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)

A 14-year-old girl with acute promyelocytic leukemia (APL) developed cardiomyopathy following chemotherapy for remission induction and subsequent consolidation consisting of cumulative doses of 644 mg/m2 of daunorubicin and 31 mg/m2 of mitoxantrone. Six months after the first complete remission, when relapse of APL was recognized an allogeneic bone marrow transplantation (BMT) from her HLA-identical brother was performed. A preconditioning regimen, consisting of cytarabine (Ara-C, 2 g/m2/day x 3 days and 4 g/m2/day x 3 days), total body irradiation (TBI, 1200 cGy) and etoposide (VP-16, 50 mg/kg) caused moderate gastrointestinal symptoms and transient hemorrhagic cystitis, but did not worsen her cardiac function. Both continuous intravenous administration of heparin to control DIC and continuous low dose dopamine infusion to prevent cardiac failure achieved their purpose. The patient is leukemia-free and has no symptoms related to cardiomyopathy at the eight month after BMT. A preconditioning regimen (Ara-C, TBI and VP-16) appeared to be suitable for BMT to a patient with anthracycline-induced cardiomyopathy.
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PMID:[A successful allogeneic bone marrow transplantation for acute promyelocytic leukemia with anthracycline-induced cardiomyopathy at relapse]. 160 7

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

To determine the relative importance of clinical factors on the efficacy of platelet transfusions, 941 pooled platelet transfusions from HLA-unmatched donors were studied prospectively in 133 patients with bone marrow failure. Multiple linear regression analyses identified the major factors influencing one-hour-corrected increments (CI) as prior splenectomy, bone marrow transplantation, disseminated intravascular coagulation, concurrent intravenous amphotericin B, splenomegaly, and HLA antibody grade. The relative impact of these factors on CI has been quantitated by using a formula developed from these data. A linear relationship was demonstrated between increasing percentage of HLA antibody grade and decreasing CI. A number of other factors were less important in the linear regression model than the aforementioned major factors. These included platelet-specific antibodies, concurrent antibacterial antibiotics, clinical bleeding grade, and temperature. Factors that did not influence CI included the number of prior platelet transfusions, prior granulocyte transfusions, prior red cell transfusions, infection, age, blood group, diagnosis, sex, pretransfusion platelet count, prior pregnancies, and concurrent antineoplastic drugs. This study identified major clinical factors that significantly influenced CI and were major causes of refractoriness to pooled platelet transfusions.
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PMID:Clinical factors influencing the efficacy of pooled platelet transfusions. 333 3

Severe disseminated intravascular coagulation was observed in a patient with Burkitt's lymphoma/leukaemia. Immunological studies on leukaemic blasts from relapsed bone marrow revealed a B-cell phenotype (B4+, B1+, HLA-Dr+, J5+) with membrane bound IgM lambda. Cytogenetic investigation revealed a variant Burkitt's translocation t(8;22)(q24;q11) involving the lambda light chain gene region and abnormalities of chromosomes 15 and 17 with breakpoints at q22 and q12 respectively, similar to those observed in the t(15;17) in acute promyelocytic leukaemia. Transmission electron microscopy of the leukaemic blasts showed crystalline cytoplasmic inclusions which may have had a role in precipitating the disseminated intravascular coagulation.
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PMID:Variant translocation t(8;22) and abnormalities of chromosome 15(q22) and 17(q12-21) in a Burkitt's lymphoma/leukaemia with disseminated intravascular coagulation. 379 Apr 45

The frequency, nature, and management of chemotherapy-associated oral hemorrhages were studied in 1,093 adult inpatients undergoing treatment for acute leukemia or the blastic phase of chronic leukemia. Of this number, 163 (14.9%) manifested gross bleeding from the mouth during the course of treatment. The most common oral bleeding sites were the lips, tongue, and gingiva. Thrombocytopenia was the underlying cause in 88% of the cases, disseminated intravascular coagulation in 6%, and combinations of thrombocytopenia and hypofibrinogenemia and of thrombocytopenia and vitamin K deficiency in 5.5% and 0.6%, respectively. The vast majority of the patients with mouth bleeding had platelet counts below 40,000/mm3. Approximately 50% had indirect evidence of a coagulation factor deficiency in the blood. The oral hemorrhages were best managed by transfusions of HLA-compatible fresh platelets and fresh frozen plasma, together with topically applied clot-promoting agents, until hemostatic control was restored.
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PMID:Chemotherapy-associated oral hemorrhages in adults with acute leukemia. 661 Jan 54

Severe thrombocytopenia and clinical bleeding remain major clinical problems in leukemic patients undergoing remission induction and those receiving high dose chemotherapy. Prophylactic platelet transfusions have made a major impact on hemorrhagic deaths over the last 20 years. The effectiveness of platelet transfusions is influenced by a number of clinical factors including the status of the spleen, prior bone marrow transplantation, the presence of disseminated intravascular coagulation and the presence of HLA antibodies. Optimal platelet transfusion therapy requires that transfusions be monitored routinely by post-transfusion counts and that a refractory group be clearly defined. The cytokine granulocyte colony stimulating factor (G-CSF) has not had a clinically significant impact on thrombocytopenia. Granulocyte-macrophage colony stimulating factor (GM-CSF) also probably has little clinical relevance, although in a randomized study, thrombocytopenia was worse in GM-CSF-treated patients. Interleukin-3 (IL-3) can increase platelet count and has the potential to protect against thrombocytopenia in patients receiving chemotherapy. This hypothesis is currently being tested in on-going clinical trials.
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PMID:Platelet support and the use of cytokines. 752 92

Refractoriness to platelet transfusions remains a significant problem for oncology patients, occurring in 30% to 70% of multiply transfused recipients with bone marrow failure. Nonimmune causes are often present and include disseminated intravascular coagulation, concurrent use of amphotericin B, infection, presence of palpable spleen, use of antibacterial antibiotics, bleeding, veno-occlusive disease, and fever. Immune causes are also commonly responsible for refractoriness, with HLA alloimmunization dominating the list of immune factors. HLA antibodies can be identified in 25% to 30% of transfused leukemia patients and can be present in as many as 80% of aplastic anemia patients. Developing a consistent approach to managing these refractory patients is essential to preventing and treating bleeding manifestations. An HLA type should be obtained for all patients anticipated to have chronic transfusion requirements. Screening for lymphocytotoxic antibodies can confirm suspected HLA alloimmunization. Histocompatible platelets (cross-match compatible and HLA matched) should be provided for all patients with HLA antibodies. A number of other therapeutic modalities have been used in an effort to manage the alloimmunized patient; most of these methods have had little or no proven benefit. When bleeding develops in the alloimmunized patient, there are few therapeutic choices. If histocompatible platelets are unavailable or unsuccessful, massive platelet transfusions of pooled platelet concentrates are commonly used, although this practice is of no proven benefit. While antifibrinolytic agents have been available for over 30 years, they are only recently being applied to control bleeding in chronic thrombocytopenia. We have successfully managed bleeding episodes in thrombocytopenic bone marrow transplant recipients with the use of epsilon aminocaproic acid. A number of these patients were platelet refractory with demonstrable platelet antibodies. Platelet refractoriness continues to plague multiply transfused oncology patients. While preventative measures may ultimately benefit some patients, this problem will continue to manifest itself. A consistent approach to transfusion support needs to be implemented to best manage this challenging patient population.
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PMID:The platelet-refractory bone marrow transplant patient: prophylaxis and treatment of bleeding. 821 Dec 11

A 75-year-old female was admitted to our hospital because of fever and hypotension. The peripheral blood showed 400 leukocytes/microliters with 13,000/microliters platelets. Bone marrow puncture revealed that NCC stood at 14,000 with 50.0% blasts. The surface characters of the blasts were CD13+, CD33+, and HLA-DR+, and blood culture tests were positive. Coagulation tests revealed DIC. Based on the foregoing results, hypoplastic leukemia was diagnosed accompanied by sepsis and DIC, and was placed on the concomitant administration of a combination of low dose Ara-C and M-CSF. After 14 days of Ara-C administration and 26 days of M-CSF, her clinical symptoms improved, with the peripheral blood showing a WBC of 2,800/microliters and platelet count of 111,000/microliters. The percentage of myeloblasts decreased to 7.0%. After the administration of Ara-C was suspended for 2 weeks, another course of low dose Ara-C plus M-CSF administration was carried out and the patient achieved full remission. M-CSF stimulates not only the production of monocytes but increases the number of neutrophils and platelets through monocytes. It is also expected that tumoricidal activity may be realized by the activation of monocytes. In this patients, the concomitant administration of M-CSF and low dose Ara-C was remarkably effective in treating hypoplastic leukemia with severe complication. This result suggests that M-CSF will be useful for the treatment of leukemia.
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PMID:[Hypoplastic leukemia which achieved remission with administration of M-CSF along with low dose ara-C]. 831 38

A case is reported of 60-year-old woman who developed transfusion refractoriness after having been transfused several times. This patient who had been transfused with 4 standard packed red cell packs (PRC) for a surgical repair of a hiatal hernia, required three further operations within two months for postoperative complications. After the first operation, she had developed anti-JK1 and anti-CW alloantibodies. Seven phenotype compatible PRC and five fresh frozen plasma (FFP) were transfused during the surgery carried out on day 32. Massive haemorrhage occurred during the fourth operation on day 48, and the patient was transfused with 31 phenotype compatible PRC, 21 fresh frozen plasma, 36 standard platelet concentrates (SPC), fibrinogen, factor VIII and anti-thrombin III. Postoperative disseminated intravascular coagulation occurred, with thrombocytopaenia (45 G.l-1). Major thrombocytopaenia persisted for 6 days (12 G.l-1 on day 52), after the other signs of intravascular coagulation had been corrected, and despite the transfusion of 40 SPC. Platelet counts progressively returned to normal (195 G.l-1 on day 56). An HLA alloimmunization was discovered, which may have been induced by leukocytes contaminating the transfused red blood cell and platelet concentrates. A fifth operation carrying a high risk of haemorrhage was therefore prepared by harvesting autologous platelet rich plasma two days before and on the morning of the operation. These were transfused intraoperatively, together with phenotyped and leukocyte-free PCR, thus avoiding massive and expensive homologous platelet transfusions. In patients with a high risk of HLA immunization (previous pregnancies, multiple transfusions), autotransfusion or leukocyte-poor blood products should be used.
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PMID:[Refractory thrombocytopenia by HLA alloimmunization in a multitransfused patient]. 833 66


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