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)

Human red blood cells (RBCs) are subject to an enormous degree of genetic diversity. The variability that occurs may result in anemia, cyanosis, polycythemia, or may cause no hematologic alterations. Genetic abnormalities affecting hemoglobin include the sickling disorders, the unstable hemoglobinopathies, hemoglobinopathies associated with polycythemia or with methemoglobinemia, and the alpha- and beta-thalassemias. The most common enzymatic abnormality of RBCs is glucose-6-phosphate dehydrogenase deficiency, but defects of many other enzymes leading to hemolytic anemia have been identified. Deficiences of RBC enzymes may also be important in the diagnosis of nonhematologic disease and in the evaluation of dietary status.
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PMID:Genetic disorders of human red blood cells. 117 73

High titers cold agglutinins were demonstrated in the serum of a 7 year old female toy Pinscher with a hemolytic anemia. In vitro, the serum did not show distinct hemolytic properties, but it fixed complement components to both the patient's own red cells and randomly sampled canine erythrocytes and agglutinated these cells at high dilutions at low temperatures (optimally at 0 degrees C). Serum electrophoresis on cellulose acetate membranes failed to reveal a paraproteinemia. Normal canine red cells sensitized with the patient's serum at 0 degrees C and eluted at 40 degrees C, released a cold agglutinin identifiable as IgM by immunoelectrophoresis. Neither IgA nor IgG were detectable in a concentrate of the eluate. The auto-antibody showed no specificity against the canine blood group A antigen and did not react with human O-erythrocytes, irrespective of whether these carried the I- or i-antigens. Following erroneous exposure of the dog to cold, cyanosis and serious gangrene developed at the acra (the ears, nose and feet). In addition, symptoms indicating diffuse intravascular coagulation were observed both hematologically and on pathological-anatomical examination. No primary disease could be demonstrated.
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PMID:Cold hemagglutinin disease in a toy Pinscher dog. 117 5

A twenty-eight day repeated oral dose toxicity test of m-nitroaniline (m-NA) was carried out in male and female F344 rats at dose levels of 0, 15, 50 or 170 mg/kg/day. Animals of both sexes were divided into 6 groups, each consisting of 30 animals, 4 groups being used for the 28 days dosing study and the remainder for investigation of subsequent recovery. Inhibition of body weight gain, and induction of cyanosis and methemoglobinemia were observed in the highest dose groups of both sexes, but there were no animal mortalities. Testicular atrophy was evident but there was no effect on the ovaries in the same group. In addition to these findings, hemolytic anemia and increases of liver, spleen and kidney weights were also observed in both sexes in a dose-related fashion. Histologically, the highest dose group showed reduction of spermatogenesis with multinucleated giant cell formation, lipofuscin deposition mainly in the proximal renal tubules, and increases in hemosiderin deposition and extramedullary hematopoiesis in the liver. Dose-related increases in the incidence of hemosiderin deposition in the spleen, erythroid hyperplasia in the bone marrow and swelling of hepatocytes were observed in treated groups. After a 14 day recovery period, these findings were attenuated or had disappeared. Based on these results obtained under the present experimental conditions, it was concluded that m-NA induces hemolytic anemia and exerts testicular toxicity in rats and that the non-observed-effect level of m-NA is less than 15 mg/kg/day.
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PMID:[Twenty-eight day repeated dose toxicity test of m-nitroaniline in F344 rats]. 136 8

Four members in two generations of a Polish-American family exhibited findings of congenital Heinz-body hemolytic anemia accompanied by cyanosis. Two of the affected family members have also developed severe pulmonary hypertension, with a fatal outcome in one of them. Blood from the affected individuals showed decreased oxygen affinity and contained elevated levels of methemoglobin. An unstable hemoglobin fraction underwent rapid precipitation following exposure of the red cell lysates to isopropyl alcohol or heat. This hemoglobin contained a newly identified abnormal beta chain with an amino acid substitution at the same position as that of Hb Hammersmith and Hb Bucuresti-Louisville.
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PMID:Hb Warsaw (beta 42 Phe----Val): an unstable hemoglobin with decreased oxygen affinity. I. Hematologic and clinical expression. 275 1

Between February 1987 and July 1988, 45 patients with advanced refractory cancer were treated with LY186641, a diarylsulfonylurea that has shown a broad spectrum of activity in preclinical testing. Patients received a weekly p.o. dose of LY186641 for 6 consecutive weeks; responding and stable patients continued weekly therapy until progression occurred. Using a standard phase I study design, the first three patients received LY186641 at 30 mg/m2 week; the dose was escalated in subsequent patients until dose-limiting toxicity occurred. Methemoglobinemia was the major toxicity observed and was dose related. Methemoglobin levels peaked approximately 24 h after LY186641 was administered and fell to low levels after 48 h. Six patients developed fatigue, cyanosis, and dyspnea associated with serum methemoglobinemia levels of greater than 20%; four of these patients were subsequently removed from the study. Hemolytic anemia was also observed but was clinically significant in only 10 patients. Other side effects were mild and infrequent. The maximum tolerated dose of LY186641, when given at this schedule, was 2550 mg/m2/week. No objective tumor responses were observed.
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PMID:Phase I clinical study of N-[(4-chlorophenyl)amino]carbonyl-2,3-dihydro-1H-indene-5-sulfonamide (LY186641). 276 90

Based on cases referred for investigation, as well as a questionnaire sent to all medical and pediatric departments in Denmark, 48 cases of hemoglobinopathy in 15 families of Danish ancestry are reviewed. 18 Danes in six families have been identified as having beta-thalassemia, and remarkably one - a homozygote - has beta-thalassemia intermedia requiring treatment with iron-chelation therapy. A further 36 Danes in 9 families have a hemoglobin variant: five unstable hemoglobins (Volga, Niteroi, and three unidentified), one hereditary methemoglobinemia (M-Arhus), one polycythemia (Ty Gard) and 2 asymptomatic (Athens-Georgia and Hafnia). Although rare in Danish families, a hemoglobinopathy should be considered in families with an unexplained chronic hemolytic anemia, cyanosis or polycythemia.
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PMID:Hemoglobinopathies in Danish families. 277 54

Signs of acute hemolytic anemia developed in 4 adult horses from 2 Georgia farms 3 to 4 days after the ingestion of wilted leaves from cut red maple trees (Acer rubrum). Clinical findings included weakness, polypnea, tachycardia, depression, icterus, cyanosis, and brownish discoloration of the blood and urine. Blood changes included methemoglobinemia, free plasma hemoglobin, decreased pcv, and Heinz bodies in erythrocytes. These findings plus hemoglobinuria suggested intravascular hemolysis. Three of the 4 horses diet 5 to 7 days after ingestion of the leaves. Gross pathologic changes included generalized icterus, splenomegaly and swollen, black kidneys. Microscopic changes including tubular nephrosis with hemoglobin casts, vacuolization of centrilobular hepatocytes, and sequestration of erythrocytes in splenic sinusoids. A disease indistinguishable from the field cases was induced in a pony by the oral administration of dried, ground red maple leaves at a dosage of 1.5 g/kg. The findings of methemoglobinemia, hemolysis, and Heinz bodies suggested that the toxic principle of the red maple leaf was an oxidant.
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PMID:Hemolytic anemia in horses after the ingestion of red maple leaves. 705 81

A case of acute Dapsone intoxication due to voluntary ingestion of 3 g of this drug as a suicide attempt is described. A severe methemoglobinemia developed, accompanied by intense cyanosis, dyspnea, headache, and nausea. Subsequently, significant sulfhemoglobinemia responsible for prolonged cyanosis was observed, as well as mild hemolytic anemia. Relapses of methemoglobinemia after methylene blue treatment required repeated administration of the reducing agent. The need of a careful follow-up for several days in this type of intoxication is emphasized.
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PMID:Delayed sulfhemoglobinemia after acute dapsone intoxication. 715 40

The authors report a case of recurrent sulfhemoglobinemia resulting from a chronic abuse of phenacetin. Cyanosis was accompanied by hemolytic anemia and numerous features of tissue aging. While phenacetin was found to be the oxidizing drug, no source of sulfur was identified. The origin of sulfhemoglobinemia in man is discussed and the possible role of intraerythrocytic glutathione is emphasized.
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PMID:Hemolytic anemia and sulfhemoglobinemia due to phenacetin abuse: a case with multivisceral adverse effects. 723 75

The study of abnormal hemoglobins was oriented towards three criteria as a function of commonly encountered clinical problems : differentiation between frequent, relatively infrequent and exceptional hemoglobins ; systematic study of high-risk ethnic groups and isolated discoveries ; silent hemoglobinopathies and those accompanied by physiopathological repercussions such as hemolytic anemia, disturbance in oxygen transport and cyanosis. The chronology and rationale for these studies was discussed, with particular attention being given both to normalized baseline measures and to the new, high-resolution techniques such as isoelectric focalization. No attempt was made to provide an exhaustive list, but rather examples were provided illustrating the various points considered. Finally, a number of particular points are brought up to where a correctly made diagnosis can avoid the necessity of subjecting patients to long and possibly dangerous tests.
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PMID:[Recent data concerning abnormal hemoglobins (author's transl)]. 730 88


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