Kaminski D L, Deshpanda Y G, Thomas L A
Hepatogastroenterology. 1987 Apr;34(2):70-3.
Prostaglandins have been postulated to be involved in the formation of gallstones and the pain and inflammation of calculous gallbladder disease. This report evaluated prostaglandin E and F levels in patients with acalculous gallbladder disease. Control gallbladders were obtained from patients undergoing cholecystectomy during insertion of hepatic artery catheters for regional, hepatic chemotherapy. Patients without gallstones and with long-standing post-prandial biliary colic with abnormal cholecystokinin administration underwent cholecystectomy for chronic acalculous cholecystitis. A third group of patients underwent cholecystectomy for acute acalculous cholecystitis. Gallbladder mucosa and muscle were separated, and prostaglandin E and F concentrations in mucosal and muscle or mucosa were identified in gallbladders from patients with chronic acalculous cholecystitis compared to gallbladders from patients without biliary tract symptoms. In gallbladders from patients with acute acalculous cholecystitis a seven-fold increase in PGE production by muscle tissue and mucosal cells was found. The more histologically inflamed gallbladders had higher mucosal and muscle prostaglandin E concentrations than were found in less inflamed gallbladders. Prostaglandin F levels were not significantly changed or were decreased, resulting in a significant increase in the ratio of PGE/PGF in acutely diseased gallbladders when compared to normal gallbladders. Prostaglandin E may be a manipulatable intermediary in the sequence of events that results in the development of acute acalculous cholecystitis.
前列腺素被推测与胆结石的形成以及结石性胆囊炎的疼痛和炎症有关。本报告评估了无结石性胆囊炎患者的前列腺素E和F水平。对照胆囊取自因进行肝动脉插管以进行区域性肝化疗而接受胆囊切除术的患者。无胆结石且长期存在餐后胆绞痛且胆囊收缩素给药异常的患者因慢性无结石性胆囊炎接受胆囊切除术。第三组患者因急性无结石性胆囊炎接受胆囊切除术。将慢性无结石性胆囊炎患者胆囊的黏膜和肌肉分离,并与无胆道症状患者的胆囊相比,测定黏膜和肌肉或黏膜中前列腺素E和F的浓度。在急性无结石性胆囊炎患者的胆囊中,发现肌肉组织和黏膜细胞产生的前列腺素E增加了7倍。组织学上炎症更严重的胆囊,其黏膜和肌肉中的前列腺素E浓度高于炎症较轻的胆囊。前列腺素F水平无明显变化或有所降低,导致与正常胆囊相比,急性患病胆囊中PGE/PGF的比值显著增加。前列腺素E可能是导致急性无结石性胆囊炎发生的一系列事件中的一个可调控的中间环节。