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Biomedical subjects

A H Waters

Publications and source records attributed to A H Waters.

At least 37 records · Page 2Linked to original sources
PubMed1992

Guidelines for platelet transfusions. British Committee for Standards in Haematology, Working Party of the Blood Transfusion Task Force.

Recommendations for the optimal transfusion support of patients likely to receive repeated platelet transfusions. 1. Determine policy for prophylactic platelet support, and select the platelet count below which platelet transfusions will be used. 2. Consider using leucocyte depletion of red cell and platelet concentrates to prevent HLA alloimmunization from the outset. 3. Type patients for HLA-A and B antigens at an early stage. 4. Use random donor platelet concentrates for initial platelet support (either single or multiple donor, depending on availability). 5. If refractoriness occurs, determine whether clinical factors, which may be associated with non-immune consumption of platelets, are present and test the patient's serum for HLA antibodies. 6. Use HLA-matched platelet transfusions if HLA alloimmunization is the most likely cause of refractoriness. 7. If there is no improvement with HLA-matched transfusions, platelet crossmatching may identify the cause of the problem and help with the selection of compatible donors. 8. Discontinue prophylactic platelet support if a compatible donor cannot be found. Use platelet transfusions from random donors to control bleeding and increase the dose, if necessary.

Blood Coagulation Disorders↗
PubMed1991

Clinical aspects of platelet transfusions.

Refractoriness is the most important complication of platelet transfusion therapy, occurring in about 50% of patients receiving repeated transfusions. The major causes are HLA alloimmunization and non-immune platelet consumption associated with clinical factors such as septicaemia. DIC and splenomegaly. Initial management of alloimmunized patients who are refractory to platelet transfusions from random donors is the use of HLA-matched platelet transfusions, which improve responses to transfusions in about 65% of patients. It may be difficult to provide effective platelet transfusion support for alloimmunized patients not responding to HLA-matched transfusions. There has been much interest in methods for the prevention of HLA alloimmunization. Primary HLA alloimmunization is dependent on the presence of HLA class II antigen-bearing cells in transfusions; pure platelet transfusions are non-immunogenic as platelets only express HLA class I antigens. The use of leucocyte-depleted blood components in multitransfused patients has resulted in a reduction in HLA alloimmunization and platelet refractioness. Improvements in the techniques for leucocyte-depletion of red cell and platelet concentrates and the possibility of inactivation of HLA class II antigen-bearing cells by UV irradiation makes prevention of alloimmunization an attainable goal.

Blood Platelets↗
PubMed1991

Alloimmune neonatal neutropenia in Australian aboriginals: an unrecognized disorder?

Alloimmune neonatal neutropenia (ANN) is reported for the first time in two Australian aboriginals. Both infants displayed the typical clinical features of ANN with profound neutropenia which persisted for 7 weeks and only minor infectious episodes. However, management strategies differed for the two infants because in one case (complicated by uncertain paternity) serological confirmation of ANN was not obtained until after recovery of the infant's neutrophil count. The maternal antibodies could not be assigned to known neutrophil antigen specificities and a new antigen may be involved. The antibodies were reactive with > 99% of neutrophils in a Caucasian population. Aboriginals comprise 1% of the total population of Australia and 1-2% of the obstetric population at our institution. Thus, ANN may be an unrecognized disorder in this ethnic group and a possible cause of neonatal infection and mortality.

Antibody Specificity↗
PubMed1990

Platelet transfusions: the problem of refractoriness.

Refractoriness is a complication of multiple platelet transfusions in 30-70% of patients with bone marrow failure. The major causes are HLA alloimmunisation and non-immune platelet consumption; the latter is usually found in patients with DIC, septicaemia or splenomegaly. Initial management of alloimmunised patients who are refractory to platelet transfusions from random donors is the use of HLA-matched platelet donors; this results in improved responses to platelet transfusions in about 65% of these patients. Platelet crossmatching may reveal the presence of platelet-specific antibodies in some patients who are refractory to platelet transfusions from HLA-matched donors and may assist in the selection of compatible platelet donors. The identification of compatible donors is not possible in all refractory patients; alternative approaches such as plasma exchange and high dose intravenous gammaglobulin have been used in such patients with variable results. Insights into the mechanism of HLA alloimmunisation have suggested methods for its prevention. Primary HLA alloimmunisation is dependent on the presence in transfusions of contaminating cells bearing HLA class II antigens; pure platelet concentrates are non-immunogenic as platelets only express HLA class I antigens. Studies using leucocyte-poor blood components for multitransfused patients have demonstrated a reduction in HLA alloimmunisation from about 50-20% and a decrease in the incidence of refractoriness. Improvements in the techniques for leucocyte depletion of red cell and platelet concentrates and the possibility of inactivation of the HLA class II antigen-bearing cells by UV irradiation might make prevention of alloimmunisation an attainable goal in the near future.

Blood Platelets↗
PubMed1990

Management of fetal alloimmune thrombocytopenia by weekly in utero platelet transfusions.

Alloimmune neonatal thrombocytopenia (ANT) may cause intracranial haemorrhage in utero as well as at delivery. Recent management has concentrated on attempts to minimise fetal thrombocytopenia and prevent its complications. This report describes further experience with the use of repeated intravascular transfusions of compatible platelets in utero. The patient studied had already had one infant with intracranial haemorrhage due to ANT. In her next pregnancy, weekly intra-uterine platelet transfusions were given from 26 weeks, but intra-uterine death occurred at 30 weeks after the mother had a heavy fall. In her most recent pregnancy, weekly intravascular transfusions of platelets were given by cordocentesis from 29 to 34 weeks. The fetal platelet count was maintained above 30 X 10(9)/l for almost all of the last 6 weeks of pregnancy before delivery of a normal infant by Caesarean section at 35 weeks' gestation. This approach is effective in preventing severe fetal thrombocytopenia in the last trimester of pregnancy and is contrasted with alternative treatments of ANT. Further data are required to determine the efficacy and risks of these treatments.

Blood Transfusion, Intrauterine↗
PubMed1990

Report on the fourth ISBT/ICSH platelet serology workshop (London 1988).

The fourth ISBT/ICSH platelet serology workshop took place in 1988. It consisted of a wet workshop carried out by the 17 participating laboratories during March 1988, followed by a discussion of the results at a meeting of the ISBT/ICSH Expert Panel on Platelet Serology at the ISBT/BBTS Congress in London in July 1988. Sixteen samples, including 1 negative control serum, were analysed by the participants using methods of their choice. There was general agreement on 10/16 samples. The results indicated progress in the following areas: (i) antibody identification; (ii) differentiation of platelet-specific and HLA antibodies; (iii) glycoprotein localisation of platelet specific antigens; (iv) identification of new platelet antigen systems.

Blood Grouping and Crossmatching↗
PubMed1989

Post-transfusion purpura.

Post-transfusion purpura (PTP) is an acute episode of severe immune thrombocytopenia occurring about a week after transfusion. It is closely associated with alloimmunisation by platelet specific antigens, and usually affects a PlA1 negative woman who has been previously immunised by a PlA1 positive pregnancy. The transfusion precipitating PTP provokes a secondary (anamnestic) response which boosts the patient's anti-PlA1 antibody, but it remains uncertain how this relates to the destruction of the patients own PlA1 negative platelets. The accumulated information gained from the intensive study of an increasing number of cases of PTP from many centres has revealed a wider clinical and serological spectrum of PTP, and this has led to a better understanding of the pathogenesis and treatment of the condition. These aspects of PTP are the subject of this review.

Humans↗