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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
ORIGINAL ARTICLE  
Year : 2013  |  Volume : 24  |  Issue : 4  |  Page : 759-763
The effect of Helicobacter pylori on vitamin B 12 blood levels in chronic renal failure patients: A single blind control trial


1 Baqiyatallah Research Center for Gastroenterology and Liver Diseases, Baqiyatallah University of Medical Sciences, Tehran, Iran
2 Department of Internal Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran

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Date of Web Publication24-Jun-2013
 

   Abstract 

Helicobacter pylori (HP) is a common infection worldwide and has been associated with severe morbidity. The level of vitamin B 12 in HP-infected chronic kidney disease (CKD) patients is reported to be lower than in the general population. The present study has been designed to evaluate the vitamin B 12 level in HP-infected CKD patients. We assessed the serum levels of vitamin B 12 in 50 CKD patients with positive HP serology, one and three months after the eradication of HP infection. There were significant differences between the serum levels of vitamin B 12 in the study patients before (806.98 ± 466.82) and after (760.36 ± 433.93) eradication treatment (P <0.001). We conclude that our study suggests the correlation between vitamin B 12 deficiency in CKD patients and the HP infection status.

How to cite this article:
Khedmat H, Amini M, Karbasi A, Azizi R. The effect of Helicobacter pylori on vitamin B 12 blood levels in chronic renal failure patients: A single blind control trial. Saudi J Kidney Dis Transpl 2013;24:759-63

How to cite this URL:
Khedmat H, Amini M, Karbasi A, Azizi R. The effect of Helicobacter pylori on vitamin B 12 blood levels in chronic renal failure patients: A single blind control trial. Saudi J Kidney Dis Transpl [serial online] 2013 [cited 2019 Oct 19];24:759-63. Available from: http://www.sjkdt.org/text.asp?2013/24/4/759/113873

   Introduction Top


Helicobacter pylori (HP) is known as one of the most common gastric infections and involves more than half of the people in the world. [1],[2] In some studies, HP infection is known as the causative factor of vitamin B 12 deficiency. [3],[4] According to previous reports, about 21% of the patients with pernicious anemia are infected with HP. [5],[6],[7]

There are several controversial studies about upper gastrointestinal diseases in chronic renal disease (CKD) patients. [8],[9],[10] Doherty et al reported that all of the CKD patients (pre-dialysis or in dialysis stages) developed upper gastrointestinal complications. [9] In contrast, a recent endoscopic study in CKD patients revealed that only 2% of them had gastrointestinal diseases, and this rate was not significantly different from that in the general population. [10]

Converting urea to ammonia by an urease enzyme is the mechanism of protection of HP against gastric acidity. [11] The gastric environment in uremic patients facilitates HP colonization and gastric mucosal damages. [12] In non-CKD patients, HP infection is associated with symptoms of peptic ulcer disease (PUD), but this association is controversial in CKD patients. Some studies showed that dyspeptic symptoms were more prevalent in CKD patients, in contrast to others that did not show such association. [13],[14]

Low levels of vitamin B 12 were found in HP-infected CKD patients. [15] The aim of our study was to determine the vitamin B 12 levels in HP-infected CKD patients and to evaluate the impact of eradication of HP on these levels.


   Materials and Methods Top


We studied 86 chronic hemodialysis patients from the dialysis center of Baqiyatallah Hospital between January and December 2008. Patients who did not tolerate hemodialysis and patients who used antibiotics except our eradication regimen were excluded from the study. Four patients were excluded from the study due to decline to participation to the study. Finally, we performed the study and statistical analysis on 82 patients. We controlled cofounding variables and matched usage of medication that could interact with the vitamin B 12 absorption or the vitamin B 12 levels. Demographic data and renal failure class and dialysis duration were recorded. Hong Kong Dyspepsia Index was used for assessment of dyspepsia symptoms in the studied patients. [16] In this index, the dyspepsia symptoms scale ranges between zero and 100 and, accordingly, the patients could be classified into four groups: No symptoms, mild symptoms, moderate symptoms and severe symptoms groups. This study was approved by the ethical committee of the Baqiyatallah University of Medical Sciences and Health Services and all the study patients consented for participation in this study.

Peripheral blood samples were obtained for diagnosis of HP infection via serologic test (IgG antibody of HP). Upper gastro-intestinal endoscopy was performed for patients with positive serologic HP tests and the infection was confirmed with gastric biopsies and urease tests. Patients received a treatment regimen consisting of three antibiotics including amoxicillin 750 mg daily, clarithromycin 500 mg daily and omeperazol 60 mg daily. We measured the levels of serum vitamin B 12 in all the patients before and one and three months after treatment of HP infection. We assessed HP infection eradication with respiratory urease test in the included patients during one and three months after treatment of HP infection.


   Statistical Analysis Top


Data of the included patients were analyzed with SPSS 16 software. We compared serum vitamin B 12 levels before and after HP infection treatment with paired sample t-test. All P-values less than 0.05 were considered as significant.


   Results Top


We found that 50 (61%) of the screened 82 CKD patients had HP infection. Dyspepsia symptoms were present in 30 (60%) patients. Mild dyspepsia symptoms were found in 20 (40%) patients and the rest complained of moderate and severe symptoms. There was no significant association between eradication status in our patients and the dyspepsia symptoms.

The mean of serum vitamin B 12 levels in our patients before HP treatment was 807 ± 466 pg/mL. The mean of vitamin B 12 levels in the male patients (850 ± 542 pg/mL) was not considerably higher than that in the female patients (747 ± 340 pg/mL) (P = 0.45). The patients without past history of PUD did not have significantly higher levels of vitamin B 12 than patients with this past history (822 ± 476 vs 696 ± 415 pg/mL; P = 0.54). The patients with mild symptoms of PUD (947 ± 609 pg/mL) had the highest and the patients with severe PUD (675 ± 237 pg/mL) had the lowest serum vitamin B 12 levels. However, there was no correlation between the past history of PUD and serum vitamin B 12 levels. (P = 0.39).[Table 1], [Table 2]
Table 1: Frequency and mean of study variables before H. pylori treatment

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Table 2: Evaluation of eradication status in our patients according to their dyspepsia symptoms.

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The mean of serum vitamin B 12 level in our patients after HP treatment was 760 ± 434 pg/mL. The mean of vitamin B 12 in male patients (776 ± 429 pg/mL) was not higher than that in female patients (739 ± 451 pg/mL) (P = 0.77). Patients without past history of PUDs did not have a significantly higher level of vitamin B 12 than patients with this past history (781 ± 443 vs 611 ± 357; P = 0.38). Patients with mild symptoms of PUDs (873 ± 503) had the highest and patients with severe PUD (503 ± 144) had the lowest serum vitamin B 12 levels. There is no significant association between past history of PUD and serum vitamin B 12 level (P = 0.25).

After treatment of CRF patients with therapeutic regimen, the urease breathing test (UBT) was performed for HP eradication assessment. The level of serum vitamin B 12 in patients with negative UBT (857 ± 475 pg/mL) was significantly higher than that in patients with positive UBT (535 ± 178 pg/mL) (P = 0.02).

Finally, there was a significant difference between serum levels of vitamin B 12 in our patients before (807 ± 467 pg/mL) and after (760 ± 434 pg/mL) HP eradication treatment (P = 0.00).


   Discussion Top


The results of our study did not show a significant association between past history of PUD in CKD patients and levels of serum vitamin B 12 . However, the levels of serum vitamin B 12 in CKD patients after HP eradication were significantly higher than those in the infected CKD patients. On the other hand, eradication of HP infection causes a significant increase of serum vitamin B 12 levels in CKD patients.

Previous reports showed that HP infection was related to adult vitamin B 12 deficiency. [3],[4] Kaptan et al [17] reported that HP eradication can improve anemia and serum vitamin B 12 levels in up to 40% of the patients and that HP plays an important role in adult vitamin B 12 deficiency. Karnes et al [18] and Varis et al [19] reported that HP infection is involved in a process that decreases the serum levels of vitamin B 12 . In contrast, some authors believed that improvement of vitamin B 12 absorption after suitable antibiotic therapy might be a result of removing aerobic and anaerobic bacterial suppression. [20] Although in countries with a high prevalence of HP infection, pernicious anemia (due to decrease in vitamin B 12) appears to be uncommon, in patients with pernicious anemia, based on serological and histological studies, evidence of HP infection is often less demonstrated as a cause compared with age-matched controls. [6],[7] [Table 3]
Table 3: Comparing mean of serum B12 level between four dyspepsia symptoms groups before and after eradication treatment.

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In previous studies, the main mechanism that links HP infection to vitamin B 12 remains undefined. HP can induce chronic antral gastritis with increasing achlorhydria and food cobalamin malabsorption. [21] However, some patients with HP infection and severe cobalamin malabsorption did not have atrophic gastritis and achlorhydria, whereas others with HP infection and hypochlorhydria maintained normal food cobalamin absorption. [20]

The pathogenesis of PUD in CKD patients remains undefined. Elevated fasting serum gastrin, which is commonly elevated in these patients, is suggested for the same. [22] Serum levels of hormones involved in the regulation of hunger and satiety, such as cholecystokinin and glucagon, and other hormone abnormalities (hypocalcemia, hypokalemia and acidosis) are raised as a result of renal failure. All these factors might play roles in motility and acid secretion abnormalities in CKD patients. [23] Luzza et al [24] and Abu Frasakh et al [25] in their studies reported that HP infection had a main role in dyspeptic symptoms in CKD patients. However, Schoonjans et al recently reported that dyspepsia and delayed gastric emptying were not related to HP infection in uremic patients. [14] Recently, Huang et al found that in CKD patients without HP infection, the prevalence of gastrointestinal discomfort was higher than that in the general population, while the prevalence of duodenal ulcer was markedly higher in HP-positive patients. [26] High concentration of urea in the gastric juice of uremic patients can affect the urease activity of HP or the modified gastric environment may favor the presence of other urease-producing organisms. [26]

In conclusion, PUD and, specially, HP infection are more prevalent in CKD patients and the infection can decrease serum levels of vitamin B 12. Therefore, a suitable antibiotic therapy for the treatment of this infection may result in an increase of the serum levels of vitamin B 12 in CKD patients.


   Acknowledgment Top


The authors would like to thank the Borhan Research Institute for grateful consultation in preparing the final draft of this manuscript.

 
   References Top

1.Cave DR. Transmission and epidemiology of Helicobacter pylori. Am J Med 1996;100:12-8S.  Back to cited text no. 1
    
2.Graham DY, Malaty HM, Evans DG, Evans DJ Jr, Klein PD, Adam E. Epidemiology of Helicobacter pylori in an asymptomatic population in the United States. Effect of age, race, and socioeconomic status. Gastroenterology 1991;100:1495-501.  Back to cited text no. 2
    
3.Carmel R, Aurangzeb I, Qian D. Associations of food-cobalamin malabsorption with ethnic origin, age, Helicobacter pylori infection, and serum markers of gastritis. Am J Gastroenterol 2001;96:63-70.  Back to cited text no. 3
    
4.Carmel R, Perez-Perez GI, Blaser MJ. Helico-bacter pylori infection and food-cobalamin malabsorption. Dig Dis Sci 1994;39:309-14.  Back to cited text no. 4
    
5.Valle J, Kekki M, Sipponen P, Ihamaki T, Siurala M. Long-term course and consequences of Helicobacter pylori gastritis. Results of a 32-year follow-up study. Scand J Gastroenterol 1996;31:546-50.  Back to cited text no. 5
    
6.Fong TL, Dooley CP, Dehesa M, et al. Helicobacter pylori infection in pernicious anemia: A prospective controlled study. Gastroenterology 1991;100:328-32.  Back to cited text no. 6
    
7.Haruma K, Komoto K, Kawaguchi H, et al. Pernicious anemia and Helicobacter pylori infection in Japan: Evaluation in a country with a high prevalence of infection. Am J Gastroenterol 1995;90:1107-10.  Back to cited text no. 7
    
8.Wee A, Kang JY, Ho MS, Choong HL, Wu AY, Sutherland IH. Gastroduodenal mucosa in uraemia: Endoscopic and histological correlation and prevalence of helicobacter-like organisms. Gut 1990;31:1093-6.  Back to cited text no. 8
    
9.Doherty CC. Gastrointestinal bleeding in dialysis patients. Nephron 1993;63:132-9.  Back to cited text no. 9
    
10.Kang JY, Ho KY, Yeoh KG, et al. Peptic ulcer and gastritis in uraemia, with particular reference to the effect of Helicobacter pylori infection. J Gastroenterol Hepatol 1999;14: 771-8.  Back to cited text no. 10
    
11.Tompkins DS, West AP. Campylobacter pylori, acid, and bile. J Clin Pathol 1987;40:1387.  Back to cited text no. 11
    
12.Lundell LR, Dent J, Bennett JR, et al. Endoscopic assessment of oesophagitis: Clinical and functional correlates and further validation of the Los Angeles classification. Gut 1999;45: 172-80.  Back to cited text no. 12
    
13.Ala-Kaila K, Vaajalahti P, Karvonen AL, Kokki M. Gastric Helicobacter and upper gastrointestinal symptoms in chronic renal failure. Ann Med 1991;23:403-6.  Back to cited text no. 13
    
14.Schoonjans R, Van VB, Vandamme W, et al. Dyspepsia and gastroparesis in chronic renal failure: The role of Helicobacter pylori. Clin Nephrol 2002;57:201-7.  Back to cited text no. 14
    
15.Trimarchi H, Forrester M, Schropp J, Pereyra H, Freixas EA. Low initial vitamin B12 levels in Helicobacter pylori--positive patients on chronic hemodialysis. Nephron Clin Pract 2004;96:c28-32.  Back to cited text no. 15
    
16.Hu WH, Lam KF, Wong YH, et al. The Hong Kong index of dyspepsia: A validated symptom severity questionnaire for patients with dyspepsia. J Gastroenterol Hepatol 2002;17: 545-51.  Back to cited text no. 16
    
17.Kaptan K, Beyan C, Ural AU, et al. Helicobacter pylori-is it a novel causative agent in Vitamin B12 deficiency? Arch Intern Med 2000;160:1349-53.  Back to cited text no. 17
    
18.Karnes WE Jr, Samloff IM, Siurala M, et al. Positive serum antibody and negative tissue staining for Helicobacter pylori in subjects with atrophic body gastritis. Gastroenterology 1991;101:167-74.  Back to cited text no. 18
    
19.Varis O, Valle J, Siurala M. Is Helicobacter pylori involved in the pathogenesis of the gastritis characteristic of pernicious anaemia? Comparison between pernicious anaemia relatives and duodenal ulcer relatives. Scand J Gastroenterol 1993;28:705-8.  Back to cited text no. 19
    
20.Cohen H, Weinstein WM, Carmel R. Heterogeneity of gastric histology and function in food cobalamin malabsorption: Absence of atrophic gastritis and achlorhydria in some patients with severe malabsorption. Gut 2000; 47:638-45.  Back to cited text no. 20
    
21.Stopeck A. Links between Helicobacter pylori infection, cobalamin deficiency, and pernicious anemia. Arch Intern Med 2000;160:1229-30.  Back to cited text no. 21
    
22.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. 22
    
23.Ravelli AM. Gastrointestinal function in chronic renal failure. Pediatr Nephrol 1995;9:756-62.  Back to cited text no. 23
    
24.Luzza F, Imeneo M, Maletta M, G, et al. Helicobacter pylori-specific IgG in chronic haemodialysis patients: Relationship of hyper-gastrinaemia to positive serology. Nephrol Dial Transplant 1996;11:120-4.  Back to cited text no. 24
    
25.Abu Farsakh NA, Roweily E, Rababaa M, Butchoun R. Brief report: Evaluation of the upper gastrointestinal tract in uraemic patients undergoing haemodialysis. Nephrol Dial Transplant 1996;11:847-50.  Back to cited text no. 25
    
26.Huang JJ, Huang CJ, Ruaan MK, Chen KW, Yen TS, Sheu BS. Diagnostic efficacy of (13)C-urea breath test for Helicobacter pylori infection in hemodialysis patients. Am J Kidney Dis 2000;36:124-9.  Back to cited text no. 26
    

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Correspondence Address:
Hossein Khedmat
Baqiyatallah Research Center for Gastro-enterology and Liver Diseases, Baqiyatallah University of Medical Sciences, Tehran
Iran
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DOI: 10.4103/1319-2442.113873

PMID: 23816726

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