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)

Serum haptoglobin has been estimated quantitatively in 25 patients with haemolytic disease, and its diagnostic value assessed by comparing the levels with those obtained in 110normal subjects, in 149 patients with other forms of anaemia, and in 37 patients with non-haematological disorders. The normal range was found to be 33 to 213 mg./100 ml.; subnormal levels were found in 80% of patients with haemolytic disease or megaloblastic anaemia, patients with haemorrhage into the tissues, and occasionally in association with other diseases. When taken in conjunction with other clinical and laboratory features this simple biochemical estimation can be of diagnostic value.
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PMID:DIAGNOSTIC VALUE OF SERUM HAPTOGLOBIN. 1424 92

Changes in the serum haptoglobin level have been reported in certain forms of anaemia (Allison and ap Rees, 1957; Allison, 1958; Nosslin and Nyman, 1958; Nyman, Gydell, and Nosslin, 1959), in hepatobiliary disease (Owen, Mackay, and Got, 1959) and in various inflammatory and chronic diseases (Jayle and Boussier, 1955; Allison and Blumberg, 1958). A simple colorimetric procedure for the determination of serum haptoglobins is presented. It is based on the peroxidase activity of haptoglobin-methaemoglobin complexes.
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PMID:A simple method for the determination of serum haptoglobins. 1442 49

Hemolysis after renal transplantation in some cases is clearly related to hemolytic-uremic syndrome (HUS) and usually attributed to cyclosporine (CsA) treatment. Acute hemolysis in other recipients is related to anti-erythrocyte autoantibodies. In most cases these patients have received ABO-compatible, although ABO-nonidentical, organs, mostly from O blood group donors. We report three cases of autoimmune hemolytic anemia after renal transplantation. Two patients (patients: 1 and 2; ABO-compatible, but nonidentical kidneys) suffered acute hemolysis in the third week after transplantation. One patient (patient 3: ABO-identical kidney) suffered a chronic, subclinical course of disease beginning 5 months after transplantation. The clinical picture of this disease was completely different from HUS. The existence of severe anemia (patients 1 and 2), hyperbilirubinemia (particularly high in patient 3), increased serum lactic dehydrogenase levels, and decreased serum haptoglobin in the presence of good graft function suggested an hemolytic anemia. In all patients the direct antiglobulin test was positive. The acute or chronic symptoms of hemolysis disappeared, at 2 and 5 weeks, respectively, after conversion from CsA to tacrolimus. Hemolysis in these patients probably relates to alloantibodies derived from passenger B lymphocytes transplanted with the organs. Because hemolysis has been most frequently related to CsA therapy, it is suggested that B lymphocytes proliferated and produced antibodies because CsA effects to inhibit T-cell function generally spares B-cell activity. It is proposed that a subtype of B cells, which are resistant to CsA, produces anti-A and/or anti-B antibodies. Treatment with tacrolimus appears to be successful, probably due to its alternate, and likely more effective, manner of B-cell suppression.
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PMID:Hemolytic anemia after renal transplantation: analysis of case reports. 1452 99

Hemolysis is a frequent complication of the implant of prosthetic valves, and is conditioned by a variety of factors, most of which related to the type of valve implanted and to the hemodynamic conditions following implantation. If sufficiently severe, it may lead to varying degrees of hemolytic anemia. The following laboratory tests are useful to diagnose and assess the severity of hemolytic anemia: hemoglobin levels; reticulocyte count; the demonstration of schistocytes on a blood smear; serum levels of lactic dehydrogenase, haptoglobin and iron. Treatment of hemolysis includes the supplementation of iron and folate when their deficiency is evident. Transfusions are necessary only in cases of severe anemia refractory to treatment. The use of beta-blockers appears to decrease the severity of hemolysis, likely because of the induction of bradycardia and of their negative inotropic effects. Some cases have been described of erythropoietin treatment for hemolytic anemia in these conditions, with favorable outcome. However erythropoietin use should currently be restricted to patients with severe hemolytic anemia in whom surgical repair or transfusions should be avoided or deferred. The recognition and the estimation of severity of hemolysis after valve implantation are important steps in the patients' follow-up and the premise for a rational treatment.
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PMID:[Hemolysis following valve surgery]. 1466 92

A 60-year-old woman with systemic sclerosis (SSc) was admitted because of severe anemia and Raynaud's phenomenon. Her anemia was associated with a low serum haptoglobin level and positive results of direct Coomb's tests, which indicated the presence of autoimmune hemolysis. Other laboratory investigations revealed positive anti-nuclear antibodies, anti-topoisomerase antibody, cold agglutinins, as well as low serum levels of IgM, C3, C4 and CH50. Bone marrow aspiration showed discrete hyperplasia of the erythropoietic system. She was diagnosed as low-titer cold agglutinin disease rousing secondarily to SSc. The anemia was alleviated with the oral administration of prednisolone. This case emphasized, in terms of pathogenesis, the close association between systemic rheumatic diseases and hematological abnormalities evoked by autoimmunity.
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PMID:Low-titer cold agglutinin disease with systemic sclerosis. 1500 58

Hemolysis presents as acute or chronic anemia, reticulocytosis, or jaundice. The diagnosis is established by reticulocytosis, increased unconjugated bilirubin and lactate dehydrogenase, decreased haptoglobin, and peripheral blood smear findings. Premature destruction of erythrocytes occurs intravascularly or extravascularly. The etiologies of hemolysis often are categorized as acquired or hereditary. Common acquired causes of hemolytic anemia are autoimmunity, microangiopathy, and infection. Immune-mediated hemolysis, caused by antierythrocyte antibodies, can be secondary to malignancies, autoimmune disorders, drugs, and transfusion reactions. Microangiopathic hemolytic anemia occurs when the red cell membrane is damaged in circulation, leading to intravascular hemolysis and the appearance of schistocytes. Infectious agents such as malaria and babesiosis invade red blood cells. Disorders of red blood cell enzymes, membranes, and hemoglobin cause hereditary hemolytic anemias. Glucose-6-phosphate dehydrogenase deficiency leads to hemolysis in the presence of oxidative stress. Hereditary spherocytosis is characterized by spherocytes, a family history, and a negative direct antiglobulin test. Sickle cell anemia and thalassemia are hemoglobinopathies characterized by chronic hemolysis.
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PMID:Hemolytic anemia. 1520 94

Four patients with paroxysmal cold hemoglobinuria (PCH) illustrate some of the difficulties in making the diagnosis. A 46-year-old male presented with anemia, a weakly positive direct antiglobulin test (DAT) with anti-IgG, a haptoglobin < 0.1 g/L, and a cold autoagglutinin showing anti-P specificity. A 9-year-old female had a 4-day coryzal illness, a 20 g/L fall in hemoglobin over 24 hours, and a haptoglobin < 0.1 g/L; the DAT was positive with anti-C3d. A 3-year-old female was referred following a rapid drop in hemoglobin of 30 g/L; the DAT was positive with anti-C3d. A 17-month-old female, unwell for 2 weeks, had a hemoglobin of 41 g/L; the DAT was strongly positive with anti-C3d and weakly positive with anti-IgG and -C3c. In all patients, PCH was confirmed by positive indirect Donath- Landsteiner tests, and the autoantibodies demonstrated P specificity. In two patients, the test was strongly positive; in the third patient, it was only positive using papainized red cells; and in the fourth patient, a two-stage papainized procedure was needed before a positive result was obtained. PCH must always be considered in a child with a rapid drop in hemoglobin, even if initial tests are negative.
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PMID:Paroxysmal cold hemoglobinuria and the elusive Donath-Landsteiner antibody. 1537 90

A 37-year-old male presented with severe anemia, mild jaundice, and hemoglobinuria during his second course of diclofenac for gout. The peripheral blood showed microspherocytes and nucleated red blood cells (RBCs). The reticulocyte count was 21 percent and haptoglobin was < 0.1 g/L. A presumptive diagnosis of diclofenac-induced immune hemolysis was made and blood, urine, and drug samples were referred for investigation. Direct antiglobulin testing showed the RBCs to be coated with IgG1, IgG4, and C3d, but an eluate only yielded weakly reacting IgG antibodies. In tests for drug-dependent antibodies, group O, R1R2 red cells were incubated with the patient's serum that had been mixed with either urine (which contained diclofenac metabolites) or diclofenac solution and then tested by an antiglobulin method. Strongly positive reactions with anti-IgG occurred in the tests using urine but only weak reactions in those tests employing diclofenac solution. All controls gave negative results. These findings support the role of diclofenac in causing hemolysis and the importance of employing urine as a source of drug metabolites. The findings also showed that an immune complex mechanism predominated and that the eluted IgG (detectable independently of the presence of the drug or its metabolites) confirmed a minor autoimmune component. Diclofenac was stopped and treatment with prednisolone and folic acid instituted; this resulted in complete recovery.
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PMID:Immune hemolytic anemia due to diclofenac. 1538 91

A 67-year-old woman with rheumatic aortic stenosis for 20 years was admitted to our hospital. Although she had no overt symptoms, she had severe aortic valve stenosis with a transvalvular pressure gradient of more than 150 mmHg. She had also been suffering from anemia and mild chronic renal failure. A peripheral blood smear showed numerous fragmented erythrocytes. Hemoglobin was 8.4 g/dl, lactate dehydrogenase was 316 IU/l, haptoglobin was less than 7.3 mg/dl, and hemosiderinuria was evident. We diagnosed intravascular hemolysis related to aortic stenosis. After we performed an aortic valve replacement, fragmentation on the peripheral blood smear dramatically disappeared.
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PMID:Intravascular hemolysis in aortic stenosis. 1557 43

Malignant lymphomas are often associated with immunological disorders. We describe here a 54-year-old woman with follicular lymphoma, simultaneously complicated with autoimmune hemolytic anemia and pure red cell aplasia. The patient had bilateral cervical, axillar and inguinal lymph node swellings. Peripheral blood analysis revealed severe anemia (Hb 3.4g/dl) and reticulocytopenia (2260/ml), and then the bone marrow showed erythroid hypoplasia. Furthermore, a direct Coombs test was positive and the serum haptoglobin level was undetectable. After treatment with CHOP followed by 1 mg/kg of prednisolone daily, the patient obtained complete remission and her anemia improved to the normal level.
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PMID:[Follicular lymphoma complicated with autoimmune hemolytic anemia and pure red cell aplasia]. 1560 89


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