| |
|
|
| Year : 2009 | Volume
: 20
| Issue : 6 | Page : 969-974 |
|
| Current knowledge on helicobacter pylori infection in end stage renal disease patients |
|
|
Hossein Khedmat1, Saeed Taheri2
1 Baqiyatallah Research Center for Gastroenterology and Liver Diseases; Baqiyatallah University of Medical Sciences, Tehran, Iran
2 Dr. Taheri Medical Research Group, Tehran, Iran
Click here for correspondence address and email
| Date of Web Publication | 27-Oct-2009 |
|
|
 |
|
 Abstract | | |
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 2018 Jun 22];20:969-74. Available from: http://www.sjkdt.org/text.asp?2009/20/6/969/57234 |
| Introduction | |  |
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 | | |
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 | | |
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 | | |
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 | | |
| 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.  |
| 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. [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. [PUBMED] [FULLTEXT] |
| 4. | Wotherspoon AC, Doglioni C, de Boni M, et al. Antibiotic treatment for low-grade gastric MALT lymphoma. Lancet 1994;343:1503. [PUBMED] |
| 5. | Misiewicz JJ. Current insights in the pathogennesis of Helicobacter pylori infection. Eur J Gastroenterol Hepatol 1995;7:701-3. [PUBMED] |
| 6. | Wyle FA. Helicobacter pylori: Current perspectives. J Clin Gastroenterol 1991;13(Suppl 1): 114-24. |
| 7. | Gasbarrini A, Franceschi F, Tartaglione R, et al. Regression of autoimmune thrombocytopenia after eradication of Helicobacter pylori. Lancet 1998; 352:878. [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. |
| 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. [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. |
| 11. | Kang JY. The gastrointestinal tract in uremia. Dig Dis Sci 1993;38(2):257-68. |
| 12. | Pupim LB, Ikizler TA. Uremic malnutrition: new insights into an old problem. Semin Dial 2003; 16(3):224-32. |
| 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. |
| 14. | Fein PA, Mittman N, Gadh R, et al. Malnutrition and inflammation in peritoneal dialysis patients. Kidney Int Suppl 2003;87:S87-91. [PUBMED] |
| 15. | Fabrizi F, Martin P. Helicobacter pylori infection in patients with end-stage renal disease. Int J Artif Organs 2000;23:157-64. [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. |
| 17. | Conz P, Chiaramonte S, Ronco C, Feriani M, La Greca G. Campylobacter pylori in uremic dialyzed patients. Nephron 1989;53(1):90. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. |
| 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. [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. [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. [PUBMED] |
| 40. | Chisholm GD, Mee AD, Williams G, Castro JE, Baron JH. Peptic ulceration, gastric secretion and renal transplantation. BMJ 1977;1:1630-3. [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. |
| 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. |
| 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. [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. [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. |
| 46. | Peterson WL. Helicobacter pylori and peptic ulcer disease. N Engl J Med 1991;324:1043-8. [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. |
| 48. | Drumm B. Helicobacter pylori in the pediatric patient. Gastroenterol Clin North Am 1993;22: 16982. |
| 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. |
| 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. |
| 51. | Hill R, Pearman J, Worthy P, Caruso V, Goodwin S, Blincow E. Campylobacter pyloridis and gastritis in children. Lancet 1986;1:387. |
| 52. | Drumm B. Helicobacter pylori in the pediatric patient. Gastroenterol Clin North Am 1993;22: 169-82. [PUBMED] |
| 53. | Bujanover Y, Konikoff F, Baratz M. Nodular gastritis and Helicobacter pylori. J Pediatr Gastroenterol Nutr 1990;11:41-4. [PUBMED] |
| 54. | Cadranel S, Goossens H, De Boeck M, Malengreau A, Rodesch P, Butzler JP. Campylobacter pyloridis in children. Lancet 1986;1: 735-6. [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. [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. [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. |
| 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. [PUBMED] |
| 59. | Morris A, Nicholson G. Ingestion of Campylobacter pyloridis causes gastritis and raised fasting gastric pH. Am J Gastroenterol 1987;82: 192-9. [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. |
| 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. [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. |
| 63. | Muto S, Murayama N, Asano Y, Hosoda S, Miyata M. Hypergastrinemia and achlorhydria in chronic renal failure. Nephron 1985;40(2): 143-8. |
| 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. |
| 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. |
| 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. |
| 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). |
| 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. |
| 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. |
| 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. [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. |
| 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. |
Correspondence Address:
Hossein Khedmat
Baqiyatallah Research Center for Gastroenterology and Liver Disease, Baqiyatallah Hospital, Mullasadra St. P.O. Box 14155-6437, Tehran
Iran
  | Check |
PMID: 19861855 
|
|
| This article has been cited by | | 1 |
Upper gastrointestinal diseases correlated to helicobacter pylori infection: Comparison between uremic and non-uremic patients. Review of the literature |
|
| De Luca, S. and Tomasello, G. and Damiano, G. and Palumbo, V.D. and Damiani, P. and Monte, A.I.L. | | Acta Medica Mediterranea. 2012; 28(3): 267-269 | | [Pubmed] | | | 2 |
Correlation between creatinine clearance and Helicobacter pylori infection eradication with sequential and triple therapeutic regimens: A randomised clinical trial |
|
| Seyyedmajidi, M. and Falaknazi, K. and Mirsattari, D. and Zojaji, H. and Roshani, M. and Lahmi, F. and Orimi, P.G. and Hadizadeh, M. and Zali, M. | | Arab Journal of Gastroenterology. 2011; 12(3): 150-153 | | [Pubmed] | | | 3 |
Epidemiology of gastroduodenal erosions in the general population: Endoscopic results of the systematic investigation of gastrointestinal diseases in China (SILC) |
|
| Ma, X. and Zhao, Y. and Wang, R. and Yan, X. and Li, Z. and Zou, D. and He, J. | | Scandinavian Journal of Gastroenterology. 2010; 45(12): 1416-1423 | | [Pubmed] | |
|
|
|
|
|
|
|
|
|
|
|
|
| Article Access Statistics | | | Viewed | 4133 | | | Printed | 145 | | | Emailed | 0 | | | PDF Downloaded | 1688 | | | Comments | [Add] | | | Cited by others | 3 | | |
|
|
