PubMed · 13352351
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F HIRSCHBERG. 1956-07-01. Achylli and constipation.. https://pubmed.ncbi.nlm.nih.gov/13352351/
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Proton pump inhibitors are potent drugs producing profound suppression of gastric acid secretion. Consequently, they are highly effective at treating acid-related disorders. There have been concerns that the suppression of gastric acid will alter the bacterial flora of the upper gastrointestinal tract and lead to complications such as cancer, enteric or other infections and malabsorption. Studies have confirmed that proton pump inhibitors do alter the bacterial population but present evidence indicates that this only rarely leads to clinical disease. As with all drugs, proton pump inhibitors should only be used for disorders shown clearly to benefit from the therapy and where the benefits will outweigh the small risks associated with them. Further research to more fully quantify the risk associated with PPI therapy is required.
Although gastric hypochlorhydria is a risk factor for gastroenteritis and for gastric cancer, no reliable, inexpensive, noninvasive test exists for screening or epidemiologic studies. We aimed to evaluate the sensitivity and specificity of the blood quininium resin test (bQRT) for hypochlorhydria, against pH monitoring. Twelve fasting adult volunteers-seven with and five without H. pylori infection-ingested 80 mg/kg of quininium resin twice, once with and once without acid suppression. Gastric pH was monitored for 75 minutes; serum samples were obtained at times 0 and 75 minutes. The bQRT levels were compared to gastric pH, controlling for omeprazole use and H. pylori infection. Subjects with a median recorded pH > or =3.5 were considered hypochlorhydric. Using a bQRT level of 10 as a cutoff for hypochlorhydria, the sensitivity and specificity of the bQRT were 100% and 37.5%, respectively. The bQRT predicted omeprazole use more accurately than pH monitoring. In conclusions, The bQRT has a high sensitivity for hypochlorhydria, making it potentially useful in populations with a high prevalence of hypochlorhydria. In its current formulation, the bQRT's low specificity makes it less useful in low-risk population.
Loss of gastric acid secretion is pathologically known as achlorhydria. Acid-secreting parietal cells are characterized by abundant expression of ezrin (Vil2), one of ezrin/radixin/moesin proteins, which generally cross-link actin filaments with plasma membrane proteins. Here, we show the direct in vivo involvement of ezrin in gastric acid secretion. Ezrin knockout (Vil2(-/-)) mice did not survive >1.5 wk after birth, making difficult to examine gastric acid secretion. We then generated ezrin knockdown (Vil2(kd/kd)) mice by introducing a neomycin resistance cassette between exons 2 and 3. Vil2(kd/kd) mice born at the expected Mendelian ratio exhibited growth retardation and a high mortality. Approximately 7% of Vil2(kd/kd) mice survived to adulthood. Ezrin protein levels in Vil2(kd/kd) stomachs decreased to <5% of the wild-type levels without compensatory up-regulation of radixin or moesin. Adult Vil2(kd/kd) mice suffered from severe achlorhydria. Immunofluorescence and electron microscopy revealed that this achlorhydria was caused by defects in the formation/expansion of canalicular apical membranes in gastric parietal cells.