Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gram-negative septicemia/endotoxemia remains a serious clinical disorder that is often complicated by disseminated intravascular coagulation (DIC). Plasma antithrombin-III (AT-III) levels usually decrease during gram-negative septicemia/endotoxemia, and even moderate decreases in this major inhibitor of the coagulation system are associated with serious DIC. We demonstrated in an earlier study that prophylactic treatment of rats with 250 U/kg of AT-III followed by endotoxin challenge markedly attenuates DIC, indices of organ damage, and metabolic dysfunction. The present study was to determine whether treatment with 250 U/kg AT-III 1 hr after endotoxin challenge would be similarly efficacious. Rats treated with 250 U/kg of AT-III inactivated by human sputum elastase (ATX) served as protein controls. Blood samples for analysis were obtained 4 hr after AT-III or ATX treatment (5 hr after endotoxin challenge). Rats in the ATX treatment group exhibited abnormalities characteristic of endotoxemia, i.e., decreased fibrinogen levels and platelet counts, increases in prothrombin time and activated partial thromboplastin time, elevated serum glutamic oxaloacetic transaminase (SGOT) and alkaline phosphatase (AKP), and hypoglycemia. Treatment with AT-III markedly and significantly (P less than .05) attenuated all of these abnormalities, although survival was not increased. This study strongly suggests that supplementation of plasma AT-III is efficacious after the development of sepsis, although not as efficacious as prophylactic treatment.
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PMID:Antithrombin-III treatment limits disseminated intravascular coagulation in endotoxemia. 273 21

Acute acalculous cholecystitis (AAC) is marked by a very high mortality rate but its relative rarity makes its features obscure to many physicians. This often contributes to a delayed diagnosis. In this study, we review one center's experience, examine the clinical features of the disorder, and describe the progression of pathological events that culminate in AAC. We performed a 10-year retrospective review of cases of AAC reported at our institution between 1988 and 1998. Fifteen cases of AAC were identified from this period, during which 5804 cardiovascular operations were performed. The mortality rate was 46.6%. Multiple organ failure was present in 12 of the 15 cases, and 9 of the patients were over 60 years of age. Prolonged hypotension occurred in 13 patients, and fever in all 15. Nine cases of gangrenous gallbladder occurred. Gram-negative septicemia was present in 12. Visceral arterial hypoperfusion was frequently evident at operation or necropsy. Thirteen patients showed clinical jaundice, a disproportionate elevation of the alkaline phosphatase, or both. Heart failure was found in 9 patients. Open cholecystectomy was most often the definitive intervention. Arterial hypoperfusion of the gut and or sepsis appear central to the pathogenesis of AAC in our series. Gallbladder inflammation and cholestasis result and bacterial invasion of the organ ensues, culminating in AAC, frequently with gangrene. A model of the pathogenesis of AAC is discussed.
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PMID:Acute acalculous cholecystitis associated with systemic sepsis and visceral arterial hypoperfusion: a case series and review of pathophysiology. 1462 41