Prevalence of Helicobacter pylori in Patients with End Stage Renal Disease
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1 2000;20: Helicobacter pylori Prevalence of Helicobacter pylori in Patients with End Stage Renal Disease Do Ha Kim, M.D., Hwoon-Yong Jung, M.D., Suk-Kyun Yang, M.D. Weon-Seon Hong, M.D. and Young Il Min, M.D. Department of Internal Medicine, University of Ulsan College of Medicine, Ulsan, Korea Background/Aims: It has been reported that patients with chronic renal failure have a tendency foward increased incidences of peptic ulcer diseases. However, it is yet unclear whether the increased incidence is due to altered gastric acidity, hypersecretin of gastrin, or increased colonization of Helicobacter pylori (H. pylori). This study was conducted to investigate the role of H. pylori in the development of peptic ulcer diseases in patients with chronic renal failure. Methods: Forty nine patients with end stage renal disease (ESRD) and 41 age-matched controls with normal renal function, were examined for H. pylori infection using a rapid urease test, histological examination with Hematoxylin, Eosin, Warthin-Starry silver stain, and culture. The presence of H. pylori was defined either as the positive culture or as positive for both CLO and histological examination. Results: Ninteen (38.8%) out of 49 ESRD patients were positive for H. pylori, which was lower than 70.7% of the controls (p 0.01). Endoscopic examination revealed that 6 ESRD patients (12.2%) had peptic ulcers, while 2.4% of the controls did, which was not statistically significant. The ESRD patients were divided into two groups by therapeutic modality: group 1 included 31 patients under dialysis, and group 2, 18 patients with maintenance therapy. The incidence of H. pylori infection in group 1 was 51.6%, which was significantly higher than the 16.7% in group 2 (p 0.05). Conclusions: The results of this study suggest that the increased incidence of peptic ulcers in ESRD patients cannot be explained by H. pylori colonization, and that there may be other factors such as a high concentration of urea in the stomach of patients with ESRD, which can suppress the colonization of H. pylori. (Korean J Gastrointest Endosc 2000;20:97 102) Key Words: Helicobacter pylori, End stage renal disease, Peptic ulcer , , : , Tel: , Fax: dhkim@uuh.ulsan.kr.,, Helicobacter pylori (H. pylori) (colonization).1 H. pylori 1984 Marshall Warren 2 97
2 ;20: (infectious disease), H. pylori, H. pylori H. pylori. Marshall urea H. pylori 4 urea 5 urea H. pylori. H. pylori.6-12 H. pylori H. pylori ,.,.,., 1 1, (NSAIDs) , , 1 6, Helicobacter pylori H. pylori, urease (CLO ), CLO H. pylori. 1) : 3, CLO.. 10% Hematoxylin and Eosin (H&E) Warthin-Starry. 2) CLO : CLO (Delta West Ltd., Western Australia, Australia) 5% O2, 10% CO2, 37oC 24,. 3) : 2 Muellier Hinton Broth 2 Chocolate agar Campy pouch (BBL) 37oC, 5% O2, 10% CO2, 100% (microaerophilic) 7, (colony) Gram stain, catalase, oxidase, urease H. pylori. 2. student' s t-test Wilcoxon rank sum test chi-square test. p
3 : Helicobacter pylori 99 Table 1. Characteristics of 49 Patients with End Stage Renal Disease and 41 Controls Table 3. The Prevalence Rate of H. pylori in 49 Patients with End Stage Renal Disease and 41 Controls ESRDs Controls Tests ESRDs Controls p value No. of cases Hemodialysis 25 Peritoneal dialysis 6 Maintenance therapy 18 Age (yr) 41 2* 46 2 Sex (M/F) 33/16 21/20 Dyspepsia 4/49 (8.2%) 5/4 (12.2%) ESRDs, patients with end stage renal disease; *, mean SD. Culture positive alone or both CLO & histology positive 38.8% 70.7% CLO positive alone 40.8% 68.3% Histology positive alone 50.0% 78.1% Culture positive alone 24.2% 35.0% 0.3 Culture positive or CLO positive or histology positive 53.1% 80.5% ESRDs, patients with end stage renal disease. Table 2. The Prevalence Rate of Peptic Ulcer in 49 Patients with End Stage Renal Disease and 41 Controls ESRDs (n=49) Controls (n=41) Peptic ulcer 6 (12.2)* 1 (2.4) Duodenal ulcer 1 (2.0) 1 (2.4) Gastric ulcer 5 (10.2) 0 (0.0) ESRDs, patients with end stage renal disease; *, no. of patients (%).. 4 (8.2%) 12.2% (Table 1) (12.2%) 50.0% 1, % 4, 2. (p 0.01). 6 3 (50.0%) H. pylori. 24.2% % (p 0.05). (Table 2). H. pylori 53.1% 3. H. pylori H. pylori 38.8% (19/49) 70.7% Figure 1. The prevalence of H.pylori infection in 31 patients under dialysis and 18 patients with maintenance therapy. 80.5% (p 0.01). (29/41) (p 0.01, Table 3). CLO 4. Helicobacter pylori 40.8% 68.3% 1 (p 0.01)., H&E Warthin-Starry 1 H. pylori. 51.6% (16/31)
4 ;20: % (3/18) H. pylori (p 0.05)(Fig. 1)..13. (acid inhibitor).14,15. H. pylori (infectious disease).16 H. pylori. H. pylori H. pylori, H. pylori. H. pylori (gastric metaplasia). H. pylori,.17, NSAIDs,. H. pylori H. pylori. H. pylori 10%. 6,7 H. pylori H. pylori. Offerhause 8 H. pylori, H. pylori 45%, 93%. H. pylori % 2.4%. H. pylori 38.8% (70.7%). H. pylori 70% H. pylori. H. pylori, urease. H. pylori. H. pylori..... H. pylori. H. pylori 20.
5 : Helicobacter pylori 101 H. pylori 10. H. pylori. H. pylori 20 70% H. pylori. H. pylori. urea. urea urea urea.5 Urea H. pylori 4, urea H. pylori 19, urea H. pylori 11. urea H. pylori. :,. H. pylori H. pylori. H. pylori H. pylori. : H. pylori urease (CLO ). : 49 ( 33, 16 ) 41. H. pylori 38.8% (19/49) 70.7% (29/41) (p 0.01). 12.2% (6/49) 2.4% (1/41)., H. pylori 51.6% (16/31) 16.7% (3/18) (p 0.01). : H. pylori. H. pylori. H. pylori. : Helicobacter pylori,, 1. Fauci AS, Braunwald E, Isselbacher KJ, et al. Harrison' s priciples of internal medicine. 14th ed. New York: McGraw- Hill, Marshall BJ. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet 1983;1: NIH Consensus Conference. Helicobacter pylori in peptic ulcer disease. JAMA 1994;272: Marshall BJ, Barrott LJ, Prakash C, McCallum RW, Guerrant RL. Urea protects Helicobacter (Campylobacter) pylori from the bactericidal effect of acid. Gastroenterology 1990;99: Neithercut WD, Rowe PA, Nujumi AM, Dahill S, McColl KE. Effect of Helicobacter pylori infection on intragastric urea and ammonium concentrations in patients with chronic renal failure. J Clin Pathol 1993;46: Tielemans C, Verhas M, Glupezynski Y, Nyst JP, Deltenre M, Dratwa M. Urea C14 breath test screening for Campylobacter pylori infection in uraemic patients. In: Magraud F, Lamouliatte H, ed. Workshop Gastroduodenal pathology and Campylobacter pylori. Abstract book 1988: Derveniotis V, Koliouskas D, Kallllokou H. Campylobacter pylori (C. p) in severely uremic hemodialyzed and successfully transplanted patients. Abstracts. XIth Int. Congress of Nephrology, Tokyo 1990:138A. 8. Offerhause GJ, Kreuning J, Valentijn RM, et al. Campylobacter pylori: Prevalence and significance in patients with chronic renal failure. Clin Nephrol 1989;32:
6 ;20: Wee A, Kang JY, Ho MS, Choong HL, Wu AY, Sutherland IH. Gastroduodenal mucosa in ureamia: endoscopic and histological correlation and prevalence of Helicobacter-like organisms. Gut 1990;31: Devenport A, Shallcross TM, Crabtree JE, Davison AM, Will EJ, Heatley RV. Prevalence of Helicobacter pylori in patients with end-stage renal failure and renal transplant recipients. Nephron 1991;59: Ala-Kaila K, Vaajalahti P, Karvonen AL, Kokki M. Gastric Helicobacter pylori and upper gastrointestinal symptoms in chronic renal failure. Ann Med 1991;23: Gladziwa U, Haase G, Handt S, Riehl J. Prevalence of Helicobacter pylori in patients with chronic renal failure. Nephrol Dial Transplant 1993;8: Shepherd AM, Stewart WK, Wormsley KG. Peptic ulceration in chronic renal failure. Lancet 1973;1: Ala-Kaila K. Gastric secretion kinetics in chronic renal failure. Scand J Gastroenterol 1987;22: Haffner J, Linnestard P, Schrumpf E, Hanssen LE, Flaten O. The immediate effect of human renal transplantation on basal and meal-stimulated levels of gastrointestinal hormones. Scand J Gastroenterol 1987;22: Lam S-K, Ching C-K, Lai K-C, et al. Dose treatment of Helicobacter pylori with antibiotics alone heal duodenal ulcer? A randomised double blind placebo controlled study. Gut 1997;41: Wyatt JI. Heicobacter pylori, duodenitis and duodenal ulceration. In: Rathbone BJ, Heatley RV, ed. Helicobacter pylori and gastroduodenal disease. London: Blackwell scientific Co, 1992: Buck GE. Campylobacter pylori and gastroduodenal disease. Clin Microbiol Rev 1990;3: ,,. Helicobacter pylori. 1996;30: Berstad A, Alexander B, Weberg R, Serck-Hassen A, Holland S, Hirschowitz B. Antacids reduce Campylobacter pylori colonization without healing the gastritis in patients with nonulcer dyspepsia and erosive prepyloric changes. Gastroenterology 1988;95:
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