Abstract
It is widely accepted that patients with aortic aneurysm (AA) show a higher incidence of peptic ulcers than those without. However, the pathogenesis of peptic ulcers associated with AA remains obscure. We measured the gastric mucosal blood flow (GMBF) endoscopically and also determined the gastric mucosal prostaglandin (PG) levels of these AA patients to investigate the mechanism behind gastric ulcer formation. Moreover, we investigated the consumption coagulopathy (CC) of AA responsible for inducing the hemorrhage from ulcers. The GMBF values of 7 AA cases, taken at the antrum, angle and corpus, were significantly decreased compared with those of control cases, while the PGE2 levels of the gastric mucosa were also significantly reduced. With regard to CC, the serum levels of fibrinogen or platelets were significantly lower than those of the control group. These results indicate that the decrease in GMBF, followed by the reduction in endogenous PG, might contribute to the gastric ulcer formation in AA patients, and that CC associated with AA could be an important factor causing the hemorrhage from these ulcers. AA patients should therefore be treated with focusing attention on the possibility of an associated ulcer and ulcer bleeding.
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References
Jones AW, Kirk RS, Bloor K. The association between aneurysm of the abdominal aorta and peptic ulceration. Gut 1970; 11: 679–684.
Bouhoutsos J, Barabas A, Martin P. The association of peptic ulcer and abdominal aortic aneurysm and its significance. Br J Surg 1973; 60: 302–304.
Euler AU, Popiela T, Tytgat GN, Kulig J, Lookabaugh JL, Phan TD, Kitt MM. A multiclinic trial evaluating arbaprostil 15R-15-methyl prostaglandin E2 as a therapeutic agent for gastric ulcer. Gastroenterology 1989; 96: 967–971.
Elkeles A. Gastric ulcer in the aged and calcified atherosclerosis. Am J Roentgenol Rad Thera Nuc Med 1964; 91: 744–750.
Darke SG, Glasgow MS, Eadie DGA. Studies on maximal acid output in patients with abdominal aortic aneurysms. J Cardiovas Surg. 1977; 18: 471–474.
Major JS, Scholes P. The localization of a histamine H2-receptor adenylate cyclase system in canine parietal cells and its inhibition by prostaglandin. Agents Actions 1983; 8: 324–331.
Soll AH. Specific inhibition by prostaglandin E2 and I2 of histamine-stimulated14C-aminopyrine accumulation and cyclic adenosine monophosphate generation by isolation canine parietal cells. J Clin Invest 1980; 65: 1222–1229.
Seidler U, Beinborn M, Sewing K-F. Inhibition of acid formation in rabbit parietal cells by prostaglandin is mediated by the prostaglandin E2 receptor. Gastroenterology 1989; 96: 314–320.
Redfern JS, Blair AJ, Lee E, Feldman M. Gastrointestinal ulcer formation in rabbits immunized with prostaglandin E2. Gastroenterology 1987; 93: 744–752.
Mulcare RJ, Royster TS, Weiss HJ, Phillips IL. Disseminated intravascular coagulation as a complication of abdominal aortic aneurysm repair. Ann Surg 1974; 180: 343–349.
Kaneko H, Sakaguchi S: Aneurysm repair and consumption coagulopathy; The importance of fibrinogen level. Jap J Cardiovas Surg 1986; 16: 58–59 (in Japanese)
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Konno, H., Sakaguchi, S., Aoki, K. et al. The formation of gastric ulcers with a tendency to hemorrhage in association with aortic aneurysms. The Japanese Journal of Surgery 21, 268–271 (1991). https://doi.org/10.1007/BF02470945
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DOI: https://doi.org/10.1007/BF02470945