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myrawjcsmicasereports · 1 month ago

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Retinal and choroidal vascular drop out in a case of severe phenotype of Flammer Syndrome. Rescue of the ischemic-preconditioning mimicking action of endogenous Erythropoietin (EPO) by off-label intra vitreal injection of recombinant human EPO (rhEPO) by Claude Boscher in Journal of Clinical Case Reports Medical Images and Health Sciences

Abstract

Background: Erythropoietin (EPO) is a pleiotropic anti-apoptotic, neurotrophic, anti-inflammatory, and pro-angiogenic endogenous agent, in addition to its effect on erythropoiesis. Exogenous EPO is currently used notably in human spinal cord trauma, and pilot studies in ocular diseases have been reported. Its action has been shown in all (neurons, glia, retinal pigment epithelium, and endothelial) retinal cells. Patients affected by the Flammer Syndrome (FS) (secondary to Endothelin (ET)-related endothelial dysfunction) are exposed to ischemic accidents in the microcirculation, notably the retina and optic nerve.

Case Presentation: A 54 years old female patient with a diagnosis of venous occlusion OR since three weeks presented on March 3, 2019. A severe Flammer phenotype and underlying non arteritic ischemic optic neuropathy; retinal and choroidal drop-out were obviated. Investigation and follow-up were performed for 36 months with Retinal Multimodal Imaging (Visual field, SD-OCT, OCT- Angiography, Indo Cyanin Green Cine-Video Angiography). Recombinant human EPO (rhEPO)(EPREX®)(2000 units, 0.05 cc) off-label intravitreal injection was performed twice at one month interval. Visual acuity rapidly improved from 20/200 to 20/63 with disparition of the initial altitudinal scotoma after the first rhEPO injection, to 20/40 after the second injection, and gradually up to 20/32, by month 5 to month 36. Secondary cystoid macular edema developed ten days after the first injection, that was not treated via anti-VEGF therapy, and resolved after the second rhEPO injection. PR1 layer integrity, as well as protective macular gliosis were fully restored. Some level of ischemia persisted in the deep capillary plexus and at the optic disc.

Conclusion: Patients with FS are submitted to chronic ischemia and paroxystic ischemia/reperfusion injury that drive survival physiological adaptations via the hypoxic-preconditioning mimicking effect of endogenous EPO, that becomes overwhelmed in case of acute hypoxic stress threshold above resilience limits. Intra vitreal exogenous rhEPO injection restores retinal hypoxic-preconditioning adaptation capacity, provided it is timely administrated. Intra vitreal rhEPO might be beneficial in other retinal diseases of ischemic and inflammatory nature.

Key words : Erythropoietin, retinal vein occlusion, anterior ischemic optic neuropathy, Flammer syndrome, Primary Vascular Dysfunction, anti-VEGF therapy, Endothelin, microcirculation, off-label therapy.

Introduction

Retinal Venous Occlusion (RVO) treatment still carries insufficiencies and contradictions (1) due to the incomplete deciphering of the pathophysiology and of its complex multifactorial nature, with overlooking of factors other than VEGF up-regulation, notably the roles of retinal venous tone and Endothelin-1 (ET) (2-5), and of endothelial caspase-9 activation (6). Flammer Syndrome (FS)( (Primary Vascular Dysfunction) is related to a non atherosclerotic ET-related endothelial dysfunction in a context of frequent hypotension and increased oxidative stress (OS), that alienates organs perfusion, with notably changeable functional altered regulation of blood flow (7-9), but the pathophysiology remains uncompletely elucidated (8). FS is more frequent in females, and does not seem to be expressed among outdoors workers, implying an influence of sex hormons and light (7)(9). ET is the most potent pro-proliferative, pro-fibrotic, pro-oxidative and pro-inflammatory vasoconstrictor, currently considered involved in many diseases other than cardio-vascular ones, and is notably an inducer of neuronal apoptosis (10). It is produced by endothelial (EC), smooth vascular muscles (SVMC) and kidney medullar cells, and binds the surface Receptors ET-A on SVMC and ET-B on EC, in an autocrine and paracrine fashion. Schematically, binding on SVMC Receptors (i.e. through local diffusion in fenestrated capillaries or dysfunctioning EC) and on EC ones (i.e. by circulating ET) induce respectively arterial and venous vasoconstriction, and vasodilation, the latter via Nitrite oxide (NO) synthesis. ET production is stimulated notably by Angiotensin 2, insulin, cortisol, hypoxia, and antagonized by endothelial gaseous NO, itself induced by flow shear stress. Schematically but not exclusively, vascular tone is maintained by a complex regulation of ET-NO balance (8) (10-11). Both decrease of NO and increase of ET production are both a cause and consequence of inflammation, OS and endothelial dysfunction, that accordingly favour vasoconstriction; in addition ET competes for L-arginine substrate with NO synthase, thereby reducing NO bioavailability, a mechanism obviated notably in carotid plaques and amaurosis fugax (reviewed in 11).

Severe FS phenotypes are rare. Within the eye, circulating ET reaches retinal VSMC in case of Blood-Retinal-Barrier (BRB) rupture and diffuses freely via the fenestrated choroidal circulation, notably around the optic nerve (ON) head behind the lamina cribrosa, and may induce all pathologies related to acute ocular blood flow decrease (2-3)(5)(7-9). We previously reported two severe cases with rapid onset of monocular cecity and low vision, of respectively RVO in altitude and non arteritic ischemic optic neuropathy (NAION) (Boscher et al, Société Francaise d'Ophtalmologie and Retina Society, 2015 annual meetings).

Exogenous Recombinant human EPO (rhEPO) has been shown effective in humans for spinal cord injury (12), neurodegenerative and chronic kidney diseases (CKD) (reviewed in 13). Endogenous EPO is released physiologically in the circulation by the kidney and liver; it may be secreted in addition by all cells in response to hypoxic stress, and it is the prevailing pathway induced via genes up-regulation by the transcription factor Hypoxia Inducible Factor 1 alpha, among angiogenesis (VEGF pathway), vasomotor regulation (inducible NO synthase), antioxidation, and energy metabolism (14). EPO Receptor signaling induces cell proliferation, survival and differentiation (reviewed in 13), and targets multiple non hematopoietic pathways as well as the long-known effect on erythropoiesis (reviewed in 15). Of particular interest here, are its synergistic anti-inflammatory, neural antiapoptotic (16) pro-survival and pro-regenerative (17) actions upon hypoxic injury, that were long-suggested to be also indirect, via blockade of ET release by astrocytes, and assimilated to ET-A blockers action (18). Quite interestingly, endogenous EPO’s pleiotropic effects were long-summarized (back to 2002), as “mimicking hypoxic-preconditioning” by Dawson (19), a concept applied to the retina (20). EPO Receptors are present in all retinal cells and their rescue activation targets all retinal cells, i.e. retinal EC, neurons (photoreceptors (PR), ganglion (RGG) and bipolar cells), retinal pigment epithelium (RPE) osmotic function through restoration of the BRB, and glial cells (reviewed in 21), and the optic nerve (reviewed in 22). RhEPO has been tested experimentally in animal models of glaucoma, retinal ischemia-reperfusion (I/R) and light phototoxicity, via multiple routes (systemic, subconjunctival, retrobulbar and intravitreal injection (IVI) (reviewed in 23), and used successfully via IVI in human pilot studies, notably first in diabetic macular edema (24) (reviewed in 25 and 26). It failed to improve neuroprotection in association to corticosteroids in optic neuritis, likely for bias reasons (reviewed in 22). Of specific relation to the current case, it has been reported in NAION (27) (reviewed in 28) and traumatic ON injury (29 Rashad), and in one case of acute severe central RVO (CRVO) (Luscan and Roche, Société Francaise d’Ophtalmologie 2017 annual meeting). In addition EPO RPE gene therapy was recently suggested to prevent retinal degeneration induced by OS in a rodent model of dry Age Macular Degeneration (AMD) (30).

Case Report Presentation

This 54 years female patient was first visited on March 2019 4th, seeking for second opinion for ongoing vision deterioration OR on a daily basis, since around 3 weeks. Sub-central RVO (CRVO) OR had been diagnosed on February 27th; available SD-OCT macular volume was increased with epiretinal marked hyperreflectivity, one available Fluorescein angiography picture showed a non-filled superior CRVO, and a vast central ischemia involving the macular and paraoptic territories. Of note there was ON edema with a para-papillary hemorrage nasal to the disc on the available colour fundus picture.

At presentation on March 4, Best Corrected Visual Acuity (BCVA) was reduced at 20/100 OR (20/25 OS). The patient described periods of acutely excruciating retro-orbital pain in the OR. Intraocular pressure was normal, at 12 OR and 18 OS (pachymetry was at 490 microns in both eyes). The dilated fundus examination was similar to the previous color picture and did not disclose peripheral hemorrages recalling extended peripheral retinal ischemia. Humphrey Visual Field disclosed an altitudinal inferior scotoma and a peripheral inferior scotoma OR and was in the normal range OS, i.e. did not recall normal tension glaucoma OS . There were no papillary drusen on the autofluorescence picture, ON volume was increased (11.77 mm3 OR versus 5.75 OS) on SD-OCT (Heidelberg Engineering®) OR, Retinal Nerve Fiber (RNFL) and RGC layers thicknesses were normal Marked epimacular hypereflectivity OR with foveolar depression inversion, moderately increased total volume and central foveolar thickness (CFT) (428 microns versus 328 OS), and a whitish aspect of the supero-temporal internal retinal layers recalling ischemic edema, were present . EDI CFT was incresead at 315 microns (versus 273 microns OS), with focal pachyvessels on the video mapping . OCT-Angiography disclosed focal perfusion defects in both the retinal and chorio-capillaris circulations , and central alterations of the PR1 layer on en-face OCT

Altogether the clinical picture evoked a NAION with venous sub-occlusion, recalling Fraenkel’s et al early hypothesis of an ET interstitial diffusion-related venous vasoconstriction behind the lamina cribrosa (2), as much as a rupture of the BRB was present in the optic nerve area (hemorrage along the optic disc). Choroidal vascular drop-out was suggested by the severity and rapidity of the VF impairment (31). The extremely rapid development of a significant “epiretinal membrane”, that we interpreted as a reactive - and protective, in absence of cystoid macular edema (CME) - ET 2-induced astrocytic proliferation (reviewed in 32), was as an additional sign of severe ischemia.

The mention of the retro-orbital pain evoking a “ciliary angor”, the absence of any inflammatory syndrome and of the usual metabolic syndrome in the emergency blood test, oriented the etiology towards a FS. And indeed anamnesis collected many features of the FS, i.e. hypotension (“non dipper” profile with one symptomatic nocturnal episode of hypotension on the MAPA), migrains, hypersensitivity to cold, stress, noise, smells, and medicines, history of a spontaneously resolutive hydrops six months earlier, and of paroxystic episods of vertigo (which had driven a prior negative brain RMI investigation for Multiple Sclerosis, a frequent record among FS patients (33) and of paroxystic visual field alterations (7)(9), that were actually recorded several times along the follow-up.

The diagnosis of FS was eventually confirmed in the Ophthalmology Department in Basel University on April 10th, with elevated retinal venous pressure (20 to 25mmHg versus 10-15 OS) (4)(7)(9), reduced perfusion in the central retinal artery and veins on ocular Doppler (respectively 8.3 cm/second OR velocity versus 14.1 mmHg OS, and 3.1/second OR versus 5.9 cm OS), and impaired vasodilation upon flicker light-dependant shear stress on the Dynamic Vessel Analyser testing (7-9). In addition atherosclerotic plaques were absent on carotid Doppler.

On March 4th, the patient was at length informed about the FS, a possible off label rhEPO IVI, and a related written informed consent on the ratio risk-benefits was delivered.

By March 7th, she returned on an emergency basis because of vision worsening OR. VA was unchanged, intraocular pressure was at 13, but Visual Field showed a worsening of the central and inferior scotomas with a decreased foveolar threshold, from 33 to 29 decibels. SD-OCT showed a 10% increase in the CFT volume.

On the very same day, an off label rhEPO IVI OR (EPREX® 2000 units, 0,05 cc in a pre-filled syringe) was performed in the operating theater, i.e. the dose reported by Modarres et al (27), and twenty times inferior to the usual weekly intravenous dose for treatment of chronic anemia secondary to CKD. Intra venous acetazolamide (500 milligrams) was performed prior to the injection, to prevent any increase in intra-ocular pressure. The patient was discharged with a prescription of chlorydrate betaxolol (Betoptic® 0.5 %) two drops a day, and high dose daily magnesium supplementation (600 mgr).

Incidentally the patient developed bradycardia the day after, after altogether instillation of 4 drops of betaxolol only, that was replaced by acetazolamide drops, i.e. a typical hypersensitivity reaction to medications in the FS (7)(9).

Subjective vision improvement was recorded as early as D1 after injection. By March 18 th, eleven days post rhEPO IVI, BCVA was improved at 20/63, the altitudinal scotoma had resolved (Fig. 5), Posterior Vitreous Detachment had developed with a disturbing marked Weiss ring, optic disc swelling had decreased; vasculogenesis within the retinal plexi and some regression of PR1 alterations were visible on OCT-en face. Indeed by 11 days post EPO significant functional, neuronal and vascular rescue were observed, while the natural evolution had been seriously vision threatening.

However cystoid ME (CME) had developed . Indo Cyanin Green-Cine Video Angiography (ICG-CVA) OR, performed on March 23, i.e. 16 days after the rhEPO IVI, showed a persistent drop in ocular perfusion: ciliary and central retinal artery perfusion timings were dramatically delayed at respectively 21 and 25 seconds, central retinal vein perfusion initiated by 35 seconds, was pulsatile, and completed by 50 seconds only (video 3). Choroidal pachyveins matching the ones on SD-OCT video mapping were present in the temporal superior and inferior fields, and crossed the macula; capillary exclusion territories were present in the macula and around the optic disc.

By April 1, 23 days after the rhEPO injection, VA was unchanged, but CME and perfusion voids in the superficial deep capillary plexi and choriocapillaris were worsened, and optic disc swelling had recurred back to baseline, in a context of repeated episodes of systemic hypotension; and actually Nifepidin-Ratiopharm® oral drops (34), that had been delivered via a Temporary Use Authorization from the central Pharmacology Department in Assistance Publique Hopitaux de Paris, had had to be stopped because of hypersensitivity.

A second off label rhEPO IVI was performed in the same conditions on April 3, i.e. approximately one month after the first one.

Evolution was favourable as early as the day after EPO injection 2: VA was improved at 20/40, CME was reduced, and perfusion improved in the superficial retinal plexus as well as in the choriocapillaris. By week 4 after EPO injection 2, CME was much decreased, i.e. without anti VEGF injection. On august 19th, by week 18 after EPO 2, perfusion on ICG-CVA was greatly improved , with ciliary timing at 18 seconds, central retinal artery at 20 seconds and venous return from 23 to 36 seconds, still pulsatile. Capillary exclusion territories were visible in the macula and temporal to the macula after the capillary flood time that went on by 20.5 until 22.5 seconds (video 4); they were no longer persistent at intermediate and late timings.

Last complete follow-up was recorded on January 7, 2021, at 22 months from EPO injection 2. BCVA was at 20/40, ON volume had dropped at 7.46 mm3, a sequaelar superior deficit was present in the RNFL with some corresponding residual defects on the inferior para central Visual Field , CFT was at 384 mm3 with an epimacular hyperreflectivity without ME, EDI CFT was dropped at 230 microns. Perfusion on ICG-CVA was not normalized, but even more improved, with ciliary timing at 15 seconds, central retinal artery at 16 seconds and venous return from 22 to 31 seconds, still pulsatile , indicating that VP was still above IOP. OCT-A showed persisting perfusion voids, especially at the optic disc and within the deep retinal capillary plexus. The latter were present at some degree in the OS as well . Choriocapillaris and PR1 layer were dramatically improved.

Last recorded BCVA was at 20/32 by February 14, 2022, at 34 months from EPO 2. SD-OCT showed stable gliosis hypertrophy and mild alterations of the external layers .

Discussion

What was striking in the initial clinical phenotype of CRVO was the contrast between the moderate venous dilation, and the intensity of ischemia, that were illustrating the pioneer hypothesis of Professor Flammer‘s team regarding the pivotal role of ET in VO (2), recently confirmed (3)(35), i.e. the local venous constriction backwards the lamina cribrosa, induced by diffusion of ET-1 within the vascular interstitium, in reaction to hypoxia. NAION was actually the primary and prevailing alteration, and ocular hypoperfusion was confirmed via ICG-CVA, as well as by the ocular Doppler performed in Basel. ICG-CVA confirmed the choroidal drop-out suggested by the severity of the VF impairment (31) and by OCT-A in the choriocapillaris. Venous pressure measurement, which instrumentation is now available (8), should become part of routine eye examination in case of RVO, as it is key to guide cases analysis and personalized therapeutical options.

Indeed, the endogenous EPO pathway is the dominant one activated by hypoxia and is synergetic with the VEGF pathway, and coherently it is expressed along to VEGF in the vitreous in human RVO (36). Diseases develop when the individual limiting stress threshold for efficient adaptative reactive capacity gets overwhelmed. In this case by Week 3 after symtoms onset, neuronal and vascular resilience mechanisms were no longer operative, but the BRB, compromised at the ON, was still maintained in the retina.

As mentioned in the introduction, the scientific rationale for the use of EPO was well demonstrated by that time, as well as the capacities of exogenous EPO to mimic endogenous EPO vasculogenesis, neurogenesis and synaptogenesis, restoration of the balance between ET-1 and NO. Improvement of chorioretinal blood flow was actually illustrated by the evolution of the choriocapillaris perfusion on repeated OCT-A and ICG-CVA. The anti-apoptotic effect of EPO (16) seems as much appropriate in case of RVO as the caspase-9 activation is possibly another overlooked co-factor (6).

All the conditions for translation into off label clinical use were present: severe vision loss with daily worsening and unlikely spontaneous favourable evolution, absence of toxicity in the human pilot studies, of contradictory comorbidities and co-medications, and of context of intraocular neovascularization that might be exacerbated by EPO (37).

Why didn’t we treat the onset of CME by March 18th, i.e. eleven days after EPO IVI 1, by anti-VEGF therapy, the “standard-of-care” in CME for RVO ?

In addition to the context of functional, neuronal and vascular improvements obviated by rhEPO IVI by that timing in the present case, actually anti VEGF therapy does not address the underlying causative pathology. Coherently, anti-VEGF IVI : 1) may not be efficient in improving vision in RVO, despite its efficiency in resolving/improving CME (usually requiring repeated injections), as shown in the Retain study (56% of eyes with resolved ME continued to loose vision)(quoted in (1) 2) eventually may be followed by serum ET-1 levels increase and VA reduction (in 25% of cases in a series of twenty eyes with BRVO) (38) and by increased areas of non perfusion in OCT-A (39). Rather did we perform a second hrEPO IVI, and actually we consider open the question whether the perfusion improvement, that was progressive, might have been accelerated/improved via repeated rhEPO IVI, on a three to four weeks basis.

The development of CME itself, involving a breakdown of the BRB, i.e. of part of the complex retinal armentorium resilience to hypoxia, was somewhat paradoxical in the context of improvement after the first EPO injection, as EPO restores the BRB (24), and as much as it was suggested that EPO inhibits glial osmotic swelling, one cause of ME, via VEGF induction (40). Possible explanations were: 1) the vascular hyperpermeability induced by the up-regulation of VEGF gene expression via EPO (41) 2) the ongoing causative disease, of chronic nature, that was obviated by the ICG-CVA and the Basel investigation, responsible for overwhelming the gliosis-dependant capacity of resilience to hypoxia 3) a combination of both. I/R seemed excluded: EPO precisely mimics hypoxic reconditioning as shown in over ten years publications, including in the retina (20), and as EPO therapy is part of the current strategy for stabilization of the endothelial glycocalix against I/R injury (42-43). An additional and not exclusive possible explanation was the potential antagonist action of EPO on GFAP astrocytes proliferation, as mentioned in the introduction (18), that might have counteracted the reactive protective hypertrophic gliosis, still fully operative prior to EPO injection, and that was eventually restored during the follow-up, where epiretinal hyperreflectivity without ME and ongoing chronic ischemia do coincide (Fig. 6 and video 6), as much as it is unlikely that EPO’s effect would exceed one month (cf infra). Inhibition of gliosis by EPO IVI might have been also part of the mechanism of rescue of RGG, compromised by gliosis in hypoxic conditions (44). Whatever the complex balance initially reached, then overwhelmed after EPO IVI 1, the challenge was rapidly overcome by the second EPO IVI without anti-VEGF injection, likely because the former was powerful enough to restore the threshold limit for resilience to hypoxia, that seemed no longer reached again during the relapse-free follow-up. Of note, this “epiretinal membrane “, which association to good vision is a proof of concept of its protective effect, must not be removed surgically, as it would suppress one of the mecanisms of resilience to hypoxia.

To our best knowledge, ICG-CVA was never reported in FS; it allows real time evaluation of the ocular perfusion and illustration of the universal rheological laws that control choroidal blood flow as well. Pachyveins recall a “reverse” veno-arteriolar reflex in the choroidal circulation, that is NO and autonomous nervous system-dependant, and that we suggested to be an adaptative choroidal microcirculation process to hypoxia (45). Their persistence during follow-up accounts for a persisting state of chronic ischemia.

The optimal timing for reperfusion via rhEPO in a non resolved issue:

in the case reported by Luscan and Roche, rhEPO IVI was performed on the very same day of disease onset, where it induced complete recovery from VA reduced at counting fingers at 1 meter, within 48 hours. This clinical human finding is on line with a recent rodent stroke study that established the timings for non lethal versus lethal ischemia of the neural and vascular lineages, and the optimized ones for beneficial reperfusion: the acute phase - from Day 1 where endothelial and neural cells are still preserved, to Day 7 where proliferation of pericytes and Progenitor Stem Cells are obtainable - and the chronic stage, up to Day 56, where vasculogenesis, neurogenesis and functional recovery are still possible, but with uncertain efficiency (46). In our particular case, PR rescue after rhEPO IVI 1 indicated that Week 3 was still timely. RhEPO IVI efficacy was shown to last between one (restoration of the BRB) and four weeks (antiapoptotic effect) in diabetic rats (24). The relapse after Week 3 post IVI 1 might indicate that it might be approximately the interval to be followed, should repeated injections be necessary.

The bilateral chronic perfusion defects on OCT-A at last follow-up indicate that both eyes remain in a condition of chronic ischemia and I/R, where endogenous EPO provides efficient ischemic pre-conditioning, but is potentially susceptible to be challenged during episodes of acute hypoxia that overwhelm the resilience threshold.

Conclusion

The present case advocates for individualized medicine with careful recording of the medical history, investigation of the systemic context, and exploiting of the available retinal multimodal imaging for accurate analytical interpretation of retinal diseases and their complex pathophysiology. The Flammer Syndrome is unfortunately overlooked in case of RVO; it should be suspected clinically in case of absence of the usual vascular and metabolic context, and in case of elevated RVP. RhEPO therapy is able to restore the beneficial endogenous EPO ischemic pre-conditioning in eyes submitted to challenging acute hypoxia episodes in addition to chronic ischemic stress, as in the Flammer Syndrome and fluctuating ocular blood flow, when it becomes compromised by the overwhelming of the hypoxic stress resilience threshold. The latter physiopathological explanation illuminates the cases of RVO where anti-VEGF therapy proved functionally inefficient, and/or worsened retinal ischemia. RhEPO therapy might be applied to other chronic ischemia and I/R conditions, as non neo-vascular Age Macular Degeneration (AMD), and actually EPO was listed in 2020 among the nineteen promising molecules in AMD in a pooling of four thousands (47).

#off-label therapy #JCRMHS #anti-VEGF therapy #Erythropoietin #Journal of Clinical Case Reports Medical Images and Health Sciences impact factor.#Primary Vascular Dysfunction

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dvar-trek · 2 years ago

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it's WiP Wednesday, my dudes

i finished the project from last week's wip wednesday:

it's a little dishcloth! i'm happy with my stitches, and the edges came out pretty neat too

i've since moved on to a little cabled project, which is taking forEVER. the pattern calls this a horseshoe cable, but tbh i don't see it unless we're talking horseshoe crabs.

also! the dmc floss color card was in stock for once in my goddamned life, and it's here!

i wish there were a little divot between colors instead of a strand of white floss, but oh well. i'm very happy to have it anyway.

and finally, i'm also working on erythropoiesis, after having donated blood this evening (i mean, i don't know. probably not yet. i don't know how long it takes before you start making extra new blood).

i'm mildly allergic to adhesives, so the phlebotomist kindly wrapped my arm in paper towel before bandaging me. we love a compassionate medical staff!

#happy wednesday i am exhausted now 😌#got no blood left #time for bed

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etlu-yume · 1 year ago

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This is just reminding me of the issues I've had with getting certain doctors to clear me to get the referral paperwork I need to have blood taken (... long story. Blood bank won't take me, so it's extra levels of beurocracy to have blood taken. One day maybe I'll just cut my losses and start a tank of leeches for medical purposes...)

And it's not even the "oh it's just anxiety"

No no no.

Instead it's "You're self medicating with periods, you're fine"

I wish I was kidding, but even the 2021 international Haemochromatosis research presentations literally start with a female researcher stating that "Women are protected from the effects of Iron Overload because of the menstruation cycle"

It's gotten to the point that from what I've seen out of the UK Haemochromatosis group, is that the GUIDELINES now are to only test "white Caucasian males" for the genetic mutation. (Which is cute!! When!! It!! Originates!! From!! Serbia/The Black Sea?!?!? Like yes, Ireland has the highest prevalence but.)

Literally all the main BBC news articles/interviews I can remember for the last few years have ALL featured young women.

I get so mad and angry when medicine wants to say this is "just a man's disease" because it's not.

(It also pisses me off that the actual "best" treatment for it also technically makes the defining feature of the condition WORSE. Like it's not an "iron overloading" condition, that's a side effect of the Hepcidin Deficiency. Which the genetic mutation does on its own. You know what else causes a temporary deficiency of hepcidin? Erythropoiesis. The process of making red blood cells. Guess what causes an increase in erythropoiesis? *removing blood*. Add to that the Estradiol component of Estrogen *also* suppressing Hepcidin production [Look I get it. Mechanically it makes sense. But just saying, body, I do not need to worry about absorbing iron to make up for what I loose during a cycle. Stop that.] and it's just a whole trifecta of deficiency in this house.)

this accidentally turned into a Haemochromatosis rant sorry OP.

tl;dr - Medical bias is a thing, and sometimes you gotta really stick to your guns to be heard. Don't give up.

The biggest male privilege I have so far encountered is going to the doctor.

I lived as a woman for 35 years. I have a lifetime of chronic health issues including chronic pain, chronic fatigue, respiratory issues, and neurodivergence (autistic + ADHD). There's so much wrong with my body and brain that I have never dared to make a single list of it to show a doctor because I was so sure I would be sent directly to a psychologist specializing in hypochondria (sorry, "anxiety") without getting a single test done.

And I was right. Anytime I ever tried to bring up even one of my health issues, every doctor's initial reaction was, at best, to look at me with doubt. A raised eyebrow. A seemingly casual, offhand question about whether I'd ever been diagnosed with an anxiety disorder. Even female doctors!

We're not talking about super rare symptoms here either. Joint pain. Chronic joint pain since I was about 19 years old. Back pain. Trouble breathing. Allergy-like reactions to things that aren't typically allergens. Headaches. Brain fog. Severe insomnia. Sensitivity to cold and heat.

There's a lot more going on than that, but those were the things I thought I might be able to at least get some acknowledgement of. Some tests, at least. But 90% of the time I was told to go home, rest, take a few days off work, take some benzos (which they'd throw at me without hesitation), just chill out a bit, you'll be fine. Anxiety can cause all kinds of odd symptoms.

Anyone female-presenting reading this is surely nodding along. Yup, that's just how doctors are.

Except...

I started transitioning about 2.5 years ago. At this point I have a beard, male pattern baldness, a deep voice, and a flat chest. All of my doctors know that I'm trans because I still haven't managed to get all the paperwork legally changed, but when they look at me, even if they knew me as female at first, they see a man.

I knew men didn't face the same hurdles when it came to health care, but I had no idea it was this different.

The last time I saw my GP (a man, fairly young, 30s or so), I mentioned chronic pain, and he was concerned to see that it wasn't represented in my file. Previous doctors hadn't even bothered to write it down. He pushed his next appointment back to spend nearly an hour with me going through my entire body while I described every type of chronic pain I had, how long I'd had it, what causes I was aware of. He asked me if I had any theories as to why I had so much pain and looked at me with concerned expectation, hoping I might have a starting point for him. He immediately drew up referrals for pain specialists (a profession I didn't even know existed till that moment) and physical therapy. He said depending on how it goes, he may need to help me get on some degree of disability assistance from the government, since I obviously shouldn't be trying to work full-time under these circumstances.

Never a glimmer of doubt in his eye. Never did he so much as mention the word "anxiety".

There's also my psychiatrist. He diagnosed me with ADHD last year (meeting me as a man from the start, though he knew I was trans). He never doubted my symptoms or medical history. He also took my pain and sleep issues seriously from the start and has been trying to help me find medications to help both those things while I go through the long process of seeing other specialists. I've had bad reactions to almost everything I've tried, because that's what always happens. Sometimes it seems like I'm allergic to the whole world.

And then, just a few days ago, the most shocking thing happened. I'd been wondering for a while if I might have a mast cell condition like MCAS, having read a lot of informative posts by @thebibliosphere which sounded a little too relatable. Another friend suggested it might explain some of my problems, so I decided to mention it to the psychiatrist, fully prepared to laugh it off. Yeah, a friend thinks I might have it, I'm not convinced though.

His response? That's an interesting theory. It would be difficult to test for especially in this country, but that's no reason not to try treatments and see if they are helpful. He adjusted his medication recommendations immediately based on this suggestion. He's researching an elimination diet to diagnose my food sensitivities.

I casually mentioned MCAS, something routinely dismissed by doctors with female patients, and he instantly took the possibility seriously.

That's it. I've reached peak male privilege. There is nothing else that could happen that could be more insane than that.

I literally keep having to hold myself back from apologizing or hedging or trying to frame my theories as someone else's idea lest I be dismissed as a hypochondriac. I told the doctor I'd like to make a big list of every health issue I have, diagnosed and undiagnosed, every theory I've been given or come up with myself, and every medication I've tried and my reactions to it - something I've never done because I knew for a fact no doctor would take me seriously if they saw such a list all at once. He said it was a good idea and could be very helpful.

Female-presenting people are of course not going to be surprised by any of this, but in my experience, male-presenting people often are. When you've never had a doctor scoff at you, laugh at you, literally say "I won't consider that possibility until you've been cleared by a psychologist" for the most mundane of health problems, it might be hard to imagine just how demoralizing it is. How scary it becomes going to the doctor. How you can internalize the idea that you're just imagining things, making a big deal out of nothing.

Now that I'm visibly a man, all of my doctors are suddenly very concerned about the fact that I've been simply living like this for nearly four decades with no help. And I know how many women will have to go their whole lives never getting that help simply because of sexism in the medical field.

If you know a doctor, show them this story. Even if they are female. Even if they consider themselves leftists and feminists and allies. Ask them to really, truly, deep down, consider whether they really treat their male and female patients the same. Suggest that the next time they hear a valid complaint from a male patient, imagine they were a woman and consider whether you'd take it seriously. The next time they hear a frivolous-sounding complaint from a female patient, imagine they were a man and consider whether it would sound more credible.

It's hard to unlearn these biases. But it simply has to be done. I've lived both sides of this issue. And every doctor insists they treat their male and female patients the same. But some of the doctors astonished that I didn't get better care in the past are the same doctors who dismissed me before.

I'm glad I'm getting the care I need, even if it is several decades late. And I'm angry that it took so long. And I'm furious that most female-presenting people will never have this chance.

#medicine #doctors #research #I've been clearly marinating in too much Haemochromatosis research this year whoops #this is how you scare doctors #(mostly joking - but they do keep asking me what the goals are)#(or just. Not knowing what certain values mean)#(Hello transferrin saturation gotta love the NTBI indicator that you are)#haemochromatosis #hemochromatosis #iron overload #hepcidin

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nursingscience · 5 days ago

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𝗟𝗶𝗳𝗲 𝘀𝗽𝗮𝗻 𝗼𝗳 𝗥𝗕𝗖

The lifespan of RBCs in circulation is approximately 120 days.

Erythrocytes originate in red bone marrow before entering the bloodstream and undergo multiple developmental stages.

Erythropoiesis is the process of RBC development from stem cells that takes around seven days.

The life cycle of erythrocytes comprises:

Production

Maturation and

Destruction

1.𝗣𝗿𝗼𝗱𝘂𝗰𝘁𝗶𝗼𝗻

Erythropoiesis primarily occurs in the bone marrow. It begins with hematopoietic stem cells (HSCs), giving rise to multipotent progenitors, which then develop into erythroid-committed precursors and mature RBCs.

Erythropoietin is the primary regulator of erythropoiesis, driving RBC precursor proliferation and differentiation and preventing erythroblast apoptosis.

2.𝗠𝗮𝘁𝘂𝗿𝗮𝘁𝗶𝗼𝗻

The maturation process involves several morphological changes to produce highly functional specialized cells. This process includes the expulsion of the nucleus and the loss of organelles, such as the smooth and rough endoplasmic reticulum, Golgi apparatus, and ribosomes, leading to the formation of mature biconcave RBCs.

3.𝗗𝗲𝘀𝘁𝗿𝘂𝗰𝘁𝗶𝗼𝗻

Mature RBCs have a lifespan of about 120 days. At the end of their lifespan, they are removed from circulation and destroyed, primarily by macrophages in the spleen and liver.

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datalyst · 1 month ago

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Iron Deficiency Anemia Therapy Market: Addressing a Global Health Challenge

The Iron Deficiency Anemia Therapy Market is one of the most prevalent nutritional deficiencies worldwide, affecting millions of people across various age groups and demographics. The condition, caused by inadequate iron levels in the body, leads to reduced red blood cell production, impacting the body's oxygen transport mechanism. Left untreated, IDA can result in severe health complications, including fatigue, developmental delays in children, impaired cognitive function, and decreased immunity. The Iron Deficiency Anemia Therapy Market, focused on providing solutions to this health issue, has witnessed substantial growth driven by increased awareness, advanced therapies, and rising incidences of iron deficiency globally. This blog post explores the current state, trends, challenges, and opportunities within the Iron Deficiency Anemia Therapy Market.

Understanding Iron Deficiency Anemia and Its Prevalence

Iron Deficiency Anemia occurs when the body lacks sufficient iron to produce hemoglobin, a protein essential for oxygen transport in the blood. This condition disproportionately affects women, children, and the elderly, although it can impact anyone. According to the World Health Organization (WHO), over 1.6 billion people globally suffer from anemia, with Iron Deficiency Anemia being the most common type.

Contributing factors include inadequate dietary intake, gastrointestinal issues hindering iron absorption, chronic blood loss (e.g., from menstruation or ulcers), and increased iron needs during pregnancy and infancy. With high prevalence rates in developing regions and notable cases in developed countries, IDA represents a major public health concern worldwide. The global Iron Deficiency Anemia Therapy Market has emerged as a critical solution provider, offering various treatment options to alleviate the burden of this condition.

Key Treatment Options in the Iron Deficiency Anemia Therapy Market

The market for Iron Deficiency Anemia Therapy encompasses a range of products, from dietary supplements to injectable solutions. Key treatment modalities include:

Oral Iron Supplements: The most commonly prescribed treatment for IDA, oral iron supplements are widely accessible and affordable. They include ferrous sulfate, ferrous gluconate, and ferrous fumarate formulations, among others. These supplements, available over-the-counter, are often the first line of treatment. However, their effectiveness can vary based on the individual’s ability to absorb iron and may lead to side effects such as gastrointestinal discomfort.

Parenteral (Intravenous) Iron Therapy: For individuals who cannot tolerate or absorb oral iron, parenteral iron therapy is often recommended. This treatment delivers iron directly into the bloodstream, providing rapid relief and increased efficacy, especially in cases of severe anemia or when quick restoration of iron levels is needed. Innovations in intravenous iron formulations, such as ferric carboxymaltose and iron isomaltoside, have enhanced the safety and convenience of these therapies.

Dietary Interventions and Functional Foods: Recognizing the role of diet in managing IDA, the market includes fortified foods and functional food products aimed at enhancing iron intake. These products, often enriched with iron and other essential nutrients, are particularly popular in regions where food insecurity and poor dietary habits contribute to anemia prevalence.

Erythropoiesis-Stimulating Agents (ESAs): ESAs are sometimes used alongside iron therapy to stimulate red blood cell production, especially in chronic kidney disease patients who experience IDA as a secondary condition. By improving red blood cell count, ESAs help to alleviate anemia symptoms and reduce dependency on blood transfusions.

Combination Therapy: For some patients, a combination of oral iron, dietary adjustments, and intravenous therapy provides the most comprehensive approach to managing IDA. Combining therapies allows for customization based on individual needs, maximizing treatment outcomes and minimizing side effects.

Factors Driving Growth in the Iron Deficiency Anemia Therapy Market

The Iron Deficiency Anemia Therapy Market has seen consistent growth due to several factors:

Increasing IDA Prevalence: The high and growing prevalence of IDA worldwide, especially in developing countries, is a primary driver for market growth. Anemia remains a significant issue in regions with limited access to nutritious food and healthcare, fueling demand for affordable and accessible therapies.

Rising Awareness and Screening Initiatives: With healthcare agencies and NGOs increasing awareness campaigns, more individuals are undergoing screening and diagnosis for IDA. Early detection has become more widespread, which in turn boosts the demand for treatment solutions. Initiatives like maternal health programs also prioritize anemia screening for pregnant women, further propelling market growth.

Product Innovation: Manufacturers are constantly innovating to provide more effective and convenient therapies for IDA. Newer intravenous formulations with fewer side effects and higher bioavailability, such as ferric carboxymaltose and iron isomaltoside, have improved patient outcomes and treatment adherence, expanding the market’s reach.

Government and NGO Support: Many governments and non-governmental organizations support anemia management programs, particularly in low- and middle-income countries. Public health policies and subsidies aimed at providing free or low-cost iron supplements contribute significantly to the market's expansion.

Demand for Non-invasive and User-Friendly Solutions: The demand for therapies that are easy to administer and have fewer side effects continues to shape the market. Innovative oral supplements that improve iron absorption and cause less gastrointestinal discomfort have gained traction, appealing to patients looking for gentler treatment options.

Challenges in the Iron Deficiency Anemia Therapy Market

While the Iron Deficiency Anemia Therapy Market is growing, it faces several challenges:

Side Effects of Oral Iron Therapy: Oral iron supplements are the most affordable treatment option but often lead to side effects such as constipation, nausea, and metallic taste. These side effects can deter adherence, particularly among pregnant women and young children who are more sensitive to these effects.

Access and Affordability in Low-Income Regions: In many low-income areas, access to advanced therapies like intravenous iron or functional foods is limited due to cost constraints and lack of healthcare infrastructure. While iron supplements are available, more effective solutions remain out of reach for a significant portion of the population.

Lack of Awareness and Education: Despite increasing awareness campaigns, many people remain unaware of IDA symptoms and risks, leading to underdiagnosis. This gap in awareness is especially evident in rural and underserved communities, where healthcare outreach is limited.

Quality Control Issues in Supplement Manufacturing: The market for oral iron supplements is vast, but not all products meet stringent quality standards. Variability in product quality can lead to inconsistent treatment outcomes, affecting consumer trust and limiting market growth.

Stigma and Misconceptions: In some communities, there are stigmas associated with taking iron supplements, especially among women. Cultural beliefs and misconceptions about anemia and its treatments can hinder patient adherence and limit market reach.

Opportunities in the Iron Deficiency Anemia Therapy Market

Despite these challenges, the Iron Deficiency Anemia Therapy Market presents numerous opportunities:

Expansion in Emerging Economies: With IDA prevalence highest in emerging economies, there is an opportunity for market players to expand their presence by offering affordable and accessible solutions. Partnerships with local governments and health organizations can further support this expansion.

Digital Health Solutions for Monitoring and Adherence: Digital health solutions such as mobile apps and telemedicine can help monitor patients' adherence to iron therapy, especially for those in remote or underserved areas. Reminders, dosage tracking, and virtual consultations can ensure consistent treatment, improving overall effectiveness.

Research and Development of Improved Therapies: Continued investment in R&D can yield innovative therapies with fewer side effects and enhanced efficacy. Improved formulations and delivery mechanisms, such as time-release capsules or high-absorption oral supplements, can cater to patient needs and boost adherence.

Incorporating Functional Foods in Diets: Fortified foods and beverages, such as cereals, juices, and dairy products with added iron, offer an innovative way to tackle IDA. These products can be integrated into everyday diets, providing a preventative approach to iron deficiency.

The Future of the Iron Deficiency Anemia Therapy Market

As awareness of IDA increases, along with the demand for effective and accessible treatments, the Iron Deficiency Anemia Therapy Market is poised for significant growth. Innovative therapies, public health initiatives, and advancements in product quality are expected to shape the future of this market. Addressing challenges such as affordability, side effects, and accessibility will be crucial to meeting the global demand for IDA therapies.

The market holds immense potential, especially as healthcare providers and manufacturers work together to improve patient outcomes and reduce the global burden of iron deficiency anemia.

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gis56 · 1 month ago

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"Market Dynamics 2024-2033: The Evolution of Renal Anemia Treatments"

Renal Anemia Market : Renal anemia is a prevalent yet often overlooked condition that affects patients with chronic kidney disease (CKD). As kidney function declines, the production of erythropoietin — a hormone responsible for stimulating red blood cell production — also decreases, leading to anemia. This can result in fatigue, weakness, and decreased quality of life for individuals battling CKD. Understanding renal anemia is crucial, as timely diagnosis and management can significantly improve patient outcomes. Advances in treatments, including erythropoiesis-stimulating agents (ESAs) and iron supplements, are empowering healthcare providers to combat anemia effectively and enhance the overall well-being of their patients.

To Request Sample Report :https://www.globalinsightservices.com/request-sample/?id=GIS26116 &utm_source=SnehaPatil&utm_medium=Article

The management of renal anemia requires a multidisciplinary approach, emphasizing the importance of regular screening and tailored treatment plans. As the awareness of this condition grows, healthcare providers are increasingly focused on integrating anemia management into comprehensive kidney care. Education and patient engagement play vital roles in ensuring adherence to treatment regimens and lifestyle modifications. With ongoing research and innovation in renal care, patients with renal anemia can look forward to improved therapies that not only alleviate symptoms but also promote better kidney health and quality of life.

#RenalAnemia #ChronicKidneyDisease #AnemiaManagement #KidneyHealth #ErythropoiesisStimulatingAgents #PatientCare #HealthAwareness #IronDeficiency #Nephrology #KidneyCare #Fatigue #ChronicIllness #HealthcareInnovation #PatientEngagement #QualityOfLife

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jcmarchi · 2 months ago

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Jane-Jane Chen: A model scientist who inspires the next generation

New Post has been published on https://thedigitalinsider.com/jane-jane-chen-a-model-scientist-who-inspires-the-next-generation/

Jane-Jane Chen: A model scientist who inspires the next generation

Growing up in Taiwan, Jane-Jane Chen excelled at math and science, which, at that time, were promoted heavily by the government, and were taught at a high level. Learning rudimentary English as well, the budding scientist knew she wanted to come to the United States to continue her studies, after she earned a bachelor of science in agricultural chemistry from the National Taiwan University in Taipei.

But the journey to becoming a respected scientist, with many years of notable National Institutes of Health (NIH) and National Science Foundation-funded research findings, would require Chen to be uncommonly determined, to move far from her childhood home, to overcome cultural obstacles — and to have the energy to be a trailblazer — in a field where barriers to being a woman in science were significantly higher than they are today.

Today, Chen is looking back on her journey, and on her long career as a principal research scientist at the MIT Institute for Medical Engineering and Science (IMES), a position from which she recently retired after 45 dedicated years.

At MIT, Chen established herself as an internationally recognized authority in the field of blood cell development — specifically red blood cells, says Lee Gehrke, the Hermann L.F. Helmholtz Professor and core faculty in IMES, professor of microbiology and immunobiology and health science and technology at Harvard Medical School, and one of the scientists Chen worked with most closely.

“Red cells are essential because they carry oxygen to our cells and tissues, requiring iron in the form of a co-factor called heme,” Gehrke says. “Both insufficient heme availability and excess heme are detrimental to red cell development, and Dr. Chen explored the molecular mechanisms allowing cells to adapt to variable heme levels to maintain blood cell production.”

During her MIT career, Chen produced potent biochemistry research, working with heme-regulated eIF2 alpha kinase (which was discovered as the heme-regulated inhibitor of translation, HRI) and regulation of gene expression at translation relating to anemia, including:

cloning of the HRI cDNA, enabling groundbreaking new discoveries of HRI in the erythroid system and, notably, most recently in the brain neuronal system upon mitochondrial stress and in cancers;

elucidating the biochemistry of heme-regulation of HRI;

generating universal HRI knockout mice as a valuable research tool to study HRI’s functions in vivo in the setting of the whole animal; and

establishing HRI as a master translation regulator for erythropoiesis under stress and diseases.

“Dr. Chen’s signature discovery is the molecular cloning of the cDNA of the heme regulated inhibitor protein (HRI), a master regulatory protein in gene expression under stress and disease conditions,” Gehrke says, adding that Chen “subsequently devoted her career to defining a molecular and biochemical understanding of this key protein kinase” and that she “has also contributed several invited review articles on the subject of red cell development, and her papers are seminal contributions to her field.”

Forging her path

Shortly after graduating college, in 1973, Chen received a scholarship to come to California to study for her PhD in biochemistry at the School of Medicine of the University of Southern California. In Taiwan, Chen recalls, the demographic balance between male and female students was even, about 50 percent for each. Once she was in medical school in the United States, she found there were fewer female students, closer to 30 percent at that time, she recalls.

But she says she was fortunate to have important female mentors while at USC, including her PhD advisor, Mary Ellen Jones, a renowned biochemist who is notable for her discovery of carbamyl phosphate, a chemical substance that is key to the biosynthesis of both pyrimidine nucleotides, and arginine and urea. Jones, whom The New York Times called a “crucial researcher on DNA” and a foundational basic cancer researcher, had worked with eventual Nobel laureate Fritz Lipmann at Massachusetts General Hospital.

When Chen arrived, while there were other Taiwanese students at USC, there were not many at the medical school. Chen says she bonded with a young female scientist and student from Hong Kong and with another female student who was Korean and Chinese, but who was born in America. Forming these friendships was crucial for blunting the isolation she could sometimes feel as a newcomer to America, particularly her connection with the American-born young woman: “She helped me a lot with getting used to the language,” and the culture, Chen says. “It was very hard to be so far away from my family and friends,” she adds. “It was the very first time I had left home. By coincidence, I had a very nice roommate who was not Chinese, but knew the Chinese language conversationally, so that was so lucky … I still have the letters that my parents wrote to me. I was the only girl, and the eldest child (Chen has three younger brothers), so it was hard for all of us.”

“Mostly, the culture I learned was in the lab,” Chen remembers. “I had to work a long day in the lab, and I knew it was such a great opportunity — to go to seminars with professors to listen to speakers who had won, or would win, Nobel Prizes. My monthly living stipend was $300, so that had to stretch far. In my second year, more of my college friends had come to the USC and Caltech, and I began to have more interactions with other Taiwanese students who were studying here.”

Chen’s first scientific discovery at Jones’ laboratory was that the fourth enzyme of the pyrimidine biosynthesis, dihydroorotate dehydrogenase, is localized in the inner membrane of the mitochondria. As it more recently turned out, this enzyme plays dual roles not only for pyrimidine biosynthesis, but also for cellular redox homeostasis, and has been demonstrated to be an important target for the development of cancer treatments.

Coming to MIT

After receiving her degree, Chen received a postdoctoral fellowship to work at the Roche Institute of Molecular Biology, in New Jersey, for nine months. In 1979, she married Zong-Long Liau, who was then working at MIT Lincoln Laboratory, from where he also recently retired. She accepted a postdoctoral position to continue her scientific training and pursuit at the laboratory of Irving M. London at MIT, and Jane-Jane and Zong-Long have lived in the Boston area ever since, raising two sons.

Looking back at her career, Chen says she is most proud of “being an established woman scientist with decades of NIH findings, and for being a mother of two wonderful sons.” During her time at MIT and IMES, she has worked with many renowned scientists, including Gehrke and London, professor of biology at MIT, professor of medicine at Harvard Medical School (HMS), founding director of the Harvard-MIT Program in Health Sciences and Technology (HST), and a recognized expert in molecular regulation of hemoglobin synthesis. She says that she is also in debt to the colleagues and collaborators at HMS and Children’s Hospital Boston for their scientific interests and support at the time when her research branched into the field of hematology, far different from her expertise in biochemistry. All of them are HST-educated physician scientists, including Stuart H. Orkin, Nancy C. Andrews, Mark D. Fleming, and Vijay G. Sankaran.

“We will miss Dr. Chen’s sage counsel on all matters scientific and communal,” says Elazer R. Edelman, the Edward J. Poitras Professor in Medical Engineering and Science, and the director of the Center for Clinical and Translational Research (CCTR), who was the director of IMES when Chen retired in June. “For generations, she has been an inspiration and guide to generations of students and established leaders across multiple communities — a model for all.”

She says her life in retirement “is a work in progress” — but she is working on a scientific review article, so that she can have “my last words on the research topics of my lab for the past 40 years.” Chen is pondering writing a memoir “reflecting on the journey of my life thus far, from Taiwan to MIT.” She also plans to travel to Taiwan more frequently, to better nurture and treasure the relationships with her three younger brothers, one of whom lives in Los Angeles.

She says that in looking back, she is grateful to have participated in a special grant application that was awarded from the National Science Foundation, aimed at helping women scientists to get their careers back on track after having a family. And she says she also remembers the advice of a female scientist in Jones’ lab during her last year of graduate study, who had stepped back from her research for a while after having two children, “She was not happy that she had done that, and she told me: Never drop out, try to always keep your hands in the research, and the work. So that is what I did.”

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tbrc34 · 2 months ago

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"Caring for the Kidney: The Evolving Landscape of Renal Anemia Therapies (2024-2033)"

Renal Anemia Market : Renal anemia is a common but often overlooked complication in patients with chronic kidney disease (CKD). As kidney function declines, the production of erythropoietin, a hormone responsible for stimulating red blood cell production, also diminishes. This can lead to anemia, characterized by fatigue, weakness, and decreased quality of life. Effective management of renal anemia is crucial, as it not only impacts patients’ overall health but also complicates their kidney disease treatment.

Download PDF Sample Report@https://www.globalinsightservices.com/request-sample/GIS26116/?utm_source=SnehaPatil-Article

Recent advancements in therapies, including erythropoiesis-stimulating agents (ESAs) and iron supplements, have significantly improved the management of renal anemia. By addressing the underlying causes and promoting healthy red blood cell production, healthcare providers can enhance patient outcomes and overall well-being. Increased awareness and proactive monitoring of renal anemia are essential in providing comprehensive care for individuals with CKD, helping them maintain a better quality of life.

Relevant Link : https://linkewire.com/2024/10/01/patient-engagement-technology-market-to-evolve-with-ai-innovations-2024-2033-forecast/

#RenalAnemia #ChronicKidneyDisease #KidneyHealth #AnemiaManagement #Erythropoietin #PatientCare #HealthcareInnovation #IronSupplements #ChronicIllness #QualityOfLife

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credenceresearchdotblog · 3 months ago

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The Erythropoietin (EPO) drug Market is poised for substantial growth, with its market size projected to expand from USD 11,728.5 million in 2024 to USD 24,205.87 million by 2032, reflecting a compound annual growth rate (CAGR) of 9.48%.The global erythropoietin (EPO) drugs market has experienced significant growth in recent years, driven by an increasing prevalence of anemia, particularly among patients with chronic kidney disease (CKD), cancer, and HIV. Erythropoietin, a glycoprotein hormone produced by the kidneys, plays a crucial role in the production of red blood cells (erythropoiesis). The synthetic forms of erythropoietin, known as erythropoiesis-stimulating agents (ESAs), are commonly used to treat anemia by stimulating the bone marrow to produce more red blood cells.

Browse the full report at https://www.credenceresearch.com/report/erythropoietin-drugs-market

Market Dynamics

The erythropoietin drugs market is primarily driven by the rising incidence of chronic diseases such as CKD and cancer. Anemia is a common complication in these diseases, leading to a growing demand for EPO drugs. According to the World Health Organization (WHO), anemia affects approximately 1.62 billion people globally, with iron deficiency anemia being the most prevalent type. This high prevalence, coupled with the increasing number of patients undergoing dialysis, chemotherapy, and antiretroviral therapy, is fueling the demand for EPO drugs.

The market is further bolstered by the growing geriatric population, which is more susceptible to chronic diseases and anemia. Additionally, advancements in biotechnology have led to the development of newer, more effective EPO formulations, enhancing treatment outcomes and expanding the market.

Regional Analysis

The erythropoietin drugs market is geographically segmented into North America, Europe, Asia-Pacific, Latin America, and the Middle East & Africa.

- North America: This region dominates the global market due to the high prevalence of CKD, well-established healthcare infrastructure, and the presence of major pharmaceutical companies. The U.S. is the largest market within this region, driven by a high rate of dialysis procedures and an aging population. - Europe: The market in Europe is also significant, with countries like Germany, the UK, and France leading due to their advanced healthcare systems and the widespread adoption of biosimilars.

- Asia-Pacific: This region is expected to witness the highest growth rate during the forecast period, attributed to a large patient population, increasing healthcare spending, and growing awareness about anemia management.

- Latin America and the Middle East & Africa: These regions are gradually emerging as potential markets due to improving healthcare infrastructure and increasing access to medical treatments.

Challenges and Opportunities

Despite the positive growth outlook, the erythropoietin drugs market faces several challenges. The high cost of biologics, side effects associated with EPO drugs, and stringent regulatory requirements are some of the key barriers to market growth. Additionally, the emergence of biosimilars poses competition to established biologics, potentially leading to price wars and reduced profit margins for manufacturers.

However, the market also presents significant opportunities. The development of next-generation EPO drugs with improved efficacy and safety profiles, coupled with the expanding applications of these drugs beyond anemia, could drive future growth. Moreover, the increasing focus on personalized medicine and targeted therapies is expected to open new avenues in the erythropoietin drugs market.

Key Player Analysis:

Amgen Inc.

Johnson & Johnson

F. Hoffmann-La Roche Ltd.

Pfizer Inc.

Novartis AG

Biocon Limited

Teva Pharmaceutical Industries Ltd.

Dr. Reddy’s Laboratories Ltd.

LG Life Sciences Ltd.

Wockhardt Ltd.

Segmentation:

by Drug Type

Biologics

Biosimilars

by Product Type

Epoetin-alfa

Epoetin-beta

Darbepoetin-alfa

Others

by Application

Haematology

Kidney Disorder

Cancer

Others

by End User

Hospitals

Homecare

Specialty Clinics

Others

Browse the full report at https://www.credenceresearch.com/report/erythropoietin-drugs-market

About Us:

Credence Research is committed to employee well-being and productivity. Following the COVID-19 pandemic, we have implemented a permanent work-from-home policy for all employees.

Contact:

Credence Research

Please contact us at +91 6232 49 3207

Email: [email protected]

Website: www.credenceresearch.com

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prudentrxdruglist · 3 months ago

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PrudentRx Drug List: Medications for Chronic Kidney Disease

Chronic Kidney Disease (CKD) is a long-term condition in which the kidneys gradually lose their ability to filter waste and balance fluids in the body. This can lead to a buildup of toxins, affecting overall health and increasing the risk of serious complications such as heart disease, anemia, and high blood pressure. Managing CKD requires a comprehensive approach, including lifestyle changes and the use of medications. The PrudentRx Drug List provides access to a range of essential medications that help slow the progression of CKD, manage its symptoms, and prevent complications. In this blog, we will explore the medications available through the PrudentRx Drug List and how they support individuals living with CKD.

Understanding Chronic Kidney Disease

CKD progresses slowly over time and is categorized into five stages, with stage 1 being mild and stage 5 indicating kidney failure. In the early stages, CKD often shows few symptoms, making it difficult to detect without regular screening. As the disease advances, symptoms such as fatigue, swelling, shortness of breath, and high blood pressure may appear.

The PrudentRx Drug List offers a wide selection of medications aimed at managing the underlying causes of CKD, such as high blood pressure, diabetes, and high cholesterol, as well as medications that help reduce the progression of the disease itself.

Key Medications for Chronic Kidney Disease

1. Angiotensin-Converting Enzyme (ACE) Inhibitors

ACE inhibitors are a class of medications commonly prescribed to help control high blood pressure, a major contributor to kidney damage in people with CKD. By lowering blood pressure, ACE inhibitors reduce the strain on the kidneys and help slow the progression of kidney disease.

PrudentRx Tip: The PrudentRx Drug List includes ACE inhibitors like lisinopril, enalapril, and ramipril, which are frequently prescribed to individuals with CKD. These medications not only lower blood pressure but also protect the kidneys by reducing the effects of high blood pressure on the delicate blood vessels in the kidneys.

2. Angiotensin II Receptor Blockers (ARBs)

Like ACE inhibitors, ARBs are another class of medications that help manage high blood pressure and protect the kidneys from further damage. ARBs are often prescribed to patients who cannot tolerate ACE inhibitors due to side effects such as a persistent cough.

PrudentRx Tip: Medications like losartan and valsartan are available through the PrudentRx Drug List. These medications work by relaxing blood vessels, allowing blood to flow more easily and reducing the pressure on the kidneys.

3. Diuretics

Diuretics, also known as water pills, help reduce fluid retention and swelling (edema), which are common symptoms of CKD. Diuretics work by helping the kidneys remove excess sodium and water from the body, lowering blood pressure and reducing the workload on the kidneys.

PrudentRx Tip: The PrudentRx Drug List includes commonly prescribed diuretics such as furosemide and hydrochlorothiazide. These medications can be especially helpful for patients experiencing swelling or fluid overload due to CKD.

4. Statins

People with CKD often have high levels of cholesterol, which increases the risk of heart disease and further kidney damage. Statins are medications that lower cholesterol levels, reducing the risk of cardiovascular complications in CKD patients.

PrudentRx Tip: The PrudentRx Drug List provides access to statins like atorvastatin and simvastatin, which help lower cholesterol and protect both the heart and kidneys from further damage.

5. Erythropoiesis-Stimulating Agents (ESAs)

As CKD progresses, the kidneys may lose their ability to produce erythropoietin, a hormone that stimulates the production of red blood cells. This can lead to anemia, a condition in which the body has too few red blood cells to carry oxygen efficiently. ESAs are medications that help stimulate red blood cell production, reducing the symptoms of anemia.

PrudentRx Tip: ESAs like epoetin alfa and darbepoetin alfa are available through the PrudentRx Drug List. These medications are essential for managing anemia in CKD patients, improving their energy levels and overall quality of life.

6. Phosphate Binders

In advanced stages of CKD, the kidneys may struggle to remove excess phosphorus from the blood. High phosphorus levels can lead to weakened bones and other complications. Phosphate binders are medications that help control phosphorus levels in the blood by preventing the body from absorbing too much phosphorus from food.

PrudentRx Tip: Phosphate binders such as sevelamer and calcium acetate are included in the PrudentRx Drug List. These medications play a crucial role in maintaining bone health and preventing complications related to high phosphorus levels in CKD patients.

Managing CKD with the PrudentRx Drug List

The PrudentRx Drug List offers a comprehensive selection of medications that help manage the various aspects of CKD, from controlling blood pressure and cholesterol to addressing anemia and phosphorus imbalances. By ensuring that individuals have access to these essential medications, the PrudentRx Drug List plays a critical role in helping CKD patients maintain their kidney function and overall health.

Additionally, the PrudentRx Program provides valuable educational resources and support for patients managing CKD. Through regular check-ins with healthcare providers and ongoing access to medications, individuals can take proactive steps to slow the progression of CKD and reduce the risk of complications.

Conclusion

Chronic Kidney Disease requires careful management, and medications play a key role in protecting kidney function and preventing further damage. The PrudentRx Drug List offers a wide range of medications that address the various challenges associated with CKD, from blood pressure control to managing anemia and phosphorus levels. By working with healthcare providers and utilizing the resources provided by the PrudentRx Drug List, individuals with CKD can take control of their condition and improve their long-term health outcomes.

#prudentrx drug list #renalhealth

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