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C H Issitt

Publications and source records attributed to C H Issitt.

13 recordsLinked to original sources
PubMed1982

Atypical presentation of acute phase, antibody-induced haemolytic anaemia in an infant.

We describe a case of 'warm' antibody-induced haemolytic anaemia (WAIHA) in which marked depression of red cell Rh antigen expression resulted in the patient presenting with severe anaemia but a negative direct antiglobulin test (DAT). The serum contained potent IgG Rh antibodies. Unlike two previously reported cases (Koscielak, 1980; Veer et al. 1981) in which the diagnosis of WAIHA was established before the DAT became negative, this patient presented with negative serological findings during his first episode of anaemia. As a result, the serum antibodies appeared to be allo- not autoimmune in nature and to be unrelated to the patient's anaemia. Confirmation of the autoimmune nature of the Rh antibodies was not possible until nearly 2 years after the first episode of anaemia.

Anemia, Hemolytic, Autoimmune↗
PubMed1976

Anti-Wrb, and other autoantibodies responsible for positive direct antiglobulin tests in 150 individuals.

Eluates from the red blood cells (and sera whenever free autoantibody was present) of 150 individuals with positive direct antiglobulin tests, have been studied for antibody specificity. Of 87 patients with AIHA, 64 had autoantibodies reacting with all red cell samples including Rhnu11. Of these 64 anti-d1 autoantibodies, two were, and 32 contained, auto-anti-Wrb. Of 33 patients being treated with alphamethyldopa, who had developed positive direct antiglobulin tests, 23 had anti-d1 autoantibodies four of which contained auto-anti-Wrb. Of 30 haematologically normal donors with positive direct antiglobulin tests, 23 had anti-d1 autoantibodies, two of which were, and six of which contained, auto-anti-Wrb. The full specificities of autoantibodies, other than anti-Wrb and anti-d1, in the 150 patients are described, as are the natures of the protein red cell coatings that caused the positive direct antiglobulin tests. The presence of free serum autoantibody as a correlate of the three clinical conditions is reported. Several observations on auto-anti-Wrb are documented. The antibody can cause gross red cell destruction in vivo, but can be benign on other occasions; it occurs with approximately the same frequency in AIHA patients and "normal" donors with positive direct antiglobulin tests, but in fewer patients with alphamethydopa induced positive direct antiglobulin tests; it does not activate complement in vivo; and finally it may eventually provide a clue to the aetiology of AIHA.

Anemia, Hemolytic, Autoimmune↗
PubMed1976

Another example of an antibody reacting optimally with p red cells.

An antibody is described that reacted strongly with red cells of the p(Tj(a-)) phenotype and moderately to strongly with cord red cells of the P2 phenotype. The antibody failed to react, or reacted very weakly, with red cells of the P1k and phenotypes and with the red cells of five children of a p individual, ahd reacted weakly with occasional red cell samples from adults of the P2 phenotype. These results suggest that the antibody does not detect a product of the p gene but instead detects a P system precursor substance. In p individuals this P system precursor substance is not altered by the p genes. In individuals of the P1 or P2 phenocursor substance is not altered by the p genes. In individuals of the P1 or P2 phenotype this precursor substance is apparently converted to P1 and/or P antigens by the P1 or P2 genes.

Aged↗
PubMedDate not supplied

Weak B antigen in a family.

A family is described in which six members were of a week subgroup of B. Presence of the subgroup in each individual was first indicated by lack of anti-B in that person's serum. Additional tests showed that the B subgroup red blood cells would adsorb anti-B and yield that antibody on elution, and that the saliva of two B subgroup persons tested contained B and H substances. The blood of one of the family members with the weak B antigen was inadvertently transfused to a group O recipient but caused no ill effects.

ABO Blood-Group System↗
PubMedDate not supplied

Resolution of red cell compatibility testing problems in patients receiving anti-lymphoblast or anti-thymocyte globulin.

Passively acquired hemagglutinating antibodies may be detected in the serum of patients receiving horse anti-lymphoblast globulin (ALG) or anti-thymocyte globulin (ATG). Thirty-seven patients receiving ALG following renal transplantation were studied. Eight patients monitored daily all developed positive direct antiglobulin tests (DAT) and positive red cell antibody screening tests. Fifteen of 32 recipients developed red cell antibodies reactive at room temperature in saline, 4 of 32 in albumin at 37 degrees C, and 33 of 37 in the antiglobulin test. Horse globulin was detected on the red cells of all six recipients tested with rabbit anti-horse globulin. Ether eluates prepared from the red cells of 20 patients showed no specificity for common red cell antigens. Anti-human globulin (AHG), absorbed with ALG-coated red cells to remove the component in the AHG which was crossreacting with horse globulin, was used successfully for antibody screening and identification, direct antiglobulin testing, and/or the antiglobulin crossmatching of 27 ALG and ATG recipients, including five with red cell alloantibodies.

Animals↗
PubMedDate not supplied

Destruction of the S antigen by sodium hypochlorite.

Low concentrations of sodium hypochlorite (chlorine bleach) destroyed S antigen on intact fresh red cells (RBCs). At levels of 0.0005 percent sodium hypochlorite in a 3 percent RBC suspension, S+s+ cells immediately became nonreactive with anti-S. S+s- cells required approximately 1.5 times this level of sodium hypochlorite to destroy S antigen reactivity. Anti-S absorbed three times with treated S+RBCs demonstrated no significant reduction in titer. In addition to its effect on S, the Rh antigens D, C, E, and e appeared slightly reduced in strength after treatment with sodium hypochlorite. However, the c antigen, as well as 20 other red cell antigens tested, appeared unaffected. Osmolality and pH determinations of supernatants from treated and untreated RBCs showed no significant differences. The proposed mechanism of S antigen destruction is an oxidation of the methionine residue in the S determinant. When sodium hypochlorite is used as a disinfectant, it should be rinsed thoroughly from all surfaces that might contaminate solutions that contact test RBCs. The destruction of the S antigen by sodium hypochlorite may be useful in testing complex antibody mixtures when a limited cell selection is available.

Epitopes↗
PubMedDate not supplied

Evaluation of commercial antiglobulin sera over a two-year period. Part I. Anti-beta 1A, anti-alpha 2D, and anti-beta 1E levels.

Antiglobulin sera from nine different manufacturers have been tested, over a two-year period, for their ability to detect the complement components beta 1A, alpha 2D, and beta 1E. The results demontrate considerable variation in the abilities of sera from different manufacturers to detect these components and indicate that not all sera on the market are suitable reagents for diagnostic use and compatibility tests. The results also show that there is considerable variation between different lots of serum from some of the manufacturers. In general, the anti-complement levels of these reagents have increased during the two-year period of study but not all companies produce suitable reagents for routine use.

Antibodies, Anti-Idiotypic↗
PubMedDate not supplied

Evaluation of commercial antiglobulin sera over a two-year period. Part II. Anti-IgG and anti-IgM levels and undesirable contaminating antibodies.

Antiglobulin sera, from nine different manufacturers, have been tested over a two-year period for their ability to detect different nonagglutinating, IgG and IgM blood group antibodies and for the presence of undesirable antibodies that cause the agglutination of nonglobulin coated red blood cells. There are not so many differences in anti-IgG levels among the sera as there are differences in anticomplement levels. Over the two-year period, there have been, in general, increases in the amounts of anti-IgM antibodies in the sera tested. Several of the sera, apparently prepared by dilution of raw rabbit serum and not by adsorption, contain antibodies that cause the agglutination of red blood cells not coated with IgG, IgM, or any of the components of complement.

Agglutinins↗