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Biomedical subjects

B Habibi

Publications and source records attributed to B Habibi.

At least 55 records · Page 3Linked to original sources
PubMed1985

Drug induced red blood cell autoantibodies co-developed with drug specific antibodies causing haemolytic anaemias.

Four individuals with anti-glafenine, anti-latamoxef and anti-teniposide antibodies were found to have an associated red blood cell autoantibody. The two components could be separated by selective absorption and showed distinct time course patterns. In three patients a well-defined blood group antigen was recognized as the receptor for both auto- and drug specific antibodies. Similarities between this type of immune response to drugs and the well-known hapten and carrier specificities developed in animals immunized by hapten-carrier conjugates are discussed.

Aged↗
PubMed1984

[Immunoallergic hemolytic anemia, thrombopenia and acute renal failure induced by aspirin].

The first case of haemolytic anaemia with thrombocytopenia and acute renal failure induced by ingestion of aspirin in a 22-year old woman is reported. An IgM anti-aspirin antibody which agglutinated erythrocytes of the patient and of ABO compatible donors in the presence of aspirin was isolated in the serum. In addition, the allergic nature of the patient's hypersensitivity to aspirin was confirmed by positive lymphocyte transformation and basophil degranulation tests in the presence of the drug.

Acute Kidney Injury↗
PubMed1984

Adverse transfusion reactions associated with a precipitating anti-C4 antibody of anti-Rodgers specificity.

A patient suffering from chronic hepatitis exhibited severe transfusion reactions after administration of fresh frozen plasma and a plasma fraction: PPSB (prothrombin complex concentrate). 1 month before these reactions, she received fresh frozen plasma during plasma exchange therapy. The patient's serum obtained 1 week and 6 months after the second reaction gave a precipitation arc against PPSB preparations when examined by double-diffusion technique in agarose gel. An antibody of IgG class present in these sera reacted with a purified preparation of the fourth complement component (C4). This was demonstrated by various experiments (protein A radioimmunoassay and passive hemagglutination) using purified C4 as antigen. The antibody had a limited specificity and reacted only with C4 of Rodgers specificity. Phenotype determination of the patient's C4 group showed that she was Chido positive and Rodgers negative. Her HLA group was A1, Aw30; B8,-; DR3,-. The patient had neither detectable anti-IgA nor other anti-immunoglobulin antibodies. She had not received blood or plasma transfusion before her hepatitis. The coexistence of a precipitating anti-C4 antibody and adverse transfusion reactions to plasma fractions containing large amounts of C4 indicates that in the absence of antibodies of other specificities, this antibody can be considered as the cause of the transfusion reaction.

Adult↗
PubMed1984

Cryoprecipitation of an anti-Pr2 monoclonal IgM cold agglutinin in the presence of GM3 ganglioside.

The mechanism of cryoprecipitation of a monoclonal IgM kappa cryoglobulin (Mou) with a cold agglutinin activity of Pr2 specificity has been studied. By immunodiffusion this cryoglobulin reacted (by its Fab' fragment) with micellar GM3, a ganglioside bearing the Pr2 antigenic determinant. In contrast to previous reports that indicated a possible temperature dependent self-association of IgM molecules via an immunological interaction leading to cold precipitation, we could not detect any affinity of this cryoglobulin for IgM when we used passive hemagglutination or an indirect enzyme-linked immunosorbent assay (ELISA). However, a GM3-like ganglioside could be extracted, by drastic methods, from the cryoglobulin studied at 22 degrees C, whereas no GM3 was extracted from two control cryoglobulins. Some minor gangliosides (representing less than 25% of total amount of bound gangliosides) were also extracted from Mou cryoglobulin and these gangliosides were shown to crossreact with GM3, as they specifically bind to Mou cryoglobulin by ELISA. After cryoprecipitation the serum still contained a monoclonal anti-Pr2 IgM kappa. A GM3-like ganglioside could be extracted from this purified IgM, and cryoprecipitability could be induced by the addition of a minute amount of micellar GM3. These results suggest that Mou cryoglobulin circulates as an immune complex and that cryoprecipitation may depend on unique IgM-GM3 (or IgM-GM3 cross-reacting gangliosides) complexes.

Agglutinins↗
PubMed1983

[Acute anuric hemolysis caused by antiajmaline antibodies].

In a 32-year old woman under ajmaline therapy for cardiac arrhythmia, a sudden episode of acute haemolytic anaemia and renal failure led to the identification of a potent agglutinating, haemolysing and lymphocytotoxic antibody specific to ajmaline and cross-reacting with quinine and quinidine. The immunological features of the antibody and the pathophysiological mechanism of blood cell destruction are presented, together with a brief synopsis of drugs incriminated so far in the induction of specific antibody formation and immune haemolytic anaemia.

Acute Kidney Injury↗
PubMed1983

[Inconvenience of planned prophylaxis of transfusion-induced alloimmunization to red cells in chronic renal insufficiency].

Records from 506 hemodialysis multitransfused patients were reviewed to evaluate the incidence of transfusion induced red cell allo-immunization. Out of 405 patients having received a total of 6 608 red cell transfusions compatible for A, B and D antigens, only 7 patients (1.72%) developed allo-antibodies which may be attributed to such transfusions. Elaborate red cell phenotyping in un-immunized recipients and selection of blood units compatible for other antigens than A, B and D in an effort to prevent red cell allo-immunization to other blood group antigens in such potentially multitransfused patients does not accordingly appear to be justified and cost-effective.

ABO Blood-Group System↗
PubMed1983

[Blood transfusion and acquired immunodeficiency syndrome (AIDS)].

This report was presented at the June 1983 meeting of the Blood Transfusion National Consultative Commission at the French Ministry of Health. Clinical and epidemiological data on AIDS as well as problems raised by the lack of specific tests for screening of blood donors were briefly summarized. Out of 49 AIDS patients recorded in France up to April 1983, only one had a history of previous blood transfusion given in Haiti, 4 years before the clinical onset of the disease. Blood donors, all Haitians, had no sign and symptom of AIDS. Retrospective review of 2 300 hemophiliacs followed up in France until April 1983 disclosed no AIDS. However, in 6 patients, the following features, more or less associated, were found to be present: thrombocytopenia, neutropenia, micropolyadenopathy, splenomegaly, hypergammaglobulinemia and low OKT4/OKT8 ratio. No clear correlation could be found between these abnormalities and the origin, commercial or national, of the coagulation factor concentrates used for the treatment. Three main recommendations were proposed: -- information of blood donors and experimental evaluation of some non specific screening tests, in the at risk donor population. -- more cautious use of coagulation factor concentrates -- reduction of importations aiming at complete national self sufficiency concerning factor VIII concentrates.

Acquired Immunodeficiency Syndrome↗
PubMed1983

[Blood group antigens may be the receptors for immunoallergic drug complexes reacting with erythrocytes].

19 antibodies specific for 11 different drugs were extensively tested in the presence of the drug against a panel of red cells including common and public minus phenotypes. High incidence blood group antigens were shown to be specific receptors for several drug-antibody complexes proving thereby that red blood cells play more than an "innocent bystander" role in drug induced immune hemolytic anemias.

Acute Kidney Injury↗
PubMed1983

[Limited indications for phenotyped blood in the prevention of transfusion-induced anti-red blood cell alloimmunization in chronic kidney failure].

Records from 506 multitransfused patients on a program of hemodialysis were reviewed to evaluate the incidence of transfusion-induced red cell alloimmunization. Out of 405 patients having received a total of 6608 red cell transfusions compatible for A, B and D antigens, only 7 patients (1.72%) developed allo-antibodies which may be attributed to such transfusions. Elaborate red cell phenotyping in non-immunized patients and selection of blood units compatible for other antigens than D does not accordingly appear to be justified and cost-effective.

Adolescent↗