Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008325 (cholecystitis)
 3,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Posttraumatic acute cholecystitis is an often unrecognized and potentially fatal complication seen among patients hospitalized for trauma, and differs in etiology from cholecystitis which develops de novo. The cause, although not yet clearly defined, is believed to be related to bile stasis, ischemia, bacterial infection, sepsis, the activation of factor XII, and the Shwarzman reaction. A case is described in which a 53-year-old man with pelvic fractures developed acute acalculous cholecystitis and died of multiple organ failure 3 weeks following cholecystectomy. The histopathological findings are also reported; these are most likely attributed to the Shwarzman reaction or the activation of the factor XII pathways. There has been a tendency to regard posttraumatic acute acalculous cholecystitis as induced by trauma, and calculous as mere coincidence. We believe, however, that it is not calculous but histopathological findings that determine whether acute cholecystitis following trauma was more than coincidence or just mere coincidence. Although progress in clinical care has improved the chances of survival of severely traumatized patients, posttraumatic acute cholecystitis has been increasing in frequency. We cannot be careful enough in judging the relationship of this fatal complication to the initial trauma.
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PMID:Posttraumatic acute cholecystitis. Relationship to the initial trauma. 360 14

Acute, acalculous cholecystitis is seen among patients suffering with bacterial sepsis, burns, trauma, or cancer; clinical conditions that could lead to activation of factor XII-dependent pathways and result in inflammation of the gall bladder. To test this hypothesis, dogs were injected intravenously with ellagic acid or rutin, known polyphenol activators of factor XII, or with Escherichia coli endotoxin, also known to activate factor XII, and monkeys were injected intravenously with ellagic acid. In both species, in vivo activation of factor XII-dependent pathways with polyphenol activator resulted in rapid and selective development of acute vasculitis in the serosa and muscularis of the gallbladder and margination of polymorphonuclear neutrophils in pulmonary blood vessels. Intravenous injection of E. coli endotoxin in dogs resulted in necrosis and thrombosis of vessels that were especially severe in the serosa and muscularis of the gallbladder but also present in vessels of many other organs. These observations indicate that blood vessels of the gall bladder and, to a lesser degree, the lung are especially sensitive to injury consequent to in vivo activation of factor XII-dependent pathways and, in view of the common ingestion of plant polyphenols, may provide important insight into the pathogenesis of cholecystitis in man.
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PMID:Induction of acute cholecystitis by activation of factor XII. 676 72

Acute acalculous cholecystitis was observed to increase in frequency between 1950 and 1979, an increase that was statistically significant. The greatest part of this increase occurred between 1965 and 1979. Acute acalculous cholecystitis was also found to be associated with a higher mortality rate, more than twice that of acute calculous cholecystitis. Acute acalculous cholecystitis occurred in a variety of clinical settings including bacterial sepsis, severe trauma including surgical trauma and burns, multiple transfusions, and severe debilitation. The lesion in the gallbladder consists of intense injury of blood vessels in the muscularis and serosa similar to those induced experimentally by in vivo activation of factor XII dependent pathways. Possibly because of the intensity of vascular injury, acute acalculous cholecystitis with minimal clinical manifestations may rapidly progress to gangrene with perforation. Undelayed surgical treatment, which has become more widely accepted over the past 50 years, is essential. It may have also contributed to the increased recognition of this clinical entity.
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PMID:Acute acalculous cholecystitis. An increasing entity. 705 88