic granulomatous disease results from a failure to perform oxidative burst. This deficiency would be most likely to interfere with A. CTL killing of viruses B. dendritic cell activation to become a mature APC C. infected cell processing of virus peptides D. macrophage intracellular killing of bacteria Answer: D 3. Difficulties with somatic gene therapy arise from all of the following except A. GVHD caused by mature T cells in the transplanted cells B. inserting a gene so that it will function properly C. limited life span of more mature hematopoietic cells D. transducing genetic material into stem cells Answer: A 4. A monoclonal antibody (mAb) specific for the 2,4-dinitrophenyl (DNP) hapten might also bind A. Leu or Ileu B. His or Pro C. Tyr or Phe D. Ser or Thr Answer: C 5. Retinoblastoma is due to a mutation in a A. kinase B. tumor supressor C. cyclin D. viral gene Answer: B 6. An autoimmune disease is A. AIDS B. Measles C. Lupus D. Mumps Answer: C 7. If Class IIMHC is not expressed in the thymus, the resulting immune deficiencies would include all of the following except reduced A. alternative complement activation. B. CD8 T cell-mediated cytotoxicity C. macrophage activation to vesicular pathogens D. IgG synthesis Answer: A 8. Specific translocations are associated with A. colon cancer B. breast cancer C. pancreatic cancer D. some leukemias Answer: D 10. The primary reason for AIDS, a deadly disease is that it A. is caused by a virus B. is caused by a bacterium C. destroys key components of the body's internal defense system D. causes a breakdown of the body's inflammatory response Answer: C

DISEASE ASSOCIATED with IMMUNE SYSTEM MCQs DISEASE ASSOCIATED with IMMUNE SYSTEM Objective type Questions with Answers 11. A selective IgA deficiency would be expected to result in problems with A. bacterial infections B. infections following dental work due to bacteria entering the bloodstream C. mucosal pathogens D. pathogens which can survive inside macrophages Answer: C 12. Combined cellular and humoral immune deficiencies result from lack of all of the following except A. a thymus B. class II MHC C. HIV infection of CD4+ T cells D. transporter of antigen peptides (TAP) Answer: D 13. An example of an immunodeficiency disorder is A. thyroiditis B. rheumatic fever C. systemic lupus erythematosus D. AIDS Answer: D 14. Bone marrow given to an infant with SCID must A. be irradiated to eliminate GVHD B. contain mature T cells that can begin making immune responses immediately C. come from a donor that shares some MHC alleles with the recipient D. come from one of the child's parents Answer: C 15. X-linked hyper IgM syndrome, resulting in high levels of serum IgM and low levels of serum IgG, is caused by a defect in CD40L expression. The specific immune event that would be prevented by a defective CD40L would be A. activation of B cells by T-independent antigens B. failure of B cells to provide co-stimulation for Th2 activation C. failure of Th2 cells to provide co-stimulation for B cell isotype switching D. failure of Th2 cells to provide co-stimulation for B cell proliferation Answer: C 16. DiGeorge's syndrome is characterized by the lack of a thymus The mouse model closest to this human disease would be a A. knock-out mouse for RAG-1 and RAG-2 B. knock-out mouse for a thymus C. nude mouse D. recombinant mouse for CD3 Answer: C 17. Which of the Rous sarcoma virus has a homologous cellular protein? A. c-src B. v-src C. v-ha-src D. v-ha-ras Answer: A 18. Infants are most susceptible to bacterial infection due to low circulating levels of IgG A. in utero (before birth) B. at 0-3 months of age C. at 3-12 months of age D. at 12-24 months of age Answer: C 19. The chemical, typically released by the body in an allergic response is A. histamine B. allergens C. antihistamines D. perforins Answer: A DISEASE ASSOCIATED with IMMUNE SYSTEM Questions and Answers pdf Download Read the full article

[juniperpublishers-oajnn-blog]

Embolic Stroke and Nephrotic Syndrome: A Case Report and Literature Review

Authored by  X Michelle Androulakis

Abstract

Nephrotic syndrome (NS) is less commonly associated with arterial thrombosis than venous thrombosis. We report a case of a 43-year- oldwomanwho presented with an acute embolic stroke confirmed on MRI, about 3 months after the diagnosis of NS. The standard stroke evaluations did not show evidence ofcardiac source of embolism, large vessel atherosclerosis or any primary hypercoagulable disorders. Laboratory tests revealed impaired renal function and extremely high nephrotic range proteinuria and a renal biopsy showed primary membranous glomerulonephropathy. Subsequently, she was discharged on anticoagulation and responded well to the treatment. This case illustrates the importance of considering hypercoagulable evaluation due to nephrotic syndrome as a potential cause of embolic stroke, and the initiation of anticoagulation therapy in a timely manner. We also present a literature review on the association between nephrotic syndrome and acute stroke.

Keywords: Stroke; Nephrotic syndrome; Hypercoagulable state; Arterial thrombosis

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Introduction

It has been shown that patients with nephrotic syndrome (NS) are prone to thrombo-embolic phenomena [1, 2]. The risk of thrombo embolism is increased during the first 6 months of the onset of NS3. In adults with NS, arterial thrombo embolic events are not as well characterized and less commonly reported than venous thrombo embolism [4]. Acute ischemic stroke is a rare complication of NS [5,6,7] and this link has not been widely reported in the literature.

Although the exact pathogenesis of cerebral infarction is not clearly understood, it has been postulated that a hyper coagulable state in NS may play an important role in ischemic stroke [3,8]. Few studies have suggested that hyper coagulability in NS is associated with the steroid and diuretic administration [9]. Although there are case reports of NS and stroke [7,10-16], we report this case to illustrate the importance of considering hypercoagulability from NS as a potential cause of embolic stroke, and to initiate anticoagulation treatment if appropriate. Additionally, we performed an extensive literature search for NS and association with ischemic stroke.

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Case Report

A 43-year-old, left-handed, woman presented with sudden onset of left sided weakness and word finding difficulty three months after the diagnosis of NS. Her other pertinent medical history included COPD, hypertension and was a smoker, with no significant family history for coagulation disorders. NS with membranous glomerulonephropathy was confirmed with biopsy during this admission. Medication history at the time of presentation included cyclophosphamide, prednisone, spironolactone, Lasix, Lisinopril and metoprolol. Her vitals were stable at presentation and general physical examination was benign. Her neurologic examwas significant for mild anomia and left sided weakness. Her laboratory tests showed significant proteinuria, mild hyperlipidemia and the standard hypercoagulable workup was normal. Other laboratory values are as detailed in Table 1.

Further work up included an MRI which revealed bi hemispheric regions of diffusion restriction, consistent with acute infarcts (Figure 1). Her cardiac work up was essentially normal. Vascular imaging of the brain was obtained with a CT angiogram which showed a left MCA occlusion at the M3- M4 segments, without evidence of any proximal large artery atherosclerosis. Given the bihemispheric infarcts, an underlying embolic source was likely. After an exhaustive cardiac work up did not reveal any source of cardio embolism, the possibility of hypercoagulability with significant proteinuria due to NS was considered the likely etiology, and anticoagulation was initiated.

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Literature Review

Systematic searches of peer-reviewed, published, research papers indexed in PubMed, EMBASE, and Science Direct from inception until Nov. 2016 were undertaken using key search terms related to ‘Nephrotic Syndrome', ‘ischemic stroke', and ‘infarction'. We identified 30 reported cases of acute ischemic strokes with NS after eliminating 10 cases with nephropathy related to DM. The age at the presentation ranged from 14 -73 years with a mean age of 40.7, and standard deviation 15.7 years. 70% of the cases (21/30) were male. Among 30 there were only 5 cases without a biopsy-proven diagnosis of NS, most of the cases (8/30) were membranous disease. The other cases were associated with Memberano proliferative Glomerulo nephritis, minimal change disease, IgA nephropathy, IgM nephropathy, Focal Segmental Glomerulo sclerosis and nodular glomerulopathy (Table 2). These infarcts have been described in various vascular distributions.

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Discussion

In this case of acute embolic stroke in the setting of NS (primary membranous glomerulopathy) with a normal coagulation profile, the initial differential diagnoses for the etiology of the embolic infarcts werecardioembolism, atherombolism and a primary hypercoagulable state. The work up for these, as outlined in the case were negative. Our standard hypercoagulable panel was normal in this case, butthis maybe confounded by the concomitant use of steroids. Other clotting factors that are not included in the standard hypercoagulable panel may be affected due to large amounts of urinary protein loss [17]. Marsh et al reported a similar case of stroke in NS with normal coagulation profile except for activated free protein S level [5]. As Fibrinogen is an acute phase reactant and has been associated with elevations in acute stroke with uncertain prognostic value, the fibrinogen level was not checked in our case. [18,19] Increased fibrinogen levels after vascular event is associated with recurrence of stroke and MI [20]. As the likelihood of hypercoagulability secondary to NS was high on the differential, she was discharged on anticoagulation and high intensity statin. She has remained stable since then, with no further vascular events.

Thrombosis is a major complication of NS. Although both arterial and venous thromboses occur, arterial thrombosis is rare and has been described in the femoral arteries commonly [7], but not in cerebral vasculature. Venous thrombosis is more common in the adult patient population while arterial thrombosis is more common in the pediatric patient population [4]. Primary hypercoagulable states like congenital or hereditary deficiencies of protein C, protein S and antithrombin-IIIare relatively rare inherited conditions that lead to endothelial dysfunction [21].

Secondary hypercoagulable states can be associated with underlying conditions such as pregnancy, malignancy, NS or oral contraceptive use [21]. Hypercoagulable states result from the imbalance between the pro-coagulant and anticoagulant factors. The primary glomerular defect in NS results in leakage of high amount of high molecular weight protein, which consist many hemostatic regulatory proteins [22,23]. The overall hypoproteinemia is compensated by increased hepatic synthesis of high molecular weight clotting factors V, VII, VIII and X [24,25]. Increased urinary excretion of natural anticoagulant protein S, anti-thrombin III [26,27] has been reported.

Taken together, the net hemostatic balance is shifted towards a pro-coagulable state. As steroids may increase the concentration of anti-thrombin III and factor VIII [10], the levels of these clotting factors can be normal in NS patients taking steroids. Furthermore, diuretics can also lead to hypercoagulability due to hypovolemia and hemoconcentration. NS is also associated with thrombocytosis and platelet hyperaggregability [25]. In addition, immunologically mediated glomerular damage triggers extrinsic coagulation pathway and thus hypercoagulability [28]. Our review of current literature suggests that most of the acute stroke cases in NS are amongst young, predominantly male patients, and have relatively fewer other vascular risk factors. Hypercoagulable panels were not consistently abnormal, which is indicative of the limitations of current standard laboratory testing for this type of patients.

Go to

Conclusion

In patients with cryptogenic ischemic stroke with concomitant nephrotic syndrome, anticoagulation for the secondary prevention of stroke and other thrombo-embolic events should be considered. Future prospective or randomized trials are needed to evaluate the link between NS and acute stroke as well as efficacy of anticoagulation therapy.

For more open access journals in juniper publishers please click https://juniperpublishers.com/

For more articles on Open Access Journal of Neurology & Neurosurgery Please click on https://juniperpublishers.com/oajnn/

Open Access Journal of Neurology & Neurosurgery in Full text in Juniper Publishers

https://juniperpublishers.com/oajnn/OAJNN.MS.ID.555591.php

[raymondmccullers]

Synthetic cells capture and reveal hidden messages of the immune system

New research is highly relevant to how antibodies are made in response to infections, vaccines and in autoimmunity due to the its analysis of a signal that is associated with hyper IgM syndrome, a genetic deficiency of CD40 ligand (CD40L) that results in profound immunodeficiency. Synthetic cells capture and reveal hidden messages of the immune system syndicated from https://triviaqaweb.blogspot.com/

[ihealthcareanalyst]

Worldwide Primary Immunodeficiency Statistics: Patients, Trends, Market

Primary immunodeficiencies (PI) are defects of the immune system that cause severe, sometimes life threatening, infections if not diagnosed and treated appropriately. Many patients with PI are undiagnosed, underdiagnosed, or misdiagnosed. There are at least 300 genetically defined single-gene inborn errors of immunity. Recent studies have shown that PI may be more common than previously estimated and that as many as 1–2% of the population may be affected with a PI when all types and varieties are considered. Over the last decade, improvements in molecular diagnosis, genetic sequencing, and cutting edge research and treatments have led to a better understanding of the immune system, as well as improved quality of life for those living with PI. However, awareness of PI among physicians and the general public remains challenging, and there continues to be a need for improved and timely management of these conditions.

The global primary immunodeficiency diseases market by disease type (Antibody deficiency – Agammaglobulinaemia, Common variable immune deficiency, IgG subclass deficiency, SIgAD; Cellular immunodeficiency – Ataxia Telangiectasia, DiGeorge syndrome, Hyper IgM syndromes, Wiskott-Aldrich syndrome; innate immune disorders – Complement deficiencies, and Hyper IgE syndrome), test type (blood and prenatal testing), treatment modality (immunoglobulin replacement therapy, antibiotics therapy, stem cell and gene therapy, etc.), and by geography (regional and country based) into North America (U.S., Canada), Latin America (Brazil, Mexico, Rest of LA), Europe (U.K., Germany, France, Italy, Spain, Rest of EU), Asia Pacific (Japan, China, India, Rest of APAC), and Rest of the World. The global primary immunodeficiency diseases market report also provides the detailed market landscape, market drivers, restraints, opportunities), market attractiveness analysis and profiles of major competitors in the global market (Baxter International, Inc., Bio Products Laboratory, Biotest AG, CSL Behring LLC, Grifols S.A., Kedrion S.p.A., LFB S.A., and Octapharma AG.) including company overview, financial snapshot, key products, technologies and services offered, and recent developments.

Global Patient Surveillance 2015

In 2015, the distribution of patients diagnosed with PI based on the categories defined by the IUIS Expert Committee for the Classification of PI, predominantly Antibody Deficiencies are reported by physicians to be 63.4% in the US, 47.7% internationally, and 53% globally. Well-defined Syndromes with Immunodeficiency was 16. % in the US, 11.2% internationally, and 12.9% globally. As a percentage of all patients identified with a specific defect, Antibody Deficiencies account for 57 % of all patients identified with a specific defect.

Based on the 15 most prevalent PI defects and percentage of each defect by region, Selective IgA deficiency is the most prevalent with 16.4% in the US, 13.0% internationally, and 14.1% globally. Common variable immunodeficiency (CVID) showed a prevalence of 15.4% in the US, 11.2% internationally, and 12.6% globally. It is noteworthy that Canada and Australia had 25.5 and 39.5% prevalence for CVID, respectively. The Middle East reported 30.5% Familial Mediterranean fever compared to 3.3% globally. Africa reports 6.5% Ataxia telangiectasia (A-T) compared to 2.6% globally, and 8.7% other combined immunodeficiencies compared to 1.5% globally.

With respect to gender and age, male patients accounted for 58.3% globally, while female patients accounted for 41.7%. In the US, 55.7% of the patients were male and 44.3% of patients were female. Globally, 63 % of the patients were 19 years of age or younger, while 37% were 20 years of age or older.

Treatment Modalities 2015

There was a 19% overall increase in patients receiving IgG. There was an increase of 7% in all patients receiving intravenous immunoglobulin therapy (IVIG) and a 100% increase in patients receiving subcutaneous immunoglobulin (SCIG). Of all patients diagnosed with a PI defect, 24.3% are on immunoglobulin replacement therapy. As to all patients with an Antibody Deficiency, 42.9% are treated with IVIG/SCIG. It is noteworthy that there was a 27% increase in the number of patients receiving IVIG in the hospital or clinic. There was a decrease of 49% in the number of patients receiving IVIG at home. This decrease was more than offset by an increase of nearly 100% in patients receiving SCIG. Latin America reported 87% of their patients receiving IgG are treated in the clinic or hospital compared to 55 % globally. In the US, 30% of patients receiving IgG are treated at home compared to 14% globally. Western Europe reported 46% of their patients requiring IgG receive SCIG compared to 28 % globally.

There were commensurate increases in patients receiving other treatments for PI as well. The number of patients treated with PEG-ADA increased by 44%. There was a 22% overall increase in patients treated by HSCT or thymus transplantation, with the number of patients receiving matched donor transplants, matched unrelated donor transplants, mismatched unrelated donor transplants, and parental haplo transplants increasing by 28.6, 17.6, 5.5, and 15.6%, respectively. Use of bone marrow as the source of stem cells increased by 17.4%, while cord blood as the stem cell source increased by 66%. While there was a 22% increase in the number of patients having received HSCT, specific stem cell sources varied significantly by region and source. Latin America reported 74% of the transplants were bone marrow, as opposed to 61% globally. Middle East reported 35% of the transplants were peripheral stem cells as opposed to 22% globally. There was a 65% overall increase in cord blood transplants in the past 2 years. Asia reported 42% of the transplants were cord blood, compared to 16% globally.

Salient Features of the report (Primary Immunodeficiency Diseases Market):

1. Botttom-up research methodology (assumptions) for market size estimation and forecast 2. Global Number of patient population for PID (subtypes) by country, 2013 & 2015 3. Global Number of patient population for treatment or therapy by country, 2013 & 2015 4. Global Number of PID Patients, by 15 Most Commonly Identified PID, 2013 & 2015 5. PID Patient’s Gender and Age – Global Comparative Analysis, 2013 & 2015

- https://www.ihealthcareanalyst.com/worldwide-primary-immunodeficiency-statistics-patients-trends-market/

[mcatmemoranda]

[healthcare-market]

Primary Immunodeficiency Market Estimated to Record Highest CAGR by 2028

Primary Immunodeficiency Market: Introduction

Transparency Market Research has published a new report titled, ‘Global Primary Immunodeficiency Market ’. According to the report, the global primary immunodeficiency market was valued at US$ 5.7 Bn in 2019 and is projected to expand at a CAGR of ~6% from 2020 to 2028. The primary immunodeficiency disorders (PIDs) are clinically heterogeneous disorders, the majority of which arise from genetic defects in immunologically relevant genes. Primary immune deficiencies are present in a heterogeneous manner, and a high index of suspicion is required to diagnose primary immune deficiencies. Any patient with a suspected or proven primary immunodeficiency disorder (PID) should be referred to the care of a clinical immunologist. Immune dysregulation phenotypes of PID are commonplace and include multiorgan autoimmunity, malignancy (particularly hematological), and autoinflammatory pathology such as periodic fever syndromes.

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In terms of type, the global primary immunodeficiency market has been segmented into antibody deficiency, cellular deficiency, and innate immune. Antibody deficiency has been categorized into agammaglobulinaemia, common variable immune deficiency, selective IgA deficiency, IgG subclass deficiency, and others. Cellular deficiency has been classified into Ataxia Telangiectasia, hyper IgM syndromes, Wiskott-Aldrich syndrome, DiGeorge syndrome, and others. Innate immune has been split into complement deficiencies, hyper IgE syndrome, and others. The antibody deficiency segment captured the largest market share in 2019. The segment is expected to expand at the highest CAGR during the forecast period, owing to rise in need and demand for diagnosis by patients.

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Based on treatment type, the global primary immunodeficiency market has been divided into immunoglobuline replacement therapy, antibiotic therapy, stem cell and gene therapy, and others (vaccines, nutritional supplements, and others). The immunoglobuline replacement therapy segment captured the largest market share in 2019. The segment is expected to expand at the highest CAGR during the forecast period due to increase in need and demand for diagnosis by patients.

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Primary Immunodeficiency Market: Prominent Regions

North America held a major share of the global primary immunodeficiency market in 2019. Highly structured healthcare industry, presence of key players, and growth strategies of these players are the major factors driving the market in the region. Rise in awareness about benefits of procedures and increase in healthcare expenditure also contribute to the growth of the market in North America. Asia Pacific held the second largest share of the global primary immunodeficiency market in 2019. Growth of the primary immunodeficiency market in the region can be attributed to rise in prevalence of chronic diseases and well-developed health care sector in the region. The market in Asia Pacific is expected to grow at a rapid pace during the forecast period. Increase in the number of people with cardiovascular diseases, product approvals, and rise in awareness about cardiovascular diseases which ultimately lead to regular checkup and diagnosis, are factors anticipated to fuel the growth of the primary immunodeficiency market in the region.

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Primary Immunodeficiency Market: Key Players

Key players are expanding their footprint to strengthen their position in the global primary immunodeficiency market. Gradual increase in incidence of primary immunodeficiency diseases globally offers lucrative opportunities to key players to increase their share in the primary immunodeficiency market. Hence, manufacturers are engaging in new product development, collaborations, and distribution to gain market share. Leading players operating in the global primary immunodeficiency market include Shire plc, CSL Behring, Kedrion Biopharma Inc, Grifols, S.A., Octapharma, China Biologic Products Holdings, Inc., Biotest AG, Sanquin, and LFB SA.

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[ruggerorespigo]

Synthetic cells capture and reveal hidden messages of the immune system

New research is highly relevant to how antibodies are made in response to infections, vaccines and in autoimmunity due to the its analysis of a signal that is associated with hyper IgM syndrome, a genetic deficiency of CD40 ligand (CD40L) that results in profound immunodeficiency. Latest Science News -- ScienceDaily https://www.sciencedaily.com/releases/2019/09/190917075826.htm

[coollanceassignments-blog]

Medical Microbiology 7th Edition Test Bank

Follow Below Link to Download File

 https://homeworklance.com/downloads/medical-microbiology-7th-edition-test-bank/

 We also Do 100% Original and Plagiarism Free Assignment / Homework and Essay

 Email us for original and Plagiarism Free Work At ( info.homeworklance@gmail.com ) or order us at (https://homeworklance.com/custom-order/ )

  View Sample Chapter Below:

 Murray: Medical Microbiology, 7th Edition

 Chapter 10: Immune Responses to Infectious Agents

 Test Bank

 MULTIPLE CHOICE

 1.    What is the first antibody produced when an invading microorganism is initially encountered?

a.

IgA

b.

IgD

c.

IgE

d.

IgG

e.

IgM

 ANS: E

 2.    A 5-day-old baby is brought back to the hospital with signs of sepsis, is not thriving, and has vesicular lesions on his scalp at the site of monitor attachment. Why is a baby susceptible to a more serious outcome with this infection than an older child or adult?

a.

Immunosuppression from the mother

b.

Infection of a site closest to the brain

c.

Lack of IgA production

d.

Low levels of interferon-γ production

e.

More rapidly growing cells

 ANS: D

 3.    Endotoxin initiates septic responses by binding to:

a.

NF-κB

b.

Complement receptor 3d

c.

Toll-like receptor 4

d.

C-reactive protein

e.

ICAM 1

 ANS: C

 4.    Endotoxin induces production of which cytokines by macrophages?

a.

IL-1, TNF-α, IL-6

b.

IL-2, IL-4, IL-6

c.

IL-4, IL-5, IL-10

d.

IL-2, IFN-γ, TNF-β

e.

TGF-β, IL-10, IL-17

 ANS: A

 5.    Which of the following cytokines is required to initiate a protective helper T cell immune response to measles virus?

a.

IL-1

b.

IL-4

c.

IL-8

d.

IL-10

e.

IL-12

 ANS: E

 6.    Treatment with which cytokine makes the macrophage more efficient at killing bacteria?

a.

Interferon alpha

b.

Interferon gamma

c.

TGF-β

d.

GM-CSF

e.

IL-2

 ANS: B

 7.    M. tuberculosis becomes reactivated in an AIDS patient because:

a.

CD8 T cells cannot kill the bacteria.

b.

Neutrophils do not become activated.

c.

Macrophages do not get an activation signal.

d.

B cells stop making protective antibody.

e.

CD4 T cells stop making TGF-β.

 ANS: C

 8.    Identify which deficiency would most compromise a protective immune response to E. coli sepsis.

a.

IgG

b.

IgE

c.

CD8 T cells

d.

Mast cells

 ANS: A

 9.    Identify which deficiency would most compromise a protective immune response to herpes simplex virus.

a.

IgG

b.

IgE

c.

CD8 T cells

d.

Neutrophils

ANS: C

10.  Identify which deficiency would most compromise a protective immune response to poliovirus.

a.

IgG

b.

IgE

c.

CD8 T cells

d.

Neutrophils

 ANS: A

 11.  Identify which deficiency would most compromise a protective immune response to S. aureus skin infection.

a.

IgA

b.

IgE

c.

CD8 T cells

d.

Neutrophils

 ANS: D

 12.  Identify which deficiency would most compromise a protective immune response to helminths.

a.

IgG

b.

IgE

c.

CD8 T cells

d.

Neutrophils

 ANS: B

 13.  A person with chronic granulomatous disease and related defects in the NADPH Oxidase enzyme complex would be most susceptible to serious outcomes from:

a.

S. aureus

b.

Herpes simplex virus

c.

Parainfluenza

d.

Neisseria meningitides

e.

All of the above

 ANS: A

 14.  A person with complement C7 deficiency would be most susceptible to serious outcomes from:

a.

S. aureus

b.

Herpes simplex virus

c.

Parainfluenza

d.

Neisseria meningitides

e.

All of the above

 ANS: D

15.  A person with hyper-IgM syndrome would be susceptible to serious outcomes from:

a.

S. aureus

b.

Herpes simplex virus

c.

Parainfluenza

d.

Neisseria meningitides

e.

All of the above

 ANS: E

 16.  A person with IgA deficiency would be most susceptible to serious outcomes from:

a.

S. aureus

b.

Herpes simplex virus

c.

Parainfluenza

d.

Strongyloides stercoralis

e.

All of the above

 ANS: C

 17.  A person with asplenia would be most susceptible to serious outcomes from:

a.

S. aureus

b.

Herpes simplex virus

c.

Parainfluenza

d.

Neisseria meningitides

e.

All of the above

 ANS: D

 18.  Match the hypersensitivity reaction with the response to poison ivy.

a.

Type I

b.

Type II

c.

Type III

d.

Type IV

 ANS: D

 19.  Match the hypersensitivity reaction with the anaphylactic response to penicillin.

a.

Type I

b.

Type II

c.

Type III

d.

Type IV

 ANS: A

 20.  Match the hypersensitivity reaction with the immune complex–induced complement activation in the kidney during hepatitis B infection.

a.

Type I

b.

Type II

c.

Type III

d.

Type IV

 ANS: C

[elizabethsimon1-blog]

Medical Microbiology 7th Edition Test Bank

Follow Below Link to Download File

 https://homeworklance.com/downloads/medical-microbiology-7th-edition-test-bank/

 We also Do 100% Original and Plagiarism Free Assignment / Homework and Essay

 Email us for original and Plagiarism Free Work At ( info.homeworklance@gmail.com ) or order us at (https://homeworklance.com/custom-order/ )

  View Sample Chapter Below:

 Murray: Medical Microbiology, 7th Edition

 Chapter 10: Immune Responses to Infectious Agents

 Test Bank

 MULTIPLE CHOICE

 1.    What is the first antibody produced when an invading microorganism is initially encountered?

a.

IgA

b.

IgD

c.

IgE

d.

IgG

e.

IgM

 ANS: E

 2.    A 5-day-old baby is brought back to the hospital with signs of sepsis, is not thriving, and has vesicular lesions on his scalp at the site of monitor attachment. Why is a baby susceptible to a more serious outcome with this infection than an older child or adult?

a.

Immunosuppression from the mother

b.

Infection of a site closest to the brain

c.

Lack of IgA production

d.

Low levels of interferon-γ production

e.

More rapidly growing cells

 ANS: D

 3.    Endotoxin initiates septic responses by binding to:

a.

NF-κB

b.

Complement receptor 3d

c.

Toll-like receptor 4

d.

C-reactive protein

e.

ICAM 1

 ANS: C

 4.    Endotoxin induces production of which cytokines by macrophages?

a.

IL-1, TNF-α, IL-6

b.

IL-2, IL-4, IL-6

c.

IL-4, IL-5, IL-10

d.

IL-2, IFN-γ, TNF-β

e.

TGF-β, IL-10, IL-17

 ANS: A

 5.    Which of the following cytokines is required to initiate a protective helper T cell immune response to measles virus?

a.

IL-1

b.

IL-4

c.

IL-8

d.

IL-10

e.

IL-12

 ANS: E

 6.    Treatment with which cytokine makes the macrophage more efficient at killing bacteria?

a.

Interferon alpha

b.

Interferon gamma

c.

TGF-β

d.

GM-CSF

e.

IL-2

 ANS: B

 7.    M. tuberculosis becomes reactivated in an AIDS patient because:

a.

CD8 T cells cannot kill the bacteria.

b.

Neutrophils do not become activated.

c.

Macrophages do not get an activation signal.

d.

B cells stop making protective antibody.

e.

CD4 T cells stop making TGF-β.

 ANS: C

 8.    Identify which deficiency would most compromise a protective immune response to E. coli sepsis.

a.

IgG

b.

IgE

c.

CD8 T cells

d.

Mast cells

 ANS: A

 9.    Identify which deficiency would most compromise a protective immune response to herpes simplex virus.

a.

IgG

b.

IgE

c.

CD8 T cells

d.

Neutrophils

ANS: C

10.  Identify which deficiency would most compromise a protective immune response to poliovirus.

a.

IgG

b.

IgE

c.

CD8 T cells

d.

Neutrophils

 ANS: A

 11.  Identify which deficiency would most compromise a protective immune response to S. aureus skin infection.

a.

IgA

b.

IgE

c.

CD8 T cells

d.

Neutrophils

 ANS: D

 12.  Identify which deficiency would most compromise a protective immune response to helminths.

a.

IgG

b.

IgE

c.

CD8 T cells

d.

Neutrophils

 ANS: B

 13.  A person with chronic granulomatous disease and related defects in the NADPH Oxidase enzyme complex would be most susceptible to serious outcomes from:

a.

S. aureus

b.

Herpes simplex virus

c.

Parainfluenza

d.

Neisseria meningitides

e.

All of the above

 ANS: A

 14.  A person with complement C7 deficiency would be most susceptible to serious outcomes from:

a.

S. aureus

b.

Herpes simplex virus

c.

Parainfluenza

d.

Neisseria meningitides

e.

All of the above

 ANS: D

15.  A person with hyper-IgM syndrome would be susceptible to serious outcomes from:

a.

S. aureus

b.

Herpes simplex virus

c.

Parainfluenza

d.

Neisseria meningitides

e.

All of the above

 ANS: E

 16.  A person with IgA deficiency would be most susceptible to serious outcomes from:

a.

S. aureus

b.

Herpes simplex virus

c.

Parainfluenza

d.

Strongyloides stercoralis

e.

All of the above

 ANS: C

 17.  A person with asplenia would be most susceptible to serious outcomes from:

a.

S. aureus

b.

Herpes simplex virus

c.

Parainfluenza

d.

Neisseria meningitides

e.

All of the above

 ANS: D

 18.  Match the hypersensitivity reaction with the response to poison ivy.

a.

Type I

b.

Type II

c.

Type III

d.

Type IV

 ANS: D

 19.  Match the hypersensitivity reaction with the anaphylactic response to penicillin.

a.

Type I

b.

Type II

c.

Type III

d.

Type IV

 ANS: A

 20.  Match the hypersensitivity reaction with the immune complex–induced complement activation in the kidney during hepatitis B infection.

a.

Type I

b.

Type II

c.

Type III

d.

Type IV

 ANS: C

[azveille]

Syndrome hyper-IgM : la greffe de cellules souches hématopoïétiques plus efficace avant 5 ans

La greffe de cellules souches hématopoïétiques semble pouvoir guérir des patients atteints d'un syndrome hyper-IgM par déficit en ligand de CD40, notamment si elle est réalisée avant l'âge de 5 ans et en l'absence de dysfonctionnement hépatique, selon des données internationales.

Le syndrome hyper-IgM dit lié à l'X ou par déficit en ligand de CD40 est un déficit immunitaire primitif qui entraîne notamment des infections récurrentes des sinus et des poumons par Pneumocystis et Cryptosporidium, rappellent le Dr Francesca Ferrua du Great North Children's Hospital à Newcastle et de l'Institut scientifique San Raffaele à Milan et ses collègues dans le Journal of Allergy and Clinical Immunology (JACI).

La survie à long terme avec un traitement conservateur était faible. Avec la greffe de cellules souches hématopoïétiques, il est possible de guérir des patients mais des complications peuvent survenir. Dans cette étude, les chercheurs ont voulu déterminer les modalités optimales du traitement par greffe de cellules souches hématopoïétiques et les facteurs de risque individuels des patients.

Pour cela, ils ont analysé de manière rétrospective les données de 130 patients ayant reçu ce traitement entre 1993 et 2015, provenant de deux registres européens (SCEIDE et EBMT) et d'un consortium de centres américains (PIDTC).

La majorité des interventions ont été réalisées après 2000. L'âge médian à la première greffe était de 4 ans (entre 0,5 et 38,3 ans), avec un délai médian de 2 ans après le diagnostic.

Globalement, il apparaît que cinq ans après la première greffe, le taux de survie globale était de 78,2%, le taux de survie sans événement (échec de la greffe et recours à une autre greffe, injection de lymphocytes, supplémentation en immunoglobuline, décès) de 58,1% et le taux de survie sans maladie de 72,3%.

Concernant la survie globale à cinq ans, elle apparaît meilleure après 2000, probablement en lien avec une amélioration des procédures de greffe et de la prise en charge des patients (82,2% vs 58,3%).

Elle est également meilleure lorsque les patients sont traités par greffe avant l'âge de 5 ans, atteignant 90%, contre 37,8% pour ceux greffés après l'âge de 10 ans. Pour ces derniers, une légère amélioration est observée après 2000, avec un taux de survie globale à 43,8%.

L'âge au diagnostic ne semble pas avoir d'effet sur la survie globale à cinq ans mais celle-ci est meilleure lorsque le délai avant l'intervention diminue.

Mauvais pronostic avec la cholangite sclérosante

Les atteintes d'organe préalables sont associées à un mauvais pronostic, en particulier les dysfonctionnements hépatiques et/ou pulmonaires chroniques, avec une survie à cinq ans de 55,6% contre 92,9% en l'absence de dysfonctionnement d'organe. La cholangite sclérosante était le facteur de risque le plus important.

Le recours à un conditionnement myélo-ablatif était associé à une meilleure survie globale par rapport au conditionnement d'intensité réduite.

Un effet significatif de l'appariement entre donneur et receveur apparaît sur la survie sans événement, avec de meilleurs résultats notamment lorsqu'ils proviennent de la même fratrie et/ou lorsqu'ils sont appariés.

La survie sans événement à cinq ans atteint 81,6% en particulier après conditionnement myélo-ablatif et greffe réalisée après 2000.

Le taux de décès dans cette cohorte était de 20%, en majorité en lien avec l'intervention. L'analyse des données indique aussi que la mortalité après greffe de cellules souches hématopoïétiques intervient dans plus des trois quarts des cas dans les six mois, principalement à cause d'une infection.

Deux patients sont décédés d'une insuffisance hépatique; ils avaient une cholangite sclérosante pré-existante. Trois autres sont décédés d'un rejet de greffe. Par ailleurs, 4 patients sont décédés de la progression de leur maladie.

Ces données sont issues de la plus grande série de patients avec un syndrome hyper-IgM par déficit en ligand de CD40. Elles montrent globalement que les progrès dans le diagnostic, la prise en charge clinique et les modalités de la greffe de cellules souches hématopoïétiques ont contribué à améliorer l'impact de ce traitement, concluent les chercheurs.

Les chances de guérir les patients atteints d'un syndrome hyper-IgM par déficit en ligand de CD40 avec une greffe de cellules souches hématopoïétiques augmentent si elle est réalisée avant la survenue d'un dysfonctionnement d'organe, avant l'âge de 10 ans, avec notamment un conditionnement myélo-ablatif, ajoutent-ils.