Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Case 1: 75 years old male was admitted to our hospital with anterior chest subcutaneous bleeding. Coagulation study revealed that fibrinogen and alpha 2-PI decreased, and FDP, FPA, B beta 15 approximately 42 and D-dimer increased. Case 2: 78 years old male was admitted to Shingu City Hospital with a left hip subcutaneous hematoma. Coagulation study revealed that fibrinogen, ATIII and alpha 2-PI decreased, and FDP increased. US and CT showed abdominal true aneurysm in both cases. Either severe infection or malignancy was not found. Ticropidine and T-AMCHA were medicated for 8 days in case 1, and for 18 months in case 2. Symptom and coagulation study improved in these cases. Due to some side effects such as appetite loss and liver dysfunction in case 1, and diarrhea in both cases, we changed the therapy to mini-dose heparin therapy. This therapy also proved effective. It is concluded that anti-platelet and anti-fibrinolytic therapy are effective for chronic DIC with abdominal true aneurysm.
 ...
PMID:[Chronic disseminated intravascular coagulation due to abdominal true aneurysm in two cases--effect of anti-platelet and anti-fibrinolytic therapy]. 262 2

Two young children with a history of diarrhea, for one and two days respectively, were admitted to our hospital due to high fever and conscious disturbance. Disseminated intravascular coagulation, abnormal hepatic and renal functions, and metabolic acidosis were noted as well. Both patients developed shock soon after arrival and expired within one day after admission. Their serum ammonia levels were normal, and their blood and cerebrospinal fluid cultures also brought negative results. Hemorrhagic shock and encephalopathy syndrome was diagnosed by their clinical manifestation and laboratory data. We also discussed their related problems.
 ...
PMID:Hemorrhagic shock and encephalopathy syndrome: Report of two cases. 263 89

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.
 ...
PMID:High-dose melphalan, misonidazole, and autologous bone marrow transplantation for the treatment of metastatic colorectal carcinoma. A phase I study. 265 May 27

Endotoxins (lipopolysaccharides, LPS) are potent bacterial poisons always present within the intestines in considerable amounts. Several pathophysiological conditions such as hypovolaemia, hypoxia, intestinal ischaemia, burns and radiation lead to a breakdown in the barrier and depending upon the extent of the injury, endotoxins enter the systemic circulation in increasing amounts. Antibiotics do not inactivate the endotoxins which continue to exert their toxic effects leading to nausea, vomiting, diarrhoea, fever, disseminated intravascular coagulation, vascular collapse and organ failure. When nonabsorbable antibiotics are given prior to the insult, systemic endotoxaemia is prevented. Immunotherapy, using anti-lipopolysaccharide IgG, inactivates plasma endotoxins, destroys gram-negative bacteria and opsonises them and may become a major form of therapy. An outline of endotoxin and anti-lipopolysaccharide and its importance to the anaesthetist and intensive care specialist is presented.
 ...
PMID:Endotoxins and anti-endotoxins (their relevance to the anaesthetist and the intensive care specialist). 265 93

Report on the first case of streptococcal toxic shock syndrome in the GDR. The patient was a 54-year-old female. One week before admission to the hospital she cut her finger. The day before admission to the hospital she presented with a painful left shoulder. Demarcation followed, and Streptococcus pyogenes (group A streptococci) was isolated from this area. The temperature rose to more than 40 degrees C and she became confused, hypotensive and anuric. There was evidence for disseminated intravascular coagulation. She died 23 h after admission. Clinical course and laboratory parameters resembles staphylococcal toxic shock syndrome, except a diarrhoea. The streptococcal strain produced a large amount of erythrogenic toxin type B (more than 20 ng/ml), but not erythrogenic toxins A or C. Erythrogenic toxins of Streptococcus pyogenes seem to play the same role in the development of streptococcal toxic shock syndrome as the toxic shock syndrome 1 (TSST-1) in staphylococcal toxic shock syndrome.
 ...
PMID:[Streptococcus-induced syndrome of toxic shock (streptococcal toxic shock syndrome)]. 269 6

Exertion-induced heat stroke is a relatively rare disorder in the moderate maritime climate of The Netherlands. Serious complications of excessive physical activity rarely occur. We describe a marathon runner with multi-organ failure after exertion-induced heat stroke. The patient developed shock, diarrhoea, coma, rhabdomyolysis, acute renal failure, liver cell damage and disseminated intravascular coagulation but recovered completely.
 ...
PMID:Multi-organ damage in exertional heat stroke. 277 93

To further define the clinical, pathologic, and biochemical features of hemorrhagic shock and encephalopathy syndrome, we studied 25 affected children (aged 3 months to 14 years) admitted to a single center between 1982 and 1985. A prodromal illness comprising vomiting, diarrhea, listlessness, and fever was present in 84% of the cases. Acute onset of shock, convulsions and coma, bleeding (or laboratory evidence of disseminated intravascular coagulation), elevated plasma activity of hepatic enzymes, acidosis, and impaired renal function was present in every case. Twenty patients died, and all the survivors are neurologically damaged. At postmortem examination, intravascular microthrombi coexisting with hemorrhages and petechiae were found in most organs. Centrilobular liver necrosis and cerebral edema were prominent features. No microbiologic cause for the disorder was identified, but decreased plasma levels of the protease inhibitors alpha 1-antitrypsin and alpha 2-macroglobulin, together with increased levels of circulating proteolytic enzymes, were frequently present. An overrepresentation of the uncommon variant phenotypes of alpha 1-antitrypsin was found in first-degree relatives of affected patients (four had the MZ phenotype, and one each the MS or MC phenotype, of 19 relatives studied). Abnormal accumulation of alpha 1-antitrypsin was detected immunohistochemically in the livers of six of the patients. Defective protease inhibitor production or release may be involved in the pathogenesis of the disorder.
 ...
PMID:Hemorrhagic shock and encephalopathy: clinical, pathologic, and biochemical features. 276 14

Thrombocytopenia was observed in 15 of 146 cases of clinically acute bovine viral diarrhea virus (BVDV) infection in adult cattle. Platelet counts ranged from 2,000 to 33,000/microliters. Clinically, a bleeding tendency was manifested by bloody diarrhea, petechial and ecchymotic hemorrhage, epistaxis, and abnormal bleeding from injection sites. Coagulation testing (six cases) gave no evidence of disseminated intravascular coagulation. Bone marrow aspirates were suggestive of active marrow necrosis (two cases) or recent repopulation (three cases). Treatment, when given, was supportive and empirical in nature. Six animals experienced complete clinical recoveries; the others died or were euthanatized. Although the pathogenesis of the thrombocytopenia was not definitively determined, thrombocytopenia associated with acute BVDV infection should be considered in the differential diagnosis for cattle with bleeding disorders.
 ...
PMID:Thrombocytopenia associated with acute bovine virus diarrhea infection in cattle. 292 19

Between July 1983 and February 1984, eight children with adenovirus Type 3 infection, proven by virus isolation from sputum, stool or nasopharyngeal swabs and a fourfold increase in complement fixation antibody titers against the virus, were treated in our department. All eight patients had fever lasting at least 7 days, hepatomegaly, diffuse pulmonary infiltrates and abnormal liver function tests. Seven of the patients exhibited dyspnea and pulmonary wheezing. Six of the patients developed changes in state of consciousness, and three had repeated convulsions. EEG patterns in three of the patients were compatible with encephalopathy. Other clinical manifestations included: follicular tonsillitis in two patients, diarrhea in two, pneumothorax in one, and shock with disseminated intravascular coagulation in one. The spectrum of adenovirus Type 3 infection reported here has been described previously only in the viral hemorrhagic fevers. This adenovirus Type 3 infection shares the potential for disseminated disease that has been described previously for Type 7, simulating Reye's syndrome.
 ...
PMID:Adenovirus type 3 infection with systemic manifestation in apparently normal children. 302 30

Cholera disease can be induced in the rabbit by ligation of the cecum (C) followed by duodenal inoculation (DI) of virulent Vibrio cholerae organisms (DIC model). When the cecum is not ligated, DI does not induce disease. In contrast, the animals are primed which becomes apparent upon challenge with live V. cholerae in the DIC model. Such animals are vibriocidally protected. This protection is characterized by absence of disease symptoms, rapid disappearance of V. cholerae from the feces and presence of high levels of anti-lipopolysaccharide Immunoglobulin A in the bile. The present study shows that primed rabbits can also be boosted by duodenal administration of killed, smooth V. cholerae cells. On the other hand, killed cells cannot prime. The minimal lethal dose of a rough derivative of a smooth strain C5, designated R5 and lacking the O antigen part of the LPS, was 100,000 times higher than that of its parent strain C5, in the DIC model. Rabbits which had been duodenally immunized with strain R5 and were subsequently challenged with the smooth strain C5, all developed diarrhea and two out of eight died. This result supports an earlier observation that the specific O antigen part of the V. cholerae LPS is an essential prerequisite for the induction of protective immunity in the rabbit.
 ...
PMID:Priming and boosting of the rabbit intestinal immune system with live and killed, smooth and rough Vibrio cholerae cells. 320 Jan 61


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>