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)

Changes of prekallikrein in the cases with DIC were investigated, i.e., DIC cases including disseminated metastasis of gastric cancer, acute promyelocytic leukemia and endotoxin shock. Therefore, the trigger substances for this paper were the pathologic cells of the leukemia, the cultured well differentiated adenocarcinoma cells and endotoxin. (1) The lysates of the pathologic cells of the leukemia and the cultured cells showed prekallikrein activation. Endotoxin showed prekallikrein activation via factor XII. (2) Serine proteases (factor Xa, thrombin, plasmin and trypsin) activated prekallikrein in the plasma and the purified prekallikrein. (3) Antithrombin III, aprotinin and FOY inhibited prekallikrein activation. Antithrombin III was promoted by heparin in its inhibitory effect.
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PMID:Changes of prekallikrein in the cases with disseminated intravascular coagulation syndrome. 16 Jan 91

A case of fulminant disseminated intravascular coagulation (DIC) in a 51-year old man, presenting with bleeding gastric adenocarcinoma, is reported. In spite of initial hematologic improvement by replacement therapy the patient died on the fifth day after admission. The rare association of DIC with adenocarcinoma of the stomach is discussed.
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PMID:Fulminant disseminated intravascular coagulation in advanced gastric carcinoma. 43 6

Thirty-one cases with malignant neoplasm and nonbacterial thrombotic endocarditis (NBTE) were studied. A threefold increase in the incidence of NBTE over the five-year period ending in 1976 was noticed. Seventy-one percent of patients with NBTE had concomitant disseminated intravascular coagulation (DIC). Adenocarcinomas of the lung or ovary were the most common tumors (48%), followed by hematologic malignancies (25%). Five patients had acute leukemia, two of whom had received bone marrow transplantation. Sudden changes in the status of cardiovascular and central nervous systems were the most common manifestations of NBTE and its complications. The possible predisposing factors included disseminated malignant neoplasms and infection with gram-negative bacilli. Identification of high-risk patients and early administration of preventive measures including anticoagulation might decrease the morbidity and mortality related to NBTE.
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PMID:Nonbacterial thrombotic endocarditis in cancer patients: comparison of characteristics of patients with and without concomitant disseminated intravascular coagulation. 66 51

Sixty-five cases of nonbacterial thrombotic endocarditis (NBTE) were discovered at autopsy during a 10 year period--an incidence of 1.6 per cent in the adult autopsy population. In 51 cases, one or more malignant neoplasms were associated; adenocarcinoma represented the most frequent histologic type of related neoplasm. Coagulation abnormalities suggestive of disseminated intravascular coagulation (DIC) were present in 18.5 per cent of the cases. It is possible that both the valvular and peripheral intravascular thromboses in at least some cases of NBTE represent the abnormal coagulation of DIC. Arterial thrombosis with infarction occurred in many peripheral organs. Splenic and renal were most frequent, but cerebral and cardiac consequences were the most significant.
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PMID:Non-bacterial thrombotic endocarditis: clinicopathologic correlations. 99 78

A 55-year-old woman was admitted to our hospital because of left hemiparesis. Brain CT and cerebral angiography demonstrated cerebral embolism due to occlusion of the sphenoidal part of the right middle cerebral artery. Two-dimensional echocardiography revealed mitral valve vegetation measuring 10 x 7 mm and slight mitral-valve regurgitation. Blood cultures were negative. She developed disseminated intravascular coagulation. Chest roentgenography and abdominal ultrasonography showed multiple liver and lung tumors, but she died before the primary lesion was detected. At autopsy, adenocarcinoma of the gall bladder was found. Friable vegetation was attached to the auricular surface of the mitral valve. Microscopic examination confirmed the diagnosis of nonbacterial thrombotic endocarditis. Although echocardiography is an important tool for diagnosing nonbacterial thrombotic endocarditis, few reports have described echocardiographic detection of nonbacterial thrombotic endocarditis. Because vegetation of nonbacterial thrombotic endocarditis is smaller than that of infective endocarditis (less than 3 mm), it is difficult for echocardiography to detect nonbacterial thrombotic endocarditis. Thus, a negative examination does not exclude the possibility of nonbacterial thrombotic endocarditis. To make an antemortem diagnosis of nonbacterial thrombotic endocarditis, we must perform echocardiography carefully in cases of cerebral infarction with carcinoma and/or DIC.
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PMID:[A case of nonbacterial thrombotic endocarditis presenting positive findings by two-dimensional echocardiography]. 143 79

A cerebral infarct due to a thrombosis of the left pericallosal artery was the first manifestation of an ovarian adenocarcinoma in a 42-year-old woman. A paraneoplastic origin was suggested by the observation that this patient had chronic intravenous coagulation and subsequently developed migratory thrombophlebitis (Trousseau's syndrome) despite high dose vitamin K antagonists therapy. This was supported by the fact that all manifestations of the hypercoagulable state disappeared following surgical cure of the cancer. Because cerebral infarction can be the first manifestation of a potentially curable cancer, patients with a cerebral infarct of an unknown etiology should be investigated for a malignant process, if there is laboratory or clinical evidence od disseminated intravascular coagulation.
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PMID:Ischemic stroke as the presenting manifestation of localized systemic cancer. 245 36

A 42-year-old male was admitted to Tokyo University Hospital because of confusion, aphasia and right hemiparesis. Cranial computed tomography and cerebral angiography demonstrated cerebral infarction due to occlusion of the left middle cerebral artery, while chest roentgenography disclosed a nodular shadow in the right upper lobe and swelling of right hilar and paratracheal lymph nodes. These findings suggested carcinoma of pulmonary origin and tumor-associated cerebral thrombosis, but a possibility of gastric cancer was raised by the finding of cervical lymph node biopsy which revealed signet ring cells in metastatic adenocarcinoma. He developed disseminated intravascular coagulation syndrome and died on the 83rd hospital day. Autopsy revealed adenocarcinoma of the lung with signet ring cells and non-bacterial thrombotic endocarditis which appeared to be responsible for the cerebral infarction. The relationship between adenocarcinoma of the lung with signet ring cells and non-bacterial thrombotic endocarditis was discussed.
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PMID:[An autopsy case of adenocarcinoma of the lung with signet ring cells, manifesting with aphasia and hemiparesis due to nonbacterial thrombotic endocarditis]. 248 83

A registry of suspected cases of cancer-associated hemolytic-uremic syndrome (C-HUS) was established in May 1984. Records of 85 patients from the registry, all with history of cancer, hematocrit less than or equal to 25%, platelet count less than 100,000, and serum creatinine greater than or equal to 1.6 mg/dL were subjected to in-depth analysis. Eighty-nine percent of patients had adenocarcinoma, including 26% with gastric cancer. Microangiopathic hemolysis was reported in 83 patients; coagulation studies were normal with rare exception. Bone marrow examination ruled out chemotherapy-induced myelosuppression in 68 of 85. Thirty-five percent of patients were without evident cancer at time of syndrome development. Mitomycin (MMC) was part of the treatment regimen in 84 patients; all but nine received a cumulative dose greater than 60 mg. Pulmonary edema, generally noncardiogenic, developed in 65% of patients, often after blood product transfusions. C-HUS has a high mortality: over 50% of patients died of or with syndrome, most within 8 weeks of syndrome development. Conventional treatment was ineffective, although ten of 21 treated with staphylococcal protein A (SPA) immunopheresis showed significant responses. Statistical analysis found only absence of obvious tumor and treatment with SPA to suggest favorable prognosis. C-HUS is distinguishable from related syndromes such as childhood HUS, thrombotic thrombocytopenic purpura (TTP), consumption coagulopathy, and microangiopathic hemolysis associated with advanced carcinoma. MMC is likely involved in the development of C-HUS; the risk of developing C-HUS after treatment with MMC is between 4% and 15%. However, possible bias in patients referred to the registry and reports of non-MMC C-HUS cases must be remembered. Recommendations include careful monitoring of renal and hematologic function in patients treated with MMC, aggressive nontransfusion in patients with suspected C-HUS, and consideration of treatment with SPA immunopheresis in patients with definite syndrome.
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PMID:Cancer-associated hemolytic-uremic syndrome: analysis of 85 cases from a national registry. 251 Dec 78

Three cases of chronic subdural hematoma (CSH) following advanced cancer are reported. Case 1. A 54-year-old male patient was referred to our clinic in a semicomatose state. Bilateral CSH was evacuated through a pair of burr holes, and consciousness was recovered. However, subependymal hemorrhage occurred at the third ventricle 6 days after the operation. Hematological examination revealed thrombocytopenia. He died 12 days after operation because of hemorrhage in the lung. Postmortem examination disclosed metastatic adenocarcinoma of unknown origin to the dura mater, lymph nodes, lung and bone marrow. Case 2. A 50-year-old male patient who was diagnosed as having gastric cancer was referred to our clinic in a state of deep coma. CT scan revealed CSH and putaminal hemorrhage at the left side. Hematological examination revealed disseminated intravascular coagulation (DIC). After the subdural hematoma was evacuated, the putaminal hematoma enlarged and hemorrhagic infarction at the left temporo-occipital lobes occurred. He died 2 days after operation. Autopsy was not carried out, but histological examination revealed poorly differentiated malignant cells in the outer membrane of the subdural hematoma. Case 3. A 53-year-old female patient who had a history of gastric cancer operated on 4 years ago was admitted to our clinic complaining of headache and vomiting. CT scan revealed bilateral subdural hematoma. Following a pair of burr-holes and irrigation of the hematoma, hemorrhage recurred alternatively at the left side on the 6th and at the right side on the 27th day after the operation. Hematological examination revealed DIC, and bone marrow puncture disclosed metastasis of the adenocarcinoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chronic subdural hematoma following advanced cancer: report of three cases]. 258 17

To augment the antitumor effect of high-dose melphalan and determine pharmacokinetics we conducted a phase I trial of escalating doses of high-dose IV melphalan with the chemosensitizer misonidazole for patients with advanced colorectal carcinoma. Fourteen patients with modified Dukes D adenocarcinoma of the colorectum were treated with a single course of melphalan (40-60 mg/m2 i.v. bolus q.d. X 3 days) and misonidazole (1-3 g/m2 p.o. q.d. X 3 days) followed by autologous bone marrow transplantation. Toxicity consisted of severe myelosuppression, moderate nausea and vomiting, and mild mucositis and diarrhea. One patient developed unexplained renal tubular acidosis, and a diffuse encephalopathy occurred in another patient. Three patients died within the first 30 days after the start of treatment, two due to tumor progression and one due to sepsis and disseminated intravascular coagulation-induced intracerebral hemorrhage. Six of 14 patients achieved a partial response, and the median response duration was 4 months (range 3-10 months). Analysis of misonidazole serum concentrations showed similar pharmacokinetics to those previously reported, suggesting no significant drug interaction with intravenous melphalan. Mean peak serum concentrations ranged from 81.8 micrograms/ml to 115.2 micrograms/ml at the second and third misonidazole dose levels, which approximate those known to provide effective chemosensitization with melphalan in animal models. In this phase I study, we showed that maximally tolerated doses of intravenous melphalan can safely be combined with oral misonidazole. In view of the large volumes of oral misonidazole required at the highest dose level, subsequent studies to determine the maximally tolerated dose of misonidazole should employ the intravenous form.
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PMID:High-dose melphalan, misonidazole, and autologous bone marrow transplantation for the treatment of metastatic colorectal carcinoma. A phase I study. 265 May 27


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