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Biomedical subjects

P D Issitt

Publications and source records attributed to P D Issitt.

At least 19 recordsLinked to original sources
PubMed1991

Hemolytic disease of the newborn caused by anti-Rh32 and demonstration that RN encodes rhi (Ce,Rh7).

A family is described in which the mother made anti-Rh32 as a result of pregnancy; her second liveborn child had hemolytic disease of the newborn and required an exchange transfusion. In investigating the family, it was found that the father's RN gene did not make rhi and that his second Rh gene made normal amounts of c and e but a reduced amount of f. In the two children of the couple, who inherited a normal r or Ro from their mother, the paternally derived RN encoded an amount of rhi that could be detected in direct typing tests. In the father, lack of production of rhi by RN may have represented a suppressive effect of the ce(f) gene in trans to RN or the presence of an unlinked suppressor of Rh that might also have been responsible for the reduced production of f by his r or Ro gene. The two children in this family are the first persons in whom RN has been shown to make rhi.

Erythroblastosis, Fetal↗
PubMed1991

An auto-anti-M causing hemolysis in vitro.

A 64-year-old white man, who had never received a transfusion, was found to have anti-M in his serum. The antibody agglutinated all M+ red cells in room-temperature tests. When the ionic strength of the test milieu was reduced by use of an additive solution and the tests were incubated at 37 degrees C, the antibody hemolyzed M + N- but not M+N+ red cells. All M+ red cells reacted in indirect antiglobulin tests using polyspecific antiglobulin reagents when such tests followed an initial incubation at room temperature. When red cells and the patient's serum were warmed to 37 degrees C before being mixed, no antibody activity was demonstrable. The antibody was adsorbed to exhaustion onto M+N- and M+N+ red cells (including the patient's own), and its activity was destroyed by dithiothreitol. There was no evidence of in vivo red cell destruction by the autoantibody. No previously reported example of anti-M has been shown to activate complement in conventional in vitro tests. This example was extraordinary in that it caused sufficient complement activation to present as an in vitro hemolysin.

Antibody Specificity↗
PubMed1991

Studies on the structures of the Tm, Sj, M1, Can, Sext and Hu blood group antigens.

The Glycophorins (GPs = sialoglycoproteins) in erythrocyte membranes from various Black individuals, some of which exhibit the M1, Can, Sj, Tm, Sext and/or Hu antigens, and several Caucasian donors, including pooled fetal red cells, were studied. Using agglutination inhibition assays with GP fractions, GP fragments and chemically modified GPs as well as trypsin treatment of intact red cells, the antigens defined by anti-M1, anti-M+M1, anti-Can and anti-Tm sera were found to be located on the N-terminal tryptic peptide (T2, residues 1-31) of the major GP (GP A = MN sialoglycoprotein). Evidence was obtained that the N-terminal amino-acid residue, NeuNAc and/or (a) different sugar residue(s) are involved in the antigens. Amino-acid sequence and composition analyses excluded an amino-acid exchange within the N-terminal region (residues 1-31) of GP A. Carbohydrate analyses revealed the attachment of GlcNAc residues (up to about five, dependent on the strength of the above-mentioned antigens) to O-glycosidically linked oligosaccharides within the N-terminal portion (residues 1-31) of GP A. As judged from the carbohydrate compositions of peptides, the alteration of the O-glycosidic oligosaccharides is associated with a slight increase of the Gal and Fuc contents and a slight decrease of the NeuNAc level. Analyses of small, secondary cyanogen bromide and V8 proteinase peptides from the N-terminal region of GP A from Blacks, Caucasians and Caucasian fetal cells suggest that the variable attachment of small quantities of GlcNAc (about 0.03 to about 0.2 residues per peptide molecule) accounts, at least in part, for the polymorphisms detected by anti-Can and the original anti-Tm (serum Sheerin). Remarkably, the GlcNAc-containing O-glycosidic oligosaccharides occur only in small quantities, or not all at, within the positions 32-61 of GP A and the glycosylated domains of GP B and GP C.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylglucosamine↗
PubMed1990

Temporary suppression of Kidd system antigen expression accompanied by transient production of anti-Jk3.

This report describes an 85-year-old woman of Russian Jewish extraction whose red cell Kidd system phenotype changed during the 2 years in which her blood was studied. Certainly once, and perhaps twice, the patient's phenotype changed from Jk(a+b-) to Jk(a-b-). On both occasions, it reverted to Jk(a+b-). During the first episode of loss of Jka, she formed anti-Jk3. Although this antibody was weak, it was capable of in vivo destruction of Jk(a+b-) and Jk(a-b+) red cells. A lack of details about the patient's clinical condition precludes speculation as to the cause of suppression of Jka expression. The phenomenon appeared to affect only the Kidd blood group system. This case should alert others that antigen loss can occur in the Kidd system as it has been shown to occur in, at least, the Rh, Kell, and Ge systems.

Aged↗
PubMed1978

Critical re-examination of the specificity of auto-anti-Rh antibodies in patients with a positive direct antiglobulin test.

Forty-eight autoantibodies with apparent 'simple' anti-Rh specificity (anti-e, -E, -c, -D, -C, -Ce, -G), have been studied by means of multiple absorption tests. The finding that 34 (70.8%) of these antibodies could bind to red blood cells lacking the antigens that the antibodies appeared to define, indicated that the antibodies had different specificities than seemed to be the case in initial antibody identification tests. Those autoantibodies that at first appeared to be directed against the Rh antigens e, E or c, most often had anti-Hr or anti-Hro specificity. These data explain why some apparent anti-Rh autoantibodies can be eluted from the red blood cells of patients negative for the antigens that the antibodi:s appear to define. However, they also illustrate that the phenomenon of autoantibodies mimicking specificities that they do not possess is common in patients positive for the antigens against which their autoantibodies appear to be directed. An explanation for the mode of action of these autoantibodies in complexing with the Rh agglutinogen is proposed, and the significance of the antibodies in transfusion therapy is considered.

Anemia, Hemolytic, Autoimmune↗
PubMed1978

The antigen Duclos. A new high frequency red cell antigen related to Rh and U.

An antibody is described which defines a new high frequency red cell antigen, Duclos, whose expression seems to require the presence of both U and Rh fundamental antigens. Apart from the antibody maker's own red cells the only nonreactive samples were from Rhnull U impaired individuals, one example of which was shown however to yield very slight amounts of antibody through absorption-elution tests. Rhmod U weak cells gave very depressed and Rhnull U positive or Rh common U negative cells moderately depressed reactions. The proposita's red cells had an apparently normal Rh-LW condition but their U antigen was significantly decreased. No further Duclos negative individual was found by screening 8,500 blood donors in the Paris area.

Aged↗
PubMed1978

Autoimmune hemolytic anemia and cold hemagglutinin disease: clinical disease and laboratory findings.

As is apparent from the length of this review, a multitude of laboratory investigations can be performed on the blood of patients with AIHA and CHD. Unfortunately, because of the considerable complexity of some of these tests, their significance is not always apparent to the physician who treats the patient. Communication gaps between the laboratory scientist and the physician at the bedside are bound to occur because of the high degree of specialization of both immunohematology and medical care. The purpose of this review has been to bridge the communication gap. The agents that cause AIHA and CHD are antibodies. Although they are often autoantibodies of complex specificity, usually reacting with all normal red cells, they nevertheless obey most of the rules explaining the action of alloantibodies that sometimes complicate transfusion therapy. By approaching AIHA and CHD as antibody-induced conditions, and by regarding autoantibodies as similar in their actions to alloantibodies, hopefully, physicians will appreciate the significance of the tests performed in the laboratory. For their part, the laboratory workers will be able not only to report test results but also to explain the findings. This review may aid in establishing the essential dialogue.

Agglutinins↗
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↗
PubMedDate not supplied

Some observations on "Bombay" bloods, with comments on evidence for the existence of two different Oh phenotypes.

Bloods from three individuals, one each of the phenotypes Oh-A, Oh-B and Oh-O have been studied. The work of Dzierzkowa-Borodej, et al.-10 was confirmed when it was shown that all three samples of Oh red blood cells had increased I antigen strength. The i, Sd-a, Le-a and Le-x antigens were not found to be increased. Attempts were made to adsorb and elute anti-A, anti-B and anti-A,B with the Oh red blood cells, using sera that contained high titered anti-I antibodies. This was done in the belief that previously reported positive results in such tests might be due to the high level of I on the Oh red blood cells, anti-I in the sera containing the ABO antibodies, and the Matuhasi-Ogata phenomenon. However, in no instance were we able to adsorb an ABO antibody onto the Oh red blood cells. Contrary to the report of others-10 the titers of anti-A, anti-B and anti-H in the sera of the three Oh individuals studied did not differ significantly. We suggest that the evidence from our findings and the work of others is sufficient to show that at least two forms of the Oh phenotype exist: one representing total suppression of H, A, and B antigens, and the other marked but not total suppression, with partial inhibition of antibody production.

ABO Blood-Group System↗
PubMedDate not supplied

Successful transfusion of Chido-positive blood to two patients with anti-Chido.

Two cases are described in this report in which patients with anti-Chido in the serum were transfused with Chido-positive blood. Since there was evidence of normal survival of the transfused red blood cells, these findings do not support a suggestion that patients with anti-Chido may require transfusion with Chido-negative blood. In spite of the apparently normal survival of the Chido-positive blood, a previous report in which it was shown that weakly Chido-positive blood can stimulate the production of anti-Chido was confirmed.

Aged↗
PubMedDate not supplied

An autoantibody with anti-Wrb specificity in a patient with warm autoimmune hemolytic anemia.

A patient with warm autoimmune hemolytic anemia (AIHA) has been found to possess an autoantibody with Wrb specificity. While this is the first known description of Wrb specificity in this disease, additional studies on the Wrb status of En(a-) cells indicate that autoantibodies previously thought to be anti-Ena are in reality also anti-Wrb. Autoantibodies with Wrb specificity may thus be a rather common finding in patients with AIHA who have been thought to have "panagglutinins" on their red blood cells. Since anti-Wra alloantibodies are found frequently in patients with AIHA, it seems possible that the Wright system holds some clue to the pathogenesis of this disease.

Anemia, Hemolytic, Autoimmune↗