Israel Medical Association Journal

Mucin gene 5AC (MUC5AC), a secreted mucin, is the most important component of the gastric mucus unstirred, protecting layer, preventing the enzymatic attack of acid and pepsin, toxins, and microorganisms. We investigated the effect of Helicobacter pylori (H. pylori) infection on MUC5AC expression in the gastric mucosa. English language medical literature searches were conducted for gastric MUC5AC expression in H. pylori infected patients compared to uninfected people, or cases after eradication. PubMed, EMBASE, Scopus, and CENTRAL databases were searched. Meta-analysis was performed and pooled odds ratios (ORs) and 95% confidence intervals (95%CIs) were calculated. Heterogeneity was evaluated and I² statistic was used to measure the proportion of inconsistency in individual studies.

We also calculated a potential publication bias. In all, 11 studies representing 13 sub-studies were selected according to the inclusion criteria. The OR of MUC5AC expression in a random effect analysis was 0.217, 95%CI 0.124–0.377, P < 0.0001, significantly lower in H. pylori gastritis than in normal mucosa. When only studies with high-quality scores were calculated, OR was 0.239, 95%CI 0.137–0.419, P < 0.0001. Heterogeneity and inconsistency were small, with no significant publication bias. MUC5AC expression is lower in H. pylori infected mucosa, which may significantly affect the effective colonization and survival of the bacterium and persistent chronic inflammation.

Background: Alkaline tide is the transient increase in blood and urine pH following stimulation of gastric acid secretion. It is attributed to HC0₃ release from parietal cells in parallel with H+ secretion. The enzyme carbonic anhydrase is thought to be responsible for HC0₃ production from CO₂ and 0H in the parietal cell.

Objective: To examine the effect of pretreatment with the carbonic anhydrase inhibitor, acetazolamide, on the alkaline tide phenomenon.

Methods: Ten patients with dyspepsia and demonstrable alkaline tide were tested on three separate days. The pH and base excess were determined in arterialized venous blood before and 45 minutes after an intramuscular injection of pentagastrin. The pH of the urine was measured before and 120 mm after pentagastrin injection. Measurements were performed after pentagastrin alone on day 1 following pretreatment with acetazolamide 60 mm before pentagastrin on day 2, and after the administration of acetazolamide alone on day 3.

Results: Following the administration of pentagastrin alone, the blood base excess increased by 1.61 +0.2 mEq/L (mean + standard deviation) and the calculated alkaline tide at 45 mm was 33.99 ±4.49 mEq. On day 2 with prior adminis­tration of acetazolamide, base excess decreased by 0.21 + 0.39 mEq/L, and the calculated alkaline tide was -3.28±7.57 mEq, which was significantly lower than on day 1 (P=0 0001). On day 3, following acetazolamide alone, the base excess values decreased by 0.53~0.2 mEq/L and the alkaline tide was -10.05 +3.33 mEq there was no significant difference compared with day 2 (P= 0.44).

Conclusion: Pretreatment with acetazolamide abolished the alkaline tide induced by pentagastrin. This finding supports the view that carbonic anhydrase has a major role in the alkaline tide phenomenon.