Hidronefrosis como causa de poliglobulia secundaria / Hydronephrosis as a cause of secondary polyglobulia

La policitemia primaria es producida por una mutación adquirida o heredada en las células progenitoras de los glóbulos rojos, mientras que la poliglobulia secundaria está relacionada con un aumento de la eritropoyetina sérica como respuesta a la hipoxia tisular o a la producción autónoma tumoral. Hace más de medio siglo que se conoce que la hidronefrosis puede actuar como una rara causa de eritrocitosis debido al aumento de producción de eritropoyetina por un riñón que censa una disminución de oxígeno, mecanismo también observado en la estenosis de la arteria renal y en los quistes renales. Se describe a continuación el caso de un paciente de 38 años con poliglobulia atendido en el Hospital Italiano de San Justo (Argentina), que presenta como hallazgo una hidronefrosis unilateral severa y cuya resolución quirúrgica a través de una nefrectomía revierte el cuadro hematológico de base. (AU)

Primary polycythemia is produced by an acquired or inherited mutation in progenitor cells of red blood cells, while secondary polyglobulia is related to an increase in serum erythropoietin in response to tissue hypoxia or autonomous tumor production. Since the middle of the twentieth century, the hydronephrosis is known to be a rare etiology of secondary polycythemia, with increased erythropoietin production caused by diminished oxygen sensing by the kidney, also seen in renal artery stenosis and kidney cysts. We describe a case of a 38 year old patient with polycythemia studied in the "Hospital Italiano de San Justo" (Argentina) that presented an incidental severe unilateral hydronephrosis, and nephrectomy was carried out as a final resolution of the hematological disorder. (AU)

Relation between anaemia and bone marrow features and serum erythropoietin in dogs with chronic kidney disease / Relação entre anemia e achados de medula óssea e eritropoetina sérica em cães com doença renal crônica

Chronic anaemia is one of the most severe complications of chronic kidney disease, contributing to morbidity and mortality caused by the disease; therefore, bone marrow cytological evaluation is needed to monitor the progression of anaemia. This study aimed to correlate the anaemia in dogs at different stages of chronic kidney disease with their serum biochemistry, myelogram results and serum erythropoietin findings. Sixty-three dogs were grouped according to International Renal Interest Society (IRIS) classification in stages 1, 2, 3 and 4. Haematologic, serum and urinary biochemistry and serum erythropoietin were performed for comparison with the findings of bone marrow cytology obtained by aspiration of the manubrium. Cytological findings for erythroid hypoplasia were described in 93.65% of dogs, and the anaemia was observed in 84.1% of them. The haematological findings were correlated with azotaemia (p<0.05). It was concluded that the erythroid hypoplasia has correlation with persistent anaemia in dogs at all stages of chronic kidney disease, with iron deficiency in dogs in the early stages and with peripheral destruction of erythrocytes caused by azotaemia.(AU)

A anemia crônica é umas das complicações mais graves da doença renal crônica, contribuindo para a morbidade e mortalidade causada pela doença; Portanto, a avaliação citológica da medula óssea é necessária para monitorar a progressão da anemia. Assim, esse estudo objetivou correlacionar a anemia em cães em diferentes estágios da doença renal crônica aos achados de bioquímica sérica, mielograma e concentração sérica de eritropoietina. Sessenta e três cães foram agrupados de acordo com a classificação da International Renal Interest Society (IRIS) em estágios 1, 2, 3 e 4. Foram realizadas análises hematológicas, bioquímicas séricas e urinárias, e dosagem sérica de eritropoetina para comparação com os achados medulares obtidos por citologia aspirativa do manúbrio. Os achados citológicos de hipoplasia eritróide foram descritos em 93,65% dos cães, e a anemia foi observada em 84,1% dos cães. Os resultados hematológicos foram correlacionados com azotemia (p<0,05). Concluiu-se que a hipoplasia eritróide teve associação com a anemia persistente em cães em todas as fases de doença renal crônica, com deficiência de ferro em cães em fases iniciais e com a destruição periférica dos eritrócitos causada pela azotemia.(AU)

Straightforward Identification of Masked Polycythemia Vera Based on Proposed Revision of World Health Organization Diagnostic Criteria for BCR-ABL1-Negative Myeloproliferative Neoplasms

No abstract available.

Diabetic Retinopathy Risk Factors: Plasma Erythropoietin as a Risk Factor for Proliferative Diabetic Retinopathy

PURPOSE: The purpose of this study was to evaluate whether any stage of diabetic retinopathy (DR) is associated with levels of plasma erythropoietin and other plasma parameters. METHODS: It was examined a representative sample of 180 type 2 diabetes patients aged 40 to 79 years. Ophthalmic examination including a funduscopic examination, performed by an experienced ophthalmologist and the retinal finding were classified according to the grading system for diabetic retinopathy of ETDRS (Early Treatment Diabetic Retinopathy Study). It was measured the levels of plasma erythropoietin, cholesterol, triglyceride, apolipoproteins A and B, C-reactive protein, fasting blood glucose and hemoglobin A1C (HbA1C) in 88 DR patients and 92 controls without DR. Risk factors correlated with DR were compared between groups. RESULTS: The study group of 180 patients included 72 males and 108 females. The mean age of the patients with and without DR was 57.36 ± 8.87 years and 55.33 ± 8.28 years, respectively. Of the 88 patients with DR, only 9 (10%) had proliferative DR and the rest suffered from non-proliferative DR. The mean plasma levels of erythropoietin in proliferative DR group showed a significant difference in comparison to other groups. The mean plasma levels of cholesterol, triglyceride, apolipoproteins A and B, C-reactive protein, and fasting blood glucose were not significantly different in the three groups except for HbA1C. The absolute relative risk (ARR) also showed that erythropoietin was an increasing risk for proliferative DR (ARR, 1.17; 95% confidence interval, 1.060 to 1.420; odds ratio,1.060). CONCLUSIONS: Of the factors studied, erythropoietin level showed significant increase in proliferative DR group. The stepwise raised in mean plasma erythropoietin level which demonstrates significant correlation with proliferative DR versus remaining two groups, will be an indication of its role in proliferative DR.

O nível sérico de Fas solúvel é preditor da necessidade de transfusão de hemácias em pacientes gravemente enfermos / Serum soluble-Fas is a predictor of red blood cell transfusion in critically ill patients

OBJETIVO: Investigar a relação entre a transfusão de hemácias e os níveis séricos de Fas solúvel, eritropoietina e citocinas inflamatórias em pacientes gravemente enfermos, com e sem insuficiência renal aguda. MÉTODOS: Os seguintes grupos foram estudados: pacientes gravemente enfermos com insuficiência renal aguda (n=30) e sem insuficiência renal aguda (n=13), pacientes portadores de doença renal crônica terminal em hemodiálise (n=25) e indivíduos saudáveis (n=21). Os níveis séricos de Fas solúvel, eritropoietina, interleucina 6, interleucina 10 e ferro, além da concentração de hemoglobina e de hematócrito, foram analisados em todos os grupos. A associação entre tais variáveis foram estudadas nos pacientes gravemente enfermos. RESULTADOS: Os níveis séricos de eritropoietina mostraram-se mais elevados nos pacientes gravemente enfermos do que nos dos demais grupos. Concentrações mais baixas de hemoglobina foram documentadas nos pacientes com insuficiência renal aguda em relação aos demais. Níveis séricos mais elevados de Fas solúvel foram observados nos pacientes com insuficiência renal aguda e doença renal crônica terminal. Pacientes gravemente enfermos transfundidos apresentaram níveis séricos mais elevados de Fas solúvel (5.906±2.047 e 1.920±1.060; p<0,001), interleucina 6 (518±537 e 255±502; p=0,02), interleucina 10 (35,8±30,7 e 18,5±10,9; p=0,02) e ferro, além de maior mortalidade em 28 dias. Os níveis séricos de Fas solúvel mostraram-se independentemente associados ao número de transfusões (p=0,02). O nível sérico de Fas solúvel foi um preditor independente da necessidade de transfusão de hemácias em pacientes gravemente enfermos (p=0,01). CONCLUSÃO: O nível sérico de Fas solúvel é um preditor independente da necessidade de transfusão de hemácias em pacientes gravemente enfermos, com ou sem insuficiência renal aguda. Mais estudos clínicos e laboratoriais são necessários para confirmar tal resultado.

OBJECTIVE: To investigate the relation between the need for red blood cell transfusion and serum levels of soluble-Fas, erythropoietin and inflammatory cytokines in critically ill patients with and without acute kidney injury. METHODS: We studied critically ill patients with acute kidney injury (n=30) and without acute kidney injury (n=13), end-stage renal disease patients on hemodialysis (n=25) and healthy subjects (n=21). Serum levels of soluble-Fas, erythropoietin, interleukin 6, interleukin 10, iron status, hemoglobin and hematocrit concentration were analyzed in all groups. The association between these variables in critically ill patients was investigated. RESULTS: Critically ill patients (acute kidney injury and non-acute kidney injury patients) had higher serum levels of erythropoietin than the other groups. Hemoglobin concentration was lower in the acute kidney injury patients than in other groups. Serum soluble-Fas levels were higher in acute kidney injury and end-stage renal disease patients. Critically ill patients requiring red blood cell transfusions had higher serum levels of soluble-Fas (5,906±2,047 and 1,920±1,060; p<0.001), interleukin 6 (518±537 and 255+502; p=0.02) and interleukin 10 (35.8±30.7 and 18.5±10.9; p=0.02), better iron status and higher mortality rates in the first 28 days in intensive care unit. Serum soluble-Fas levels were independently associated with the number of red blood cell units transfused (p=0.02). Serum soluble-Fas behaved as an independent predictor of the need for red blood cell transfusion in critically ill patients (p=0.01). CONCLUSIONS: Serum soluble-Fas level is an independent predictor of the need for red blood cell transfusion in critically ill patients with or without acute kidney injury. Further studies are warranted to reconfirm this finding.

Study the relationship of erythropoietin and chronic obstructive pulomonary disease

It has long been known that COPD causes polycythemia secondary to erythrocytosis caused by hypoxia present in advanced cases of COPD. However, it was shown in several studies that some COPD patients had anemia rather than erythrocytosis. Revealing the changes which occur in erythropoiesis in response to COPD was the aim of the current study. 41 COPD patients of different groups according to the inclusion and exclusion criteria and ten healthy control subjects age and sex matched were enrolled in the study. For all, history taking and full Clinical exam were performed, also ABGs, PFT [spirometry], routine labs [CBC, liver and renal function] and determination of EPO should be performed on human serum by ELISA. Showed that the erythropoietin level was 15.24 +/- 2.6 in stage 1, 22.61 +/- 5.68 in stage 2, 33.59 +/- 4, in stage 3, then 17.9 +/- 3.3 in stage 4. Also the total percentage of anemia in COPD patients was 46.3% [19/41], in comparison to 51.3% [21/41] non anemic and 2.4% [1/41] polycythemic. And that the percentage of anemia was 27.3% in stage 1, followed by 38.0% in stage 2, 100% in stage 3 then dropped to 58.33% in stage 4 with emergence of polycythemia in 8.33% of cases. Although COPD was thought to cause polycythemia, the current study showed that almost half of patients have anemia, and polycythemia occurred only in the advanced stages. It also appeared that response to erythropoietin in COPD is probably blunted especially with increased severity of the condition. This might be considered as a contributing factor in the development of anemia in COPD which is considered as anemia of chronic disease

Hb E/beta-thalassaemia: a common & clinically diverse disorder.

Haemoglobin E-beta thalassaemia (Hb E/β-thalassaemia) is the genotype responsible for approximately one-half of all severe beta-thalassaemia worldwide. The disorder is characterized by marked clinical variability, ranging from a mild and asymptomatic anaemia to a life-threatening disorder requiring transfusions from infancy. The phenotypic variability of Hb E/β-thalassaemia and the paucity of long-term clinical data, present challenges in providing definitive recommendations for the optimal management of patients. Genetic factors influencing the severity of this disorder include the type of beta-thalassaemia mutation, the co-inheritance of alpha-thalassaemia, and polymorphisms associated with increased production of foetal haemoglobin. Other factors, including a variable increase in serum erythropoietin in response to anaemia, previous or ongoing infection with malaria, previous splenectomy and other environmental influences, may be involved. The remarkable variation, and the instability, of the clinical phenotype of Hb E beta-thalassaemia suggests that careful tailoring of treatment is required for each patient, and that therapeutic approaches should be re-assessed over-time.

Consequences of hypoxia-reoxygenation phenomena in patients with obstructive sleep apnea syndrome

Obstructive sleep apnea syndrome [OSAS] is a common disorder characterized by numerous episodes of absence of respiratory flow during sleep, which can be followed by a decrease in SaO2, which is rapidly normalized when ventilation resumes. We hypothesize that this hypoxia-reoxygenation phenomena may affect the generation of vascular endothelial growth factor [VEGF], erythropoietin [EPO], endothelin-1 [ENDO-1], and inducible nitric oxide synthase [iNOS]. Prospective, patients referred to sleep disorders center. The presence and severity of OSAS were determined using the standard overnight polysomnography. Diagnosis of OSAS was made when the apnea-hypopnea index [AHI] was >/= 15, independent of the appearance of symptoms. Serum levels of VEGF, EPO, ENDO-1, and nitrite-nitrate were measured after overnight fasting in 69 patients with OSAS and in 17 healthy control subjects. Serum levels of VEGF and nitrite-nitrate were measured again after 12 weeks of treatment with continuous positive airway pressure [CPAP] in OSAS patients. Serum VEGF levels were found to be significantly higher and nitrite-nitrate levels were found to be significantly lower in OSAS patients than in controls [P=.003, .008, respectively], but no differences in EPO and ENDO-1 levels were found between the groups. We demonstrated that in OSAS patients, the serum VEGF levels were decreased and nitrate levels were increased after 12 weeks of CPAP treatment [P=.001, .002, respectively]. According to our data, it is likely that hypoxia-reoxygenation phenomena affect the VEGF and nitrite-nitrate levels, which may be pathogenic factors in generating cardiovascular complications in OSAS

role of hepcidin in iron overload in children with beta-thalassemia

Thalassemias are a group of inherited blood disorders with defective production of hemoglobin. Patients with beta-thalassemia develop iron overload due to increased iron absorption and transfusion therapy. Hepcidin is a hepatic hormone released in case of iron overload to regulate systemic iron homeostasis by inhibiting iron absorption from diet and recycling of iron by macrophages. To determine role of hepcidin in the pathogenesis of iron overload in 13-thalassemia. Setting: Departments of Clinical Pathology, and Pediatrics, Faculty of Medicine, Tanta University, Egypt. 20 patients with beta thalassemia major [TM] included 10 males and 10 females, 20 patients with beta thalassemia intermedia [TI] included 10 males and 10 females and twenty healthy children of matched age and sex were included in this study. We assessed iron overload by measuring serum ferritin, assessed erythropoietic activity by measuring serum erythropoietin levels, and correlated these with urinary hepcidin measurements. We found severe urinary hepcidin deficiency in TI with strong inverse relationship between urinary hepcidin and serum erythropoietin levels in comparison with control group. In contrast, urinary hepcidin levels were elevated in TM with decrease of erythropoietin levels. In addition, serum ferritin level was significantly higher in TM than TI and significantly higher in TM and TI compared with normal control. Hepcidin deficiency may be the key factor allowing excessive iron absorption and iron overload in TI while in TM, chronic hemolysis and frequent blood transfusions may be the main factors that increase iron load

Anemia in COPD patients and its relation to serum levels of erythropoietin

Although chronic obstructive pulmonary disease [COPD] is traditionally associated with polycythemia, its systemic inflammatory components can interfere with erythropoietin and result in anemia of chronic disease. We assessed the frequency of anemia and its relation to serum erythropoietin [EPO] levels and severity of the disease in a group of COPD patients. Eighty patients with the mean age of 66.48 +/- 11.55 years and mean forced expiratory volume in first second [FEV1] of 45.14 +/- 16.88% predicted were enrolled in this study. Severity of the disease was defined according to the global initiative for chronic obstructive lung disease [GOLD] guidelines. Hemoglobin and erythropoietin levels were assessed in all patients. Anemia of chronic disease was present in 13 of 80 patients [16%]. The mean serum levels of EPO were 59 +/- 203 [SD] micro/l and 70.3 +/- 255 [SD] micro/l in anemic and nonanemic COPD patients, respectively. There was no significant difference between the two groups [p=0.13]. A significant correlation was seen between hemoglobin and serum EPO in all COPD and nonanemic patients [r = - 0.86, p < 0.001 and r = - 0.28, p = 0.02]. No significant correlation was seen between hemoglobin and serum erythropoietin levels in the anemic group [r = 0.07, p = 0.82]. This study showed that anemia occurred relatively frequently in COPD patients. In addition to erythropoietin resistance, other factors are probably involved in the pathogenesis of anemia in these patients

Enteral erythropoietin increases plasma erythropoietin level in preterm infants: a randomized controlled trial.

OBJECTIVE: To evaluate the effects of enteral administration of recombinant human erythropoietin (rhEPO) on serum level of erythropoietin and erythropoiesis in preterm infants. STUDY DESIGN: Randomized controlled trial. SETTING: Level III NICU. SUBJECTS: 16 preterm infants less than 34 wk with birth weight less than 1800 g. INTERVENTION: Enteral rhEPO 400 U/kg, three times/week, plus FeSO4,3-6 mg/Kg/day ( Study group, n = 7) or FeSO4 only (Control group, n = 9). OUTCOME MEASURES: Hemoglobin, serum erythropoietin (EPO), reticulocyte count, and serum ferritin levels, measured at baseline, after 10 days and at discharge. RESULTS: Mean birth weight and gestational age for the Study and the Control groups were 1328.5 +/- 267.4 vs. 1392.8 +/- 196.7 g and 30.7 +/- 2.5 vs. 30.2 +/- 0.9 weeks, respectively. At discharge, there was no difference in hemoglobin or hematocrit but the reticulocyte counts were significantly higher in the Study group (1.4 +/- 0.7 vs. 0.7 +/- 0.4, P = 0.03). Serum erythropoietin level was significantly higher in the Study group (18 +/- 11 vs. 8.6 +/- 3.9 mU/mL, P = 0.006). Conversely, serum ferritin level was lower in the study group but did not achieve statistical significance. CONCLUSIONS: Enteral administration of rhEPO in preterm infants resulted in increase in serum erythropoietin and reticulocyte counts at the time of discharge without significantly affecting hemoglobin or hematocrit.

Anemia, interleukin-10, tumor necrosis factor alpha, and erythropoietin levels in children with acute, complicated and uncomplicated malignant malaria in Jazan, Saudi Arabia

To gain insight into potential relationships between tumor necrosis factor alpha [TNF-alpha], interleukin 10 [IL-10], erythropoietin [EPO], and anemia in acute malaria, 90 children 3 to 11 years with acute malaria were studied. According to parasitemia and hemoglobin levels, they were divided into 3 groups: Gl [mild]: asexual low-density Plasmodium falciparum parasitemia <8000 parasites/ul and hemoglobin levels >8g/dl. G2 [high-density uncomplicated]: asexual high-density parasitemia [>8000 parasites/ul, with hemoglobin levels >8 g/dl. G3 [anemia]: with severe malaria symptoms and parasitemia with anemia [hemoglobin levels <8 g/dl]. Hospital controls included 10 children with matching age group who required inpatient management but had no malaria parasitemia. Good marrow response was in Gl and G2 showed by elevation of serum EPO and soluble transferring receptors [sTfR] and increased red cell distribution width [RDW]. In G3, bone marrow suppression was in spite of increased EPO level in response to anemia. TNF-alpha level was significantly higher G2 and G3 [P.05]. IL-10 levels in Gl were significantly higher than in hospital control group [P<0.05]. The highest level of IL-10 was in G2. The mean EL-10 to TNF- alpha ratio in G2 [4.64] was significantly higher [P<.005] than in G3 [mean ratio, 1.77]

role of hepcidin level in iron overload in children with beta-thalassemia

Thalassemias are a group of inherited blood disorders with defective production of hemoglobin. Patients with beta-thalassemia develop iron overload due to increased iron absorption and transfusion therapy. Hepcidin is a hepatic hormone released in case of iron overload to regulate systemic iron homeostasis by inhibiting iron absorption from diet and recycling of iron by macrophages. To determine role of hepcidin in the pathogenesis of iron overload in 6-thalassemia. 20 Patients with beta thalassemia major [TM] included 10 males and 10 females, 20 patients with beta thalassemia intermedia [TI] included 10 males and 10 females and twenty healthy children of matched age and sex were included in this study. We assessed iron overload by measuring serum ferritin, assessed erythropoietic activity by measuring serum erythropoietin levels, and correlated these with urinary hepcidin measurements. We found severe urinary hepcidin deficiency in TI with strong inverse relationship between urinary hepcidin and serum erythropoietin levels in comparison with control group. In contrast, urinary hepcidin levels were elevated in TM with decrease of erythropoietin levels. In addition, serum ferritin level was significantly higher in TM than TI and significantly higher in TM and TI compared with normal control. Hepcidin deficiency may be the key factor allowing excessive iron absorption and iron overload in TI while in TM, chronic hemolysis and frequent blood transfusions may be the main factors that increase iron load

estimation of erythropoietin levels in the blood serum and cystic fluid in patients with solitary renal cysts

Renal cysts are common among people older than 50 years. A hypothesis that erythropoietin may be produced in renal cysts as a defense mechanism to prevent anemia was put forwards, thus erythropoietin concentration in cystic fluid should be higher than the serum level. Our study aimed to explain this phenomenon. Levels of erythropoietin were estimated in serum and cystic fluid of 33 patients with renal cysts and were compared to results from 33 controls. Results showed a 35 times higher level of erythropoietin in cystic fluid compared to serum. Serum levels of erythropoietin from renal cyst patients were comparable to those from control group. Thus we concluded that there is no erythropoietin penetration from the cystic fluid into the blood serum; and the role of high erythropoietin concentration in renal cystic fluid is not clear yet

study of some clinical and biochemical markers of epileptic seizures

The adverse effects of anticonvulsant drugs, duration and expense of therapy and social implications make it essential for accurate discrimination of epileptic from non epileptic seizures [NES]. There is still no single biochemical marker for epileptic seizures and many patients being treated as epileptics are not actually so. Moreover, the coexistence of pseudoseizures with epilepsy is high. Recently few studies had investigated the neuroprotective erythropoietin [EPO] system in the central and peripheral nervous systems. However, the clinical importance of EPO as a specific biochemical marker for epileptic fits is not yet investigated. Sixty children divided into 3 groups were studied. Group I included 20 recently diagnosed epileptics, aged 3.5-15 years. Group II involved 20 children with recent NES, aged 2-14 years. Twenty children suffering fever of unknown origin with lumbar puncture as part of its diagnostic work up, aged 3-15 years represented group III [control group]. All children were suffering no other neurological, hematological or renal diseases. Thorough history, clinical examination and routine investigations, confirmed diagnosis and established exclusion criteria. CT brain, EEG and EMG were done for all patients. Peripheral white blood cells [WBCs], serum creatine kinase [CK] and serum and CSF albumin and erythropoietin [EPO] were measured 24 hours Post-ictally for all patients and on admission of control children. Family history was positive for epilepsy in 20% of epileptic children. Post-ictal symptoms followed more than a half of epileptic seizures and less than a quarter of NES. The most common types of epileptic seizures were generalized tonic-clonic [GTC], generalized tonic [GT], myoclonic then focal seizures. CT brain was normal among most epileptic and all non epileptic patients; with hemorrhage in two epileptics and calcification in only one. EEG showed focal [FEA], generalized [GEA] and multifocal epileptogenic activities [MFEA] among our recent epileptics. Peripheral WBCs, serum CK and CSF levels of EPO showed a significant elevation 24 hours Post-ictally following generalized tonic-clonic epileptic fits and to a lower extent following focal and non epileptic fits. The 3 parameters showed a significant positive correlation with seizure duration. Serum CK levels were markedly elevated [more than 200 U/L] and CSF levels of EPO increased by more than 2 standard deviations in a high percentage of epileptic seizures especially so; GTC seizures, with this marked degree of elevation as a more sensitive factor discriminating epileptic from non epileptic seizures. Post-ictal symptoms, peripheral WBCs, serum CK and CSF levels of EPO are important discriminative factors between epileptic and non epileptic seizures before proceeding to more sophisticated and expensive investigations

Effect of hyperhomocysteinemia on erythrocyte function and its impact on erythropoiesis in experimental rats

The current work was conducted to study the possible effect of hyperhomocysteinemia [HHcy] on some erythrocytic functions as a cause of anemia and its impact on erythropoietin [EPO] release in experimental rats. Forty adult male albino rats were divided into two main groups, the control group [Group I] and the hyperhomocysteinemic group [HHcy] [Group II]. Hyperhomocysteinemia was induced by subcutaneous injection of DL- homocysteine at a dose of 100 mg/kg/day for 4 weeks. At the end of the fourth week each main group was subdivided into two subgroups, [Ia] control, [Ib] Hypoxic-control [IIa] and HHcy, [IIb] Hypoxic-HHcy. Hypoxia was induced by a single intra-peritoneal injection of desferrioxamine [200 mg/kg] 22 hours before decapitation. Whole blood was used for determination of erythrocytic fragility, hematological parameters, reticulocyte percentage. Homocysteine, erythropoietin [EPO], urea and creatinine were estimated in plasma. Erythrocytes were used for estimation of lipid peroxidation, G6PDH activity and membrane separation for deten-nination of Na[+] K[+] ATPase enzymatic activity. Homocysteine, EPO and creatinine plasma levels, and reticulocyte% and erythrocytic lysis in addition to erythrocyte lipid peroxidation were all significantly higher, while G6PDH and Na[+] K[+]- ATPase enzymatic activities were significantly lower in the HHcy group as compared to the control group. A significant positive correlation was found between total Hcy plasma levels and erythrocyte lipid peroxidation. EPO plasma levels showed a significant increase in response to hypoxic stimulation in the control group, while blunted response was observed in the HHcy group. It could be concluded that disturbance in erythrocyte membrane and enzymatic functions in HHcy increases the susceptibility of RBCs to hemolysis and reduces its life span. Hyperhomocysteinemia also impacts EPO release to hypoxic stimulation which may be due to damaging effect of HHcy on renal cells

An insight on pathogenesis of systemic lupus erythmatosus-induced anemia of chronic diseases

The present study was designed to evaluate the frequency of anemia of chronic diseases [ACD] in patients with systemic lupus erythematosus [SLE] and to estimate serum levels of interleukin-6 [IL-6] and erythropotien [EPO] and to determine the serum positivity for antibodies to human EPO [anti-EPO antibodies] in patients with ACD so as to evaluate their probable role in pathogenesis of ACD. The study included 200 patients with SLE; all underwent clinical evaluation of disease activity using the British Isles Lupus Assessment Group [BILAG] score and laboratory assessment of immunologic parameters. Hemoglobin concentration [Hb cone.] was determined and anemia was defined by haemoglobin concentration [Hb cone.] of

Evaluation of hepcidin level and its relation to iron status, inflammation and liver function in hemodialyzed patients

Hepcidin, a key regulator of iron metabolism by blocking its intestinal absorption and its release by the reticuloendothelial system, and modulated in response to anemia, hypoxia or inflammation. The aim of the study was to assess hepcidin correlations with markers of iron status, erythropoietin therapy, liver function and markers of inflammation in hemodialyzed [HD] patients. Fifty patients on regular HD [30 patients treated with erythropoietin and 20 patients without erythropoietin therapy] and 20 healthy controls were studied. Hepcidin and C-reactive protein [CRP] were measured. Iron status, complete blood count, liver function and lipid profile were assessed. The weekly erythropoietin dose and the patients demographics were recorded. In comparison to the healthy controls, the HD patients had higher serum ferritin, CRP and hepcidin levels. Serum iron, total iron binding capacity [TIBC], transferrin saturation [TSAT], erythrocyte count, hemoglobin [Hb], hematocrit [Hct], platelet count and albumin were low in HD patients. In the patient group, hepcidin level were positively correlated with leukocyte count, triglyceride, albumin, aspartate aminotransferase, ferritin and erythropoietin dose and negatively correlated with erythrocyte count, Hb and HCt values. In multiple regression analysis, triglyceride [beta value was 0.27, p <0.05] and albumin [beta value was - 0.30, p < 0.05] were correlated with hepcidin in HD patients. In conclusion, high serum levels of hepcidin in HD patients may be due to accumulation in the serum, low - grade inflammation, frequently found in HD patients may also contributed. Elevated hepcidin levels in HD patients could be responsible for functional iron deficiency and anemia and may be considered as a sensitive tool for functional iron deficiency in these patients

Evaluation of serum erythropoeitin response to anaemia in macroalbuminurics of diabetic and non-diabetic etiologies.

This case-control study was undertaken in 75 subjects categorized into 3 equal groups (A: diabetic subjects with macroalbuminuria, B: non-diabetic subjects with macroalbuminuria and C; control subjects). Serum erythropoietin (EPO) was estimated and analyzed in relation to hemoglobin levels in the three groups. The Pearson's coefficient (r) for hemoglobin and log natural EPO was significant for groups A (0.01), B (0.05) and C (0.01). Linear regression analysis of hemoglobin and log natural EPO showed significant differences between the study and control groups; however no significant difference could be demonstrated amongst the study groups. Hence, it was concluded that an inadequate EPO production occurs in renal failure, which accounts for the anaemia and diabetes does not confer an additional discrepancy in this mechanism over non-diabetic macroalbuminuria.