| 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 2020 May 29];22:282-5. Available from: http://www.sjkdt.org/text.asp?2011/22/2/282/77604
| Introduction|| |
Helicobacter pylori infection affects approximately 50% of the world population. , H. pylori has been shown to play an important role in the development of gastritis and gastric ulcer. ,,,,,,, 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. , 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. ,,,,,
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%).  About one-third of the circulating Mg is bound to plasma proteins, with the remaining two-thirds free, and presumably biologically a vailable. ,,,,, 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.  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.  This study was performed to investigate the association of serum Mg with H. pylori infection among T2DM patients having different GFRs.
| Material and Methods|| |
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).
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. 
| Statistical Analysis|| |
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|| |
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|| |
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.  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. , 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. , 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. ,, 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.  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. , 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. 
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,  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|| |
|1.||Megraud F. Epidemiology of H. pylori infection. Gastroenterol Clin North Am 1993;22:73-88. |
|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. |
|3.||Nakajima F, Sakaguchi M, Oka H, et al. Prevalence of Helicobacter pylori antibodies in longterm dialysis patients. Nephrology 2004;9:73-6. |
|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. |
|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. |
|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. |
|7.||Nasri H. Aggravation of anemia by helicobacter pylori infection in maintenance hemodialysis patients. Pak J Nutr 2006;5(2):172-5. |
|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. |
|9.||Nasri H. Close association between helicobacter pylori infection and serum homocysteine in stable hemodialysis patients Adv Mol Med 2005;1(4):171-5. |
|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. |
|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. |
|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. |
|13.||Oldenburg B, Diepersloot RJ, Hoekstra JB. High seroprevalence of Helicobacter pylori in diabetes mellitus patients. Dig Dis Sci 1996;41: 458. |
|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. |
|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. |
|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. |
|17.||Levine C, Colburn JW. Magnesium, the mimic/ antagonistof calcium. N Engl J Med 1984;19: 1253-4. |
|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. |
|19.||Nasri H, Baradaran HR. Lipids in association with serum magnesium in diabetes mellitus patients. Bratisl Lek Listy 2008;109:7. |
|20.||Nasri H. Baradaran A. Correlation of serum magnesium with dyslipidemia in maintenance hemodialysis patients. Acta Medica 2004;47(4):263-5. |
|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. |
|22.||Gums JG. Clinical significance of magnesium: a review. Drug Intell Clin Pharm 1987;21:240-6. |
|23.||Nasri H. Helicobacter pylori infection and its relationship to plasma magnesium in hemodialysis patients. Bratisl Lek Listy 2007;108 (12):506-9. |
|24.||Cockcroft DW, Gault MH. Prediction of creatinin clearance from serum creatinine. Nephron 1976;16:31-41. |
|25.||Dunn BE, Cohen H, Blaser MJ. Helicobacter pylori. Clin Microbiol Rev 1997;10:720-41. |
|26.||McGee DJ, Mobley HL. Mechanisms of Helicobacter pylori infection: Bacterial factors. Curr Top Microbiol Immunol 1999;241:155-80. |
|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. |
|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. |
|29.||Greger R, Windhorst U, eds. Comprehensive human physiology. New York, NY: Springer; 1996:2432. |
|30.||Moncrief MB, Maguire ME. Magnesium transport in prokaryotes. J Biol Inorg Chem 1999; 4:523-7. |
|31.||Smith RL, Maguire ME. Microbial magnesium transport: unusual transporters searching for identity. Mol Microbiol 1998;28:217-26. |
|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. |
Department of Internal Medicine, Shahrekord University of Medical Sciences, Hajar Hospital, P.O. Box 88155-468, Shahrekord