Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The administration of recombinant human erythropoietin (rHuEPO) to anemic hemodialysis patients is usually followed by a rapid increase in hemoglobin. Initial 'nonresponders' may either respond to higher doses of rHuEPO or rarely may remain totally unresponsive. Schematically, one can distinguish between a state of relative and absolute resistance to the action of the hormone. The most common causes of resistance are iron deficiency, aluminium overload, episodes of infection or other inflammatory processes, probably severe hyperparathyroidism, acute or chronic hemolytic conditions, acute or chronic blood loss, folate deficiency, and hemoglobinopathies in exceptional instances. Antibody formation against rHuEPO or marrow fibrosis secondary to rHuEPO treatment can be discarded as potential causes of resistance.
 ...
PMID:Resistance to recombinant human erythropoietin in hemodialysis patients. 226 Jun 16

Therapy with recombinant human erythropoietin (rHuEPO) can reverse anemia and improve the quality of life in anemic hemodialysis patients. However, therapy is costly and must be used efficiently. An initial rHuEPO dose less than 50 U/kg intravenously three times weekly may be adequate to achieve a hematocrit of 30-33% in many patients. Acquired iron deficiency is a common problem during rHuEPO therapy and must be prevented with oral and parenteral iron replacement to maintain the efficacy of rHuEPO. Patients should be monitored carefully for additional problems including: an increase in blood pressure; onset of seizures or headaches; increased blood potassium, phosphate, and creatinine concentrations; enhanced coagulability resulting in dialyzer and vascular access clotting; and myalgias with a 'flu-like' syndrome.
 ...
PMID:Practical approach to initiation of recombinant human erythropoietin therapy and prevention and management of adverse effects. 226 Jun 19

Erythroid colony growth in the presence and absence of erythropoietin was compared in 23 patients with primary proliferative polycythaemia (PPP), nine with idiopathic erythrocytosis, 10 with secondary polycythaemia, 15 with pseudopolycythaemia and in 76 normal subjects. Erythroid colonies growing without erythropoietin stimulation (endogenous erythroid colonies) from peripheral blood (BFU-E) were found in 20 of 22 patients with PPP and in two of seven with idiopathic erythrocytosis. None was found in secondary polycythaemia, pseudopolycythaemia, or in normal subjects. Small numbers of endogenous colony forming units-erythroid (CFU-E) (though not BFU-E) were cultured from the bone marrow of three of 24 normal subjects, suggesting that peripheral blood cultures provide a more specific indicator of clonal erythropoiesis. Peripheral blood endogenous erythroid colony growth is an effective and convenient means of distinguishing patients with clonal erythrocytosis and may be of particular value when iron deficiency obscures the diagnosis of PPP on conventional criteria.
 ...
PMID:Erythroid colony growth from peripheral blood and bone marrow in polycythaemia. 226 65

Thirty six patients with rheumatoid arthritis (RA) (25 with anaemia) were studied to establish the role of iron, vitamin B12, and folic acid deficiency, erythropoietin responsiveness, and iron absorption in the diagnosis and pathogenesis of anaemia in RA. Iron deficiency, assessed by stainable bone marrow iron content, occurred in 13/25 (52%), vitamin B12 deficiency in 7/24 (29%), and folic acid deficiency in 5/24 (21%) of the anaemic patients. Only 8/25 (32%) had just one type of anaemia. The iron deficiency of anaemia of chronic disease (ACD) was distinguished by ferritin concentration, which was higher in that group. Mean cell volume (MCV) and mean cell haemoglobin (MCH) were lower in both anaemic groups, but most pronounced in iron deficient patients. Folic acid, and especially vitamin B12 deficiency, masked iron deficiency by increasing the MCV and MCH. Iron absorption tended to be highest in iron deficiency and lowest in ACD, suggesting that decreased iron absorption is not a cause of ACD in RA. No specific causes were found for vitamin B12 or folic acid deficiency. Haemoglobin concentration was negatively correlated with erythrocyte sedimentation rate in the group with ACD. Erythropoietin response was lower in ACD than in iron deficient patients. It was concluded that generally more than one type of anaemia is present simultaneously in anaemic patients with RA. The diagnosis of each type may be masked by another. Studies on pathogenesis of the anaemia are difficult as deficiencies generally coexist with ACD. Disease activity and, possibly, erythropoietin responsiveness are major factors in ACD pathogenesis.
 ...
PMID:Anaemia in rheumatoid arthritis: the role of iron, vitamin B12, and folic acid deficiency, and erythropoietin responsiveness. 231 22

Therapy with recombinant human erythropoietin (rEPO) can correct anemia in RDT patients. However, iron deficiency can develop making treatment unsuccessful. Eighteen non-transfused RDT patients with hematocrit less than 26% were treated with rEPO to raise the HCT to 30-35%; then the dose was individually adjusted to maintain the HCT. The mean HCT rose from 22.3% to 31.5%. Ten patients received iron substitution before rEPO. During rEPO therapy five further patients had to be supplemented with iron; all patients needed an increase in the oral iron doses and three required i.v. iron. During the correction phase mean serum ferritin dropped from 203 micrograms/l to a minimum of 71 micrograms/l and was 102 micrograms/l after six months. Serum iron and TIBC changed only moderately. It thus appears that iron demand rises markedly during rEPO therapy, requiring iron substitution in most patients. Serum ferritin is the most sensitive parameter for development of iron deficiency.
 ...
PMID:Iron metabolism under rEPO therapy in patients on maintenance hemodialysis. 234 53

The article gives an account of contemporary knowledge of the treatment of anaemia in dialyzed patients by human recombinant erythropoietin. It was obtained by genetic engineering. It is very effective in the treatment of anaemia in patients included in a dialyzation programme, unless factors are present which reduce its effect (iron deficiency, Al cumulation and others). Along with red cell haematopoiesis, some other organs and systems are affected. The main undesirable effects may be hypertension and vascular thrombosis. In case of correct treatment and careful monitoring of treatment, these effects are outweighed by the assets of treatment. The drug is very expensive and it is important to pay attention to its effective use not only with regard to the patients but also to wider aspects associated with the care of dialyzed patients and the operation of dialyzation centres.
 ...
PMID:[Chronic kidney failure, anemia and erythropoietin]. 235 Jul 72

Immunoreactive serum erythropoietin concentrations were measured in 35 patients with anaemia associated with active rheumatoid arthritis. Based on an evaluation of stainable iron in the bone marrow (marrow iron grade 0-4) and serum ferritin concentrations (concentrations less than or equal to 60 micrograms/l compatible with iron deficiency) the anaemia was found to be complicated by iron deficiency in 19/35 (54%) of the patients. The mean serum erythropoietin level (57.6 (SD) 27.3) U/l) was sufficiently raised for the degree of anaemia irrespective of the size of the marrow iron stores. Thus the data do not support the contention that suppressed secretion of erythropoietin is involved in the pathogenesis of anaemia of chronic disorders. There was a significant inverse correlation between the haemoglobin concentration and log serum erythropoietin in the patients with rheumatoid arthritis. In the patients with adequate iron stores, but not in the iron depleted patients, there was a tendency for serum erythropoietin concentrations to correlate positively both with C reactive protein and erythrocyte sedimentation rate. Red cell distribution width (mean (SD) 16.3 (1.8)%) was above normal (11.5-14.5%) both in the iron replete and the iron depleted patients, and the mean red cell distribution width values did not differ significantly among the two subpopulations. The plasma lactoferrin concentration (mean (SD) 137.6 (109.9) micrograms/l) was normal and did not differ significantly between the iron deficient patients and those with adequate iron.
 ...
PMID:Anaemia of rheumatoid arthritis: serum erythropoietin concentrations and red cell distribution width in relation to iron status. 238 57

The baseline hematologic status of 27 patients with modest degrees of aluminum overload was examined. In addition, hematologic data were evaluated in 19 of these patients during and after treatment with DFO. Although neither severe anemia nor microcytosis was observed pretreatment, there was a significant correlation between hemoglobin level and degree of aluminum burden as determined by bone surface aluminum staining (r = -0.58; P less than 0.007). Following treatment with DFO, hemoglobin concentration increased dramatically by 1.3 to 4.4 g/dl in eight patients but did not change in the remaining eleven. Responders and nonresponders were similar with regard to the degree of aluminum overload both before and after chelation therapy but differed with regard to baseline levels of erythropoietin (higher in responders) and degree of iron overload (greater in nonresponders). Pretherapy levels of red cell ALA dehydratase were depressed in all patients (32 +/- 4 vs. 56 +/- 5 U/g Hb in normals) but did not correlate with the degree of aluminum overload and did not change with chelation therapy. Pretherapy levels of red cell protoporphyrin were elevated in 15 of 24 patients (62%) and were higher in responders than in nonresponders. Following DFO therapy, levels fell by 25 to 50% in 7 of 8 patients with elevated pretherapy values, despite the tendency in several patients to develop iron deficiency with treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Aluminum induced anemia: pathogenesis and treatment in patients on chronic hemodialysis. 261 92

Terminal renal dysfunction (TRD) was induced in 2 groups of dogs by partial surgical ablation of the kidney. Dogs of a control group and of 1 of the TRD groups were maintained on a diet containing normal phosphorus concentration, whereas dogs of the other TRD group were maintained on a low-phosphorus diet. Mild anemia developed in dogs of both TRD groups and could not be attributed to iron deficiency, increased erythrocyte concentration of 2,3-diphosphoglycerate, or absolute deficiency of erythropoietin (EP). Subsequently, all dogs were acutely depleted of approximately 25% of their blood volume. Erythropoietin concentration in dogs of the TRD groups was lower than that of controls, however, erythroid regenerative capacity was comparable with that of control dogs when plasma parathyroid hormone (PTH) concentration was lowered by reduced dietary intake of phosphorus. The PCV in dogs of the chronic TRD groups had a slight positive correlation with serum EP concentration, and a significant (P less than 0.05) negative correlation with plasma PTH and serum phosphorus and creatinine concentrations, using a correlation matrix. There was no longer a significant correlation between plasma PTH concentration and PCV after controlling for serum creatinine concentration by use of a multiple linear regression analysis. A significant (P less than 0.05) negative correlation also was observed between plasma PTH and serum EP concentrations, but not between serum EP and phosphorus or creatinine concentrations. Significance of the EP and PTH association was reduced when analyzed, using a multiple linear regression analysis that included serum creatinine values.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Role of parathyroid hormone in the anemia of chronic terminal renal dysfunction in dogs. 261 21

Several factors contribute to the pathogenesis of anemia due to renal failure. Hypoproliferation of red cell progenitors may be caused partially by an inhibitory effect of some 'uremic toxins' whose existence certainly is very controversial. Iron deficiency due to gastrointestinal and dialysis-related blood losses and occasionally aluminum intoxication may interfere with the maturation of the erythron. Moderate hemolysis with shortening of red cell survival to some 50% of normal may be an additional factor. The main cause of anemia is, however, inadequate production of erythropoietin by the diseased kidney. This latter factor has now become amenable to treatment.
 ...
PMID:[Pathogenesis of anemia due to kidney disease]. 264 77


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>