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)

The records of 104 patients with culture-proven enteric fever were reviewed and evaluated as to the clinical signs, laboratory findings, pathologic features and complications of the disease. One patient with fatal disseminated intravascular coagulation and enteric fever is also presented. Fever and bradycardia were the leading clinical signs followed by splenomegaly, hepatomegaly and rose spots. The principal complications of enteric fever included anemia, typhoid hepatitis, relapse and bleeding. Evidence of typhoid hepatitis was present in 30% of the patients tested. The pathology consisted of typhoid nodules of variable frequency and size depending upon the severity of the condition. The relationship of typhoid hepatitis to relapse seems to be more than coincidental as four out of seven patients who had relapse had abnormal liver tests. The occurrence of disseminated intravascular coagulation in enteric fever is rare; however, awareness of such a potential complication may be life-saving to the patient.
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PMID:Enteric fever: a clinicopathologic study of 104 cases. 64 89

When in a patient who is receiving random donor platelet infusions there is an inadequate rise in platelet count and anti-human HL-A antibodies are noted in the serum, it is natural to assume that platelet destruction results from an immunologic cause. Nonimmunologic causes of such failure do occur, however. Two of the most common are disseminated intravascular coagulation and splenomegaly.
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PMID:Unrecognized causes of platelet transfusion failure in the presence of anti-HL-A antibodies. 85 18

Between 1969 and 1988, 146 children with immune thrombocytopaenic purpura (ITP) were seen in the outpatient clinic. The diagnosis was based upon an isolated thrombocytopaenia, without disseminated intravascular coagulation, splenomegaly or systemic disease and a normal bone marrow. Patients who required treatment (116/146) received either steroids (105/116) or IV gammaglobulins (IV-Ig) (11/116) as initial therapy. The long term outcome was similar in both groups. IV-Ig had the advantage to give a rapid increase in the platelet count without major side effects and to be very useful in chronic ITP either as maintenance therapy or as preparation for splenectomy.
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PMID:Treatment of immune thrombocytopaenic purpura in childhood. A review of 146 patients. 169 54

A 33-year-old man was hospitalized because of thrombocytopenia and severe splenomegaly. On admission 78% of peripheral lymphoid cells were abnormally large, with pale cytoplasm. Flow cytometry of the abnormal lymphocytes showed that they expressed CD 2, CD 3, CD 11, CD 16, and CD 56, but not CD 4 nor CD 8, so they were T-cell large granular lymphocytes (T-LGL). Abnormal lymphocytes obtained from a lymph node expressed CD 2, CD 16, CD 38, and CD 56, but not CD 3, CD 4, and CD 8, so they were natural killer(NK) cells. Splenectomy was performed and the operative specimen showed diffuse infiltration of pleomorphic lymphocytes, probably chronic lymphocytic leukemia cells. After splenectomy, the platelet count returned to normal but the lymphocytosis continued. Two years after discharge, chemotherapy was done because of thrombocytopenia and hepatomegaly. The patient died of disseminated intravascular coagulation arising from sepsis. The differences and similarities between peripheral and lymph-node lymphocytes suggest that LGL and NK cells may be differentiated from the same kind of cell, somewhat differentiated from stem cells.
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PMID:[Chronic lymphocytic leukemia with peripheral T lymphocytes expressing CD 2+, CD 3+, CD 4-, CD 8-, CD 16+, and CD 56+ and lymph-node lymphocytes expressing CD 2+, CD 3-, CD 4-, CD 8-, CD 16+, CD 38+, and CD 56+]. 171 68

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

A 46-year-old woman was admitted to our hospital because of hemorrhagic tendency. Normal coagulation test results conflicted with the diagnosis of disseminated intravascular coagulation (DIC). Furthermore, we saw no evidence of autoantibodies, including antinuclear antibodies and splenomegaly, and there was no past history of infection or medication. Peripheral blood test showed marked decrease of platelets only. Bone marrow aspiration revealed increased megakaryocytes. Morphology of other blood components was normal. Thus, we diagnosed this case as idiopathic thrombocytopenic purpura (ITP). Administration of prednisolone and an immunosuppressants did not improve symptoms. So patient was temporarily discharged and treated with 6-MP at the outpatient department. She was rehospitalized for liver damage caused by the drug. Patient then developed sepsis from acinetobactor. We administered gabexate mesilate (FOY, 2,000 mg/day) for four days to prevent DIC. Platelet count, which was 1.5 X 10(4)/microliter before FOT administration, began increasing on the second day, reaching 25. 5 X 10(4)/microliter on the fourth. Count rapidly decreased to 2.8 X 10(4)/microliter on the seventh day after administration had been discontinued. Two-time FOY administration after patient's recovery from sepsis led to a definite, similar transient increase in platelet count. As ITP patients with transient increase in platelet count by FOY administration had not been reported, this case is thought to be an interesting case in the pathogenesis and treatment of ITP.
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PMID:[Gabexate mesilate induced remarkable transient reversal of thrombocytopenia in a ITP patient]. 190 8

Sixteen cases of nodular regenerative hyperplasia of the liver in children are presented. The patients, 10 girls and 6 boys, were between the ages of 7 months and 13 years, with a median of 6 years. Clinically, nine children presented with hepatomegaly or splenomegaly, with and without signs of portal hypertension. A history of anticonvulsant drug therapy was obtained in four patients. Associated conditions in the remaining three cases were Donohue's syndrome, disseminated intravascular coagulation, and angiomyolipoma of the kidney. In five patients a clinical diagnosis of primary intra-abdominal tumor was made. Follow-up showed that six patients died of causes unrelated to the nodular hyperplasia. Two patients were asymptomatic when last seen 5 and 18 years after the initial diagnosis of nodular hyperplasia. Both patients underwent shunt surgery. No follow-up was available for eight patients. The importance of recognizing this entity in the pediatric age group, as well as its histopathologic differential diagnosis, is stressed.
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PMID:Nodular regenerative hyperplasia of the liver in children. 203 39

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

Thirty-four new cases of acute promyelocytic leukaemia (M3) were diagnosed at the authors' Centre between 1970 and 1988 (19 males and 15 females) with ages between 5 and 73 years (median age, 32 years). Three cases were of the hypogranular variant or M3-v (8.8%). The clinical picture included: haemorrhagic diathesis (85%), pallor/malaise (82%), fever/infection (41%), hepatomegaly (26%), splenomegaly (12%). Leucopenia of less than 5 x 10(9)/L was present in 23/34 cases, laboratory signs of DIC in 26/31, increased LDH, over 400 U/mL, in 6/31, and abnormal karyotype in 7/15. One of the patients rejected any treatment; two others died of brain haemorrhage before therapy was started, and seven died in the first two weeks of treatment. Of the 31 patients treated, complete remission (CR) was achieved in 21 cases (67.7%). Allogeneic BMT was carried out in two of them, with further relapse and death. Post-remission treatment was given to the remaining 19 patients, and there were 13 relapses. Six patients have been in CR, 5 of them after cessation of therapy, for the last 1.5-11.5 years. Age under 50 years and leucocyte count below 5 x 10(9)/L at diagnosis were favourable prognostic factors according to the univariate statistical analysis performed. The survival plateau of the actuarial curve was reached beyond 2.75 years by 15% of all the patients treated (33 cases), 23% of the patients who achieved CR (21 cases), 31% of the patients under 50 years of age and 5 x 10(9)/L leucocyte count at diagnosis (15 cases) and 36% of these last achieving CR (13 cases).
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PMID:[Acute promyelocytic leukemias: clinico-biological aspects, prognostic factors, therapeutic response, and possibilities of cure in 34 cases (1970-1988)]. 218 63

DIC in patients affected by cirrhosis, accompanied by portal hypertension and splenomegaly, has been suspected in the past. The main aim of this study is to ascertain the incidence of this phenomenon. We carried out coagulation and fibrinolytic tests in 113 cirrhotic patients and 20 healthy control persons. We found chronic consumption coagulopathy at analysis level in 28 cases (24.8%) with a decrease of fibrinogen, factor V, kallikrein, platelets, prothrombin complex activity, increase of PDF, partial thromboplastic time and euglobulin lysis. 25 cases had active cirrhosis, with ascites, variceal bleeding and/or hepatic encephalopathy; 3 were non-active cirrhosis. Only 7 patients had clinical DIC. We observed that coagulation disorders increased with more active cirrhosis.
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PMID:[The incidence of consumption coagulopathy in liver cirrhosis]. 256 20


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