Saudi Journal of Gastroenterology
Home About us Instructions Submission Subscribe Advertise Contact Login    Print this page  Email this page Small font sizeDefault font sizeIncrease font size 
Users Online: 223 

ARTICLES Table of Contents   
Year : 2004  |  Volume : 10  |  Issue : 2  |  Page : 78-85
Does helicobacter pylori infection in chronic renal failure increase the risk of gastroduodenal lesions? A prospective study

1 Department of Medicine, King Fahad Hospital of the University, P 0 Box 40032, Al Khobar, 31952, Saudi Arabia
2 Department of Radiology, King Fahad Hospital of the University, P 0 Box 40032, Al Khobar, 31952, Saudi Arabia

Click here for correspondence address and email

Date of Submission06-Sep-2003
Date of Acceptance22-Oct-2003


Background: Helicobacter pylori (H.pylori) plays an important role in gastroduodenal disease. However, there are few data concerning the epidemiology of H.pylori in patients with chronic renal failure and on hemodialysis (HD) treatment. Aim of the study: This study is aimed to determine the epidemiology of H.pylori infection in patients with end stage renal disease (ESRD) on Hemodialysis (HD). Patients and Methods: Ninety­six patients with dyspeptic complaints were included in the study. They were divided into two groups; group one consisted of 46 patients with ESRD on HD and group two (control) of 50 patients without renal disease. All patients were subjected to upper gastrointestinal endoscopies, and gastric biopsies were obtained for histological evidence of H. pylori infection. Results: The mean age of both groups was similar. The prevalence of H.pylori among the two groups was not significantly different (45.7%Vs48%=p>0.05). The prevalence of duodenal ulcers was significantly higher in H.pylori positive than in H.pylori negative ESRD patients (p<0.05). GERD was significantly lower in H.pylori positive patients in both groups (p<0.001 and p<0.01 respectively). Conclusion: This study showed a similar prevalence of H.pylori infection in both groups. H.pylori infection in patients with ESRD is probably associated with increased risk of gastroduodenal lesions

Keywords: Helicobacter pylori, gastroduodenal lesions, chronic renal failure, hemodialysis.

How to cite this article:
Abdulrahman IS, Al-Mueilo SH, Ismail MH, Yasawy MI, Al-Qahtani FN, Al-Qorain AA. Does helicobacter pylori infection in chronic renal failure increase the risk of gastroduodenal lesions? A prospective study. Saudi J Gastroenterol 2004;10:78-85

How to cite this URL:
Abdulrahman IS, Al-Mueilo SH, Ismail MH, Yasawy MI, Al-Qahtani FN, Al-Qorain AA. Does helicobacter pylori infection in chronic renal failure increase the risk of gastroduodenal lesions? A prospective study. Saudi J Gastroenterol [serial online] 2004 [cited 2022 Dec 2];10:78-85. Available from:

Helicobacter pylori Scientific Name Search ri) has been identified as a major factor in the pathogenesis of peptic ulcer disease and gastritis in general population[1],[2] . Various reports have been published from the Kingdom of Saudi Arabia regarding H.pylori prevalence and its relation to upper gastrointestinal pathology [3],[4] . H.pylori is known to alter acid secretory physiology in chronically infected patients, in particular basal and postprandial elevation of serum gastrin concentration [5],[6],[7],[8],[9]. Hypergastrinemia and subsequent acid hypersecretion are thought to be key factors in the pathophysiology of peptic ulcer disease and gastroduodenal lesions in these patients, and more obvious in patients with ESRD[10]. Dyspeptic symptoms are quite common in chronic hemodialysis patients, a considerable number of whom are infected with H.pylori[6],[8]. Thus, detection and treatment of gastroduodenal lesions are very important in this group, especially in terms of preventing complications after renal transplantation [11],[12] Various studies were performed to investigate whether uremia or urea concentration in gastric secretion creates a favorable environment for H. pylori infection [12],[13] Some reports have indicated that there is no relationship between uremia and H.pylori infection rate [14],[15] whereas others have reported an H.pylori infection frequency of 34-47% in uremia [16],[17] and 38% [18] in renal transplant patients. The few published studies addressed small number of patients, which were insufficient to get a strong conclusion. This prospective study is aimed to determine the following: (1) the prevalence of H.pylori infection among patients with ESRD on HD, and compare it with the control, (2) whether H.pylori infection in patients with ESRD on HD, is associated with increased risk of gastroduodenal lesions.

   Patients and methods Top

This study was conducted in the period between January first, and December thirty­first, 2002, in King Fahad Hospital of the University, Al-Khobar, Saudi Arabia, and was carried out according to Helsinki Declaration. After obtaining the written informed consent, the ninety-six patients with dyspeptic symptoms were included in this prospective study. They were divided into two groups: group one consisted of 46 patients on HD; 22 (47.8%) males and 24 (52.2%) females. Group two (control) consisted of 50 non-renal disease patients; 23 (46%) males and 27 (54%) females. Forty-one patients (89.1%) in group one and 46 (92%) in group two were Saudis. The mean age in group 1 was 48.6+16.3 years and in group 2 was 46.9 + 19. Patients who had received a proton pump inhibitors or antibiotics within the last three months were excluded from the study. Information about duration and frequency of hemodialysis sessions and predialysis renal functions were obtained from the patient's charts. All patients were subjected to upper gastrointestinal endoscopy with Olympus GIF Q 230 videofiberscope; gastric biopsies were obtained and examined histologically for evidence of H. pylori. Gastric biopsy specimens were obtained from ulcer edge, erosions sites, body, and antrum. The formalin-fixed, paraffin-embedded tissue sections were stained with hematoxylin and eosin, as well as modified Giemsa stain to detect H-pylori. All biopsy specimens were interpreted by one histopathologist. Patients were considered to be infected with H pylori if the histological examination was positive. Anti-H.pylori IgG antibodies were detected by Enzyme-Linked Immunosorbent Assays (ELISA) (PathoDx Pylori TRAK (DPC Diagnostic Product Corp. Los Angeles, CA). The statistical analysis was performed using SPSS for Windows version 5.0 (SPSS Inc. Chicago, IL). Numerical values were given as mean 4­SD, and t-test was used when appropriate. For nominal data, chi-square test was utilized. Fisher exact test was applied, and p values less than 0.05 were accepted as significant.

   Results Top

The mean age of the two groups and male/female ratio showed no statistical differences (p>0.05) [Table - 1]. All patients on chronic HD showed endoscopic gastroduodenal lesions. Twenty-one (45.7%) of the 46 patients on HD and 24 (48.0%) of the 50 non-renal disease patients with dyspepsia were positive for H.pylori infection. The difference of H.pylori prevalence among the two groups was statistically insignificant (p>0.05). The mean predialysis level of serum blood urea nitrogen in H.pylori positive HD patients was 67.3+19.5 mg/dl compared with 70.1+18.9 mg/dl in H.pylori negative HD patients (p>0.05). The most frequent endoscopic findings in the HD group were antral gastritis (38.1%), duodenal ulcer (28.6%), erosive gastritis (23.8%), and gastro-esophageal reflux disease (GERD) (9.5%) respectively. In the non-renal patients, antral gastritis was still the leading pathology (37.4%), followed by duodenal ulcer (29.2%), GERD (16.7%), and erosive gastritis (16.7%) [Table - 2]. Sixteen (76.2%) of the H.pylori positive patients in group one had haemodialysis for less than 36 months (28.6% had dialysis for 12 months or less, 23.8% from 13-less than 24 months & 23.8% from 24- less than 36 months) (p<0.01) [Figure - 1].

The prevalence of duodenal ulcer was significantly higher (28.6% vs 12.0%) in HD patients who are positive for H.pylori infection (p<0.05), while GERD was lower in the symptomatic ESRD patients than in the symptomatic controls (41.5% vs 59%). the difference, however was statistically insignificant (p>0.05).

   Discussion Top

Helicobacter pylori is a gram-negative bacterium and closely associated with type B gastritis, peptic ulcer disease, and linked to mucosa-associated lymphoid tissue lymphoma (MALT), and gastric adenocarcinoma [1],[19],[20] . Various studies have reported a prevalence of H.pylori infection in patients with ESRD on HD of 34% to 75%, similar to that in the general population [21] this suggests that greater urea levels in the gastric juice and blood of patients with ESRD is not a risk factor for H.pylori infection [16],[22]. Most hemodialysis patients suffer from upper gastrointestinal symptoms [8],[23] . Similar results were found in our study, and almost all patients with ESRD undergoing HD experienced gastrointestinal discomfort. These dyspeptic symptoms were even greater in our patients with ESRD without H.pylori infection compared with those infected (54.3% vs 45.7%). There may be factors other than H.pylori infection that cause dyspepsia in this population. Among the possible factors are chronic use of steroids, nonsteroidal anti-inflammatory drugs, iron therapy and high level of urea, in addition to the elevated serum level of gastrin which results in an increased gastric acid secretion [24],[25] . Peptic ulcer prevalence in HD patients is also comparable with that in the general population. However, the frequency of peptic ulcer remained clearly higher among our patients with ESRD infected with H.pylori than our noninfected patients (28.6% versus 12.0 %) p<0.05. This greater incidence indicates that H.pylori infection remains an important cause of peptic ulcer disease in both patients with ESRD and controls [Table - 2]. There are few reports on the prevalence of H.pylori in the HD patients indicating an increase of H.pylori prevalence among patients undergoing hemodialysis treatment [26],[27] . The low gastric motility and hypochlorhydria in uremic patients could be synergistic risk factors for gastric colonization with H.pylori. However our results did not confirm these theoretical assumptions. Yildiz et al reported that the mean duration of dialysis was 26.6 months and 44.1 months in H.pylori positive and H.pylori negative patients, respectively, suggesting that the proportion of H.pylori- positive patients was significantly lower in patients receiving dialysis for a prolonged period (p=0.038) [12] . Other investigators found a lower prevalence of H.pylori among dialysis patients than in individuals with normal renal functions and concluded that patients with renal dysfunction appear to be partially protected against H.pylori [9],[28] . Possible postulated protective mechanisms might include antibiotic use [9] or aluminium-containing antacids prescribed for HD patients during the course of their illness [29] . Also, uremia could change bacterial colonization of the upper gastrointestinal tract and thus reducing H.pylori infection [30] In our study the H.pylori prevalence was rather high, but similar to non-renal disease patients (45.7 vs 48.0%, p>0.05). Age is a factor closely involved in the proportion of H.pylori­ positive patients [31] and since our study mainly included elderly patients; no relation between age and the incidence of H.pylori infection was found. We did not find a difference in the mean blood urea nitrogen levels between H.pylori positive and negative patients on HD. This indicates that high levels of urea are not a risk factor for acquiring H.pylori in our population, as previously mentioned by other investigators [32] . The simplest tests for the diagnosis of H.pylori infection are serologic, involving the assessment of specific IgG levels in serum. The best of these tests are as accurate as other diagnostic methods, but many commercial tests, especially rapid office tests perform poorly. [33] It is well known that the level of antibodies specific for H.pylori decreases progressively after eradication of the bacteria. This decrease may take months or years and is probably parallel to the decreasing inflammation in the gastric mucosa, which also heals very slowly. For this reason serology cannot provide a "yes" or "no" answer regarding the presence of H.pylori after eradication [34] , in contrast to 13C-Urea breath test and perhaps the antigen stool test [35] . In a previous study [36],[37] the test yielded 81 % sensitivity and 89% specificity, which leaves more than 20% of false positivity. H.pylori serologic testing is cheap and widely used for the diagnosis of H.pylori infection in patients before treatment. Although approved laboratory-based tests have sensitivity and specificity similar to those of urea breath test, inconsistent results have been reported with some office based tests. Because H pylori strains differ among geographic locations, local validation is necessary. Serologic testing is however useful in confirming H.pylori eradication after therapy. A 25% or more decline in titer 6 months after therapy is a sensitive marker for eradication of infection [38]. It is however not reliable in young children [39] GERD is the most common esophageal disease seen in primary care settings [40]. Although findings have been inconsistent regarding the relationship between gastric acid secretion and uremia, most authors are of the opinion that chronic renal failure is associated with hypochlorhydria [41],[42] . The prevalence of GERD therefore is expected to be lower in symptomatic ESRD patients than in symptomatic controls. The role of H.pylori in GERD is highly controversial [43]. It is known that the distribution of H.pylori affects acid secretion in the stomach, and that corpus gastritis causes hypochlorhydria [44] . El­ Serag et al reported that corpus gastritis is protective against reflux oesophagitis [45] Cekin et al reported the same conclusion [46] . Thus we may argue that H.pylori infection protects against the development of GERD not only in ESRD but also in the controls. However, wide scale control trials are definitely needed to consolidate this conclusion.

The authors think that sample size is small; this is due to the limited number of patients on regular hemodialysis in one center. However the facts that there are only few reports dealing with H.pylori infection in hemodialysis patients, and that in most of them the sample size was also small (45-51 patients) may add to the validity of this study [46],[47],[48]. Nevertheless we believe that multicenter trials which include more patients will definitely make it more valuable.

   Conclusion Top

This prospective study has shown that the prevalence of H.pylori infection in ESRD and control is similar. There is some evidence that infection with H.pylori in ESRD patients might increase the risk of gastroduodenal lesions. Long term hemodialysis might decrease the prevalence of H.pylori infection. GERD is significantly lower in H.pylori positive patients of both groups. The value of the serological test for the diagnosis of H.pylori infection should be interpreted cautiously in ESRD patients on hemodialysis. Further extensive as well as multicenter trials are needed to address the various aspects of these results before a final conclusion is reached.

   References Top

1.NIH Consensus Conference. Helicobacter pylori in peptic ulcer disease. NIH Consensus Development Panel on Helicobacter pylori in peptic ulcer disease. JAMA 1994; 272: 65-9.  Back to cited text no. 1    
2.Dooley CP, Cohen H. The clinical significance of Campylobacter pylori. Ann Intern Med 1988;108:70-4.  Back to cited text no. 2  [PUBMED]  
3.Al-Qurain A, Satti MB, Al-Hamdan A, et al. Pattern of upper gastrointestinal disease in the Eastern Province of Saudi Arabia: Endoscopic evaluation of 2982 patients. Trop Geog Med 1991; 43: 203-8.  Back to cited text no. 3    
4.Mohammad AE, Al-Karawi MA, Al-Juma AA, et al. Helicobacter pylori: prevalence in 352 consecutive patients with dyspepsia. Ann Saudi Med 1994; 14: 134-5.  Back to cited text no. 4    
5.Brady CE 3rd, Hadfield TL, Hyatt JR, et al. Acid secretion and serum gastrin levels in individuals with Campylobacter pylori. Gastroenterol 1988; 94: 923-7.  Back to cited text no. 5    
6.Kang JY, Ho KY, Yeoh KG, et al. Peptic ulcer and gastritis in uremia, with particular reference to the effect of Helicobacter pylori infection. J Gastroenterol Hepatol 1999; 14: 771-8.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Luzza F, Imeno M, Maletta M, et al. Helicobacter pylori-specific IgG in chronic hemodialysis patients: relationship of hypergastrinemia to positive serology. Nephrol Dial Transplant 1996; 11: 120-4.  Back to cited text no. 7    
8.Offerhaus GJA, Kreuning J, Valentijn RM, et al. Campylobacter pylori: prevalence and significance in patients with chronic renal failure. Clin Nephrol 1989; 32: 239-41.  Back to cited text no. 8    
9.Shousha S, Arnaout AH, Abbas SH, et al. Antral Helicobacter pylori in patients with chronic renal failure. J Clin Path 1990; 43: 397­9.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Smith JT, Pounder RE, Nwokolo CU, et al. Inappropriate hypergastrinemia in asymptomatic healthy subjects infected with Helicobacter pylori. Gut 1990; 31: 522-5.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.El-Omar E, Penman I, Dorrian CA, et al. Eradicating Helicobacter pylori infection lowers gastrin mediated acid secretion by two thirds in patients with duodenal ulcer. Gut 1993; 34: 1060-5.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]
12.Yildiz A, Besisik F, Akkaya V, et al. Helicobacter pylori antibodies in hemodialysis patients and renal transplant recipients. Clin Transplantation 1999; 13: 13-6.  Back to cited text no. 12    
13.Kim H, Park C, Jong WI, et al. The gastric juice urea and ammonia levels in patients with Campylobacter pylori. Am J Clin Pathol 1990; 94: 187-90.  Back to cited text no. 13    
14.Conz P, Feriari M, Milan M, et al. Campylobacter pylori infection in uremic dialyzed patients. Nephron 1990; 55: 442.  Back to cited text no. 14    
15.Watson RG, Bhatt BM, McCaugley C, et al. Helicobacter pylori and chronic renal failure. Eur J Gastroenterol Hepatol 1991; 3: 325-9.  Back to cited text no. 15    
16.Gladziva U, Haase G, Hanolt S, et al. Prevalence of Helicobacter pylori in patients with chronic renal failure. Nephrol Dial Transplant 1993; 8: 301-6.  Back to cited text no. 16    
17.Davenport A, Shallcross TM, Crabtree JE, et al. Prevalence of Helicobacter pylori in patients with end stage renal disease and renal transplant recipients. Nephron 1991; 59: 587-91.  Back to cited text no. 17    
18.Teenan RP, Burgayne M, Brown IL, et al. Helicobacter pylori in renal transplant recipients. Transplantation 1993; 56: 100-4.  Back to cited text no. 18    
19.Atherton JC, Blaser MJ. Helicobacter infections, in Harrison's Principles of Internal Medicine, edited by Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, Hauser SL, Longo DL. New York, NY, McGraw-Hill, 1998; 14: 931-43  Back to cited text no. 19    
20.Lim JT, Wang JH, Wu MS, et al. Seroprevalence study of Helicobacter pylori infection in patients with gastroduodenal disease. J Formos Med Assoc 1994; 93: 122-7.  Back to cited text no. 20    
21.Bustillo MD, Tomero JAS, Sanz JC, Moreno JA, et al. Eradication and follow-up of Helicobacter pylori infection in hemodialysis patients. Nephron 1998; 79: 55-60.  Back to cited text no. 21    
22.Di Giorgio P, Rivellini G, D'Alessio L, et al. The influence of high blood levels of urea on the presence of Campylobacter pylori in the stomach: A clinical study. Ital J Gastroenterol 1990; 22: 64-5.  Back to cited text no. 22  [PUBMED]  
23.Ala-Kaila K, Vaajalahati P, Karvonen AL, et al. Gastric Helicobacter and upper gastrointestinal symptoms in chronic renal failure. Ann Med 1991; 23: 403-6.  Back to cited text no. 23    
24.Muto S, Asano Y, Hosoda S, et al. Hypochlorhydria and hypergastrinemia and their association with gastrointestinal bleeding in undialyzed and hemodialyzed patients. Nephron 1988; 50: 10-3.  Back to cited text no. 24  [PUBMED]  
25.Akmal M, Sawelson S, Karubian F, et al. The prevalence and significance of occult blood loss in patients with predialysis advanced chronic renal failure, or receiving dialytic therapy. Clin Nephrol 1994; 42: 198-202.  Back to cited text no. 25    
26.Kao CH, Hsu YH, Wang SJ. Delayed gastric emptying and Helicobacter pylori infection in patients with chronic renal failure. Eur J Nucl Med 1995; 22: 1282-5.  Back to cited text no. 26  [PUBMED]  
27.Wee A, Kang JY, Ho MS, et al. Gastroduodenal mucosa in uremia: Endoscopic and histological correlation and prevalence of Helicobacter like organisms. Gut 1991; 31:1093-6.  Back to cited text no. 27    
28.Jasperson D, Fassbinder W, Heinkele P, et al. Significantly lower prevalence of Helicobacter pylori in uremic patients than in patients with normal function. J Gastroenterol 1995; 30: 585-­8.  Back to cited text no. 28    
29.Berstad A, Alexander B, Weber G, et al. Antacids reduce Campylobacter pylori colonization without healing the gastritis in patients with non-ulcer dyspepsia and erosive prepyloric changes. Gastroenterol 1988; 95: 619-24.  Back to cited text no. 29    
30.Simenhoff MI, Sankonen JJ, Burke JF, et al. Bacterial populations of the small intestine in uremia. Nephron 1978; 22: 63-7.  Back to cited text no. 30    
31.Haruma K, Okamoto S, Kawaguchi H, et al. Reduced incidence of Helicobacter pylori in young Japanese persons between the 1970s and the 1990s. J Clin Gastroenterol 1997; 25: 583-6.  Back to cited text no. 31  [PUBMED]  [FULLTEXT]
32.Conz P, Chiaramonte S, Ronco C, et al. Campylobacter pylori in uremic dialyzed patients. Nephron 1989; 53: 90-4.  Back to cited text no. 32  [PUBMED]  
33.Von Wulfen H. An assessment of serological tests for the detection of Helicobacter pylori. Eur J Clin Microbiol Infect Dis 1992; 11: 577­-82.  Back to cited text no. 33    
34.Bergey B, Marchildon P,Peacock J,et al. What is the role of serology in assessing Helicobacter pylori eradication?. Aliment Pharmacol Ther 2003; 18: 635-9.  Back to cited text no. 34    
35.Vaira D, Malfertheiner P, Megraud F, et al. Noninvasive antigen-based assay for assessing Helicobacter pylori eradication: a European multicenter study. The European Helicobacter pylori HpSA Study Group. Am J Gastroenterol 2000; 95: 925-9.  Back to cited text no. 35    
36.Van de Wouw BAM, de Boer WA, and Jansz AR. Serodiagnosis of Helicobacter pylori infection in the Netherlands: an evaluation of a commercially available ELISA for detection of serum IgG antibodies. Neth J Med 1995; 46: 76-7.  Back to cited text no. 36    
37.Branka AM, Van De Wouw, Wink A, et al. Comparison of three commercially available enzyme-linked immunosorbent assays and biopsy-dependent diagnosis for detecting Helicobacter pylori infection. J Clin Microbiol 1996; 34: 94-7.  Back to cited text no. 37    
38.Marchildon P, Balaban DH, Sue M, et al. Usefulness of serological IgG antibody determination for confirming eradication of Helicobacter pylori infection. Am J Gastroenterol 1999; 94: 2105-08.  Back to cited text no. 38  [PUBMED]  
39.Sebastian S and Pierre M. Helicobacter pylori infection. N Engl J Med 2003; 47: 1175-86.  Back to cited text no. 39    
40.Locke GR, Talley NJ, Fett SL, et al. Prevalence and clinical spectrum of gastroesophageal reflux: A population-based study in Olmsted country, Minnesota. Gastroenterology 1997; 112: 1448-56.  Back to cited text no. 40  [PUBMED]  [FULLTEXT]
41.Muto S, Murayama N, Asano Y, et al. Hypergastrinemia and achlorhydria in chronic renal failure. Nephron 1985; 40: 143-8.  Back to cited text no. 41  [PUBMED]  
42.Paronen I, Ala-Kaila K, Rantala I, et al. Gastric parietal, chief, and G-cell densities in chronic renal failure. Scand J Gastroenterol 1991; 26 696-700.  Back to cited text no. 42    
43.Metz DC, Kroser JA. Helicobacter pylori and gastroesophageal reflux disease. Gastroentero Clin North Am 1999; 28: 971-85.  Back to cited text no. 43    
44.El-Omar E, Oien K, El-Nujumi, et al. Helicobacter pylori infection and chronic gastric hyposecretion. Gastroenterology 1997; 113: 15­-24.  Back to cited text no. 44    
45.El-Serag HB, Sonnenberg A, Jamal MM, et al. Corpus gastritis is protective against reflux oesophagitis. Gut 1999; 45: 181-5.  Back to cited text no. 45  [PUBMED]  [FULLTEXT]
46.Cekin AH, Boyacroglu S, Gursoy M, et al. Gastroesophageal reflux disease in chronic renal failure patients with upper GI symptoms:Multivariate analysis of pathogenetic factors. Am J Gastrointerol 2002; 97: 1352-6.  Back to cited text no. 46    
47.Gur G, Boyacioglu S, Cetin G, et al. Impact of Helicobacter pylori infection on serum gastrin in hemodialysis patients. Nephrol Dial Transplant 1999; 14: 2688-91.  Back to cited text no. 47    
48.Fumitaka N, Masahiro S, Kanji A, et al. Helicobacter pylori in patients receiving long­term dialysis. Am J Nephrol 2002; 22: 468-72.  Back to cited text no. 48    

Correspondence Address:
Ibrahim Saeed Abdulrahman
King Fahad Hospital of the University, P 0 Box 40032, Al Khobar, 31952
Saudi Arabia
Login to access the Email id

Source of Support: None, Conflict of Interest: None

PMID: 19861830

Rights and PermissionsRights and Permissions


  [Figure - 1]

  [Table - 1], [Table - 2]


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Email Alert *
    Add to My List *
* Registration required (free)  

    Patients and methods
    Article Figures
    Article Tables

 Article Access Statistics
    PDF Downloaded0    
    Comments [Add]    

Recommend this journal