Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Clinical aspects of platelet transfusions. 189 71

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.
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PMID:Platelet transfusions: the problem of refractoriness. 218 45