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)

An 80-year-old woman was admitted with anemia, jaundice and a bleeding tendency about 5 weeks after starting omeprazole. On admission, the hemoglobin was 6.4 g/dl, platelets 0.1 x 10(4)/microliter, leukocyte count 7,500/microliter, and reticulocyte count 325/1000. The total bilirubin was 1.9 mg/dl, indirect bilirubin 0.6 mg/dl, lactate dehydrogenase 572 IU/l, and haptoglobin < 10 mg/dl. Both the direct and the indirect Coombs' tests were positive. The platelet-associated IgG (PAIgG) was 1,100.0 ng/10(7) cells. A decrease in the complement value was observed. There was an increase in the number of megakaryocytes and erythroblasts in the marrow film. After omeprazole administration was halted, her hemoglobin and platelet levels gradually returned to normal. On the 27th hospital day, the direct Coombs' test was positive but the indirect Coombs' test became negative. The PAIgG value also returned to normal, and she was discharged on the 59th hospital day. The acute phase of the drug-induced lymphocyte stimulation test was negative, however, we detected the IgG antibody to omeprazole. In the recovery phase, the IgG value decreased. Forty days after discharge, the direct Coombs' test had become negative. This is apparently the first report of a patient with acute hemolytic anemia and thrombocytopenia due to omeprazole through an immune complex mechanism.
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PMID:[Hemolytic anemia and thrombocytopenia associated with anti-omeprazole antibody]. 969 74

We describe a 27-month-old boy who was first admitted to our hospital on 7 January 1995 with nasal bleeding. From 6 months of age he has had lymphadenopathy, low levels of serum uric acid, increased levels of serum lactate dehydrogenase and hyper gamma-globulinemia. From the age of 18 months he has had persistent Epstein-Barr virus (EBV) infection (target cells; B cells), recurrent episodes of thrombocytopenia, anemia and hepatosplenomegaly. Dysmobility of the left leg and arm from a central nervous system complication during a relapse with pancytopenia on March 1995, was also observed. Relapses of thrombocytopenia with increases of platelet-associated immunoglobulin G and hepatosplenomegaly have been observed approximately every 2 months, and two relapses of pancytopenia were accompanied with weak positivity of Coombs test and low level of haptoglobin. These recurrent episodes were improved with prednisolone. However, now in June 1997 we have not been able to diagnose what underlies the above clinical symptoms, except that the patient has a persistent EBV infection.
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PMID:Recurrent hepatosplenomegaly and peripheral blood cytopenia, persistent Epstein-Barr virus infection and central nervous system manifestation in a patient with lymphadenopathy and low serum uric acid. 974 82

Haptoglobin phenotypes have been shown in human medicine to be related to the prevalence of various diseases. Furthermore, abnormal glycosylation of haptoglobin has been reported as a consequence of liver disease, cancer and immunological disorders in man. To our knowledge, similar findings have not, so far, been reported in canine disease. The present paper describes a method for investigation of canine haptoglobin phenotypes and of microheterogeneity caused by altered glycosylation. The method consisted of isoelectric focusing (IEF) of dog serum, followed by immunoblotting. The results indicated the existence of only one canine haptoglobin phenotype with a characteristic microheterogeneity pattern in healthy dogs. Changes in this pattern were found in serum from dogs with liver disease, predominantly chronic progressive hepatitis, and with different kinds of anaemia. Pretreatment of serum with neuraminidase or glycopeptidase F (PNGase F) resulted in identical IEF patterns of haptoglobin from healthy and diseased dogs. Moreover, a fucose-specific lectin was capable of binding to some of the abnormal haptoglobin fractions, mainly those found in association with anaemia. The changes described were interpreted as alterations of the carbohydrate content, with or without fucosylation, of some haptoglobin fractions.
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PMID:Disease-related variations of the glycosylation of haptoglobin in the dog. 980 25

The first known human case of heme oxygenase-1 (HO-1) deficiency is presented in this report. The patient is a six-year-old boy with severe growth retardation. He has been suffering from persistent hemolytic anemia characterized by marked erythrocyte fragmentation and intravascular hemolysis, with paradoxical increase of serum haptoglobin and low bilirubin. An abnormal coagulation/fibrinolysis system, associated with elevated thrombomodulin and von Willebrand factor, indicated the presence of severe, persistent endothelial damage. Electron microscopy of renal glomeruli revealed detachment of endothelium, with subendothelial deposition of an unidentified material. Iron deposition was noted in renal and hepatic tissue. Immunohistochemistry of hepatic tissue and immunoblotting of a cadmium-stimulated Epstein-Barr virus-transformed lymphoblastoid cell line (LCL) revealed complete absence of HO-1 production. An LCL derived from the patient was extremely sensitive to hemin-induced cell injury. Sequence analysis of the patient's HO-1 gene revealed complete loss of exon-2 of the maternal allele and a two-nucleotide deletion within exon3 of the paternal allele. Growth retardation, anemia, iron deposition, and vulnerability to stressful injury are all characteristics observed in recently described HO-1 targeted mice. This study presents not only the first human case of HO-1 deficiency but may also provide clues to the key roles played by this important enzyme in vivo.
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PMID:Oxidative stress causes enhanced endothelial cell injury in human heme oxygenase-1 deficiency. 988 42

The severity of anaemia associated with acute, Plasmodium falciparum malaria and the extent to which haemolysis, bone-marrow suppression, and pre-existent iron deficiency contribute to the anaemia were assessed in 102 Indian children aged 2-12 years. Blood haemoglobin (Hb), plasma unconjugated bilirubin and haptoglobin, serum iron and transferrin concentrations and transferrin saturation, red cell morphology and reticulocyte response were investigated in the patients and in 50 control children. Twenty-three patients with severe anaemia (< 70 g Hb/litre) were investigated further, by bone-marrow biopsy followed by iron staining of sections or touch smears of the biopsy material. There was evidence of haemolysis in the malaria cases: in the peripheral blood smears and the significantly higher plasma concentrations of unconjugated bilirubin, lower plasma concentrations of haptoglobin and lower blood concentrations of Hb than those seen in the controls. Haemoglobin concentration correlated directly with haptoglobin (r = 0.489; P < 0.001) and inversely with unconjugated bilirubin in malaria patients (r = -0.526; P < 0.001) but not in controls (r = -0.140 and -0.061, respectively). Parasitaemia (parasites/microliter) was not significantly correlated with Hb, haptoglobin or unconjugated bilirubin. Compared with the earlier samples, follow-up samples from the patients, collected 2 weeks after discharge from hospital and antimalarial therapy, showed significant increase in Hb, haematocrit, haptoglobin and decreases in both total and unconjugated bilirubin. There was evidence of hypercellularity and mild-moderate erythroid hyperplasia, mainly of normoblastic maturation with adequate reticulocyte response, in the bone-marrow samples from the cases of severe anaemia; dyserythropoiesis was only noticed in one case and no stainable iron was detectable in 17 of the 23 cases. These observations indicate that haemolysis is the prime cause of the anaemia seen in acute falciparum malaria, although destruction of parasitised erythrocytes is not the sole cause of the haemolytic process. Bone-marrow suppression appears to have an insignificant role but pre-existent iron deficiency aggravates the severity of the anaemia.
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PMID:Anaemia in acute, Plasmodium falciparum malaria in children from Orissa state, India. 1047 36

To assess the extent of oxidative stress in erythrocytes of patients with acute Plasmodium falciparum malaria, erythrocyte thiobarbituric acid-reactive substance (ETBAR), and intracellular, membrane and extracellular antioxidants were estimated in 102 cases of P. falciparum malaria and 50 control subjects. The mean concentration of ETBAR was significantly higher (P < 0.001) and many of the antioxidants were significantly lower in patients than controls. Among the erythrocyte antioxidants, catalase, reduced glutathione (GSH) and tocopherol were significantly lower in the patients (P < 0.05, 0.001, 0.001, respectively). Erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were not reduced to a statistically significant level. Similarly, the plasma antioxidants ascorbate and albumin were significantly lower (P < 0.001) but not urate. ETBAR correlated inversely with erythrocyte GSH and tocopherol (P < 0.001), and plasma ascorbate and albumin (P < 0.001) but not with the erythrocyte enzymic antioxidants. However, on multiple regression analysis only tocopherol correlated strongly with ETBAR, followed by GSH and plasma ascorbate. ETBAR also correlated well with haemolytic indices such as haemoglobin, plasma unconjugated bilirubin and haptoglobin concentrations (P < 0.001, for all). On follow-up after 2 weeks, ETBAR and different antioxidants reached near control levels. These observations indicate an enhanced oxidative stress on erythrocytes in acute falciparum malaria that may contribute substantially to haemolysis and anaemia.
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PMID:Evidence for erythrocyte lipid peroxidation in acute falciparum malaria. 1049 92

Anaemia has been associated with aluminium (Al) accumulation in plasma and/or bone tissue in patients with chronic renal insufficiency. Nevertheless, in previous works, we have found shortened red-cell life span, increased osmotic resistance and inhibition of colony-forming units-erythroid (CFU-E) development in Al-overloaded rats with normal renal function. To elucidate further the action of Al on in vivo erythropoiesis, aluminium citrate was provided to Sprague Dawley rats (n = 18) in the drinking water for 8 months. Significant decreases in haematocrit (38.8 +/- 4.29 versus 43.1 +/- 3.58%, p < 0.05) and blood haemoglobin concentration (137 +/- 10.1 versus 148 +/- 8.5 g/l, p < 0.05), reticulocytosis (1.8/1.3-4.2 versus 1.2/0.4-3.7%, p < 0.05), and severe inhibition of CFU-E growth (670/120-950 versus 1530/810-2440 CFU-E/2 x 10(5) cells, p < 0.005) were found. Anysocytosis, poikilocytosis and schistocytosis were detected in peripheral blood stained films. Scanning electron microscopy revealed the presence of erythrocytes with abnormal shape, including crenated and target cells. Aluminium was localised specially inside the schistocytes by EDAX analysis. Decreased haptoglobin concentration (107/83-127 versus 139/89-169 mg/l, p < 0.05) supports the assumption of haemolytic nature of the anaemia. Rats were not iron depleted, as plasma iron concentration and total iron binding capacity were found in the range of control values, and sideroblasts and haemosiderin deposits were observed in bone marrow smears. Total 59Fe uptake and 59Fe incorporated to haem by the bone marrow cells were found decreased. In conclusion, the erythropoiesis impairment induced by Al may be a combined effect of direct action on circulating erythrocytes and interference with the cellular iron metabolism in erythroid progenitors.
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PMID:Morphologic and functional alterations of erythroid cells induced by long-term ingestion of aluminium. 1061 63

We encountered 4-year-old boy who developed paroxysmal cold hemoglobinuria (PCH) in the middle of August. He was admitted due to progressive jaundice and pallor following fever and nausea. Laboratory data revealed severe anemia, increased serum indirect bilirubin and LDH, and decreased serum haptoglobin. Direct/indirect Coombs tests were positive. These findings yielded a diagnosis of autoimmune hemolytic anemia. Serological test for syphilis was negative. The patient's symptoms and signs promptly subsided after treatment with prednisolone, which was started on the 2nd hospital day. The patient has been in a disease-free state for 16 months without any medication. After discharge, he was finally given a diagnosis of PCH because a Donath-Landsteiner test was positive. The antibody belonged to an IgM subclass and showed anti-I specificity. Considering that development of PCH is common in winter, this case was unique because it developed in August. We speculated that exposure to a cool air-conditioned atmosphere prior to hospitalization and the cooling mechanism of the body after admission were involved in the summer onset of PCH and its prolonged clinical course.
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PMID:[A boy with summer onset paroxysmal cold hemoglobinuria induced by Donath-Landsteiner antibody with anti-I specificity]. 1069 97

The haptoglobin (Hp) phenotypes were determined by polyacrylamide-gel electrophoresis in plasma samples obtained in 1997 from 113 Plasmodium falciparum malaria patients (aged 1-12 years) with strictly defined cerebral malaria, severe malarial anaemia, or uncomplicated malaria and 42 age-matched healthy controls from the same area (coastal Ghana). Hp1-1 was significantly more prevalent among the patients (43%) than among healthy controls (7.1%), whereas Hp2-1 and Hp2-2 were underrepresented among the patients (11% and 2%, respectively) compared to the control donors (33% and 14%, respectively). No significant difference in frequency of Hp0 was observed between patients and controls. Among the malaria patients, the Hp1-1 phenotype was significantly more prevalent among patients with the complications of cerebral malaria and severe anaemia compared to patients with uncomplicated disease, whereas the reverse was seen with respect to Hp2-1 and Hp2-2. Our data suggest that the Hp1-1 phenotype is associated with susceptibility to P. falciparum malaria in general, and to the development of severe disease in particular.
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PMID:Haptoglobin 1-1 is associated with susceptibility to severe Plasmodium falciparum malaria. 1089 72

A 57-year-old woman was found to have rheumatoid arthritis (RA) in 1996. Treatment with different immunoregulatory agents, including actarit and bucillamine, produced no improvement. Therefore, combined therapy with methotrexate (MTX) (5 mg/week oral) and low-dose prednisolone (PSL) (5 mg/day) was started in April 1997. Sulindac and famotidine were also administered. In August 1997, she was admitted to our hospital because of palpitations and shortness of breath due to severe anemia. Results of laboratory studies were hemoglobin, 2.9 g/dl; reticulocyte count, 225/1000; and haptoglobin, less than 10 mg/dl. The direct and indirect Coombs'tests were positive. A diagnosis of autoimmune hemolytic anemia (AIHA) was made on the basis of the laboratory findings. Treatment with high-dose PSL (50 mg/day) was started, and the anemia improved. The hemoglobin level increased to 6.0 g/dl within the 1st week and to 12.6 g/dl 6 weeks later. We believe that the most likely explanation for this anemia was the low-dose MTX because the anemia appeared soon after treatment was started.
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PMID:[A case of rheumatoid arthritis associated with autoimmune hemolytic anemia due to weekly low-dose methotrexate therapy]. 1102 Nov 73


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