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  • Title: [Influence of impaired renal function and Helicobacter pylori infection on serum pepsinogen concentrations].
    Author: Murakawa M.
    Journal: Nihon Jinzo Gakkai Shi; 1999 Jun; 41(4):399-405. PubMed ID: 10441989.
    Abstract:
    It has been known that patients with chronic renal failure have elevated concentrations of serum pepsinogens, which are raised by Helicobacter pylori (H. pylori) infection of the stomach. This study was conducted to examine how renal dysfunction and H. pylori infection affect serum pepsinogen (PG) concentrations. The subjects consisted of 93 patients with renal disease (60 males and 33 females with a mean age of 55 +/- 1.3 years). Dialysis patients were not included. Twenty-four-hour urinary collection was performed, and creatinine clearance (Ccr) was calculated for all the subjects. Status of H. pylori infection was assessed by serum IgG antibody against H. pylori. Fasting serum PG I and PG II were measured by RIA. The subjects were divided into 4 groups based on Ccr: group A: Ccr > or = 71 ml/min; group B: 30-70 ml/min; group C: 11-30 ml/min; group D: Ccr < or = 10 ml/min. Regardless of the H. pylori status, serum PG I concentrations were elevated as the renal function declined; serum PG I levels of groups C and D (177.5 +/- 15.2 ng/ml and 234.0 +/- 32.2 ng/ml, respectively) were significantly higher than those of group A (66.1 +/- 9.6 ng/ml, p < 0.01); Group D also had a significantly higher concentration of PG I than group B (106.0 +/- 17.2 ng/ml, p < 0.01). The same tendency was found in serum PG II concentrations. However, the differences among the 4 groups were not statistically significant (16.2 +/- 2.3, 24.2 +/- 4.0, 28.3 +/- 3.5, 34.3 +/- 5.6 ng/ml for group A, B, C, and D, respectively). There was a negative correlation between Ccr and serum PG I concentrations (r = -0.45, p < 0.01). In comparison between H. pylori-infected patients and uninfected patients, serum levels of PG II were higher in the former patients than in the latter. This difference was significant in groups A and C. Serum PG I concentrations were the same between H. pylori-infected patients and their uninfected counterparts for the 4 groups. The present study has shown that serum PG I concentrations are raised by a loss of renal function, while PG II levels are elevated mainly by H. pylori infection of the stomach. It is concluded that renal function and H. pylori infection should be taken into account when serum PG concentrations are evaluated in patients with renal diseases.
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