Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002878 (hemolytic anemia)
 7,530 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of acute immune hemolytic anemia associated with non-traumatic rhabdomyolysis (NTR) induced by streptomycin (SM) reinjection, which developed acute renal failure, has been reported. A 70-year-old female was admitted to our hospital because of sudden macroscopic hematuria after reinjection of 1g. SM. Laboratory findings on admission were as follows; hemoglobin and myoglobin were positive in urine. RBC 129 x 10(4)/microliters, Hb 4.9g/dl, Ht 11.1%, reticulocytes 52/1000, serum indirect billirubin 3.8g/dl, LDH 9, 230 WU, BUN 149mg/dl, Cr 7.9mg/dl, myoglobin 1, 400ng/ml and haptoglobin 10.6mg/dl. The drug lymphocyte stimulating test of SM was positive (215%). A direct antiglobulin test was also positive. An indirect antiglobulin test was negative, but became positive after incubation with SM. These observations made the diagnosis of SM-induced hemolytic anemia associated with NTR. On the second hospital day she developed anuria, and was put on hemodialysis treatment. Two months after the acute hemolytic episode and acute renal failure she recovered and is presently in good health without recurrence.
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PMID:[A successfully treated case of acute renal failure due to acute immune hemolytic anemia and nontraumatic rhabdomyolysis induced by streptomycin reinjection]. 129 78

Hemolysis can be induced by two general mechanisms. In the first one, erythrocytes lyse intravascularly due to complement fixation, trauma, or other extrinsic factors. In the second mechanism, which is the most common, the red cells are removed from the circulation by the mononuclear-phagocytic system either because they are intrinsically defective or because of the presence of bound immunoglobulins to their surfaces. The diagnosis of hemolysis is not difficult to establish and is based on the presence of anemia with sustained reticulocytosis in the absence of blood loss. Additional findings can include marrow erythroid hyperplasia; increased unconjugated bilirubin, LDH, and free hemoglobin; decreased haptoglobin and hemopexin; hemoglobinuria and hemosiderinuria; and decreased 51Cr red cell half-life. Hemoglobinemia, hemoglobinuria, and hemosiderinuria occur only in the setting of severe and rapid intravascular hemolysis. Conditions associated with significant lysis of red cells in the circulation include incompatible transfusion, G6PD deficiency, PNH, severe burns, and certain infections. The morphology of the red cell is abnormal in almost all cases of hemolytic anemia. However, the morphologic abnormality can be, in certain cases, diagnostic of the underlying condition. Treatment is usually supportive, with effective therapy directed to treat the underlying cause of hemolysis.
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PMID:Hemolytic anemias. Diagnosis and management. 157 62

Microangiopathic haemolytic anaemia was diagnosed in the course of haematopoietic and lymphatic disorders such as chronic granulocytic leukemia, chronic myelofibrosis, chronic lymphatic leukemia, Osler's disease, chronic monocytic leukemia, and lymphoplasmocytic lymphoma, in 11 patients (6 women and 5 men) aged between 33 and 81 years (mean age 58.8 years) treated at the Haematological Out-Patient Clinic of the Postgraduate Medical Education Centre within 1977-1987. The following laboratory tests were carried out: 1) morphology of the peripheral blood and bone marrow, especially some haematological parameters concerning erythrocytes and blood platelets; 2) biochemical tests reflecting erythrocytes disintegration; 3) haemostasis. All examined patients suffered from haemolytic anaemia of various degree with characteristic changes in erythrocyte shape (helmets, tear-drops etc.). Haemolytic origin of anaemia was confirmed by the increased LDH activity. In the majority of patients no compensative stimulation of haematopoiesis (reticulocytosis, red blood cells hyperproliferation in bone marrow) was seen. Clinical symptoms of haemostatic disorders such as haemorrhagic diathesis and vein thrombosis were diagnosed in 50% of the patients. Blood platelet counts ranged from markedly decreased to significantly increased. Bone marrow smears did not show increased number of megacariocytes. Bleeding time was prolonged in the majority of examined patients while prothrombin index--decreased). Abnormal fibrinogen levels (decreased or increased) were found in the majority of patients with fibrin degradation products. Microangiopathic haemolytic anaemia in these patients differ from the typical Moschowitz's disease clinically probably due to the lack of compensative stimulation of erythropoiesis and lower thrombocytopenia.
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PMID:[Microangiopathic hemolytic anemia in patients with diseases of the hematopoietic and lymphatic systems]. 262 5

A case of microangiopathic hemolytic anemia (MHA) associated with the immunosuppressive agent, cyclosporine, is reported herein. The patient manifested anemia with red blood cell fragmentation, hypertension, thrombocytopenia, elevation of serum LDH levels and glomerular capillary thromboses within a few days of his transplantation. Extensive treatments with urokinase and heparin proved ineffective and graftectomy was performed 7 days after his transplantation. Immunofluorescent staining failed to show immunoglobulin (IgG or IgM) or complement (C3) deposition within the glomeruli, which discriminated MHA from acute humoral-vascular rejection.
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PMID:Cyclosporine-associated microangiopathic hemolytic anemia in a renal transplant recipient. 265 53

Factors affecting the response to plasma therapy (plasma exchange and plasma infusion) were studied in four cases of thrombotic thrombocytopenic purpura (TTP) treated in our hospital. Plasma therapy led to recovery from advanced TTP, but three of the patients exhibited chronic relapse. The longer the period from onset, the more marked was the progression of TTP, from the first stage (thrombocytopenia alone) to the second stage in which thrombocytopenia was accompanied by microangiopathic hemolytic anemia (MHA), and the third stage in which neurological abnormalities appeared. Platelet thrombi, which are thought to be the primary pathogenetic feature, probably enlarge leading to stenosis of the vessels during the progression of TTP. Although the severity of TTP in the early stages could be judged from two markers, LDH and the platelet count, it was impossible to determine the severity of advanced TTP by these two markers. However, the severity of advanced TTP could be judged by including the grade and period of neurological abnormalities. The dose of plasma needed to induce recovery was small in the early stage, but as the period from onset lengthened, the dose had to be increased. Though the early platelet thrombi might be easily eliminated by plasma infusion, larger and well-established platelet thrombi might not be lysed even by massive doses of plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Factors affecting the response to plasma therapy in thrombotic thrombocytopenic purpura. 272 41

The lactate dehydrogenase mouse mutant Ldh-1c/Ldh-1c is afflicted with a severe hemolytic anemia associated with extreme reticulocytosis (95%) and splenomegaly. Ninety-one percent of the total body colony-forming units--erythroid (CFU-E) have been quantified in the seven- to ten-times enlarged spleens of the mutant mice. Moreover, the splenic fraction of morphologically recognizable erythroid precursors was 134 times normal. From these data it was apparent that the spleen crucially contributes to the maintenance of steady state erythropoiesis in the mutants. On the other hand, an enhanced sequestration of red blood cells in the enlarged spleen may augment the anemia. Splenectomy experiments were performed with LDH mutant and wild type mice in order to investigate the role of the spleen in this particular hemolytic disease. Following splenectomy, the peripheral blood values and the frequency of femoral stem and progenitor cells were determined, and histological investigations were carried out. The life span of the splenectomized mutants was not shortened, in spite of a very low red blood cell count (25% of the untreated mutant value). Compared to the splenic loss only a moderate increase in bone marrow erythropoiesis was observed, such as a 250% increase of CFU-E. It is concluded that the reduction in red blood cell survival due to splenic sequestration in the mutants is of such a magnitude that it counterbalances a significant portion of splenic erythropoiesis.
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PMID:The role of the spleen in a lactate dehydrogenase mutant mouse (Ldh-1c/Ldh-1c) with hemolytic anemia. 336 65

Following a three-week administration of alpha-interferon (IFN-alpha), a 62-year-old woman with chronic hepatitis C manifested fever and dyspnea and showed diffuse infiltrative opacities on chest roentgenograms. Her laboratory data included results of anemia with reticulocytosis, a decreased complement level and hepatitis with elevated ALP, LDH and gamma-GTP. Because laboratory data also revealed a positive lymphocyte stimulation test for IFN-alpha, this cytokine was considered to be responsible for the development of interstitial pneumonia, hemolytic anemia and cholestatic liver dysfunction due to its immunomodulatory effects. Although these three disorders have been reported to develop singly after IFN-alpha therapy, this is the first report of a patient in whom these disorders occurred simultaneously.
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PMID:A patient with chronic hepatitis C who simultaneously developed interstitial pneumonia, hemolytic anemia and cholestatic liver dysfunction after alpha-interferon administration. 791 19

In a 63-year old patient with a history of aortic valve replacement in 1986, a reduced hemoglobin of 91 g/l was found by a family physician. Since serum LDH was also increased, the patient was diagnosed to suffer from mechanically induced, hemolytic anemia and presented at our hospital for further diagnosis and evaluation of the aortic valve prosthesis.
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PMID:Anemia with LDH-elevation in a patient with aortic valve replacement. 792 25

Hemolytic uremic syndrome (HUS) is characterized by microangiopathic hemolytic anemia, thrombocytopenia and acute renal failure. Most cases of HUS are caused by E. coli O157:H7 verotoxin. In the case reported here, diarrhea continued for twenty days after an E. coli 0157:H7 infection and was followed by acute renal failure and thrombocytopenia. Examination of percutaneous renal biopsy tissue showed typical HUS findings, e.g., mesangiolysis in glomeruli and thickening of capillary walls with prominent double outlines, but there was no indication of hemolytic anemia. LDH and haptoglobin, indications of hemolytic anemia, were in the normal range throughout the patient's clinical course. The patient's red blood cells had P1 antigen, which reportedly provides protection by adsorption of toxin into the red blood cells thereby preventing or limiting toxic damage to other organs. Therefore, we assumed that because of the expression of P1 antigen in this patient, the kidneys were not severely damaged and microangiopathic hemolytic anemia was thereby avoided.
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PMID:Hemolytic uremic syndrome without hemolytic anemia: a case report. 795 84

Aldolase deficiency of red blood cell is a rare cause of hereditary hemolytic anemia and now there exists only three patients in the world. We had a 24-year-old man operated on for gallbladder stone secondary to this uncommon disease. He underwent a cholecystectomy under general anesthesia combined with thoracic epidural block, using isoflurane, fentanyl, vecuronium, midazolam and lidocaine. During the surgery serum concentrations of bilirubin, free hemoglobin and LDH showed no change, suggesting a lower incidence of drug-induced hemolysis in the case of aldolase deficiency than in other enzyme deficiency. This fact also provides a useful guide to the choice of anesthetics and related agents. In the postoperative period, however, we found a hemolytic response to fever with a drop in hemoglobin level to 2.5 g.dl-1. Aldolase activity of his red cell is heat labile and an increase in body temperature may aggravate a disturbance in the glycolytic pathway leading to hemolytic crisis. It is thus important to prevent the body temperature from rising when a patient is suffering from hemolytic anemia due to red cell aldolase deficiency.
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PMID:[Anesthesia for a patient with red cell aldolase deficiency]. 851 55


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