Search PubMed⌕ Search

Biomedical subjects

A H Waters

Publications and source records attributed to A H Waters.

At least 55 records · Page 3Linked to original sources
PubMed1987

Disappearance of HLA and platelet-specific antibodies in acute leukaemia patients alloimmunized by multiple transfusions.

Alloimmunization by platelet transfusions was studied in 154 patients with acute leukaemia. 17 patients had HLA antibodies at initial presentation induced by previous transfusions or pregnancies; one of these also had platelet-specific antibodies and one other patient had platelet-specific antibodies alone. A further 38 patients developed HLA antibodies during therapy; three also had platelet-specific antibodies and two patients developed platelet-specific antibodies alone. Of these, 37 patients with HLA antibodies including three with platelet-specific antibodies and one patient with platelet-specific antibodies alone survived their initial therapy and formed the basis of this study. Antibodies once detected persisted throughout the study in seven of the 37 patients with HLA antibodies including one patient with platelet-specific antibodies and in the patient with platelet-specific antibodies alone. HLA antibodies disappeared after discontinuation of transfusions in six patients, and after switching to HLA matched platelet transfusions and leucocyte-poor blood in eight patients; two of the latter patients also had platelet-specific antibodies which disappeared. The other 16 patients with HLA antibodies lost their antibodies despite continued transfusions.

Acute Disease↗
PubMed1987

Incidence and mechanism of neutropenia and thrombocytopenia in patients with human immunodeficiency virus infection.

The incidence of lymphopenia, thrombocytopenia and neutropenia was studied in 105 homosexual men with HIV infection. Lymphopenia was common in patients with AIDS (75%), but its incidence in PGL (24%) was not significantly different from that in asymptomatic anti-HIV positive (15%) homosexual men. Neutropenia and thrombocytopenia were found in patients with AIDS or PGL, but not in asymptomatic anti-HIV positive homosexuals. The study suggests that the neutropenia and thrombocytopenia in these patients were due to autoimmune destruction of neutrophils and platelets.

Acquired Immunodeficiency Syndrome↗
PubMed1987

A survey of anti-platelet antibody detection--report of the UK Platelet and Granulocyte Serology Working Group, 1985.

In 1985, serum samples were distributed to 27 laboratories within the UK and Eire with the objective of determining the current state of anti-platelet antibody detection. The sera included five unknown samples for blind assessment and four well-characterized reference reagents. The laboratories involved used a wide range of different methods but the most commonly used techniques were the fluorescent antiglobulin test and the enzyme-linked immunosorbent assay. In the trial, all responding laboratories were able to detect potent anti-platelet alloantibodies but there was a 43% incidence of 'false positive' results with samples which had been designated as inert. There were no apparent differences in performance between assays using fluorescein- or enzyme-labelled antiglobulin reagents or between assays which utilized PFA-treated rather than untreated platelets.

Antibodies↗
PubMed1987

Post-transfusion purpura associated with anti-Baka and anti-PIA2 platelet antibodies and delayed haemolytic transfusion reaction.

The occurrence of post-transfusion purpura (PTP) in a 16-year-old girl with sickle/beta-thalassaemia is described. Clinically this was a typical case of PTP, but it was unusual serologically. Anti-Baka and anti-PIA2 platelet-specific antibodies were identified and the patient's platelets were typed as homozygous PIA1-positive and Baka-negative. The patient also developed red-cell, granulocyte and lymphocytotoxic antibodies in response to the blood transfusion and had a delayed haemolytic transfusion reaction.

Adolescent↗
PubMed1986

Use of leucocyte-poor blood components and HLA-matched-platelet donors to prevent HLA alloimmunization.

Recent studies have shown that the incidence of alloimmunization due to repeated platelet transfusions from random donors may be reduced by the use of leucocyte-poor blood components. These results were confirmed by this study, where 16% of patients with acute leukaemia undergoing initial chemotherapy and receiving leucocyte-poor blood components developed lymphocytotoxic antibodies, compared with 48% of patients in a control group receiving standard (non-leucocyte-depleted) blood components. In a third group, who received leucocyte-poor blood components and HLA-matched platelets, none of the patients developed lymphocytotoxic antibodies. There was a low incidence of platelet-specific antibodies (8%) but no difference between the three groups. Improved methods of removing leucocytes from blood components appear to offer the best approach for minimizing HLA alloimmunization, as the provision of HLA-matched platelet donors for prophylactic platelet support of all patients is not feasible.

Adolescent↗
PubMed1986

Autoimmune thrombocytopenia and neutropenia after remission induction therapy for acute leukaemia.

Patients with acute leukaemia who are exposed to intensive chemotherapy, with or without radiotherapy, may remain thrombocytopenic or neutropenic in remission. The incidence of these prolonged cytopenias was examined retrospectively in 46 patients in remission and prospectively in 14 patients. The patients were tested for the presence of autoantibodies to platelets and neutrophils using a fluorescent antihuman globulin technique with paraformaldehyde-fixed cells. In the retrospective study nine patients (20%) had neutrophil autoantibodies and seven (15%) had platelet autoantibodies; only one of the former had neutropenia and one of the latter thrombocytopenia. In the prospective study three (21%) had neutrophil autoantibodies and seven (50%) had platelet autoantibodies. One of the patients with platelet autoantibodies had transient thrombocytopenia, and shortened platelet survival was demonstrated. None of the patients with neutrophil autoantibodies had neutropenia. The rare occurrence of cytopenias in association with these autoantibodies was possibly due to bone marrow compensation for antibody-mediated cell destruction, although other possible mechanisms are discussed.

Acute Disease↗
PubMed1985

Post-transfusion purpura responding to high dose intravenous IgG: further observations on pathogenesis.

A typical case of post-transfusion purpura (PTP) is described in a 61-year-old woman. Treatment with steroids corrected the purpuric manifestations, but the patient remained thrombocytopenic in spite of steroid therapy and plasma exchange. However, an intravenous infusion of high dose IgG led to a rapid and sustained increase in the platelet count. The mechanism of thrombocytopenia in PTP is still a matter for speculation, as the platelet specific antibody usually cannot be shown to react with the patient's own platelets in vitro. Therefore, the finding of a coexistent platelet specific IgM autoantibody in this patient, first detected during the early recovery phase, is of particular interest and suggests a possible autoimmune basis for the profound thrombocytopenia.

Autoantibodies↗
PubMed1985

Cephalosporin-induced immune neutropenia.

Neutropenia is an occasional complication of treatment with cephalosporin antibiotics. This report describes two patients who had neutropenia while receiving high doses of cephalosporins. The neutrophil counts returned to normal after stopping the drug, and cephalosporin-dependent neutrophil antibodies were demonstrated in both cases, using the granulocyte immunofluorescence test. In one patient, the immune neutropenia appeared to be due to a drug adsorption mechanism similar to penicillin-induced haemolytic anaemia, while an immune complex mechanism may have been involved in the second patient.

Adult↗
PubMed1985

Use of chloroquine-treated granulocytes and platelets in the diagnosis of immune cytopenias.

A chloroquine modification of the fluorescent antiglobulin technique has been used to demonstrate cell-specific antibodies in the presence of HLA antibodies. This is of particular value in the diagnosis of alloimmune neonatal thrombocytopenia and neutropenia, post-transfusion purpura, and in the investigation of febrile non-haemolytic transfusion reactions and of patients refractory to platelet transfusions.

Adult↗