Inability to produce gastric acid. Most commonly caused by gastric atrophy. Gastric atrophy, with or without autoimmune gastritis, is present in about 15% of older people and is thought to be initiated by infection with Helicobacter pylori.
Usually asymptomatic but may present with signs and/or symptoms of iron, cobalamin (vitamin B12), or calcium deficiency and may predispose to enteric infection with organisms such as Clostridium difficile, Salmonella, and Campylobacter.
May interfere with the absorption of certain drugs including thyroxine, ketoconazole, itraconazole, and dipyridamole.
The most common cause of hypergastrinemia.
Although the prognosis is excellent, it carries a small increased risk for the development of gastric adenocarcinoma and gastric carcinoid tumor.
Achlorhydria indicates the inability to produce gastric acid (i.e., hydrochloric acid [HCl]), even after stimulation with secretagogues (e.g., pentagastrin [gastrin analog], histamine, betazole [histamine analog], or a meal). Serum gastrin is a marker for gastric acid output. A decrease in gastric acid interrupts a negative feedback pathway controlling gastrin secretion and leads to elevated serum gastrin levels (hypergastrinemia). The most common cause of achlorhydria is chronic atrophic gastritis of the fundus and corpus (body) of the stomach (also termed gastric corpus atrophy, oxyntic gastric atrophy, chronic atrophic gastritis, and gastric atrophy), which is characterized histopathologically as loss of oxyntic glands. It is the oxyntic (oxys: Greek for acid) glands that contain the acid-producing parietal cells.
History and exam
- age >60 years
- female gender
- autoimmune disorders
- decreased exercise tolerance
- skin and conjunctival pallor
- paresthesias and difficulty ambulating
- nutritional deficiency (cobalamin, iron, calcium, vitamin D)
- enteric infection
- memory loss, irritability, depression, and dementia
- ataxia, shuffling gait, decreased position sense, decreased vibration sense
- pale, smooth, and glossy tongue
- serum gastrin
- gastric acid secretory test (gastric analysis)
- parietal cell antibodies
- intrinsic factor antibodies
- urea breath test: Helicobacter pylori infection
- histology: Helicobacter pylori infection
- rapid urease test on biopsy samples: Helicobacter pylori infection
- stool antigen test: Helicobacter pylori infection
- serology: Helicobacter pylori infection
- polymerase chain reaction (PCR): Helicobacter pylori infection
- fluorescence in situ hybridization: Helicobacter pylori infection
Professor of Medicine and Physiology
Virginia Commonwealth University Health System
Chief of Gastroenterology
MLS is an author of several studies referenced in this monograph.
Dr Mitchell L. Schubert would like to gratefully acknowledge Dr Juan Diego Baltodano, a previous contributor to this monograph. JDB declares that he has no competing interests.
Professor of Medicine
David Geffen School of Medicine at UCLA
JP declares that he has no competing interests.
Associate Professor of Gastroenterology and Internal Medicine
Medical University of Graz
University Hospitals Graz
HFH has been reimbursed by Astra Zeneca, Nycomed, and Janssen, the manufacturers of proton-pump inhibitors, for attending several conferences and speaking, and has been paid by Astra Zeneca for running educational programs.
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