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Year : 2009  |  Volume : 20  |  Issue : 6  |  Page : 969-974
Current knowledge on helicobacter pylori infection in end stage renal disease patients

1 Baqiyatallah Research Center for Gastroenterology and Liver Diseases; Baqiyatallah University of Medical Sciences, Tehran, Iran
2 Dr. Taheri Medical Research Group, Tehran, Iran

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Date of Web Publication27-Oct-2009


Gastric infection with Helicobacter Pylori in end-stage renal disease patients is of rele­vance because of its potential impact on the quality of life as well as morbidity and mortality of patients. Existed data on the issue are controversial, and we attempt in this article to evaluate the available data to approach extended perception of the current knowledge on the epidemiology, relevance, and optimum therapeutic strategies.

How to cite this article:
Khedmat H, Taheri S. Current knowledge on helicobacter pylori infection in end stage renal disease patients. Saudi J Kidney Dis Transpl 2009;20:969-74

How to cite this URL:
Khedmat H, Taheri S. Current knowledge on helicobacter pylori infection in end stage renal disease patients. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2022 Aug 13];20:969-74. Available from: https://www.sjkdt.org/text.asp?2009/20/6/969/57234

   Introduction Top

Helicobacter Pylori (H. pylori) is a gram­negative spiral flagellate bacillus that resides usually in the gastric mucosa and can cause chro­nic active gastritis and peptic ulcer disease. [1] In addition, chronic H. pylori infection has close associations with gastric hyperplastic polyps, gastric adenoma, gastric cancer, and gastric mu­cosa associated lymphoid tissue lymphoma. [2],[3],[4],[5],[6] Recently, increasing evidence suggests that some extra-gastrointestinal disorders including chro­nic idiopathic urticaria, iron deficiency anemia and idiopathic thrombocytopenic purpura (ITP) are also related to H. pylori infection. [7],[8],[9]

Uremia triggers considerable clinical symp­toms as well as pathological changes in the gas­trointestinal (GI) system. [10],[11] Dyspepsia defined as discomfort in the upper part of the abdomen is a common complication in chronic renal di­sease (CKD) patients, especially in regular dia­lysis patients, and it affects the quality of life in these patients. [12],[13],[14] H. Pylori infection is the single most reported responsible factor for dyspepsia by the studies that investigated the causes of this complaint in end-stage renal disease (ESRD) patients. [1]

   Epidemiology Top

H. pylori infection is the most common chronic bacterial infection in humans. Estimates indicate that approximately 60% of the world population is colonized with this agent. [15] However; the epi­demiological data concerning H. pylori infection in ESRD patients are controversial. The repor­ted frequency of anti H. pylori antibody in pa­tients with renal failure ranges from 21-64%. [16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26] These conflicting results may be related to va­rious factors including the methods of detecting H. pylori infection, the size of the study popu­lation, the local prevalence of the organism in the general population, and the various features of the study population. Several studies of the epidemiological features of H. pylori infection have revealed similar findings in ESRD and non­uremic patients. [15] However, higher or lower pre­valence rates of H pylori infection in ESRD pa­tients than the general population have been reported by other investigations. [1],[27],[28],[29],[30],[31],[32],[33] There are different explanations for the variable preva­lence. In a previous study on hemodialysis (HD) and renal transplant patients in compari­son with healthy controls, we found a signifi­cantly higher prevalence of H. pylori infection in the HD patients than that in the other two groups. [1] Investigators who detected similar re­sults to ours have mostly related it to the im­paired immune system function. [15],[27],[28] Some in­vestigators focused on the higher concentration of urea in the gastric juice of renal failure pa­tients raising the local gastric pH and providing abundant substrate for H. pylori.[1],[20] On the other hand, other investigators concluded that the higher levels of urea in the mucus of stomach in ESRD patients may result in a lower prevalence of H. pylori colonization in these patients. [29] Further­more, fluctuations in the gastric blood supply, [1] low gastric motility, and hypo [15] as well as hyper­chlohydria [30] have also been proposed for the higher the prevalence of H. pylori infection in the uremic patients. [31] Schoonjans et al [28] repor­ted that positive H. pylori antibodies by serolo­gical tests may not be related to dyspepsia or gastroparesis in uremic patients.

Leffeld et al, [18] Luzza et al, [19] Fabrizi et al, [15] and Hosseini et al [32] found no difference of pre­valence of H. pylori infection between patients on HD and healthy controls. They concluded that the levels of urea in ESRD patients do not represent a risk factor for acquiring H. pylori infection in this patient population. Altay et al [33] reported a 26.6% prevalence rate of H. pylori infection among chronic ambulatory peritoneal dialysis (CAPD) patients complaining of dys­pepsia. Although they did not compare their finding with healthy individuals, one may ob­serve that peritoneal dialysis patients have lo­wer rate of H. pylori infection than the general population.

On the other hand, lower prevalence of H. pylori in HD patients has repeatedly been re­ported. [1],[18],[24],[25],[29],[34] Patients with renal dysfunction may be partially protected against H. pylori; the reasons include increased prescription of anti­biotics [24] and aluminum-containing anti-acids [35] in addition to uremia that can change bacterial colonization of the upper gastrointestinal tract with reduced H. pylori and overgrowth of other bacteria. [36] In a recent long-term prospective study by Sugimoto et al [29] on 539 Japanese HD pa­tients, the prevalence of H. pylori infection was significantly lower than the general population, but it increased with the increased duration on HD. With respect to this finding, they presented three explanations: 1) blood urea levels as well as urea nitrogen levels in gastric secretions are higher in dialysis patients than in patients with normal renal function as high urea levels inhibit H. pylori growth in the stomach; [20] 2) H. pylori might be eradicated upon antibiotic treatment because antibiotics are commonly used or their concentrations are higher in patients with renal failure; 3) Patients receiving dialysis have higher levels of proinflammatory cytokines, including interleukin-1b, -6, -8, and tumor necrosis factor from activated inflammatory cells infiltrating the gastric mucosa. [37] As a result, gastric atrophy progresses with increased pH, and finally H. pylori cannot live in the gastric mucosa. [38]

   Children with ESRD and Helicobacter Pylori Top

Gastrointestinal symptoms are quite common in children with ESRD, and under nutrition re­sulting from these symptoms contributes to their poor growth. [39] Several studies have investigated gastric H. pylori infection in adult HD patients, but scarce data exist regarding the above men­tioned issue in infancy and childhood.[40],[41],[42],[43],[44]

The role of H. pylori in the pathogenesis of gastric diseases is well known in both adults and children. [45],[46],[47],[48] However, there are several im­portant differences in pediatric H. pylori infection compared to adults; [49],[50],[51],[52],[53] evidence suggests a lower incidence of H. pylori infection in chil­dren undergoing endoscopy. [45],[48],[49],[54],[55],[56]

In a study on 37 chronic HD pediatric patients of whom 40% had gastrointestinal complaints, Emir et al detected H. pylori infection in 27%; 80% of H. pylori-positive patients were symp­tomatic, while only 14% of asymptomatic pa­tients revealed H. pylori infection in their gas­tric tissues. In addition, H. pylori were detected in 62.5% of the patients with gastroduodenal le­sions. Moreover, H. pylori positivity was asso­ciated with endoscopic abnormalities. Emir et al also reported comparable results for H. pylori infection among ESRD children with gastritis to children with normal kidney function. [49],[55],[57],[58],[59] With regard to all their findings, they recom­mended that upper gastrointestinal examination should be considered for symptomatic pediatric ESRD patients most notably in areas where H. pylori is known to be endemic.

Mortazavi et al, [60] in a study on 31 HD chil­dren, found that 17 (55%) had gastrointestinal symptoms and 20 (65%) were positive for H. pylori antibody, and children with longer dura­tion on dialysis were more likely to be negative for H. pylori infection. These investigators, as other studies, [57] recommended gastrointestinal eva­luations for all ESRD children, emphasizing the unreliability of symptoms in these patients.

   Relevance of Helicobacter Pylori Infection in ESRD Patients and Impact of Treatment Top

H. pylori have a notable relationship with CRF and HD in several ways: 1) HP contributes to the development of peptic ulcer disease, esophago­gastro-duodenal erosions, and anemia due to gastro-duodenal blood loss, which is common in HD patients. 2) HP produces gastric muco­sal inflammation and, hence, may contribute to dyspepsia, anorexia, malignancies, and malnu­trition in HD patients. [27],[61] 3) HP may have an independent role in anemia of HD patients. [62]

An increased concentration of fasting serum gastrin is observed in patients with impaired re­nal function. [63],[64] The mechanisms for the hyper­gastrinemia revealed in such patients are be­lieved to be the declined renal clearance of gas­trin and the increase in gastric G cell density. [63],[64] It has been shown that H. pylori in the stomach plays a crucial role in the elevation of serum gastrin concentration. [65],[66] However, scientific reports regarding the influence of H. pylori in­fection on the serum gastrin concentration in patients with ESRD have been limited and the results are conflicting. Luzza et al [19] and Toku­shima [67] reported that dialysis patients with H. pylori infection had significantly higher serum gastrin levels than those who were not infected, while other studies did not find such diffe­rences. [68],[69] Furthermore, Tokushima et al repor­ted in two other studies that successful eradi­cation of H. pylori using a combination therapy of amoxicillin, lansoprazole and plaunotol in patients on dialysis would induce a significant reduction in the serum gastrin concentrations. [70],[71] The serum gastrin level was normalized in over 90% of patients who became H. pylori negative after treatment. The restoration of normal gas­trin levels was associated with a marked reduc­tion in the gastric juice ammonia levels and pH. Regarding these findings, Tokushima et al sug­gested that H. pylori infection might be res­ponsible, at least in part, for the hypergastrine­mia observed frequently in patients on dialysis. The same findings were reported in a study by Gur et al. [72]

In conclusion, in the context of the current knowledge, we suggest that eradication of H. pylori in uremic patients should be considered in all patients with upper GI symptoms, and the efficacy of this approach should be further eva­luated in controlled prospective clinical trials. Moreover, although routine evaluation of asy­mptomatic adult ESRD patients for H. pylori infection does not seem warranted, it should be considered for all pediatric ESRD patients irres­pective of symptoms.

   References Top

1.Khedmat H, Ahmadzad-Asl M, Amini M, et al. Gastro-duodenal lesions and Helicobacter pylori infection in uremic patients and renal transplant recipients. Transplant Proc 2007;39(4):1003-7.  Back to cited text no. 1      
2.Uemura N, Okamoto S, Yamamoto S, et al.Helicobacter pylori infection and the develop­ment of gastric cancer. N Engl J Med 2001;345: 784-9.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]  
3.Hopkins RJ, Girardi LS, Turney EA. Relationship between Helicobacter pylori eradication and reduced duodenal and gastric ulcer recurrence: a review. Gastroenterology 1996;110:1244-52.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]  
4.Wotherspoon AC, Doglioni C, de Boni M, et al. Antibiotic treatment for low-grade gastric MALT lymphoma. Lancet 1994;343:1503.  Back to cited text no. 4  [PUBMED]    
5.Misiewicz JJ. Current insights in the pathogen­nesis of Helicobacter pylori infection. Eur J Gastroenterol Hepatol 1995;7:701-3.  Back to cited text no. 5  [PUBMED]    
6.Wyle FA. Helicobacter pylori: Current perspec­tives. J Clin Gastroenterol 1991;13(Suppl 1): 114-24.  Back to cited text no. 6      
7.Gasbarrini A, Franceschi F, Tartaglione R, et al. Regression of autoimmune thrombocytopenia after eradication of Helicobacter pylori. Lancet 1998; 352:878.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]  
8.Tebbe B, Geilen CC, Schulzke JD et al. Helico­bacter pylori infection and chronic urticaria. J Am Acad Dermatol 1996;34:685-6.  Back to cited text no. 8      
9.Annibale B, Marignani M, Monarca B, et al. Reversal of iron deficiency anemia after Helico­bacter pylori eradication in patients with asymp­tomatic gastritis. Ann Intern Med 1999;131: 668-72.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]  
10.Var C, Giiltekin F, Candan F, et al. The effects of HD on duodenal and gastric mucosal changes in uremic patients. Clin Nephrol 1996;45(5): 310-4.  Back to cited text no. 10      
11.Kang JY. The gastrointestinal tract in uremia. Dig Dis Sci 1993;38(2):257-68.  Back to cited text no. 11      
12.Pupim LB, Ikizler TA. Uremic malnutrition: new insights into an old problem. Semin Dial 2003; 16(3):224-32.  Back to cited text no. 12      
13.Locatelli F, Fouque D, Heimburger O, et al. Nut­ritional status in dialysis patients: a European consensus. Nephrol Dial Transplant 2002;17(4): 563-72.  Back to cited text no. 13      
14.Fein PA, Mittman N, Gadh R, et al. Malnutri­tion and inflammation in peritoneal dialysis patients. Kidney Int Suppl 2003;87:S87-91.  Back to cited text no. 14  [PUBMED]    
15.Fabrizi F, Martin P. Helicobacter pylori infection in patients with end-stage renal disease. Int J Artif Organs 2000;23:157-64.  Back to cited text no. 15  [PUBMED]    
16.Kang JY, Wu AY, Sutherland IH, Vathsala A. Prevalence of peptic ulcer in patients under­going maintenance HD. Dig Dis Sci 1988;33(7): 774-8.  Back to cited text no. 16      
17.Conz P, Chiaramonte S, Ronco C, Feriani M, La Greca G. Campylobacter pylori in uremic dialyzed patients. Nephron 1989;53(1):90.  Back to cited text no. 17      
18.Loffeld RJ, Peltenburg HG, vd Oever H, Stobberingh E. Prevalence of Helicobacter pylori antibodies in patients on chronic inter­mittent haemodialysis. Nephron 1991;59(2):250-3.   Back to cited text no. 18      
19.Luzza F, Imeneo M, Maletta M, et al. Helico­bacter pylori-specific IgG in chronic haemodia­lysis patients: Relationship of hypergastrinaemia to positive serology. Nephrol Dial Transplant 1996;11(1):120-4.  Back to cited text no. 19      
20.Gladziwa U, Haase G, Handt S, et al. Prevalence of Helicobacter pylori in patients with chronic renal failure. Nephrol Dial Transplant 1993;8 (4):301-6.  Back to cited text no. 20      
21.Ozgur O, Boyacioglu S, Ozdogan M, Giir G, Telatar H, Haberal M. Helicobacter pylori infec­tion in haemodialysis patients and renal trans­plant recipients. Nephrol Dial Transplant 1997; 12(2):289-91.  Back to cited text no. 21      
22.Davenport 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(4):597-601.  Back to cited text no. 22      
23.Offerhaus GJ, Kreuning J, Valentijn RM, et al. Campylobacter pylori: prevalence and signifi­cance in patients with chronic renal failure. Clin Nephrol 1989;32(5):239-41.  Back to cited text no. 23      
24.Shousha S, Arnaout AH, Abbas SH, Parkins RA. Antral Helicobacter pylori in patients with chro­nic renal failure. J Clin Pathol 1990;43(5):397­-9.  Back to cited text no. 24      
25.Jaspersen D, Fassbinder W, Heinkele P, et al. Significantly lower prevalence of Helicobacter pylori in uremic patients than in patients with normal renal function. J Gastroenterol 1995;30 (5):585-8.  Back to cited text no. 25      
26.Antoniou S, Dimitriadis A, Kliridou M, Pavlitou K, Batzili H, Malaka E. Prevalence of Helico­bacter pylori antibodies in CAPD patients. Nephron 1997;75(3):358-9.  Back to cited text no. 26      
27.Schoonjans R, Van VB, Vandamme W, et al. Dyspepsia and gastro paresis in chronic renal failure: the role of Helicobacter pylori. Clin Nephrol 2002;57(3):201-7.  Back to cited text no. 27      
28.Aydemir S, Boyacioglu S, Gur G, et al. Helico­bacter pylori infection in HD patients: suscep­tibility to amoxicillin and clarithromycin. World J Gastroenterol 2005;11(6):842-5.  Back to cited text no. 28      
29.Sugimoto M, Sakai K, Kita M, Imanishi J, Yamaoka Y. Prevalence of Helicobacter pylori infection in long-term HD patients. Kidney Int2009;75(1):96-103.  Back to cited text no. 29      
30.Paronen I, Ala-Kaila K, Rantala I, Kainulainen H, Karvonen AL. Gastric parietal, chief, and G­cell densities in chronic renal failure. Scand J Gastroenterol 1991;26(7):696-700.  Back to cited text no. 30      
31.McNamee PT, Moore GW, McGeown MG, Doherty CC, Collins BJ. Gastric emptying in chronic renal failure. Br Med J (Clin Res Ed) 1985;291(6491):310-1.  Back to cited text no. 31      
32.Asl MK, Nasri H. Prevalence of Helicobacter pylori infection in maintenance HD patients with non-ulcer dyspepsia. Saudi J Kidney Dis Transpl 2009;20(2):223-6.  Back to cited text no. 32      
33.Altay M, Turgut F, Akay H, et al. Dyspepsia in Turkish patients on continuous ambulatory peri­toneal dialysis. Int Urol Nephrol 2008;40(1): 211-7.  Back to cited text no. 33      
34.Korzonek M, Szymaniak L, Giedrys-Kalemba S, Ciechanowski K. Is it necessary to treat Helicobacter pylori infection in patients with end-stage renal failure and in renal transplant recipients? Pol Arch Med Wewn 2004;111(3): 297-304.  Back to cited text no. 34      
35.Berstad A, Alexander B, Weberg R, Serck­Hanssen A, Holland S, Hirschowitz BI. Antacids reduce Campylobacter pylori colonization with­out healing the gastritis in patients with non­ulcer dyspepsia and erosive prepyloric changes. Gastroenterology 1988;95(3):619-24.  Back to cited text no. 35      
36.Simenhoff ML, Saukkonen JJ, Burke JF, Wesson LG Jr, Schaedler RW, Gordon SJ. Bacterial populations of the small intestine in uremia. Nephron 1978;22(1-3):63-8.  Back to cited text no. 36      
37.Hwang IR, Kodama T, Kikuchi S, et al. Effect of interleukin 1 polymorphisms on gastric mucosal interleukin 1beta production in Helicobacter pylori infection. Gastroenterology 2002;123:1793­-803.  Back to cited text no. 37  [PUBMED]  [FULLTEXT]  
38.Wesdorp RI, Falcao HA, Banks PB, Martino J, Fischer JE. Gastrin and gastric acid secretion in renal failure. Am J Surg 1981;141:334-8.  Back to cited text no. 38  [PUBMED]  [FULLTEXT]  
39.Simmons JM, Wilson CJ, Potter DE, Holliday MA. Relationship of calorie deficiency to growth failure in children on haemodialysis and the growth response to calorie supplementation. N Engl J Med 1971;285:653-6.  Back to cited text no. 39  [PUBMED]    
40.Chisholm GD, Mee AD, Williams G, Castro JE, Baron JH. Peptic ulceration, gastric secretion and renal transplantation. BMJ 1977;1:1630-3.  Back to cited text no. 40  [PUBMED]  [FULLTEXT]  
41.Margolis D, Saylor JL, Geisse G, DeSchryver­Kecskemeti K, Harter HR, Zuckerman GR. Upper gastrointestinal disease in chronic renal failure. A prospective evaluation. Arch Intern Med 1978;138:1214-7.  Back to cited text no. 41      
42.Musola R, Franzin G, Mora R, Manrfrini C. Prevalence of gastroduodenal lesions in uremic patients undergoing dialysis and after renal trans­plantation. Gastrointest Endosc 1984;30:343-6.  Back to cited text no. 42      
43.Andriulli A, Malfi B, Recchia S, Ponti V, Triolo G, Segoloni G. Patients with renal failure are not at risk of developing chronic peptic ulcers. Clin Nephrol 1985;23:245-8.  Back to cited text no. 43  [PUBMED]    
44.Wee A, Kang JY, Ho MS, Choong HL, Wu AY, Sutherland IH. Gastroduodenal mucosa in uremia: endoscopic and histological correlation and prevalence of Helicobacter-like organisms. Gut 1990;31:1093-6.  Back to cited text no. 44  [PUBMED]  [FULLTEXT]  
45.Kilbridge DM, Dahms BB, Czinn SJ. Campy­lobacter pylori-associated gastritis and peptic ulcer disease in children. Am J Dis Child 1988; 142:1149-52.  Back to cited text no. 45      
46.Peterson WL. Helicobacter pylori and peptic ulcer disease. N Engl J Med 1991;324:1043-8.  Back to cited text no. 46  [PUBMED]    
47.Valle J, Seppale K, Sipponen P, Kosunen T. Disappearance of gastritis after eradication of Helicobacter pylori. A morphometric study. Scand J Gastroenterol 1991;26:1057-65.  Back to cited text no. 47      
48.Drumm B. Helicobacter pylori in the pediatric patient. Gastroenterol Clin North Am 1993;22: 16982.  Back to cited text no. 48      
49.Prieto G, Polanco L, Larrauri J, Rota L, Lama R, Carrasco S. Helicobacter pylori infection in children: clinical, endoscopic and histologic correlations. J Pediatr Gastroenterol Nutr 1992; 14:420-5.  Back to cited text no. 49      
50.Mitchell HM, Bohane TD, Tobias V, et al. Heli­cobacter pylori infection in children: potential clues to pathogenesis. J Pediatr Gastroenterol Nutr 1993;161:120-5.  Back to cited text no. 50      
51.Hill R, Pearman J, Worthy P, Caruso V, Goodwin S, Blincow E. Campylobacter pyloridis and gastritis in children. Lancet 1986;1:387.  Back to cited text no. 51      
52.Drumm B. Helicobacter pylori in the pediatric patient. Gastroenterol Clin North Am 1993;22: 169-82.  Back to cited text no. 52  [PUBMED]    
53.Bujanover Y, Konikoff F, Baratz M. Nodular gastritis and Helicobacter pylori. J Pediatr Gastroenterol Nutr 1990;11:41-4.  Back to cited text no. 53  [PUBMED]    
54.Cadranel S, Goossens H, De Boeck M, Malengreau A, Rodesch P, Butzler JP. Campy­lobacter pyloridis in children. Lancet 1986;1: 735-6.  Back to cited text no. 54  [PUBMED]  [FULLTEXT]  
55.Thomas JE, Whatmore AM, Barer MR, Eastham EJ, Kehoe MA. Serodiagnosis of Helicobacter pylori infection in children. J Clin Microbiol 1990;28:2641-6.  Back to cited text no. 55  [PUBMED]  [FULLTEXT]  
56.Glassman MS, Dallal S, Berezin SH, et al. Helicobacter pylori-related gastroduodenal disease in children: diagnostic utility of enzyme linked immunoabsorbent assay. Dig Dis Sci 1990;35: 993-7.  Back to cited text no. 56  [PUBMED]    
57.Emir S, Bereket G, Boyacioglu S, Varan B, Tunali H, Haberal M. Gastroduodenal lesions and Helicobacter pylori in children with end­stage renal disease. Pediatr Nephrol 2000;14(8­9):837-40.  Back to cited text no. 57      
58.Hardikar W, Davidson PM, Cameron DJ, Gilbert GL, Campbell PE, Smith AL. Helicobacter pylori infection in children. J Gastroenterol Hepatol 1991;6:450-4.  Back to cited text no. 58  [PUBMED]    
59.Morris A, Nicholson G. Ingestion of Campylo­bacter pyloridis causes gastritis and raised fasting gastric pH. Am J Gastroenterol 1987;82: 192-9.  Back to cited text no. 59  [PUBMED]    
60.Mortazavi F, Rafeey M. Endoscopic findings and Helicobacter pylori in children on long-term HD. Pak J Biol Sci 2008;11(14):1840-3.  Back to cited text no. 60      
61.Aguilera A, Codoceo R, Bajo MA, et al. Helico­bacter pylori infection: a new cause of anorexia in peritoneal dialysis patients. Perit Dial Int 2001;21 Suppl 3:S152-6.  Back to cited text no. 61  [PUBMED]  [FULLTEXT]  
62.Fabbian F, Catalano C, Bordin V, Balbi T, Di Landro D. Esophagogastroduodenoscopy in chronic HD patients: 2-year clinical experience in a renal unit. Clin Nephrol 2002;58(1):54-9.  Back to cited text no. 62      
63.Muto S, Murayama N, Asano Y, Hosoda S, Miyata M. Hypergastrinemia and achlorhydria in chronic renal failure. Nephron 1985;40(2): 143-8.  Back to cited text no. 63      
64.Ala-Kaila K, Kekki M, Paronen I, Paakkala T. Serum gastrin in chronic renal failure: its rela­tion to acid secretion, G-cell density, and upper gastrointestinal findings. Scand J Gastroenterol 1989;24(8):939-48.  Back to cited text no. 64      
65.Levi S, Beardshall K, Haddad G, Playford R, Ghosh P, Calam J. Campylobacter pylori and duodenal ulcers; the gastrin link. Lancet 1989;1 (8648):1167-8.  Back to cited text no. 65      
66.Smith JT, Pounder RE, Nwokolo CU, et al. Inappropriate hypergastrinaemia in asympto­matic healthy subjects infected with Helico­bacter pylori. Gut 1990;31(5):522-5.  Back to cited text no. 66      
67.Tokushima H. Role of Helicobacter pylori in gastro-duodenal mucosal lesions in patients with end-stage renal disease under dialysis treat­ment. Nippon Jinzo Gakkai Shi 1995;37(9):503-­10 (abstract).  Back to cited text no. 67      
68.Ala-Kaila K, Vaajalahti P, Karvonen AL, Kokki M. Gastric Helicobacter and upper gastrointes­tinal symptoms in chronic renal failure. Ann Med 1991;23(4):403-6.  Back to cited text no. 68      
69.el Nujumi AM, Rowe PA, Dahill S, Dorrian CA, Neithercut WD, McColl KE. Role of ammonia in the pathogenesis of the gastritis, hypergastrinaemia, and hyperpepsinogenaemia I caused by Helicobacter pylori infection. Gut 1992;33(12):1612-6.  Back to cited text no. 69      
70.Tokushima H. Role of Helicobacterpylori in gastro-duodenal mucosal lesions in patients with end stage renal disease under dialysis treat­ments. Nippon Jinzo Gakkai Shi 1995;37:503.  Back to cited text no. 70  [PUBMED]    
71.Tokushima H, Tamura H, Murakawa M, et al. Eradication of Helicobacter pylori restores elevation of serum gastrin concentrations in patients with end-stage renal disease. Intern Med 1998;37(5):435-9.  Back to cited text no. 71      
72.Gur G, Boyacioglu S, Giil C, et al. Impact of Helicobacter pylori infection on serum gastrin in haemodialysis patients. Nephrol Dial Transplant 1999;14(11):2688-91.  Back to cited text no. 72      

Correspondence Address:
Hossein Khedmat
Baqiyatallah Research Center for Gastroenterology and Liver Disease, Baqiyatallah Hospital, Mullasadra St. P.O. Box 14155-6437, Tehran
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