Home About us Current issue Back issues Submission Instructions Advertise Contact Login   

Search Article 
  
Advanced search 
 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 706 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 
 


 
Table of Contents   
ORIGINAL ARTICLE  
Year : 2011  |  Volume : 22  |  Issue : 2  |  Page : 282-285
Helicobacter pylori specific IgG antibody and serum magnesium in type-2 diabetes mellitus chronic kidney disease patients


Department of Internal Medicine, Shahrekord University of Medical Sciences, Hajar Hospital, Shahrekord, Iran

Click here for correspondence address and email

Date of Web Publication18-Mar-2011
 

   Abstract 

Infection with Helicobacter pylori (H. pylori) is common in diabetics with inade­quately controlled blood sugar. Evidence has been published suggesting that the prevalence of H. pylori infection is higher in patients with type-2 diabetes mellitus (T2DM) as opposed to the normal population. This study was conducted to investigate the association between serum magnesium (Mg) levels and H. pylori infection in T2DM patients with various glomerular function rates (GFRs). A total of 94 patients with mean age of 62 (±12) years and the duration of diabetes of 7.9 (±6.9) years (median: 7 years), were studied. The mean HbA1c in the study patients was 7.8 (±1.9) g/dL. The mean serum Mg was 2 (±0.50) mg/dL (median: 2 mg/dL), and the mean creatinine clea­rance was 62 (±23) mL/min (median: 64 mL/min). The mean value of serum H. pylori specific IgG antibody titers in the study patients was 3.9 ± 4 U/mL (median 1.9 U/mL). No significant relation­ship was found between the serum H. pylori specific IgG antibody titers and serum Mg levels and the age of the patients, creatinine clearance and duration of diabetes mellitus (DM). We could not find any significant positive association between serum Mg and H. pylori infection even among patients who had GFR below 40 mL/min. In a previous study on a group of patients on hemo­dialysis (HD), we had found a positive correlation between serum Mg and H. pylori infection. Thus, the high serum Mg level as well as its higher concentration in the gastric mucosa might facilitate the colonization of H. pylori in the stomach of patients on HD, but not in patients with various stages of renal failure that were not on HD.

How to cite this article:
Baradaran A, Nasri H. Helicobacter pylori specific IgG antibody and serum magnesium in type-2 diabetes mellitus chronic kidney disease patients. Saudi J Kidney Dis Transpl 2011;22:282-5

How to cite this URL:
Baradaran A, Nasri H. Helicobacter pylori specific IgG antibody and serum magnesium in type-2 diabetes mellitus chronic kidney disease patients. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2019 Aug 23];22:282-5. Available from: http://www.sjkdt.org/text.asp?2011/22/2/282/77604

   Introduction Top


Helicobacter pylori infection affects approxi­mately 50% of the world population. [1],[2] H. py­lori has been shown to play an important role in the development of gastritis and gastric ulcer. [3],[4],[5],[6],[7],[8],[9][10] Infection with H. pylori is common in diabe­tics who do not have adequately controlled hy­perglycemia and these individuals are prone to colonization by this organism in the gastric an­trum. [11],[12] Evidence has been published sugges­ting that the prevalence of H. pylori infection might be increased in patients with type-2 dia­betes mellitus (T2DM) when compared with the normal population. [11],[12],[13],[14],[15],[16]

Magnesium (Mg) is an important intracellular cation that is distributed into three major com­partments: mineral phase of bones (65%), in­tracellular space (34%) and extracellular fluid (1%). [17] About one-third of the circulating Mg is bound to plasma proteins, with the remaining two-thirds free, and presumably biologically a­ vailable. [17],[18],[19],[20],[21],[22] Magnesium seems to be an impor­tant factor both for gastric acid secretion regu­lation (together with Ca 2+ ) and for survival and virulence of H. pylori. [23] Therefore, it is impor­tant to assess if H. pylori infection is accom­panied by variations in the serum Mg levels in patients with T2DM, who have different glome­rular function rates (GFRs).

Few reports are available regarding the factors that promote H. pylori infection in diabetic pa­tients. Previously, we had shown the relation­ship between H. pylori infection and plasma Mg in patients on HD. [17] This study was performed to investigate the association of serum Mg with H. pylori infection among T2DM patients having different GFRs.


   Material and Methods Top


Patients

This cross-sectional study was conducted on patients with diabetes mellitus (DM) and on treatment with oral hypoglycemic agent and/or insulin. Patients who had hypertension in addi­tion were on anti-hypertensive drugs consisting of calcium channel blockers, angiotensin-con­verting enzyme (ACE) inhibitors or angiotensin receptor antagonists (ARA) in varying doses. The exclusion criteria included use of diuretics and the presence of chronic or acute infections. The study was carried out at the Hajar Medical Educational and Therapeutic Center, Shahre­kord University of Medical Sciences, Iran. All patients signed the consent form for participa­tion in this study. After admission, the medical history of all patients was studied, particularly concerning the duration of diabetes and the me­dications they were taking for DM and hyper­tension (HTN). Patients were also examined for blood pressure (BP) and body mass index (BMI).

Laboratory Methods

Blood samples were collected after overnight fasting. The blood samples were centrifuged within 15 min of collection. The glycosylated hemoglobin (HbA1c) was measured by chroma­tography using Hb-Gold of UK (the normal va­lue in our laboratory is less than or equal to 6.1%). Levels of serum Mg, serum creatinine, and blood urea nitrogen (BUN) were measured using standard methods. H. pylori specific IgG antibody titer was measured by enzyme linked immunosorbent assay (ELISA). A titer >10 U/ mL was interpreted as positive according to the manufacturer's instructions. The BMI was cal­culated using the standard formula (weight in kilograms/height in meters squared: kg/m 2 ). The creatinine clearance (CrcL) was calculated from serum creatinine, age and body weight. [24]


   Statistical Analysis Top


Results are expressed as mean ± SD and me­dian values. Statistical correlations were assessed using a partial correlation test. Comparison of data between female and male patients was made using Student's t-test. All analyses were performed with the SPSS statistical package (version 11.500 for Windows; SPSS, Chicago, USA). Statistical significance was determined at a P value of <0.05.


   Results Top


The present study included 94 patients (32 males, 62 females) with a mean age of 62 (±12) years. The mean length of time they were dia­betic was 7.9 (±6.9) years (median: 7 years). The mean HbA1c of the study patients was 7.8 (±1.9) g/dL, the mean BMI was 25 (±2.9) kg/ m 2 , the mean serum Mg was 2 (±0.50) mg/dL (median: 2 mg/dL), the mean creatinine clea­rance was 62 (±23) mL/min (median: 64 mL/ min) and the mean serum H. pylori specific IgG antibody titer was 3.9 ± 4 U/mL (median: 1.9 U/mL). In this study population, there was no significant association between the H. pylori specific IgG antibody titers and serum Mg le­vels between males and females. Also, there was no significant association between the se­rum H. pylori specific IgG antibody titers and serum Mg levels on the one hand, and the age of the patients, creatinine clearance, duration of DM and BMI, on the other; no significant asso­ciation was found even among patients with creatinine clearance below 40 mL/min.


   Discussion Top


In this study, no correlation was found bet­ween serum anti H. pylori IgG antibody levels and serum Mg in patients with DM. Also, there was no significant difference in H. pylori spe­cific IgG antibody and serum Mg titers between males and females. In an earlier report on a group of HD patients, we had shown a positive correlation between serum Mg level and H. p­ylori infection. [23] It seems that the cation meta­bolism of the gastric pathogen H. pylori is of substantial importance for survival in the hos­tile and changing environment of the gastric mucosa. [25],[26] Although the essential biological functions of serum Mg point toward a rele­vance of its acquisition in the adaptation to the gastric environment, proteins involved in the uptake and metabolism of serum magnesium by H. pylori have not been studied in detail. [27],[28] The complete lack of growth of H. pylori in ex­ternal media without Mg supplementation shows that H. pylori CorA is essential for serum Mg acquisition, which in turn is required for survi­val in low serum Mg environments. [29],[30],[31] These findings underscore the role of H. pylori cation metabolism in maintaining metabolic functions and highlight the substantial importance of se­rum Mg acquisition in gastric adaptation. [28] As mentioned previously, serum Mg acquisition by CorA is essential for H. pylori in vitro. Serum Mg is a co-factor of many enzymes involved in central biochemical pathways within the human host; pathogenic bacteria express specific serum Mg uptake systems, which are essential for their viability. [30],[31] Magnesium also seems to be an important factor both for regulation of gastric acid secretion (together with Ca 2+ ) and for sur­vival and virulence of H. pylori. [32]

In this study, we could not find any significant positive association between serum Mg and H. pylori infection even among patients with T2DM who had GFR below 40 mL/min. Com­paring these data with our previous study, [23] we may confirm the hypothesis that high serum Mg levels, and probably its higher concentration in the gastric mucosa, might facilitate the coloni­zation of H. pylori in the stomach of patients on HD but not in patients with various stages of renal failure who were not undergoing HD. Fur­ther investigation is needed to define the cli­nical significance of these findings.

 
   References Top

1.Megraud F. Epidemiology of H. pylori infec­tion. Gastroenterol Clin North Am 1993;22:73­-88.  Back to cited text no. 1
    
2.Bener A, Uduman SA, Ameen A, et al. Preva­lence of Helicobacter pylori infection among low socio-economic workers. J Commun Dis 2002;34:179-84.  Back to cited text no. 2
[PUBMED]    
3.Nakajima F, Sakaguchi M, Oka H, et al. Preva­lence of Helicobacter pylori antibodies in long­term dialysis patients. Nephrology 2004;9:73-6.  Back to cited text no. 3
[PUBMED]  [FULLTEXT]  
4.Nasri H, Baradaran A. The influence of serum 25-hydroxy vitamin D levels on Helicobacter Pylori Infections in patients with end-stage renal failure on regular hemodialysis. Saudi J Kidney Dis Transpl 2007;18(2):215-9.  Back to cited text no. 4
    
5.Baradaran A. Nasri H. Correlation of serum leptin with circulating anti-helico bacter Pylori IgG antibodies in end-stage renal failure pa­tients on regular hemodialysis. Pak J Nutr 2005; 4(6):389-92.  Back to cited text no. 5
    
6.Baradaran A. Nasri H. Helicobacter pylori IgG specific antibodies in association with serum albumin in maintenance hemodialysis patients. Pak J Nutr 2005;4(4):265-9.  Back to cited text no. 6
    
7.Nasri H. Aggravation of anemia by helicobacter pylori infection in maintenance hemodialysis patients. Pak J Nutr 2006;5(2):172-5.  Back to cited text no. 7
    
8.Baradaran A. Nasri H. Helicobacter pylori IgG antibodies in association with secondary hyper­parathyroidism in end-stage renal failure pa­tients undergoing regular hemodialysis. Arch Med Sci 2005;1(3):148-51.  Back to cited text no. 8
    
9.Nasri H. Close association between helicobacter pylori infection and serum homocysteine in stable hemodialysis patients Adv Mol Med 2005;1(4):171-5.  Back to cited text no. 9
    
10.Nasri H. The association between helicobacter pylori infection and body mass index in hemo­dialysis patients. Acta Facultatis Medicae Nais­sensis 2006;23(3):129-33.  Back to cited text no. 10
    
11.Bytzer P, Talley NJ, Leemon M, et al. GI symp­toms in diabetes mellitus are associated with both poor glycemic control and diabetic compli­cations. Am J Gastroenterol 2002;97:604-11.  Back to cited text no. 11
    
12.Bytzer P, Talley NJ, Leemon M, et al. Prevalence of gastrointestinal symptoms associated with diabetes mellitus: A population-based survey of 15,000 adults. Arch Intern Med 2001;161:1989­-96.  Back to cited text no. 12
[PUBMED]  [FULLTEXT]  
13.Oldenburg B, Diepersloot RJ, Hoekstra JB. High seroprevalence of Helicobacter pylori in dia­betes mellitus patients. Dig Dis Sci 1996;41: 458.  Back to cited text no. 13
[PUBMED]    
14.Malecki M, Bien AI, Galicka-Latala D, et al. The prevalence of Helicobacter pylori infection and types of gastritis in diabetic patients. The Krakow study. Exp Clin Endocr Diab 1996;104: 365-9.  Back to cited text no. 14
    
15.Talley NJ, Howell S, Jones MP, Horowitz M. Predictors of turnover of lower gastrointestinal symptoms in diabetes mellitus. Am J Gastro­enterol 2002;97:3087-94.  Back to cited text no. 15
    
16.Perdichizzi G, Bottari M, Pallio S, et al. Gastric infection by Helicobacter pylori and antral gas­tritis in hyperglycemic obese and diabetic sub­jects. New Microbiol 1996;19:149- 54.  Back to cited text no. 16
[PUBMED]    
17.Levine C, Colburn JW. Magnesium, the mimic/ antagonistof calcium. N Engl J Med 1984;19: 1253-4.  Back to cited text no. 17
    
18.Baradaran A, Nasri H. Correlation of serum magnesium with serum parathormone levels in patients on regular hemodialysis. Saudi J Kidney Dis Transpl 2006;17(3):344-50.  Back to cited text no. 18
    
19.Nasri H, Baradaran HR. Lipids in association with serum magnesium in diabetes mellitus pa­tients. Bratisl Lek Listy 2008;109:7.  Back to cited text no. 19
    
20.Nasri H. Baradaran A. Correlation of serum mag­nesium with dyslipidemia in maintenance hemo­dialysis patients. Acta Medica 2004;47(4):263­-5.  Back to cited text no. 20
    
21.Nasri H, Kheiri S. Effects of diabetes mellitus, age, and duration of dialysis on parathormone in chronic hemodialysis patients. Saudi J Kidney Dis Transpl 2008;19(4):608-13.  Back to cited text no. 21
    
22.Gums JG. Clinical significance of magnesium: a review. Drug Intell Clin Pharm 1987;21:240-6.  Back to cited text no. 22
[PUBMED]    
23.Nasri H. Helicobacter pylori infection and its relationship to plasma magnesium in hemo­dialysis patients. Bratisl Lek Listy 2007;108 (12):506-9.  Back to cited text no. 23
    
24.Cockcroft DW, Gault MH. Prediction of crea­tinin clearance from serum creatinine. Nephron 1976;16:31-41.  Back to cited text no. 24
[PUBMED]    
25.Dunn BE, Cohen H, Blaser MJ. Helicobacter­ pylori. Clin Microbiol Rev 1997;10:720-41.  Back to cited text no. 25
[PUBMED]  [FULLTEXT]  
26.McGee DJ, Mobley HL. Mechanisms of Helico­bacter pylori infection: Bacterial factors. Curr Top Microbiol Immunol 1999;241:155-80.  Back to cited text no. 26
[PUBMED]    
27.Nolan KJ, McGee DJ, Mitchell HM, et al. In­vivo behavior of a Helicobacter pylori SS1nixA mutant with reduced urease activity. Infect Immun 2002;70:685-91.  Back to cited text no. 27
[PUBMED]  [FULLTEXT]  
28.Pfeiffer J, Guhl J, Waidner B, et al. Magnesium uptake by CorA is essential for viability of the gastric pathogen Helicobacterpylori. Infect Immun 2002;70:3930-4.  Back to cited text no. 28
[PUBMED]  [FULLTEXT]  
29.Greger R, Windhorst U, eds. Comprehensive human physiology. New York, NY: Springer; 1996:2432.  Back to cited text no. 29
    
30.Moncrief MB, Maguire ME. Magnesium trans­port in prokaryotes. J Biol Inorg Chem 1999; 4:523-7.  Back to cited text no. 30
[PUBMED]  [FULLTEXT]  
31.Smith RL, Maguire ME. Microbial magnesium transport: unusual transporters searching for identity. Mol Microbiol 1998;28:217-26.  Back to cited text no. 31
[PUBMED]  [FULLTEXT]  
32.Abbasciano V, Sartori S, Trevisani L, et al. Comparison of magnesium concentration in serum, erythrocytes and gastric tissue in two groups of patients affected by chronic gastritis, Helicobacter pylori negative and positive. Magnes Res 2003;16:281-6.  Back to cited text no. 32
[PUBMED]    

Top
Correspondence Address:
Hamid Nasri
Department of Internal Medicine, Shahrekord University of Medical Sciences, Hajar Hospital, P.O. Box 88155-468, Shahrekord
Iran
Login to access the Email id


PMID: 21422626

Rights and Permissions




 

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


 
    Abstract
    Introduction
    Material and Methods
    Statistical Analysis
    Results
    Discussion
    References
 

 Article Access Statistics
    Viewed2794    
    Printed90    
    Emailed0    
    PDF Downloaded639    
    Comments [Add]    

Recommend this journal