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Doctors Using Vitamin Therapy On Covid-19 With 100% Cure Rate On Old People
- Thread starter mimmo123
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md_a
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- Aug 31, 2015
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Oral Vitamin C Supplementation Reduces Erythropoietin Requirement in Hemodialysis Patients With Functional Iron Deficiency
Abstract
Purpose: Functional iron deficiency (FID) is a major cause of persistent anemia in dialysis patients and also contributes to a suboptimal response to erythropoietin (Epo) administration. Vitamin C acts as an enzyme cofactor and enhances mobilization of the ferrous form of iron to transferrin thus increasing its bioavailability. High-dose intravenous vitamin C has been shown to decrease the Epo requirement and improve hemoglobin levels in previous studies. This study assessed the effect of low-dose oral vitamin C on possible reduction in Epo dose requirements in stable hemodialysis patients with FID.
Methods: This prospective study included 22 stable hemodialysis patients with FID defined as transferrin saturation (T sat) <30 % and ferritin levels of >100 mcg/L with Epo requirement of ≥4000 U/HD session. Patients received oral vitamin C 250 mg daily for 3 months. Hemoglobin, iron and T sat levels were recorded monthly. No one received iron supplementation during the study period.
Results: There was a significant reduction in median Epo dose requirement in the 15 patients who completed the study, from 203.1 U/kg/week (95 % CI 188.4-270.6) to 172.8 U/kg/week (95 % CI 160.2-214.8), (P = 0.01). In the seven responders, there was 33 % reduction in Epo dose from their baseline. Despite adjustment of Epo dose, the mean hemoglobin level was significantly increased from 10.1 ± 0.6 to 10.7 ± 0.6 mg/dL (P = 0.03). No adverse effects of oral vitamin C were observed.
Conclusion: Daily low-dose oral vitamin C supplementation reduced Epo dose requirements in hemodialysis patients with FID. Limitations of this study include a small sample size and the lack of measurements of vitamin C and oxalate levels. Despite concerns regarding oral vitamin C absorption in dialysis patients, this study indicates vitamin C was well tolerated by all participants without reported adverse effect.
Oral Vitamin C Supplementation Reduces Erythropoietin Requirement in Hemodialysis Patients With Functional Iron Deficiency - PubMed
...
Does recombinant human erythropoietin administration in critically ill COVID‐19 patients have miraculous therapeutic effects?
Abstract
An 80‐year‐old man with multiple comorbidities presented to the emergency department with tachypnea, tachycardia, fever, and critically low O2 saturation and definitive chest computerized tomography scan findings in favor of COVID‐19 and positive PCR results in 48 hours. He received antiviral treatment plus recombinant human erythropoietin (rhEPO) due to his severe anemia. After 7 days of treatment, he was discharged with miraculous improvement in his symptoms and hemoglobin level. We concluded that rhEPO could attenuate respiratory distress syndrome and confront the severe acute respiratory syndrome coronavirus 2 virus through multiple mechanisms including cytokine modulation, antiapoptotic effects, leukocyte release from bone marrow, and iron redistribution away from the intracellular virus.
Highlights
DISCUSSION
As mentioned above rhEPO was prescribed for an 80‐year‐old confirmed case of COVID‐19 due to his initial severe anemia in addition to antivirals.
Subsequently, a very fast response considering his age and past medical history both in anemia correction (from Hb:6.7 to Hb:9) and COVID‐19 symptom relief was observed that could not be elaborated simply as a result of anemia correction.
The patient had Iron deficiency anemia and perhaps a mixed component of chronic disease anemia according to the lab results, however a thorough assessment of his anemia was reserved for after his discharge from the hospital.
Erythropoietin (EPO) is a hormone/cytokine produced mainly by the kidneys via hypoxia‐inducible factor‐2 as its primary transcription factor, and through inhibition of RBC precursors’ apoptosis, increases the red cell mass. However, EPO has other beneficial cytoprotective effects including anti‐ischemic, regenerative and antiapoptotic effects in a variety of tissues including lung, kidney, cardiac muscle, nervous system, retina, pancreas, and endothelial cells.3 Through a special receptor; EPOR‐βcR, it conducts its protective effects following trauma and in critically ill patients.4
Few animal studies have been conducted to explain the molecular pathways underlying the nonhematopoietic effects of EPO.
In 2019, Zhang et al5 conducted an animal study on rats and grouped them into three groups of Sham, sepsis‐caused acute lung injury, and an intervention group with sepsis‐caused acute lung injury receiving EPO. The intervention group showed less severe pulmonary interstitial, and alveolar edema, hemorrhage, or lung collapse compared to Sham and sepsis‐caused lung injury groups. The protective effects of EPO towards lung tissue were attributed to its effects in inhibiting expression of nuclear factor‐κB (NF‐κB) in lung tissues, inhibition of interleukin‐6 (IL‐6) and tumour necrosis factor alpha as proinflammatory cytokines, and improvement of anti‐inflammatory cytokine IL‐10 levels. A similar study was also conducted to assess rhEPO effect on human respiratory epithelial cell apoptosis and detected cytoprotective effects of rhEPO through induction of an antiapoptotic Bcl‐xL/Bax phenotype6 (Figure 2).
In another animal study of lipopolysaccharide (LPS) induced sepsis model,7 EPO effect on hepatic mitochondrial damage was assessed and it was shown that EPO suppressed the LPS effect on the increase of IL‐1β and reactive oxygen species levels, mitochondrial DNA copy number, and also decreased protein expressions of caspase‐1, and NLRP3 (NLR Family Pyrin Domain Containing 3) gene. EPO alleviated LPS‐induced cellular edema in hepatic lobules, lymphocytic infiltration, and hepatocellular necrosis.
Renoprotective effects of EPO in mice with septic acute kidney injury has been observed and has been linked to attenuation of microvascular damage, reducing renal inflammatory response and improvement of renal tissue oxygenation through the decrease of hypoxia‐inducible factor‐1 alpha, inducible nitric oxide synthase, and NF‐κB and also enhancement of erythropoietin receptor (EPO‐R), PeCAM‐1, vascular endothelial growth factor, and VEGFR‐2 expression.8
Another study conducted earlier by Heitrich et al9 on a murine model of sepsis‐caused acute lung injury and acute kidney injury demonstrated beneficial protective EPO effects on pulmonary and renal outcomes through EPO‐R and VEGF/VEGFR‐2 expression. Moreover, it has been shown that EPO has cardioprotective effects by reducing the myocardial inflammatory response in septic rats and attenuates the reduction in mitochondrial membrane potential and inhibits myocardial cell apoptosis through mitochondrial pathway and by reducing NF‐κB p65 expression.10
NF‐κB is a principle factor of multiple inflammatory pathways, and according to the above‐mentioned studies, it can be considered an important target for treatment. Blocking the activation of NF‐κB by EPO may prevent further deterioration caused by the COVID‐19 disease through cytokine modulation and its regenerative and antiapoptotic effects
Another mechanism for an explanation of EPO effect on the improvement of the clinical condition of the presented case could be rooted to the findings of Ito et al11 on an animal study that revealed that 24 hours after EPO administration, the number of IgDlow immature B cells and mature B cells, as well as CD4+ and CD8+ T cells in the bone marrow, decreased significantly due to their egress into the peripheral blood. This backup leukocyte release into the peripheral bloodstream might be a reason for the optimized viral confrontation of the immune system. Thus in the presented case, after the first dose of rhEPO and packed RBC transfusion, absolute lymphocyte count increased from 333 to 933/μL of blood; a rise quite larger than to be elucidated only by 250 mL of packed RBCs transfusion.
During inflammation, serum Hepcidin levels increase the following stimulation by IL‐6, downregulating cellular ferroportin and this leads to decreased iron absorption and its detainment in liver and spleen macrophages12 which could promote the survival of intracellular microorganisms. EPO by downregulating IL‐6 and Hepcidin levels could lead to an increased release of iron from macrophages and increased absorption of iron by the bone marrow, thus decreasing iron availability for intracellular organisms like Coronavirus for their required enzymatic activities. This antiviral strategy of keeping iron out of infected cells has previously been explored and considered to be potentially effective in human infections by hepatitis C virus, human immunodeficiency virus‐1, hepatitis B virus, and cytomegalovirus viral infections.13
Although the above‐mentioned novel mechanisms of EPO effect in septic states could elaborate the rapid clinical improvement of the presented COVID‐19 case, we should not underestimate the definitive effects of rising hemoglobin from 6.7 to 9 g/dL in the improvement of pulmonary oxygenation and thus relieving the existing respiratory symptoms. However, the 2.3 g/dL rise in hemoglobin level in only 7 days with the mentioned dose of rhEPO is both profound and questionable considering the reported peak effects of rhEPO in 2 to 6 weeks after the starting dose.14, 15
In spite of the aforementioned benefits for EPO, it can aggravate the formation of microthrombosis and subsequent septic multiorgan failure and coagulopathy.16 Besides, in patients with chronic kidney disease‐associated anemia, EPO increases thrombotic events and risk of death when administered for Hb more than 12 g/dL.17 Other side effects of rhEPO in patients receiving large doses have been reported to be hypertension, hyperviscosity, enhancement of tumor progression, and in rare instances pure red blood cell aplasia.18
Regarding the probable benefits of rhEPO in reversing ARDS and its side effects, it seems to be a reasonable choice to use this agent in critically ill COVID‐19 patients to save their lives from imminent death, however, to determine the optimal dose with maximum cytoprotective and antiapoptotic effects and minimum potential toxicity of rhEPO, more clinical studies are required.
Therefore, we recommend the designation of well‐organized clinical trials with careful consideration of rhEPO administration in anemic COVID‐19 patients to further evaluate its clinical benefits in this critical patient population group without imposing further adverse effects associated with this drug.
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Abstract
Purpose: Functional iron deficiency (FID) is a major cause of persistent anemia in dialysis patients and also contributes to a suboptimal response to erythropoietin (Epo) administration. Vitamin C acts as an enzyme cofactor and enhances mobilization of the ferrous form of iron to transferrin thus increasing its bioavailability. High-dose intravenous vitamin C has been shown to decrease the Epo requirement and improve hemoglobin levels in previous studies. This study assessed the effect of low-dose oral vitamin C on possible reduction in Epo dose requirements in stable hemodialysis patients with FID.
Methods: This prospective study included 22 stable hemodialysis patients with FID defined as transferrin saturation (T sat) <30 % and ferritin levels of >100 mcg/L with Epo requirement of ≥4000 U/HD session. Patients received oral vitamin C 250 mg daily for 3 months. Hemoglobin, iron and T sat levels were recorded monthly. No one received iron supplementation during the study period.
Results: There was a significant reduction in median Epo dose requirement in the 15 patients who completed the study, from 203.1 U/kg/week (95 % CI 188.4-270.6) to 172.8 U/kg/week (95 % CI 160.2-214.8), (P = 0.01). In the seven responders, there was 33 % reduction in Epo dose from their baseline. Despite adjustment of Epo dose, the mean hemoglobin level was significantly increased from 10.1 ± 0.6 to 10.7 ± 0.6 mg/dL (P = 0.03). No adverse effects of oral vitamin C were observed.
Conclusion: Daily low-dose oral vitamin C supplementation reduced Epo dose requirements in hemodialysis patients with FID. Limitations of this study include a small sample size and the lack of measurements of vitamin C and oxalate levels. Despite concerns regarding oral vitamin C absorption in dialysis patients, this study indicates vitamin C was well tolerated by all participants without reported adverse effect.
Oral Vitamin C Supplementation Reduces Erythropoietin Requirement in Hemodialysis Patients With Functional Iron Deficiency - PubMed
...
Does recombinant human erythropoietin administration in critically ill COVID‐19 patients have miraculous therapeutic effects?
Abstract
An 80‐year‐old man with multiple comorbidities presented to the emergency department with tachypnea, tachycardia, fever, and critically low O2 saturation and definitive chest computerized tomography scan findings in favor of COVID‐19 and positive PCR results in 48 hours. He received antiviral treatment plus recombinant human erythropoietin (rhEPO) due to his severe anemia. After 7 days of treatment, he was discharged with miraculous improvement in his symptoms and hemoglobin level. We concluded that rhEPO could attenuate respiratory distress syndrome and confront the severe acute respiratory syndrome coronavirus 2 virus through multiple mechanisms including cytokine modulation, antiapoptotic effects, leukocyte release from bone marrow, and iron redistribution away from the intracellular virus.
Highlights
Recombinant human erythropoietin can rapidly correct anemia and symptoms associated with COVID‐19
Through cytokine modulation, rhEPO exerts its cytoprotective and anti‐apoptotic effects in COVID pneumonia.
rhEPO takes iron away from intracellular virus into the bone marrow, undermining the viral enzymatic requirements.
DISCUSSION
As mentioned above rhEPO was prescribed for an 80‐year‐old confirmed case of COVID‐19 due to his initial severe anemia in addition to antivirals.
Subsequently, a very fast response considering his age and past medical history both in anemia correction (from Hb:6.7 to Hb:9) and COVID‐19 symptom relief was observed that could not be elaborated simply as a result of anemia correction.
The patient had Iron deficiency anemia and perhaps a mixed component of chronic disease anemia according to the lab results, however a thorough assessment of his anemia was reserved for after his discharge from the hospital.
Erythropoietin (EPO) is a hormone/cytokine produced mainly by the kidneys via hypoxia‐inducible factor‐2 as its primary transcription factor, and through inhibition of RBC precursors’ apoptosis, increases the red cell mass. However, EPO has other beneficial cytoprotective effects including anti‐ischemic, regenerative and antiapoptotic effects in a variety of tissues including lung, kidney, cardiac muscle, nervous system, retina, pancreas, and endothelial cells.3 Through a special receptor; EPOR‐βcR, it conducts its protective effects following trauma and in critically ill patients.4
Few animal studies have been conducted to explain the molecular pathways underlying the nonhematopoietic effects of EPO.
In 2019, Zhang et al5 conducted an animal study on rats and grouped them into three groups of Sham, sepsis‐caused acute lung injury, and an intervention group with sepsis‐caused acute lung injury receiving EPO. The intervention group showed less severe pulmonary interstitial, and alveolar edema, hemorrhage, or lung collapse compared to Sham and sepsis‐caused lung injury groups. The protective effects of EPO towards lung tissue were attributed to its effects in inhibiting expression of nuclear factor‐κB (NF‐κB) in lung tissues, inhibition of interleukin‐6 (IL‐6) and tumour necrosis factor alpha as proinflammatory cytokines, and improvement of anti‐inflammatory cytokine IL‐10 levels. A similar study was also conducted to assess rhEPO effect on human respiratory epithelial cell apoptosis and detected cytoprotective effects of rhEPO through induction of an antiapoptotic Bcl‐xL/Bax phenotype6 (Figure 2).
In another animal study of lipopolysaccharide (LPS) induced sepsis model,7 EPO effect on hepatic mitochondrial damage was assessed and it was shown that EPO suppressed the LPS effect on the increase of IL‐1β and reactive oxygen species levels, mitochondrial DNA copy number, and also decreased protein expressions of caspase‐1, and NLRP3 (NLR Family Pyrin Domain Containing 3) gene. EPO alleviated LPS‐induced cellular edema in hepatic lobules, lymphocytic infiltration, and hepatocellular necrosis.
Renoprotective effects of EPO in mice with septic acute kidney injury has been observed and has been linked to attenuation of microvascular damage, reducing renal inflammatory response and improvement of renal tissue oxygenation through the decrease of hypoxia‐inducible factor‐1 alpha, inducible nitric oxide synthase, and NF‐κB and also enhancement of erythropoietin receptor (EPO‐R), PeCAM‐1, vascular endothelial growth factor, and VEGFR‐2 expression.8
Another study conducted earlier by Heitrich et al9 on a murine model of sepsis‐caused acute lung injury and acute kidney injury demonstrated beneficial protective EPO effects on pulmonary and renal outcomes through EPO‐R and VEGF/VEGFR‐2 expression. Moreover, it has been shown that EPO has cardioprotective effects by reducing the myocardial inflammatory response in septic rats and attenuates the reduction in mitochondrial membrane potential and inhibits myocardial cell apoptosis through mitochondrial pathway and by reducing NF‐κB p65 expression.10
NF‐κB is a principle factor of multiple inflammatory pathways, and according to the above‐mentioned studies, it can be considered an important target for treatment. Blocking the activation of NF‐κB by EPO may prevent further deterioration caused by the COVID‐19 disease through cytokine modulation and its regenerative and antiapoptotic effects
Another mechanism for an explanation of EPO effect on the improvement of the clinical condition of the presented case could be rooted to the findings of Ito et al11 on an animal study that revealed that 24 hours after EPO administration, the number of IgDlow immature B cells and mature B cells, as well as CD4+ and CD8+ T cells in the bone marrow, decreased significantly due to their egress into the peripheral blood. This backup leukocyte release into the peripheral bloodstream might be a reason for the optimized viral confrontation of the immune system. Thus in the presented case, after the first dose of rhEPO and packed RBC transfusion, absolute lymphocyte count increased from 333 to 933/μL of blood; a rise quite larger than to be elucidated only by 250 mL of packed RBCs transfusion.
During inflammation, serum Hepcidin levels increase the following stimulation by IL‐6, downregulating cellular ferroportin and this leads to decreased iron absorption and its detainment in liver and spleen macrophages12 which could promote the survival of intracellular microorganisms. EPO by downregulating IL‐6 and Hepcidin levels could lead to an increased release of iron from macrophages and increased absorption of iron by the bone marrow, thus decreasing iron availability for intracellular organisms like Coronavirus for their required enzymatic activities. This antiviral strategy of keeping iron out of infected cells has previously been explored and considered to be potentially effective in human infections by hepatitis C virus, human immunodeficiency virus‐1, hepatitis B virus, and cytomegalovirus viral infections.13
Although the above‐mentioned novel mechanisms of EPO effect in septic states could elaborate the rapid clinical improvement of the presented COVID‐19 case, we should not underestimate the definitive effects of rising hemoglobin from 6.7 to 9 g/dL in the improvement of pulmonary oxygenation and thus relieving the existing respiratory symptoms. However, the 2.3 g/dL rise in hemoglobin level in only 7 days with the mentioned dose of rhEPO is both profound and questionable considering the reported peak effects of rhEPO in 2 to 6 weeks after the starting dose.14, 15
In spite of the aforementioned benefits for EPO, it can aggravate the formation of microthrombosis and subsequent septic multiorgan failure and coagulopathy.16 Besides, in patients with chronic kidney disease‐associated anemia, EPO increases thrombotic events and risk of death when administered for Hb more than 12 g/dL.17 Other side effects of rhEPO in patients receiving large doses have been reported to be hypertension, hyperviscosity, enhancement of tumor progression, and in rare instances pure red blood cell aplasia.18
Regarding the probable benefits of rhEPO in reversing ARDS and its side effects, it seems to be a reasonable choice to use this agent in critically ill COVID‐19 patients to save their lives from imminent death, however, to determine the optimal dose with maximum cytoprotective and antiapoptotic effects and minimum potential toxicity of rhEPO, more clinical studies are required.
Therefore, we recommend the designation of well‐organized clinical trials with careful consideration of rhEPO administration in anemic COVID‐19 patients to further evaluate its clinical benefits in this critical patient population group without imposing further adverse effects associated with this drug.
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HealthisWealth
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- Dec 10, 2015
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did not yet play the video. Why hydrogen peroxide? I just bought the other day 20volumes
EMF Mitigation - Flush Niacin - Big 5 Minerals
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