Abstract Background: The relationship between Helicobacter pylori ( H. pylori ) eradication and atrophic changes in the gastric mucosa has not yet been fully defined. Although studies report a partial restoration of serum pepsinogen I (sPGI) levels after eradication, it is not clear if this finding reflects gastric mucosal healing on a morphological level. Aim: To assess alterations in gastric function after H. pylori eradication on moderate/severe body atrophic gastritis by determination of sPGI levels. Methods: Twenty‐three dyspeptic patients, selected from 284 consecutive H. pylori positive patients, with histological features of moderate/severe body atrophic gastritis and sPGI < 25 µg/L (11 men, mean age: 51.8 years, range: 29–79 years), underwent an upper gastrointestinal endoscopy with gastric biopsies and sPGI determination at baseline. All patients underwent eradication therapy. Serum pepsinogen I was measured again after 6 months, and at 1, 2, 3 and 4 years after eradication therapy. Results: Mean sPGI levels prior to eradication were 11.9 µg/L (range: 4–23 µg/L). Six months after eradication therapy, mean sPGI levels significantly increased to 17.4 µg/L ( P = 0.04). At the completion of the study, 4 years after eradication, sPGI levels increased from 17.4 to 32.7 µg/L ( P = 0.01). A significant progressive increase in sPGI levels was observed from 6 months to 1 year (17.4 to 23.9 µg/L) and from 1 to 2 years (23.9 to 26.0 µg/L, P = 0.01). Serum pepsinogen I levels higher than the cut‐off value of 25 µg/L were observed at various time‐points: 6.3% of patients at 6 months (1/16), 33.3% (5/15) at 1 year, 50% (7/14) at 24 months, 66.7% (6/9) at 36 months and 87.5% (7/8) at 4 years. Conclusion: After H. pylori eradication, subjects with body atrophic gastritis showed long‐term improvement of physiological gastric function, reflected by significantly and continually increasing sPGI levels over a 4‐year period.
Abstract A protective role of the transient potential vanilloid receptor 1 (TRPV1) in intestinal inflammation induced by dinitrobenzene sulphonic acid (DNBS) has been recently demonstrated. Curcumin, the major active component of turmeric, is also able to prevent and ameliorate the severity of the damage in DNBS‐induced colitis. We evaluated the possibility that curcumin (45 mg kg −1 day p.o. for 2 days before and 5 days after the induction of colitis) was able to reduce DNBS‐induced colitis in mice, by acting as a TRPV1 agonist. Macroscopic damage score, histological damage score and colonic myeloperoxidase (MPO) activity were significantly lower (by 71%, 65% and 73%, respectively; P < 0.01), in animals treated with curcumin compared with untreated animals. Capsazepine (30 mg kg −1 , i.p.), a TRPV1 receptor antagonist, completely abolished the protective effects of curcumin. To extend these data in vitro , Xenopus oocytes expressing rat TRPV1 were examined. Capsaicin‐evoked currents (3.3 μ mol L −1 ) disappeared subsequent either to removal of the agonist or subsequent to the addition of capsazepine. However, curcumin (30 μ mol L −1 ) was ineffective both as regard direct modification of cell membrane currents and as regard interference with capsaicin‐mediated effects. As sensitization of the TRPV1 receptor by mediators of inflammation in damaged tissues has been shown previously, our results suggest that in inflamed, but not in normal tissue, curcumin can interact with the TRPV1 receptor to mediate its protective action in DNBS‐induced colitis.
