Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To date 88 abnormal hemoglobins have been described with altered oxygen affinities. Of these, 60 variants have high affinity and 28 have low affinity. Twenty-six of these abnormal hemoglobins are chemically unstable. Twenty-seven of the high affinity hemoglobins are associated with erythrocytosis. An equal number are not associated with increased red cell mass. Anemia has been reported with 13 of the low affinity variants; however, the primary cause of the anemia of many may be the concurrent chemical instability. A strong correlaton can be shown for stable variants with altered oxygen affinity between the P50 value of the red cell and the hemoglobin concentration of the affected individual's blood. Hemoglobin variants with altered oxygen affinity can be classified into groups depending upon the amino acid change in specific structural sites. The sites include subunit interfaces, heme contacts, central cavity, DPG binding site, C-terminus, and other external and internal residues. Functional studies of six abnormal hemoglobins, four at the beta 101 residue in the central cavity near the alpha 1 beta 2 interfce, one near the DPG binding site and one at the C-terminus of the beta chain, indicate that the exact explanation of the structure-function relationship in hemoglobin depends upon the specific residue that is altered and the chemical properties of the substituted group. Comparative studies of multiple variants of the same position should provide insight into the role of critical residues in the binding of oxygen by hemoglobin.
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PMID:Hemoglobin variants with altered oxygen affinity. 741 21

Angiotensin-converting enzyme (ACE) inhibitor therapy has recently been shown to be effective in the treatment of post-renal transplant erythrocytosis (PTE). In an attempt to assess the effect of drug treatment on serum erythropoietin level, glomerular filtration rate, and urinary protein excretion, we prospectively evaluated 8 consecutive cadaveric renal transplant recipients with PTE treated with ACE inhibitor therapy for 3 months. In response to ACE inhibition, the mean hematocrit (HCT) value decreased from 53.7 +/- 0.6% before treatment to 42.7 +/- 2.2% at the conclusion of the study (p = 0.03). However, 1 patient failed to respond to ACE inhibition (HCT > 50%), and 2 patients with PTE developed anemia (HCT < 35%) while maintained on drug treatment. Although the mean serum erythropoietin level decreased during ACE inhibition (from 22.8 +/- 8.4 to 9.4 +/- 5.3 mU/ml; p = 0.06), a consistent change in individual erythropoietin levels was not identified. At the conclusion of the study, the serum erythropoietin levels were undetectable in 4 patients, decreased in 1, unchanged in 2, and increased in the only patient with PTE who failed to respond to drug treatment. All patients tolerated the ACE inhibitor therapy without developing cough or hyperkalemia. In addition, serum creatinine levels, 125I-iothalamate clearances, and mean arterial blood pressures were unchanged throughout the study. Microalbuminuria (spot urinary albumin/creatinine ratio between 30 and 200 mg/g) developed in 5 patients with PTE and coincided with the onset of erythrocytosis (25.2 +/- 7 mg/g before PTE and 76.3 +/- 36.7 mg/g at the time of PTE detection).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association of post-renal transplant erythrocytosis and microalbuminuria: response to angiotensin-converting enzyme inhibition. 757 90

Anaemia of end-stage chronic renal failure improves following successful kidney transplantation. However, erythrocytosis occurs in 6.8-17.3% of transplanted patients. Mechanism of post-transplant erythrocytosis (PTE) and its erythropoietin (Epo) dependence are still controversial. Firstly, we compared basal serum Epo levels of 10 PTE patients, 14 non-erythrocytosic renal transplant (non-PTE) patients and 12 healthy blood donors. Then we performed venesection in PTE patients and healthy blood donors and compared their Epo response to venesection 5 hours later. The mean basal serum Epo of 24.3 mU/ml was significantly higher in the PTE group than the 10.8 mU/ml in the non-PTE and 8.6 mU/ml in the healthy blood donor group (p < 0.01). Epo levels in the non-PTE group did not differ significantly from those of healthy blood donors (p > 0.05). Following venesection the mean serum Epo levels increased significantly in both groups, from 24.3 mU/ml to 67.7 mU/ml (p < 0.001) in the PTE group and from 8.6 to 12.1 mU/ml (p < 0.01) in the healthy blood donor group, but the increment in the PTE group was more marked. We conclude that PTE patients have elevated basal serum Epo levels and there is a feedback regulation of Epo secretion in these patients like in healthy blood donors, but in an exaggerated way.
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PMID:Increased erythropoietin response to venesection in erythrocytosic renal transplant patients. 759 83

Erythrocytosis is not rare in renal transplant recipients, and phlebotomy is still the main treatment. Recently, the occurrence of angiotensin-converting enzyme (ACE) inhibitor induced anemia in patients on chronic hemodialysis and in renal transplant recipients has been reported. We herein report 5 transplant recipients whose hematocrit levels decreased while taking ACE inhibitors, including 2 patients treated with ACE inhibitors for erythrocytosis. The individual mean hematocrit values ranged from 35.0% to 54.7% before treatment and from 27.6% to 42.0% after treatment. The hematocrit level in the 2 patients with erythrocytosis decreased from 54.7% to 39.8% and 47.5% to 27.6%, respectively. Anemia improved after discontinuation or dosage reduction of the drugs. The patients were given the same immunosuppressive drugs, and had good renal function. ACE inhibitor-induced conspicuous anemia was not observed in the transplant recipient who received a kidney from a twin sibling and had not been taking any immunosuppressive drugs, nor in the 8 other patients with diabetes mellitus or chronic glomerulonephritis who served as controls. We conclude that ACE inhibitor-induced anemia may frequently arise in an immunosuppressed state. Based on these events, the ACE inhibitor can be used as a potent drug for erythrocytosis in post-transplant recipients.
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PMID:Angiotensin-converting enzyme inhibitor-induced anemia and treatment for erythrocytosis in renal transplant recipients. 766

Although full blood counts (FBC) are among the most commonly performed laboratory tests, the contribution of routine FBCs to the diagnosis of new problems is controversial. This study represents a unique linkage of a consultant haematology team, reviewing all abnormal blood counts, to an organization providing ambulatory health care to 350,000 patients. The objective was to establish the underlying clinical disorders responsible for all abnormal FBCs during a 2-month period, and to estimate the impact of the haematology team on the diagnostic work-up and management of newly identified problems. 572 (2.55%) of the 22,454 FBCs were abnormal. Of these, 357 showed microcytosis, caused by iron deficiency (58%), thalassaemia minor (35%), inflammation (6%) or chronic renal failure (1%). The most common causes of normocytic anaemia (25 patients) were disseminated malignancy and acute blood loss; of macrocytosis (27 patients), chronic liver disease and cancer; of erythrocytosis (16 patients), chronic hypoxia; of thrombocytopaenia (48 patients), chronic liver disease and ITP; of thrombocytosis (47 patients), iron deficiency and inflammation; of leukopaenia or pancytopaenia (20 patients), cirrhosis and disseminated malignancy; and of leukocytosis (26 patients), chronic leukaemias in the elderly and infection in children. Major new haematological abnormalities were encountered in 0.24% of all blood counts, representing about one new diagnosis per day. Routine blood counts do contribute to the health care of a population. Screening for haematological disease through a central clinical laboratory covering a large high-risk ambulatory population offers a cost-effective way of searching for serious clinical problems, alerting the primary physicians of their existence, and offering advice in continued evaluation and problem management.
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PMID:The haematologist as watchdog of community health by full blood count. 779 88

Patients with HIV infection frequently develop clinically significant anemia, either as a manifestation of the HIV or as a result of therapy with medications such as zidovudine. Therapy with recombinant human erythropoietin can increase hemoglobin levels in these patients, decreasing transfusion requirements and improving some aspects of the quality of life. Once erythropoietin therapy is started, it is important to monitor patients carefully for the development of iron deficiency and erythrocytosis.
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PMID:The clinical application of recombinant erythropoietin in the HIV-infected patient. 785 17

Posttransplant erythrocytosis (PTE) represents a common complication in allograft recipients with normal renal function. Although the pathogenesis is not completely known, an alteration in the regulation of erythropoietin production by native kidneys or by renal allograft have been implicated as the main causes. Traditional therapies include repeated phlebotomies, bilateral native nephrectomies, and anticoagulant therapy. Recently, theophylline has been proposed as an effective therapy, although without general acceptance. Also, angiotensin-converting enzyme inhibitors have been involved in the development of anemia in chronic renal failure and dialysis patients. The aim of the present study was to demonstrate the efficacy of captopril on long-term treatment of PTE. Nineteen renal allograft recipients affected with severe PTE were included in the study. All patients had their native kidneys and none had a renal tumor or hydronephrosis. Restrictive criteria for PTE were applied to all patients and other causes of erythrocytosis were rationally excluded. Captopril was administered at a dose of 25 mg/24 hr (12.5 mg b.i.d.) during 12 months and no change on the initial dose was made during follow-up. After 3 months of captopril therapy and during the study period, significant reductions in hematocrit (P < 0.001), hemoglobin (P < 0.001), and RBC count (P < 0.001) were obtained in all patients. Erythropoietin levels decreased significantly during the study period, although the values were within the normal range of our laboratory. Captopril was well tolerated and only 1 patient had to be withdrawn from the drug because of dry cough. The present study has shown that captopril, at a low dose, represents a safe and effective therapy for PTE, without remarkable side effects or graft dysfunction. Long-term treatment with captopril in PTE did not induce anemia.
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PMID:Efficacy of captopril on posttransplant erythrocytosis. Long-term follow-up. 805 53

Erythrocytosis (i.e., elevation in red cell mass) frequently develops after renal transplantation and is associated with increased risk of thromboembolic incidents and hypertension. Because it has been reported that enalapril may induce anemia in renal allograft recipients, we have undertaken a prospective study to estimate the efficacy and safety of enalapril therapy for erythrocytosis and to establish the mechanism by which enalapril reduces red cell mass. Seventeen (12 male and 5 female) long-term renal allograft recipients with increased hematocrit value (> 55% for male and > 50% for female) and elevated red cell mass as determined with 51Cr-labeled autologous erythrocytes were treated with enalapril. After 3 months of therapy, enalapril was withdrawn and patients were observed in order to differentiate spontaneous remission of erythrocytosis from effects of enalapril therapy. After 3 months of the treatment, mean hematocrit decreased from 51.1% (range 47-56%) to 42.9% (range 37-51%; P < 0.01). Red cell mass significantly decreased during this period (from 46.7 ml/kg, range 32.5-60.7 ml/kg, to 32.9 ml/kg, range 20.1-60.1 ml/kg; P < 0.01). Serum erythropoietin levels also changed from 12.2 mIU/ml (range 1.0-33.0 mIU/ml) at baseline to 5.4 mIU/ml (range 0.7-24.2 mIU/ml; P < 0.05). During the following 3 months without enalapril treatment, an increase in hematocrit was noted, reaching 51.7% (range 46-58%; P < 0.05). No serious side effects of enalapril were observed during the study, but there was a need to reduce other hypotensive drugs in some patients. Serum creatinine did not change significantly during enalapril therapy (1.49 mg/dl, range 0.9-2.3 mg/dl, and 1.55 mg/dl, range 1.0-2.3 mg/dl; before and after 3 months of therapy, respectively). Our study proves that enalapril can be safely and effectively used to treat posttransplant erythrocytosis. The effect of enalapril on red cell mass results from reducing erythropoietin production.
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PMID:Correction of posttransplant erythrocytosis with enalapril. 816 3

We evaluated a newly developed enzymeimmunoassay for serum erythropoietin (Epo) and investigated relationship between Epo levels and hematological disorders. This method has several advantages including simplicity, high sensitivity, good precision. Moreover, the procedure requires only about 2.5 hours. Samples from 134 healthy subjects showed a normal logarithmic distribution, and its normal range was 4.5 approximately 21.3 mU/ml. The levels of Epo in normal subjects and various hematological disorders were as follows: 10.5 +/- 4.1 (mean +/- SD mU/ml) in normal subjects, 2.2 +/- 1.7 in polycythemia vera (PV), 6.1 +/- 3.1 in essential thrombocythemia, 17.8 +/- 27.3 in chronic myelogeneous leukemia, 3.6 +/- 1.8 in stress erythrocytosis, 39.4 and 14.1 in two cases of primary myelofibrosis, 1289 +/- 4798 in iron deficiency anemia and 6564 +/- 10870 in aplastic anemia. In patients with PV, serum Epo were low and did not correlate with hemoglobin concentration. However, inverse correlation was found between changes of Epo levels and hemoglobin levels in most patients. In cases in which PV progressed into myelofibrosis, anemia developed and Epo levels increased accordingly. These results suggest that the method is thought to be useful and reliable for the diagnosis and monitoring of PV and related hematological disorders.
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PMID:[Evaluation of a one step sandwich enzymeimmunoassay for serum erythropoietin--serum erythropoietin values in polycythemia vera and related hematological disorders]. 835 12

Erythropoietin is the only hematopoietic growth factor that behaves like a hormone. Produced in the kidneys and the liver, erythropoietin interacts with erythroid progenitor cells in the bone marrow to promote their proliferation and maintain their viability. Erythropoietin production is regulated at the level of its gene by tissue oxygenation; hypoxia or anemia stimulates erythropoietin production, and erythrocytosis suppresses it, but never completely. The plasma erythropoietin concentration reflects erythropoietin production and can be used to define erythropoietin-deficient states in which anemia may be amenable to correction by administration of recombinant human erythropoietin.
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PMID:Recombinant erythropoietin. 847 46


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