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)

In septic shock, hypotension, disseminated intravascular coagulation, and neutrophil activation are related to the activation of the blood coagulation contact system. This study evaluates in dogs the effect of the C1-esterase inhibitor (C1-INH), a main inhibitor of the blood coagulation contact system, on the cardiovascular and respiratory dysfunction associated with endotoxic shock. Two groups were included: controls, which received Escherichia coli endotoxin, and a C1-INH group in which C1-INH was infused before E. coli endotoxin administration. In both groups, endotoxin produced hypodynamic shock; however, the decrease in the systolic index and the ventricular systolic work indexes were greater in controls than the C1-INH group. In controls, the arterial O2 partial pressure decreased by 30% and the alveolo-arterial O2 difference increased by 625%, these parameters remained unchanged in the C1-INH group. Hypoxemia was associated with increased intrapulmonary shunt, decreased blood coagulation contact factors, and decreased C3c. In contrast, C1-INH administration prevented endotoxin-induced hypoxemia, the increase in intrapulmonary shunt, and the decrease in blood coagulation contact factors. This study shows that, in dogs with endotoxic shock, pulmonary dysfunction is associated with an activation of the blood coagulation contact phase system. An inhibition of this system by C1-INH prevented the hypoxemia induced by endotoxic shock.
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PMID:Endotoxin-induced pulmonary dysfunction is prevented by C1-esterase inhibitor. 851 83

We evaluated retrospectively the causes of death from active pulmonary tuberculosis by the review of records and chest radiograohs of 364 patients (male 282, female 82) with active pulmonary tuberculosis, who were admitted to our hospital during 1995 to 1998. 43 patients (male 33, female 10) were died under anti-tuberculous chemotherapy. 20 cases were tuberculous death; death from acute progression of tuberculosis without response to chemotherapy (acute progression group) in eight cases and death from debility in spite of partial response to chemotherapy (debility group) in eight cases. 23 cases were died from underlying diseases; death from malignant neoplasmas (malignant group) in nine cases and death from complication of bacterial pneumonia (pneumonia group) in seven cases. In acute progression group, the age (mean +/- SE) was 64.8 +/- 5.2 years old and the survival period from admission was 11.8 +/- 4.2 days. Five cases were laborer or unemployed. This group was characterized with far advanced diseases presenting extensive lung lesions complicated with DIC or hepatic dysfunction, low performance status (PS), severe malnutrition and lymphocytepenia. In debility group, the age was 70.8 +/- 3.9 years old and the survival period from admission was 254.6 +/- 90.7 days. Five cases were laborer or unemployed. This group was characterized with multiple underlying diseases, low PS, previous anti-tuberculous chemotherapy and resistance to INH and/or RFP. In malignant group, the age was 69.3 +/- 3.2 years old and the survival period from admission was 99.9 +/- 21.2 days. This group was characterized with relatively well nourished, relatively good PS in comparison with other groups, and lymphocytepenia. In pneumonia group, the age was 82.8 +/- 1.7 years old and the survival period from admission was 153.3 +/- 54.5 days. This group was characterized with remarkably advanced age, low PS related to underlying disorders of central nervous system. In the causes of death with active pulmonary tuberculosis under chemotherapy, inhomogenous groups were included. Extensive disease, low PS, malnutrition, lymphocytopenia, previous chemotherapy, resistance to INH and/or RFP, and poorer social circumstances seemed to be risk factors for tuberculous death. In contrast, underlying malignant nepolasma, lower PS, and far advanced age were seemed to be the risk factors for non-tuberculous death.
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PMID:[A clinical study of causes of death from active pulmonary tuberculosis with chemotherapy]. 1002 8