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)

Thirty-six children with duodenal ulcer were examined for the coagulation and thrombocytic components of hemostasis. Use was made of the new coagulologic research methods based on administration of the synthetic tri- and tetrapeptides containing a chromoform group. The high sensitivity of the synthetic peptides enables the use of plasma in high dilutions, owing to which the effect of inhibitors is decreased and a small amount of blood is only required, being of paramount importance in carrying out serial tests. In acute ulcer 1/3 of the children show the signs of the DIC syndrome compensated at the expense of the high content of anticoagulants. At the same time 4 patients were discovered to have coagulologic disorders characteristic of Willebrand's disease (3 cases) and thrombasthenia (1 case). The coagulologic alterations should be taken into consideration in treatment administration, since the compensated DIC syndrome untreated by anticoagulant therapy aggravates the course of the ulcerous process and gives rise to hemorrhagic diathesis. Meanwhile in children with hemorrhagic diathesis, peptic ulcer may cause severe, life-threatening hemorrhages.
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PMID:[Blood aggregation in duodenal ulcer]. 186 48

We reported 5 patients with renal failure associated with polyarteritis nodosa (PN). In all patients the renal dysfunction became apparent from 2 to 4 weeks after the onset of fever or neuromuscular symptoms with laboratory findings supporting marked inflammatory process and took the course of either acute or rapidly progressive renal failure. The clinical diagnoses on admission were variable; fever of unknown origin, peptic ulcer disease, polyneuritis multiplex, disseminated intravascular coagulation and Buerger's disease. Microscopic examination of the kidneys in 3 by renal biopsy and in 2 by autopsy revealed crescentic glomerulonephritis without immunoglobulin deposit, segmental necrotizing glomerulonephritis, marked inflammatory infiltrate around the glomeruli, granulomatous lesion, tubular necrosis and cortical necrosis other than necrotizing vasculitis. The outcomes were favorable with prednisolone monotherapy in two patients who had biopsy-proven diagnosis and treatment early in the course. Of all PN the prevalence of renal involvement is considered to be about 70%, the prognosis of which has been considered very poor. However it seems possible to alter fatal outcome of this disease by starting treatment with confident histological proof early in the disease process.
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PMID:[Renal failure associated with polyarteritis nodosa]. 197 42

Coagulation studies were performed in patients who underwent abdominal surgery. One hundred and twenty six patients with cholelithiasis, peptic ulcer and gastric cancer were examined. Although fibrinogen increased up to 560 mg/dl postoperatively, DIC did not occur among these patients, at all. For 30 patients who underwent hepatectomy, esophageal transection or pancreatoduodenectomy, HPT, PT, fibrinogen, platelet count, alpha 2-PI, AT-III, plasminogen and DIC score were investigated until 10 postoperative days. As for 13 patients without liver cirrhosis in this group, deterioration of HPT, PT and AT-III was noted on the second postoperative day, however these parameters improved on the fifth postoperative day and all patients recovered uneventfully. On the contrary, as to patients with liver cirrhosis, changes of coagulation parameters were drastic. Significant decrease of HPT, PT, AT-III, plasminogen and increase of FDP and DIC score were noted after operation and these values deteriorated with time in certain cases. Seven patients out of 17 died of DIC and multiple organ failure. More than half of these patients received Gabexate Mesilate (GM) injection in a dose of 1200 mg/day postoperatively for more than 5 days to prevent DIC. In patients who underwent hepatectomy due to hepatocellular carcinoma with liver cirrhosis, the increase of FDP and DIC score seemed to be inhibited by GM on the fifth postoperative day.
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PMID:[Coagulation studies in patients after abdominal surgery]. 308 4

Current management of hemorrhage in cirrhotic patients is disappointing, probably because it deals only with the portal hypertension, while the coagulation disorders are neglected. Some new suggestions can be made : 1) Hemorrhage originates in coagulation disorders. The mechanical lesion of the mucosa is only the opportunity for these disorders to become apparent. The lesion may be : infrequently, a ruptured esophageal varix or a gastroduodenal peptic ulcer ; a lesion of the cardia (hiatal hernia, reflux, esophagitis, minimal traumatic tears) ; a gastric anomaly (hemorrhagic gastritis, superficial ulcerations, petechiae) ; in some cases no mucosal lesion is apparent. 2) Any widespread liver disease results in lasting hypercoagulability which is responsible for : permanent lysis, consumption, DIC. The spleen is responsible for the functional alteration of the platelets. Splenectomy is followed by permanent recovery. 3) Changes involving the platelets are responsible for most hemorrhages. Thrombopenia and severe anomalies of platelet aggregation are common findings in liver cirrhosis. Further deterioration can be induced by acetylsalicylic acid, especially if it is absorbed after an immoderate ingestion of alcohol. Emergency treatment consists in platelet transfusions. 4) Stasis in the portal system may, however, result in permanent activation of coagulation. 5) Cirrhosis results in chronic hypercoagulability and severe platelet deterioration. Any stress involving coagulation mechanisms may therefore induce hemorrhage : infection, acetyl salicylic acid, respiratory distress, estrogens, massive transfusion. It is always dangerous to "feed" consumption or to restrain lysis. 6) Coagulation tests should be performed rapidly, in order to evaluate hypercoagulability, consumption, lysis, and evidence of DIC ; FDP can probably be responsible for inflammatory changes in the liver and spleen. 8) Coagulation disorders are permanent since the hepatic alterations are irreversible.
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PMID:[Hemorrhage in liver cirrhosis : new suggestions (author's transl)]. 627 81

We describe the second example of a duodenal-caval fistula in a patient with peptic ulcer disease. This condition was complicated by embolization of intestinal contents to the lung, with abundant intravascular mucin. This is the first histological documentation of intravascular mucin apart from amniotic fluid embolism. It is well known that mucin may activate coagulation. We propose that intravascular mucin activated the coagulation cascade in our patient, causing disseminated intravascular coagulation and adult respiratory distress syndrome.
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PMID:Spontaneous duodenal-caval fistula with embolization of intestinal contents. 978 59

Blood coagulation and fibrinolysis were studied in 34 patients with diffuse peritonitis treated in intensive care wards of common profile. Forced ventilation of the lungs was carried out for 2-26 days in 32 of 34 patients. The causes of peritonitis were perforating gastroduodenal ulcers (22 cases), acute perforating ulcers of the small intestine (5 cases), and acute phlegmonous perforative cholecystitis (7 cases). Disseminated intravascular coagulation, depressed fibrinolysis first in the plasma and then in whole blood were observed early (2-16 h) after surgery in all patients (17 survived and 17 died). These changes progressed by days 3-5 of treatment in all patients, being the most pronounced in cases with complications (failure of sutures after gastroduodenal ulcer suturing, acute gastroduodenal ulcers complicated by hemorrhages, acute perforating ulcers of the small intestine, etc.), particularly in the patients who died.
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PMID:[Dynamics of indicators of blood coagulation and fibrinolysis in patients with diffuse peritonitis]. 1185 59

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

Symptomatic gastric malignancy usually presents with symptoms which mimic peptic ulcer disease.Usual presenting features include weight loss and abdominal pain. Other symptoms include nausea, vomiting, dysphagia, melena and early satiety. Gastric malignancy presenting with hemetemesis, macular skin lesions of DIC and low backache due to bone metastasis from the primary is rare. Also bone metastasis in gastric cancer in the absence of hepatic metastasis is also rare.
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PMID:An unusual presentation of carcinoma stomach. 2364 20