Frequency of peptic ulcer and erosion in patients with different types of cholestasis

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Group: 2008
Subgroup: Volume 10, Issue 1
Date: January 2008
Type: Letter to Editor
Start Page: 44
End Page: 45

Authors:

  • F Mansour-Ghanaei
  • Department of Gastroenterology and Hepatology, Gastrointestinal and Liver Diseases Research Center (GLDRC), Guilan University of Medical Sciences, Rasht, Gilan, Iran
  • M Yousefi-Mashhour
  • Department of Gastroenterology and Hepatology, Gastrointestinal and Liver Diseases Research Center (GLDRC), Guilan University of Medical Sciences, Rasht, Gilan, Iran
  • A Mahjoob
  • Department of Internal Medicine, Guilan University of Medical Sciences, Rasht, Gilan, Iran
  • F Joukar
  • School of Nursing and Midwifery, Guilan University of Medical Sciences, Rasht, Gilan, Iran
  • M Jamali
  • General Practitioner, Rasht, Gilan, Iran

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Dear Editor,

Cholestasis is a state of obstruction in bile duct and accumulation of bile salts in the body.1 It primarily leads to bile retention, regurgitation of bile into serum, and reduction of bile delivery into the intestine. These effects give rise to the worsening of the patient’s underlying liver disease and a systemic illness.2 The vascular changes due to cholestasis are partly explained by several factors such as an increase in prostaglandins in bile salts, and in the level of endogenous opoids, endotoxinemia, and NO production.1 By regarding these complications, this study was conducted to determine the frequency of peptic ulcer in patients with various types of cholestasis. Peptic mucosal lesions were observed in 42.3% (36) of patients in the mechanical cholestatic group and in 17.6% (15) of subjects in the non-mechanical cholestatic group (Table 1). 51 out of 170 patients with cholestasis (30%) had mucosal lesions. Table 2 shows that out of 38 cases with mucosal damage, 25 (65.7%) were in the mechanical cholestasis and 13 (34.3%) were in the non-mechanical cholestasis groups. Of 25 patients with mucosal damage in the mechanical cholestasis group, 17 (68%) had duodenal ulcer and 8 (32%) gastric ulcer. Therefore, the frequency of peptic ulcer in patients with mechanical cholestasis was more than that in those with non-mechanical cholestasis and in the mechanical cholestasis patients, the frequency of mucosal damage was more in the duodenum than that in the stomach. It is well known that the frequency of gastrointestinal ulceration is higher in jaundiced patients than that in the normal population. A previous report revealed an increase in gastric acid output and free radical formation, but a decrease in gastric wall blood flow3 in in rats with cholestasis.4 It was indicated that gastric mucosal susceptibility to injury is dependent on the normal flow of bile into the duodenal lumen, which appears to be a requirement for adaptive gastric cytoprotection.2 In another study, function of the liver and billiary system was evaluated in 130 patients with peptic ulcer, showing that 84.6% of the patients had some disorders in the hepatobilliary system.5 The results of this study showed significantly more mucosal erosions in patients with mechanical cholestasis than in those with non-mechanical cholestasis. The frequency of duodenal ulcer and peptic erosion was significantly more in patients with mechanical cholestasis than in those with non-mechanical cholestasis. It is concluded that mechanical obstruction is a risk factor for mucosal peptic erosion especially in patients with duodenal ulcer.

References: (5)

  1. Borhani A, Houshmand G, Samini M, Narimanian K, Hajrasouliha A, Tavakoli S, Ebrahimi F, Dehpour A. α2-adenoreceptor subsensitivity in mesenteric vascularbed of cholestatic rats: The role of nitric oxid and endogenous opioids. Eur J Pharmacol 2005;514(2-3):183-9.
  2. Cinigi A, Ahiskali R, Oktar B, Gulpinar M, Yegen C, Yegen B. Billiary decompression reduced the susceptibility to ethanol induced ulcer in jaundiced rats. Physiological Res J 2002;51:619-27.
  3. Nahavandi A, Mani AR, Homayounfar H, Akbari MR, Dehpuor AR. The role of the interaction between endogenous opioids and nitric oxide in the pathophisiology of ethanol–induced gastric damage in colestatic rats. Fundamental Clin Pharmacol 2001;15(3):181-7.
  4. Canturk NZ, Canturk Z, Ozbilim G, Yenisey C. Protective effect of vitamine E on gastric mucosal injury in rats with billiary obstruction. Can J Gastroenterol.2000;14(6):499-503.
  5. Vakhrushev I, Mufazdalova IV. Study of functional state of the hepathobilliary system in the dynamics of treatment of patients with peptic ulcer. EKSP Klin Gastroentrol 2005;(2):44-8.