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 morphologic and clinical findings in seven fatal cases of meningococcal septicemia are described and interpreted in light of recent experimental and clinical studies. We include evidence that suggests the disease has two distinct pathogenetic mechanisms. First, a shock-like terminal phase is associated with the development of widespread pulmonary microvascular thrombosis. These thrombi, composed largely of platelets and leukocytes, produce severe cor pulmonale that cannot be prevented with heparin sodium treatment. Meningococcal endotoxin also produces disseminated intravascular coagulation, which includes the rapid consumption of fibrinogen and the formation of fibrin thrombi in adrenal and renal glomerular capillaries, causing hemorrhagic infarction of the adrenal glands and renal cortical necrosis. This secondary phase of the disease can be modified with heparin therapy, but its control does not improve survival because the parenchymal lesions produced are not immediately life threatening.
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PMID:Fatal meningococcal septicemia. 57 4

The results of the clinical observations over 127 patients with mucoviscidosis and chronic (primary and secondary) pneumonia are presented. The children were aged from 1 to 15 years. Study of the plasma and platelet links of hemostasis permitted one to reveal considerable disorders seen during exacerbation in all the groups. The intensity of the disorders correlated well with the gravity of the patient's condition and with the bronchopulmonary process spreading as well as with the presence of complications on the part of the cardiovascular system (cor pulmonale) and the hepatobiliary system (liver cirrhosis). The chronic form of the disseminated intravascular coagulation (DIC) syndrome was diagnosed in 50 percent of the patients with mucoviscidosis, in 1/3 of the patients with secondary and in 18 percent of the patients with primary chronic pneumonia. The subacute form of the DIC syndrome was diagnosed in 15 percent of the patients with mucoviscidosis and in 4.5 percent of the patients with secondary chronic pneumonia. The multimodality treatment without heparin made it possible to correct the hemostatic disturbances in the majority of the patients under observation. In some children with mucoviscidosis and secondary chronic pneumonia, the use of heparin in the form of intravenous injections or ultrasonic inhalations permitted making such a correction more rapidly and more completely.
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PMID:[Clinical significance of disorders of hemostasis in children with chronic pneumonia and mucoviscidosis]. 272 62

A child with respiratory failure and cor pulmonale secondary to the obesity hypoventilation syndrome (OHS) was found to have abnormal beta-endorphin levels in cerebrospinal fluid (CSF) and serum. A single iv dose of 10 microgram/kg of naloxone early in the course of respiratory failure resulted in dramatic improvement which lasted approximately 3 to 4 h. The patient failed to response to progesterone, and because of deteriorating respiratory status a low-dose continuous infusion of naloxone, 2 microgram/kg.h, was begun and gradually increased to 10 microgram/kg.h, during which time there was a dramatic improvement in respiratory status and clinical condition. After 5 days, naloxone infusion was discontinued and progressive respiratory deterioration recurred. The child died of over-whelming sepsis and disseminated intravascular coagulation.
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PMID:Narcotic antagonist therapy of the obesity hypoventilation syndrome. 628 52

Pulmonary tumor thrombotic microangiopathy (PTTM) is a rare clinical entity where tumor cell embolisms in pulmonary circulation induce thrombotic microangiopathy (TMA), respiratory failure, and subacute cor pulmonale.We describe 3 cases of PTTM that presented as the initial manifestation of metastatic gastric adenocarcinoma with TMA and pulmonary infiltrates.All 3 cases had similar clinical and laboratory features, which included moderate thrombocytopenia without renal failure, hemolysis with extremely high serum lactate dehydrogenase levels, leukoerythroblastosis in peripheral blood smear, altered coagulation tests, lymphadenopathies, and interstitial pulmonary infiltrates. All patients died within 2 weeks of diagnosis. Two cases were initially misdiagnosed as idiopathic thrombotic thrombocytopenic purpura and treated with plasma exchange with no response. One patient had bone marrow infiltration by malignant cells. Autopsies revealed PTTM associated with gastric disseminated adenocarcinoma (signet-ring cell type in 2 patients and poorly differentiated type in 1).PTTM should be considered in the differential diagnosis of patients with fulminant microangiopathic hemolytic anemia, such as atypical thrombotic thrombocytopenic purpura, mainly those with pulmonary infiltrates, disseminated intravascular coagulation, or Trousseau syndrome.
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PMID:Pulmonary tumor thrombotic microangiopathy: report of 3 cases and review of the literature. 2550 Jul 5