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At least 19 recordsLinked to original sources
PubMed1981

Incidence and cause of aplastic anemia, hemolytic anemia, agranulocytosis and thrombocytopenia.

A total of 745 patients with cytopenia (aplastic anemia 157, hemolytic anemia 101, agranulocytosis 136, thrombocytopenia 351) were diagnosed during a 5-year period in a health care region comprising 16% of the Swedish population. The total incidence was for aplastic anemia 24.6, hemolytic anemia 15.8, agranulocytosis 21.3 and thrombocytopenia 55.0 cases per 10(6) and year. Compared to 10 years earlier, aplastic anemia and agranulocytosis have become more common, thrombocytopenia occurs with unchanged frequency while hemolytic anemia is rarer. The overall incidence is 5 times higher in elderly (greater than 65 y.) than in younger patients and 1.3 times higher in women than in men, figures that make total incidence figures rather meaningless. The most common cause is "unknown" (45%), the next drug-induced (25-36% including cytostatic drugs). Disregarding cytostatics, the drugs most often encountered are oral diuretics, analgesics, antiphlogistics and sulfonamides.

Adolescent↗
PubMed1975

Intestinal iron absorption under the influence of available storage iron and erythroblastic hyperplasia. Comparative studies in children with hereditary spherocytosis, nonspherocytic enzymopenic hemolytic anemia, acquired hemolytic anemia, vitamin B12 deficiency induced megaloblastic anemia, erythroblastic hypoplasia and aplastic anemia.

A high negative correlation (coefficient similar to 0.9) between increased 59Fe absorption from a diagnostic 0.56 mg 59Fe2+ dose and the depletion of available storage iron was observed in menstruating and pregnant women, fullterm and premature infants, blood donors, patients with infections, inflammations, tumors, hepatic cirrhosis, gastric surgery, increased urogenital or gastrointestinal blood loss. The increased diagnostic 59Fe2+ absorption is a reliable and sensitive indicator of at least depleted iron stores or prelatent iron deficiency as caused by iron malnutrition or maldigestion, increased iron requirement in pregnancy, infancy, urogenital or gastrointestinal blood loss. Although the messenger system which signalyzes the depletion of iron stores to the iron absorbing enterocytes of the duodenal and jejunal mucosa is not yet known available storage iron seems to control intestinal iron absorption under normal and the great majority o pathological condition in humans. Anemia per se or high erythropoietin levels in blood do not influence iron absorption since patients with even severe erythroblastic hypoplasia, aplastic anemia and megaloblastic anemia due to vitamin B12 deficiency absorb iron according to their iron stores. An only mild hyperplasia of the erythropoietic system in the bone marrow does also not effect iron absorption which was still under the control of available storage iron in patients with hereditary spherocytosis, nonspherocytic congenital hemolytic anemia due to glucose-6-phosphate dehydrogenase deficiency, acquired hemolytic anemia and vitamin B12 deficiency induced megaloblastic anemia..

Adolescent↗
PubMed1999

Several mutations including two novel mutations of the glucose-6-phosphate dehydrogenase gene in Polish G6PD deficient subjects with chronic nonspherocytic hemolytic anemia, acute hemolytic anemia, and favism.

DNA sequencing revealed seven different glucose-6-phosphate dehydrogenase (G6PD) mutations in G6PD deficient subjects from 10 Polish families. Among them we found two novel mutations: 679C-->T (G6PD Radlowo, class 2) and a 1006A-->G (G6PD Torun, class 1). Variant G6PD Radlowo was characterized biochemically. Both novel mutations were analyzed using a model of the tertiary structure of the human enzyme. The main chain of G6PD Torun is different from the wild-type G6PD. The remaining mutations identified by us in deficient Polish patients were: 542A-->T (G6PD Malaga), 1160G-->A (G6PD Beverly Hills), 1178G-->A (G6PD Nashville), 1192G-->A (G6PD Puerto Limon), and 1246G-->A (G6PD Tokyo). Variant Tokyo was found in four families. In one of them favism was the first clinical sign of G6PD deficiency and chronic nonspherocytic hemolytic anemia (CNSHA) was diagnosed later. Variants G6PD Nashville and G6PD Puerto Limon were accompanied by the silent mutation 1311C-->T of the G6PD gene.

Acute Disease↗
PubMed2004

Immune-mediated hemolytic anemia.

Hemolytic anemia due to immune function is one of the major causes of acquired hemolytic anemia. In recent years, as more is known about the immune system, these entities have become better understood and their treatment improved. In this section, we will discuss three areas in which this progress has been apparent. In Section I, Dr. Peter Hillmen outlines the recent findings in the pathogenesis of paroxysmal nocturnal hemoglobinuria (PNH), relating the biochemical defect (the lack of glycosylphosphatidylinositol [GPI]-linked proteins on the cell surface) to the clinical manifestations, particularly hemolysis (and its effects) and thrombosis. He discusses the pathogenesis of the disorder in the face of marrow dysfunction insofar as it is known. His major emphasis is on innovative therapies that are designed to decrease the effectiveness of complement activation, since the lack of cellular modulation of this system is the primary cause of the pathology of the disease. He recounts his considerable experience with a humanized monoclonal antibody against C5, which has a remarkable effect in controlling the manifestations of the disease. Other means of controlling the action of complement include replacing the missing modulatory proteins on the cell surface; these studies are not as developed as the former agent. In Section II, Dr. Alan Schreiber describes the biochemistry, genetics, and function of the Fc gamma receptors and their role in the pathobiology of autoimmune hemolytic anemia and idiopathic thrombocytopenic purpura due to IgG antibodies. He outlines the complex varieties of these molecules, showing how they vary in genetic origin and in function. These variations can be related to three-dimensional topography, which is known in some detail. Liganding IgG results in the transduction of a signal through the tyrosine-based activation motif and Syk signaling. The role of these receptors in the pathogenesis of hematological diseases due to IgG antibodies is outlined and the potential of therapy of these diseases by regulation of these receptors is discussed. In Section III, Dr. Wendell Rosse discusses the forms of autoimmune hemolytic anemia characterized by antibodies that react preferentially in the cold-cold agglutinin disease and paroxysmal cold hemoglobinuria (PCH). The former is due to IgM antibodies with a common but particular structure that reacts primarily with carbohydrate or carbohydrate-containing antigens, an interaction that is diminished at body temperature. PCH is a less common but probably underdiagnosed illness due to an IgG antibody reacting with a carbohydrate antigen; improved techniques for the diagnosis of PCH are described. Therapy for the two disorders differs somewhat because of the differences in isotype of the antibody. Since the hemolysis in both is primarily due to complement activation, the potential role of its control, as by the monoclonal antibody described by Dr. Hillmen, is discussed.

Anemia, Hemolytic, Autoimmune↗
PubMed2002

Evidence for a susceptibility gene (SLEH1) on chromosome 11q14 for systemic lupus erythematosus (SLE) families with hemolytic anemia.

Hemolytic anemia is a forme fruste of systemic lupus erythematosus (SLE), being observed months or even years before the onset of other clinical manifestations in some patients. We hypothesized that hemolytic anemia in those SLE-affected patients would identify a group of SLE pedigrees that share a high degree of genetic homogeneity. From 160 multiplex SLE pedigrees, we sought evidence for linkage in 35 (16 African-American, 17 European-American, and 2 Hispanic) who had at least one SLE-affected patient with hemolytic anemia. Significant linkage was present at 11q14 in the 16 African-American pedigrees, yielding a maximum two-point logarithm of odds (LOD) score of 4.5 at D11S2002. The segregation pattern of SLE in these African-American pedigrees suggested a dominant mode of inheritance and, when maximized across penetrance and disease allele frequencies, produced a multipoint LOD of 4.7. Multipoint analysis yielded a multipoint heterogeneity LOD score of 3.6 (alpha = 0.63), again with maximum LOD at D11S2002. Finally, markers typed 7 centimorgans to either side of D11S2002 achieved LOD scores of 3 or better by using the maximized model, supporting linkage to 11q14. Clearly, pedigree ascertainment based on select clinical manifestations is an important tool, capable of revealing otherwise cryptic genetic linkages in complex genetic diseases. Thus, we show strong evidence for an SLE susceptibility gene, SLEH1, near D11S2002 in African-American pedigrees multiplex for SLE that have at least one SLE-affected patient with hemolytic anemia.

Anemia, Hemolytic↗
PubMed1974

Sulfhydryl groups of the erythrocyte membrane and their relation to glycolysis and drug-induced hemolytic anemia.

Hemolytic anemia caused by oxidative drugs is thought to result from the oxidation of intracellular and membrane sulfhydryl groups of the erythrocyte. This process is more likely to occur in those erythrocytes in which the intracellular mechanism for reduction of disulfides is abnormal (e.g., glucose-6-phosphate dehydrogenase deficiency). If a membrane sulfhydryl group is critical in the pathogenesis of druginduced hemolytic anemia, it follows that this specific group must be dependent on intracellular reductive mechanisms for maintenance of the reduced state. This report describes a sulfhydryl group(s), involved in membrane structure, which is (are) dependent on intracellular metabolism for maintenance of the reduced state. It is postulated that this metabolically dependent membrane sulfhydryl group may play a role in the pathogenesis of drug-induced hemolytic anemia. Membrane sulfhydryl groups were studied by observing the effect of sulfhydryl blocking agents, e.g., N-ethyl-maleimide (NEM), on the recovery of erythrocyte ghosts after osmotic lysis. It was shown that NEM interfered with ghost recovery by reacting with membrane sulfhydryl groups. The concentration of NEM (as determined by [(14)C] NEM binding) necessary to cause this effect was lower than that necessary to produce changes in osmotic fragility or cation permeability, or to cause Heinz body formation. In the absence of glucose, these sulfhydryl groups became disulfides, but could be returned to the reduced state by restoring glycolysis or by adding dithiothreitol. Phenylhydrazine hemolytic anemia was induced in pigs, and membrane changes of the type described above occurred early in the pathogenesis of the disease.

Anemia, Hemolytic↗
PubMed1996

[Mycoplasma infection and hemolytic anemia].

Hemolytic anemia due to cold agglutinin disease is a known complication of Mycoplasma pneumoniae infection but is rarely observed. An example of the clinical course of such hemolytic anemia is presented, and laboratory findings of the cases reported mainly in Japanese journals, are summarized. Autoantibodies against erythrocyte membrane "I" antigen arise by the interaction of "I" antigen with M. pneumoniae is suspected, since "I" antigen is shown to be a receptor of this agent. Corticosteroid therapy is sometimes necessary for the treatment of marked anemia.

Adult↗
PubMed1986

Role of aniline metabolites in aniline-induced hemolytic anemia.

Hemolytic anemia after aniline and aniline-related drugs such as dapsone and primaquine is thought to be mediated by active/reactive metabolite(s) formed during the hepatic clearance of the parent compounds. To determine whether any of the known metabolites of aniline contribute to the hemolytic response seen in rats given aniline, rats were infused with isologous 51Cr-labeled erythrocytes 24 hr before administration of aniline or aniline metabolites. The time course of blood radioactivity was followed in individual rats by serial sampling from the orbital sinus and the time required for blood radioactivity to fall by 50% (T50Cr) was used as a measure of in vivo erythrocyte survival. Aniline HCl produced a dose-dependent reduction in the T50Cr. Acetanilide also reduced the T50Cr, but was less potent than aniline. Aminophenols (2-, 3- and 4-) in similar doses did not significantly alter the T50Cr. In contrast, phenylhydroxylamine produced a dose-dependent decrease in the T50Cr with approximately 10 times the potency of aniline. The T50Cr was also decreased in a concentration-dependent manner for labeled erythrocytes incubated in vitro with phenylhydroxylamine, then readministered to rats, indicating a direct toxic effect of phenylhydroxylamine on erythrocytes. In addition, the area under the blood time course curve for phenylhydroxylamine plus nitrosobenzene was equivalent in rats administered equitoxic doses of aniline or phenylhydroxylamine, indicating that sufficient phenylhydroxylamine is formed in vivo during aniline clearance to account for aniline's toxicity. These results suggest that phenylhydroxylamine is the active metabolite that mediates aniline-induced hemolytic anemia.

Anemia, Hemolytic↗
PubMed1991

Role of metabolites in propanil-induced hemolytic anemia.

Hemolytic anemia and methemoglobinemia induced by exposure to certain arylamines, such as aniline and dapsone, are known to be mediated by their N-hydroxylamine metabolites. The arylamide propanil (3,4-dichloropropionanilide), a herbicide used extensively in rice fields, is also thought to induce methemoglobinemia through the action of metabolites. However, the hemolytic potential of this compound has not previously been reported. The present studies were undertaken to determine the hemolytic potential of propanil, and, if positive, the role of metabolites in this hemotoxicity. The survival of previously administered 51Cr-labeled erythrocytes in rats was reduced in a dose-dependent manner by ip administration of both propanil and its deacylated metabolite, 3,4-dichloroaniline (ED50 for both ca. 1.8 mmol/kg). When labeled erythrocytes were exposed in vitro to propanil or 3,4-dichloroaniline and then readministered to rats, no decrease in erythrocyte survival was observed, which indicated that these compounds were not direct-acting hemolytic agents. In contrast, erythrocyte survival was markedly reduced by ip administration or in vitro exposure to N-hydroxy-3,4-dichloroaniline. In addition, N-hydroxy-3,4-dichloroaniline was detected in the blood of propanil-treated rats in amounts sufficient to account for the hemolytic activity of the parent compound. These data indicate that N-hydroxy-3,4-dichloroaniline mediates propanil-induced hemolytic anemia, and that occupational exposure to propanil may result in an increased risk of hemolytic episodes.

Anemia, Hemolytic↗
PubMed1993

Clinical features and splenic pathologic changes in patients with autoimmune hemolytic anemia and congenital hemolytic anemia.

We characterized the pathologic changes in 50 spleens from patients with autoimmune hemolytic anemia and in 13 spleens from patients with congenital hemolytic anemia. The major pathologic findings in autoimmune hemolytic anemia were mild to pronounced cord congestion and variable white pulp area, erythrophagocytosis in conjunction with an increased polymorphonuclear neutrophil reaction, and increased deposition of hemosiderin and extramedullary hematopoiesis. In contrast, both the severity and the frequency of polymorphonuclear neutrophil reactions, deposition of hemosiderin, and extramedullary hematopoiesis were less in patients with congenital hemolytic anemia, and prominent cord congestion associated with an empty or collapsed sinus was noted in patients with hereditary spherocytosis. The activity of erythrophagocytosis in the sinus was more distinct in patients with congenital hemolytic anemia, especially those with nonspherocytic congenital hemolytic anemia, than in patients with autoimmune hemolytic anemia. These findings are consistent with the existence of different mechanisms of trapping and destruction of erythrocytes in autoimmune hemolytic anemia and congenital hemolytic anemia.

Adolescent↗