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)

Coagulation factor XIII and plasma fibrinogen chromatographic assays have been performed serially in patients suffering from acute myocardial and cerebral infarction, and in others with disseminated intravascular coagulation. The findings were compared with 2 groups of "controls"; normal clinically-well subjects and hospitalized patients with cerebral infarction who exhibited minimal, stable, or improving neurological deficits. Substantial depression of factor XIII concentrations developed in the 3 patient groups, together with concomitant significant increases in the proportion and concentration of plasma high molecular weight fibrin(ogen) complexes (HMWFC). An inverse correlation (p less than 0.05) between coagulation factor XIII concentration and percentage of HMWFC was demonstrated in the early stages of the illness. These findings suggest that depression of coagulation factor XIII concentration in these states, is secondary to extravascular or intravascular coagulation and may reflect its degree.
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PMID:Reduction of coagulation factor XIII concentration in patients with myocardial infarction, cerebral infarction, and other thromboembolic disorders. 57 91

We report a 31-year-old female who had repeated thrombosis and was diagnosed as having congenital homozygous protein C deficiency based on decreased protein C antigen and activity, and the findings of family history. This patient had shown no symptom of thrombosis until the age of 27 years, when she had cerebral infarction as the first symptom. Low molecular weight heparin was useful for disseminated intravascular coagulation (DIC) that complicated protein C deficiency in this patient.
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PMID:Late-onset homozygous protein C deficiency manifesting cerebral infarction as the first symptom at age 27. 133 7

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 48-year-old female received serial combination chemotherapy including L-asparaginase (L-ASP) for acute lymphoblastic leukemia. After administration of L-ASP, the prothrombin time and activated partial thromboplastin time were prolonged, while fibrinogen and antithrombin III levels markedly decreased, so she was given fresh frozen plasma (FFP). But subsequently, she developed cerebral infarction in the left parietal region and further hemorrhagic infarction in the right parietal region, and died. Autopsy revealed superior sagittal sinus thrombosis and bilateral cerebral infarction, but no obvious thrombus in other organs. Coagulopathy following L-ASP therapy is well-known. In this case, the coagulation studies at the first attack showed that the plasma protein levels of coagulation and fibrinolysis factors decreased in spite of administration of FFP. Fibrin-fibrinogen degradation products (FDP) slightly increased. However there were no significant abnormalities in the platelet count, nor soluble fibrin monomer, which suggested no evidence of disseminated intravascular coagulation. Thus, these findings suggest that L-ASP might be associated with the pathogenesis of thrombosis in this case.
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PMID:[Superior sagittal sinus thrombosis following L-asparaginase therapy of acute lymphoblastic leukemia]. 157 39

To evaluate the clinical usefulness of D-dimer, various effects on the measurement of D-dimer were examined. Although both fibrinolytic and fibrinogenolytic products were detected by the measurement of FDP, only fibrinolytic products were detected by the measurement of D-dimer. In patients with DIC and other thrombo-embolic diseases, plasma D-dimer levels were significantly higher than in normal persons. A significant positive correlation between plasma D-dimer and serum FDP was found in DIC patients. In patients with DIC associated with acute promyelocytic leukemia, which is thought to be an increased fibrinogenolysis state, serum FDP was higher than the plasma D-dimer which suggests that increased fibrinogenolysis affects the result of serum FDP measurement. Plasma D-dimer significantly increased 5 minutes after endoscopic embolization with thrombin in the patients with esophageal varices. However serum FDP increased 30 minutes after the treatment, which suggests that the D-dimer is more useful for rapid detection of coagulo-fibrinolytic change than serum FDP. Plasma D-dimer was significantly higher in patients with cerebral infarction and increased with age. These finding suggest the usefulness of plasma D-dimer measurement for the specific and rapid evaluation of coagulo-fibrinolytic activation and thrombo-embolic state.
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PMID:[Clinical usefulness of the measurement of plasma D-dimer levels]. 192 Aug 61

We report a case of potentially survivable closed head injury, which was complicated by disseminated intravascular coagulation and bilateral cerebral infarction. Autopsy disclosed pulmonary emboli composed of cerebral tissue. We suggest that the entry of brain tissue into the systemic blood circulation caused severe disseminated intravascular coagulation, with consequent thrombosis of cerebral veins and spreading infarction.
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PMID:Embolism of cerebral tissue: a cause of coagulopathy and cerebral infarction? Report of a case. 199 Apr 85

A case of systemic lupus erythematosus (SLE) with subarachnoid hemorrhage due to a ruptured intracranial aneurysm is reported. A 31-year-old woman who had been treated with steroid for SLE was admitted to our department with severe headache, and nausea. CT scan showed subarachnoid hemorrhage and the left carotid angiogram revealed a small aneurysm at the supraclinoid portion of the left internal carotid artery. She had no neurological deficit. Hematological examination on admission showed disseminated intravascular coagulation (DIC), therefore, we decided to perform an intentionally delayed operation. In the meantime we treated the patient for DIC with FOY and methylprednisolone. The operation was performed after two weeks, when DIC had been eliminated completely. Postoperative hematological examination showed severe thrombocytopenia. We considered that SLE had come to the fore again, so we used Danazol in company with FOY and steroid. It seemed that Danazol was very effective for her. She was discharged about two months after admission with no problem. Cerebral apoplexy, such as cerebral infarction and cerebral hemorrhage, has often been seen in SLE, but subarachnoid hemorrhage due to a ruptured aneurysm is very rare. We could find only five reports of this phenomenon. Their prognoses were all, unfortunately, poor. It should be born in mind for therapy that a patient in SLE has a tendency to bleed. It seems that repeated hematological examinations and quick and proper management are important. We think that the aneurysmal formation in SLE is due to lupus vasculitis or the fragility of blood vessels due to a long use of Steroid.
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PMID:[A case of systemic lupus erythematosus with subarachnoid hemorrhage due to ruptured aneurysm]. 220 86

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

We performed a clinical study by measuring the plasma levels of D-dimer, which is derived from the degradation of cross linked fibrin, in some thrombotic disorders using Dimertest EIA kit obtained from AGEN Corp. (Australia). The level of D-dimer in disseminated intravascular coagulation (DIC) were greater than that in thrombotic thrombocytopenic purpura (TTP). These levels of D-dimer in two thrombotic disorders showed a different pathogenesis between them. And also, the levels of D-dimer in some arteriosclerotic disorders, i.e.; aortic aneurysm , cerebral infarction and coronary insufficiency, and in venous thrombosis significantly increased compared with normal subjects. The level of D-dimer measured by Dimertest EIA kit was useful marker for detecting a thrombotic tendency in the low level of D-dimer, in which latex agglutination test for fibrin/fibrinogen degradation products (FDPL test) could not usually detect.
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PMID:[Clinical significance of cross linked fibrin degradation products in thrombotic disorders]. 267 36


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