Helicobacter pylori infection: protective against increased interdialytic weight gain in asymptomatic hemodialysis
Baris Afsar1, Rengin Elsurer, Bulent Huddam
1Department of Nephrology, Zonguldak Atatürk Government Hospital, Zonguldak, Turkey. afsarbrs@yahoo.com
Objective:
Infection with Helicobacter pylori, which induces persistent and uncontrolled gastric inflammation leading to decreased appetite, might be protective against obesity. There is a close relationship between interdialytic weight gain (IDWG) and nutritional parameters, confirming the role of IDWG as a marker of calorie and protein intake in hemodialysis (HD) patients. Hypothesis of the present study was that infection with H pylori in subjects with uremia might cause inflammation, diminished appetite, anorexia, and decreased IDWG.
Design:
A cross-sectional study was conducted.
Settings:
This trial involved HD patients from a state hospital.
Methods:
Demographic, laboratory, and clinical parameters were collected. All patients were clinically stable and euvolemic and their average IDWG percent was calculated. Malnutrition inflammation score, spKt/V, and normalized protein equivalent of total nitrogen appearance were determined. Patients were asked to rate their appetite status from 1 to 5 on a Likert scale (very good, good, fair, poor, and very poor appetite, respectively). An H pylori infection was detected by the H pylori stool antigen (HpSA) in all the patients.
Results:
HpSA was positive in 18 (30%) patients. None of the demographic and laboratory parameters differed between patients infected with HpSA and the noninfected patients. Stepwise linear regression analysis of independent factors related with IDWG% revealed that daily urine output (β = -0.432, P < .0001), serum phosphorus (β = +0.343, P = .004), and hemoglobin (β = +0.358, P = .003) were related with IDWG%.
Conclusions:
Infection with H pylori is not related with IDWG% and nutritional parameters in HD patients.
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Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
