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)

A 75-year-old man presented with a rare case of chordoma in the sella turcica of the skull base. He had been treated for hypertension and chronic renal failure since 1990. Computed tomography detected a tumor in the sella turcica in 1994, but the patient had no clinical complaints and the serum pituitary hormone levels were normal. He died of disseminated intravascular coagulation, myocardial infarction, pulmonary infection, and multiple cerebral infarctions in 2000. At autopsy, the tumor in the sella turcica was 3.1 cm in greatest diameter and had compressed the pituitary gland posteriorly. Histological examination found oval cells and vacuolated short spindle-shaped cells which showed morphological changes similar to myxoma cells. The tumor was lobulated by narrow connective tissues. The tumor did not contain any cartilaginous tissue components, and was stained positively for epithelial membrane antigen but negatively for S-100 protein. The final diagnosis was chordoma. There was no association between the tumor and the cause of death.
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PMID:Chordoma in the sella turcica. 1216 Mar 11

The authors report on a 2-year-old boy with atypical Kawasaki disease (KD) and thrombocytopenia who developed 3 coronary artery aneurysms. The mechanism of thrombocytopenia in KD seems to be consumption coagulopathy. Review of the 30 reported cases of KD and thrombocytopenia revealed that this combination is more common in girls and in young age groups, and is associated with an increased risk of coronary artery aneurysm and myocardial infarction.
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PMID:Thrombocytopenia in Kawasaki disease: a risk factor for the development of coronary artery aneurysms. 1457 29

Platelets are anucleate cells that fragment from mature megakaryocytes and play an essential role in thrombosis and hemostasis. Platelets are among the first cell types to be recruited to an injured blood vessel, assisting in endothelial repair. Platelet hyperactivation contributes to the development of atherosclerosis, myocardial infarction, and ischemia of peripheral limbs. A fall in platelet counts, due to a variety of conditions, including disseminated intravascular coagulation, chemotherapy or genetic disorders, may lead, in most severe cases, to death from hemorrhage. This review focuses on the late stages of megakaryocyte differentiation and platelet fragmentation, including associated cytoskeletal changes, and on the importance of apoptotic events for these processes. Studies point to a unique biological system in which programmed cell death may be linked with biogenesis of new cells.
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PMID:Role of apoptotic processes in platelet biogenesis. 1464 46

The author presents the results of an examination of 106 patients with myocardial infarction (MI) of various severity, who also had a peptic ulcer relapse. Patients with moderate and severe MI in the majority of cases had solitary duodenal ulcers whereas those with extremely severe MI often had multiple ulcers in the body and the cardial part of the stomach, which were bleeding in 43.5% of cases. The pathogenetic basis of the ulcerogenesis was focal microcirculation disorders in the mucosa of the gastroduodenal zone of thrombohemorragic or thromboischemic type. In patients with moderate or severe MI they appeared against the background of hemostatic disturbances typical of the first stage of thrombohemorragic syndrome (hypercoagulation). In extremely severe MI they corresponded to the second stage i.e. partial consumption coagulopathy. In patients with moderate coronary pathology these changes were promoted by the activation of acid-peptic factor, the depression of mucopolysaccharide production, hypo- and hyperkinetic dyskinesis, and in those with extremely severe coronary pathology --the depression of all gastric function except normal acid production. One of the trigger mechanisms of ulcerogenesis could be changes in the activity of sympathoadrenal and histaminereactive systems, which increased in cases of moderate and severe MI and decreases to a certain extent in cases of extremely severe MI.
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PMID:[The condition of sympathoadrenal and histaminoreactive systems and the influence of their changes on the peculiarities of a peptic ulcer relapse in patients with myocardial infarction]. 1588 39

Protein C, protein S, and antithrombin III were measured in 35 patients with acute leukemia (13 with AML and 22 with ALL). Low levels of proteins C and S were present in 15 (42.9%) and 20 (57.1%) patients, respectively, and 6 patients had low levels of antithrombin (ATIII). Seven patients also had DIC at presentation. There were no significant differences in the levels of protein C, protein S, and ATIII in patients with or without DIC. Twenty patients were available for re-evaluation at the end of induction therapy. The low levels of protein C and ATIII found at diagnosis had risen to normal levels at the end of the induction therapy, while low =levels of protein S remained in 75% of the patients. One patient with low protein C at presentation developed myocardial infarction on day 15, and another patient died of progressive neuropathy. No other thrombotic manifestations were seen. Whether the low protein C, protein S, or antithrombin levels predispose patients with acute leukemia to thrombosis in the absence of DIC is not known.
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PMID:Roles of protein C, protein S, and antithrombin III in acute leukemia. 1649 9

A thorough review of the literature and of personal files has allowed the gathering of 81 patients with rare congenital bleeding disorders and thrombotic phenomena. Sixteen of these patients had congenital afibrinogenemia, eight involved factor V deficiency, 20 factor VII defects, 33 factor XI deficiencies and only one, a factor XIII defect. Altogether 42 patients showed arterial thrombosis (myocardial infarction [MI] in 28 cases; ischemic stroke in 4; arterial occlusion in 8; 2 patients with disseminated intravascular coagulation (DIC)). Ages varied between 13 and 74. Twenty-two patients were males and 16 females. In four cases, sex was not reported. There were three fatalities: two after a MI and one because of heart failure. With regard to venous thrombosis: 9 patients had pulmonary embolism, 15 patients had deep vein thrombosis, 9 patients had both pulmonary embolism and deep vein thrombosis; 1 patient had superficial vein thrombosis, whereas, 5 cases had an unusual site venous thrombosis (two portal systems, two cerebral sinuses, one inferior vena cava) for a total of 39 cases. Age varied between 3 and 86. In this case, 20 patients were males and 17 were females. In two cases, sex was not reported. There were three fatalities: two because of pulmonary embolism and one because of inferior vena cava thrombosis. The fact that thrombosis has never been described in patients with factor II or factor X seems to underscore the central antithrombotic role that these two factors have in the coagulation system.
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PMID:Arterial and venous thrombosis in rare congenital bleeding disorders: a critical review. 1683 33

Ischaemic stroke in thromboembolic mechanism may be a first sign of neoplastic disease, as in the presented case of a 56-year-old woman. Progressive trombocytopenia, anaemia with reticulocytosis and schistocytes in peripheral blood smear, elevated serum LDH activity as well as coexisting myocardial infarction initially suggested Moschcowitz syndrome. However, plasma exchange did not improve her neurological status and D-dimer values increase in subsequent evaluations indicated chronic DIC. At the same time, on transesophageal echocardiography, thrombotic endocarditis was diagnosed. Screening for cancer showed high CA 125 marker and chest computed tomography revealed lung tumor, not visible on earlier chest X-ray. In further treatment she underwent palliative radiotherapy and continued low molecular weight heparin. The neoplastic process had an unfavorable course and she died after four months. The authors point out that in case of multifocal ischaemic stroke and coexistent thrombocytopenia, neoplastic hypercoagulable state and thrombotic endocarditis should be considered.
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PMID:[Multifocal ischaemic stroke and myocardial infarction in a woman with occult lung cancer complicated with chronic DIC and thrombotic endocarditis]. 1719 80

We present a case of emphysematous pyelonephritis (EPN) with sepsis and disseminated intravascular coagulation (DIC). An 87-year-old man with a history of uncontrolled diabetes mellitus (DM) for more than 25 years was admitted to our hospital for altered mental status and high fever. The initial diagnosis was acute pyelonephritis based on the findings of pyuria and right costovertebral angle knock pain. DIC developed rapidly even though empirical antimicrobial therapy had been started immediately. The abdominal CT revealed the presence of gas in the right renal parenchyma; the definitive diagnosis was EPN. Escherichia coli (E. coli) was identified from both blood and urine cultures. We selected medical conservative therapy with antibiotics because of his advanced age and a history of myocardial infarction three months previously. With only noninvasive therapy and no surgical therapy, his condition improved and he was discharged four months after admission. EPN is a rare, severe gas-forming, necrotizing infection of the renal parenchyma and surrounding areas. Over 90% of the cases occur in DM patients and the most common causative organism is E. coli (60%). The mortality rate with only medical conservative therapy is approximately 20% and transurethral and/or percutaneous drainage or nephrectomy are generally reported to be necessary. To our knowledge, no case with EPN over the age of 84 years has been reported. Although his condition was very severe on admission and long-term antimicrobial therapy was necessary, he was ambulatory at the time of discharge. Herein, we report the pertinent EPN literature and discuss the management of EPN.
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PMID:[Case of emphysematous pyelonephritis with sepsis and disseminated intravascular coagulation]. 1842 71

Prostate cancer is the most prevalent malignancy in men and the third leading cause of cancer deaths worldwide. Disorders of hemostasis are commonplace in patients with prostate cancer and include disseminated intravascular coagulation, venous thromboembolism, acute coronary syndrome, and postsurgical bleeding. These hemostatic disorders contribute to the mortality and morbidity of prostate cancer. The leading mechanisms proposed to underlie prostate cancer-related coagulopathies are thought to be a hyperexpression of tissue factor, cancer procoagulant, and platelet-activating factor, which is then accompanied by release of large amounts of both prothrombotic and profibrinolytic substances into the bloodstream. Given the generally accepted notion that prostate-specific antigen (PSA) represents an important biomarker in prostate cancer diagnostics, large population screenings were initiated for early detection of cancer. However, recent clinical and economic drawbacks have been recently raised, including evidence that screening exposes patients to a significant risk of both overdiagnosis and overtreatment. Nevertheless, several lines of evidence suggest that PSA may have tumor-suppressing activities. Despite being a member of the vast kallikrein family, which actively interplays with the coagulation cascade, the role of PSA in the pathogenesis of hemostatic disorders observed in prostate cancer patients remains circumstantial and speculative. However, observations that the levels of this cancer marker tend to correlate positively with those of several markers of thrombin generation, and with postsurgical bleeding as well as with coronary atherosclerosis and negative outcomes of myocardial infarction, raise a new and intriguing scenario regarding the pathophysiological role of this serine protease.
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PMID:Prostate-specific antigen, prostate cancer, and disorders of hemostasis. 2001 32

Heat stroke is defined by central nervous system abnormalities and failure of proper maintenance of thermoregulation as a result of high core body temperature ensuing from exposure to high environmental temperatures or strenuous exercise. Common complications include acute respiratory distress syndrome, disseminated intravascular coagulation, acute renal injury, hepatic injury, and rhabdomyolysis. Myocardial injury may also occur during heat stroke, resulting in cardiac enzyme increase and ST-segment changes on the ECG. Such findings might behave as diagnostic pitfalls by mimicking the presentation of coronary artery occlusive myocardial infarction. A previous case report described a patient with heat stroke and ST-segment elevation, in which the definite cause of the ST-segment elevation was unclear; however, acute myocardial infarction caused by coronary artery disease was ruled out according to the clinical signs, serial ECG changes, and serum level of cardiac biomarkers. Stress-induced cardiomyopathy (Takotsubo cardiomyopathy) was suspected, but it could not be confirmed because of the lack of coronary angiography. We herein report a case of heat stroke presenting with ST-segment elevation and cardiogenic shock. Coronary angiography was performed and coronary artery occlusive myocardial infarction was ruled out because of the presence of patent coronary arteries. Left ventriculography showed midventricular and apical hypokinesis, and stress-induced cardiomyopathy was then determined to be the appropriate diagnosis. Heat stroke causes increase of serum catecholamine levels, in which oversecretion and abnormal responses to catecholamines are a possible cause of stress-induced cardiomyopathy. Catecholamines may therefore be the key in linking heat stroke and stress-induced cardiomyopathy.
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PMID:Stress-induced cardiomyopathy caused by heat stroke. 2215 97


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