Disease relevance of Achlorhydria

• Gastric mucosal biopsy specimens taken from subjects during hypochlorhydria revealed severe fundal and antral gastritis; however, even when acid secretion was severely depressed, parietal cells were abundant and appeared normal histologically [1].
• Finally, the argyrophil-cell hyperplasia occurring in fundic atrophic gastritis with achlorhydria is associated not with the gastritis intensity, as assessed by histologic and secretory criteria, but with a circulating hypergastrinemia and an increase of both fundic histamine content and histidine decarboxylase activity [2].
• It is concluded that multicentric ECL gastric carcinoids in patients with pernicious anemia and achlorhydria appear to be gastrin dependent and disappear after normalization of serum gastrin by antrectomy [3].
• This is the first documented case of a duodenal ulcer with pentagastrin-fast achlorhydria [4].
• Objective responses (more than 50% reduction in tumour markers or tumour size) were seen in 7/7 with watery diarrhoea/hypokalaemia/achlorhydria syndrome, 3/4 with the Zollinger-Ellison syndrome, 6/9 with "non-functioning" tumours, and 1 with a mixed tumour mainly producing somatostatin [5].

High impact information on Achlorhydria

• Absorption of calcium from carbonate in patients with achlorhydria was significantly lower than in the normal subjects and was lower than absorption from citrate in either group; absorption from citrate in those with achlorhydria was significantly higher than in the normal subjects, as well as higher than absorption from carbonate in either group [6].
• Reciprocal regulation of antral gastrin and somatostatin gene expression by omeprazole-induced achlorhydria [7].
• Exogenous somatostatin, however, did not influence the decrease in antral somatostatin mRNA levels seen with achlorhydria [7].
• On resolution of the gastritis, a decrease in parietal and gastrin-expressing (G) cells was observed despite sustained hypochlorhydria in the presence of omeprazole [8].
• Acute infection is associated with transient hypochlorhydria, whereas chronic infection is associated with hypergastrinemia and decreased somatostatin levels [9].

Chemical compound and disease context of Achlorhydria

• Mean calcium absorption (+/- S.D.) in the patients with achlorhydria was 0.452 +/- 0.125 for citrate and 0.042 +/- 0.021 for carbonate (P less than 0.0001) [6].
• Achlorhydria was induced in rats by the gastric H+/K+ ATPase inhibitor, omeprazole (100 mumol/kg) [7].
• Gastric analysis revealed pentagastrin-fast achlorhydria [4].
• Studies in fasting subjects have suggested that cimetidine therapy might lead to nocturnal hypochlorhydria, allowing bacterial overgrowth and the production of intragastric carcinogens [10].
• The very low ascorbic acid concentrations in hypochlorhydria may be a consequence of oxidation by bacterial nitrite [11].

Biological context of Achlorhydria

• The results suggest that in drug-induced achlorhydria, the progressive increase of enterochromaffinlike cells is explained by an enhanced mitosis, whereas other factors in addition to proliferation are responsible for the augmentation of gastrin cells [12].
• This suggests that CYP2C19 genotype testing will not be useful in proton-pump inhibitor therapy of GERD, except perhaps in identifying patients at risk for hypochlorhydria and consequent hypergastrinemia [13].
• In twelve patients with achlorhydria with a spared antrum, PCA was positive and basal gastrin was elevated [14].
• Since hypochlorhydria can induce hypergastrinemia, and gastrin has a trophic effect on some gastrointestinal cells, states that cause elevated plasma gastrin levels are of interest in terms of effects on cell growth and function [15].

Anatomical context of Achlorhydria

• Omeprazole-induced achlorhydria reduced D-cell activity as shown by a threefold decrease in antral somatostatin mRNA levels that began after 24 h [7].
• Infection was accompanied by a transient hypochlorhydria but a sustained fall in gastric juice ascorbic acid concentration [16].
• A patient with watery diarrhea, hypokalemia, hypochlorhydria, and a non-beta islet cell carcinoma of the pancreas (Verner-Morrison syndrome) was found to have an elevated vasoactive intestinal peptide (VIP) concentration in the plasma as well as in the tumor [17].
• Against a background of omeprazole-induced achlorhydria hypergastrinemia appears to influence differentiation rather than growth of normal colon mucosa [18].
• Achlorhydria was considered to be present if plasma gastrin measured on a sample obtained with the patient fasting was over 200 ng/l. Serum was tested for intrinsic factor and gastric parietal cell antibodies [19].

Gene context of Achlorhydria

• Polymorphisms of the IL-1B and IL-1RN genes (which encode interleukin [IL]-1beta and IL-1 receptor antagonist, respectively) have been associated with hypochlorhydria and gastric cancer [20].
• In another patient, the serum gastrin concentration was elevated secondary to achlorhydria [21].
• After induction of achlorhydria, however, neither the amount of alpha-amidated gastrin nor the total progastrin product increased in the fat/fat mice [22].
• Augmentation of the inhibitory effect of FK480, a CCK-A receptor antagonist, on pancreatic exocrine secretion by achlorhydria [23].
• Based on these known biological actions of TGF alpha, we have examined TGF alpha production in Ménétrier's disease, a disorder characterized by foveolar hyperplasia, hypochlorhydria, and increased gastric mucin content [24].
• Toxigenic (vacA type s1/m1) H. pylori was associated with precancerous gastric hypochlorhydria (P<0.01) [25].

Analytical, diagnostic and therapeutic context of Achlorhydria

• 1-Phenyl-1-hydroxy-N-pentane may be a useful agent for release of secretin in subjects with achlorhydria, severe hyposecretory state, or total gastrectomy [26].
• The purpose of this study was to determine whether gastric achlorhydria or hypochlorhydria has any significant gross effects on the urinary recovery of dietary nitrate and to what extent the inclusion of such individuals would compromise the results of potential epidemiological studies [27].
• CONCLUSION: The modified endoscopic Congo red is an accurate, simple, fast, inexpensive, and well-tolerated chromoendoscopic method for identification of patients with hypo/achlorhydria during routine upper endoscopy [28].
• Pentagastrin given during upper gastrointestinal endoscopy: a simple screening method for hypo- and achlorhydria [29].
• Basal serum gastrin (mean +/- SEM) was progressively higher for each group; normal (42 +/- 3 pg/ml), duodenal ulcer (53 +/- 4 pg/ml), vagotomy (226 +/- 54 pg/ml), hypochlorhydria (346 +/- 92 pg/ml), achlorhydria (844 +/- 100 pg/ml) [30].

References