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)

Thrombocytopenia frequently complicates systemic infection and results from multiple possible mechanisms. We and others have demonstrated that platelet-associated IgG (PAIgG) levels are elevated in the majority of patients with septic thrombocytopenia. Corticosteroids may be undesirable as a treatment for thrombocytopenia for patients with severe infection because of their potential for suppressing the immune response. We hypothesized that septic thrombocytopenia is, in most cases, an immune disorder analogous to idiopathic thrombocytopenic purpura (ITP) which might respond to intravenous gamma-globulin as a treatment for increasing the platelet count in this disorder. Intravenous immune globulin (IVIG), 400 mg/kg daily for 3 days, was administered in a randomized double-blind placebo-controlled trial. Twenty-nine patients who developed thrombocytopenia during a documented, septic episode were studied. Patients with disseminated intravascular coagulation (DIC), hypersplenism, or drugs known to cause thrombocytopenia were excluded. Elevated PAIgG levels were documented in 52% of evaluable patients. Mean platelet counts in the IVIG group rose from 43K at study entry to 178K (411% rise) by Day 9. In the placebo group platelets rose from 51K to 125K (261% rise; P = 0.02). Seventy-seven percent of the IVIG group had a minimum peak rise of 35K, vs 56% of the placebo group. Three patients in the placebo group had a serious bleeding episode, vs one in the IVIG group. The use of IVIG to treat septic thrombocytopenia not associated with DIC leads to a more rapid, more sustained, and greater increase in platelet count than placebo. Its use is recommended in the septic patient who is bleeding or is likely to need invasive or surgical procedures.
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PMID:Treatment of septic thrombocytopenia with immune globulin. 176 42

Platelet abnormalities associated with hepatobiliary diseases include increased (thrombocytosis) and decreased (thrombocytopenia) numbers of platelets as well as abnormalities in function (thrombocytopathy or thrombasthenia). Hepatic diseases that are accompanied by platelet abnormalities include hepatitis, cirrhosis, portal hypertension, and neoplastic disorders both benign and malignant. The objective of this work is to examine the platelet abnormalities that occur with a variety of hepatobiliary disorders. Thrombocytosis is seen as a reactive entity following splenectomy. Thrombocytopenia is associated with hypersplenism, dysproteinemias and liver disease related disseminated intravascular coagulation (DIC). Qualitative platelet abnormalities are found in hepatic failure, liver diseases associated with high or low levels of lipid, and with medications given for a variety of hepatocellular diseases. Clinically common and significant platelet abnormalities associated with liver disease are thrombocytopenia secondary to portal hypertension and the thrombasthenias following metabolic changes and/or therapeutic interventions of liver disease.
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PMID:Platelet abnormalities in hepatobiliary diseases. 218 3

Hematologic dysfunction occurs commonly in patients with malignancy. Over half are anemic, often because of acute or chronic blood loss, marrow involvement by the malignancy, marrow suppressive effects of chemotherapy or radiation therapy, or because of the anemia of chronic disease. Less frequently, anemia may result from red cell aplasia, folate or B12 deficiency, hemolytic processes, or hypersplenism. Occasional patients may become polycythemic because of erythropoietin-producing tumors such as renal adenocarcinomas or cerebellar hemangiomas. Elevation of the white cell count is commonly seen, especially in patients with lung cancer. Monocytosis and thrombocytosis, which may be early signs of an underlying malignancy, are also very common and occur in up to half of patients. Thrombocytopenia is commonly a result of therapy or marrow replacement; a few patients may have a syndrome resembling immune thrombocytopenic purpura. Abnormalities of coagulation are present in many patients, and may lead to superficial or deep venous thromboses, pulmonary emboli, nonbacterial thrombotic endocarditis with arterial emboli, bleeding, or acute disseminated intravascular coagulation. A sound understanding of the potential hematologic complications that can result from the malignant process is essential to the clinician caring for cancer patients.
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PMID:Hematologic manifestations of malignancy. 268 Mar 58

Very few data on the frequency and diversity of haematological abnormalities occurring in brucellosis in children have been reported. In the present study 110 children (56 boys and 54 girls; age range, 2 months to 14 years) with proven brucellosis were investigated to determine the haematological changes during the active course of this infection. Anaemia was detected in 48 (44%) patients, of whom four had evidence of haemolysis. Leukopenia occurred in 33% of the cases, with neutropenia and/or lymphopenia being the most striking features encountered. Thrombocytopenia was found in six (5%) patients and pancytopenia in 15 (14%) patients, of whom one developed disseminated intravascular coagulation. Clinically detectable bleeding occurred in five (4.5%) patients whose platelet counts were significantly low. Hypersplenism, haemophagocytosis and granulomatous lesions of the bone marrow appear to play a fundamental role in producing these abnormalities of the peripheral blood. Brucellosis may be considered in patients whose blood picture reveals haemolytic anaemia, leukopenia, thrombocytopenia or pancytopenia, particularly when the disease is epidemiologically suspected.
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PMID:Haematological manifestations of childhood brucellosis. 844 76

Recent experimental studies suggested that hematopoietic cell proliferation and differentiation are under a neuroendocrine control and that they change in relation to the 24-hour period. Moreover, it has been shown that the pineal hormone melatonin (MLT) plays a role in mediating the influence of the psychoendocrine system and of the lighting conditions on the hematopoiesis. Finally, MLT has appeared to regulate hematopoietic cell growth by influencing apoptosis-related mechanisms. In particular, preliminary studies have shown that the pineal hormone MLT may determine some benefits in blood cell disorders, mainly platelet diseases. On this basis, a pilot phase II study of MLT therapy was performed in patients suffering from persistent thrombocytopenia due to different causes. The study included 14 patients, and thrombocytopenia was due to bone metastatic involvement in 5, hypersplenism in 3, myelodysplastic syndrome in 3, DIC in 1, genetic factors in 1, and Werlhof's disease in the last case. MLT was given orally at 20 mg/day in the evening for 2 months. No MLT-related toxicity occurred. A normalization of platelet number was achieved in 8/14 (57%), and platelet mean number significantly increased on MLT therapy. This preliminary study would suggest that MLT may be effective in the treatment of thrombocytopenia due to different reasons, for which no effective standard therapy is available.
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PMID:The pineal hormone melatonin in hematology and its potential efficacy in the treatment of thrombocytopenia. 906 51

Patients with hematologic malignancies or aplastic anemia may have reduced responses to platelet transfusions after multiple transfusions of standard red blood cells or platelet components. This situation, conventionally described as 'refractoriness' to platelet transfusions, may result from immune or non-immune causes. Non-immune causes include fever, infections, hypersplenism, disseminated intravascular coagulation, antibiotics, or veno-occlusive disease. Immune causes include platelet-reactive alloantibodies, which are typically antibodies to human leukocyte antigens (HLA) or, less commonly, antibodies to human platelet antigens (HPA). Transfused HLA-matched platelets often have satisfactory posttransfusion survivals, but few transfusion services have the donor and logistical resources to sustain a prolonged course of platelet transfusions requiring four-antigen matches. The availability of commercially marketed kits for crossmatching samples of potential donors' platelets with a recipient's serum has facilitated donor-recipient matching. Also, platelet crossmatching may be used to select a suitable unit of from several candidates platelets that have been identified to be partial HLA matches. The high likelihood of decreased efficacy of platelet transfusions in HLA-alloimmunized recipients makes avoidance of exposure to HLA-bearing leukocytes a priority. This goal is facilitated by lowering transfusion 'triggers' for cellular blood components, particularly for prophylactic platelet transfusions, by reducing the leukocyte content of components by leukocyte-reduction filters and, possibly by ultraviolet-B irradiation of leukocyte-containing products.
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PMID:Management of patients with hematologic malignancies and aplastic anemia who are refractory to platelet transfusions. 970 52

Splenectomy in patients with non-Hodgkin's lymphoma (NHL) is performed for either diagnostic or therapeutic reasons. We report on a series of 29 patients with NHL and splenomegaly who underwent splenectomy during the years 1979-1998 in our hospital. According to the indication for splenectomy our patients were categorized in three groups. Group A: In 20 patients splenectomy was performed for diagnostic reasons. Group B: Three patients were splenectomized for autoimmune haemolytic anaemia (AIHA). Group C: Six patients underwent splenectomy because of hypersplenism. A definitive histopathological diagnosis of NHL was obtained in all patients of group A. Hypersplenism and AIHA were resolved in all patients after splenectomy. One (3.5%) patient died postoperatively because of septicemia complicated by disseminated intravascular coagulation. Six postoperative complications were observed in 4 (14%) patients. Splenectomy, with an acceptable surgical risk, has the potential to establish the diagnosis of NHL in patients with splenomegaly without lymphadenopathy and negative bone marrow findings. Moreover, splenectomy has the capacity to modify the disease course in patients with NHL complicated by AIHA or hypersplenism.
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PMID:Splenectomy in patients with malignant non-Hodgkin's lymphoma. 1099 79

A 45-year-old Japanese woman with splenomegaly and thrombocytopenia was referred to our hospital. The diagnosis of Osler-Weber-Rendu disease (Osler's disease) was made because of spotty telangiectasia on her tongue, recurrent epistaxis since childhood, and a diathesis indicated by her family history. The patient's laboratory examination revealed anemia, thrombocytopenia, and other data consistent with chronic disseminated intravascular coagulation (DIC). Bone marrow examination was normal. Abdominal computed tomography showed marked enlargement of the spleen with deformity and calcified plaque, not homogeneously enhancing. Hypersplenism was not observed. Platelet scintigraphy indicated a remarkable uptake in the spleen. She was diagnosed as having chronic DIC associated with vascular lesions of Osler's disease in the spleen. Splenectomy was performed and the subsequent pathological findings indicated that fragility of the fine vascular architecture of the splenic red pulp might have been responsible for pathogenesis. The large pooling of blood with coagulation was thought to be secondary.
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PMID:Splenomegaly and chronic disseminated intravascular coagulation in Osler-Weber-Rendu disease: a case report. 1107 62

A 59-year-old woman was admitted to our hospital with a picture of high fever and dyspnea. Pneumonia was diagnosed by chest CT scan and was treated. Laboratory findings showed pancytopenia and examination of aspirated bone marrow showed mature histiocytes with marked hemophagocytosis. She was treated with prednisolone, but her respiratory condition worsened, so she was ventilated. An acid-fast bacterial smear of bronchoalveolar lavage fluid from the left lingula showed Gaffky's scale No. 5, and so tuberculosis was diagnosed. Though anti-tuberculosis therapy was started, she died after eight days of hospitalization. Infection-associated hemophagocytic syndrome is caused by various infections. Until now, 26 cases of tuberculosis-associated hemophagocytic syndrome have been reported, and many of these diseases were caused by severe tuberculosis. If a patient with severe tuberculosis presents with leucocytopenia or thrombocytopenia, investigations should serve a differential diagnosis that takes into account disseminated intravascular coagulation, tuberculous granuloma of the bone marrow, side effects of anti-tuberculous drugs, and hypersplenism from hemophagocytic syndrome.
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PMID:[A case of hemophagocytic syndrome caused by tuberculosis]. 1264 10

From 1995-2002, 14 patients with predominantly prehepatic, noncirrhotic portal hypertension were evaluated. At presentation, the eight females and six males had a mean age of 9 years (range 2-18). Seven were admitted with gastrointestinal, mostly esophageal bleeding, three with splenomegaly, three with hepato-pulmonary syndrome, and one with hyperammonemia. Imaging studies showed portal vein obstruction in six patients and non-obstructed but frequently anomalous vascular patterns, including hypoplasia of the portal vein, in the remaining eight patients. At the onset, liver function was marginally abnormal in all patients, but thrombocytopenia of approximately 100 x 10(9)/L was consistently observed, probably reflecting chronic mild consumption coagulopathy and hypersplenism. The most striking and frequent histopathologic finding in 25 liver samples, was the presence of hypoplastic portal triads with collapsed portal vein radicles. In contrast, other triads showed markedly distended and misshapen portal vein radicles and likely lymphatics. These two patterns of collapse and distention presumably reflect areas of impaired versus overloaded intrahepatic portal venous flow. Some of the biopsies showed variable portal/sinusoidal fibrosis. Four patients (two with intestinal bleeding, two with hepatopulmonary syndrome) required liver transplants and are doing well. Eight patients are doing well clinically after surgical or spontaneous vascular shunting. Two patients with intestinal bleeding and hepato-pulmonary syndrome, respectively) who had congenital dyskeratosis, underwent bone marrow transplantation and died of nonhepatic-related complications. It is possible to suggest prehepatic causes of portal hypertension even in needle biopsies when collapsed portal vein radicles are present in portal triads, but more than one biopsy sample with larger bore bioptomes may be required to see the changes. Conversely, identifying these changes may suggest to the clinicians the need to work-up a patient for portal hypertension.
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PMID:Pathology of noncirrhotic portal hypertension: clinicopathologic study in pediatric patients. 1470 35


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