Achlorhydria

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

Last reviewed: 20 Aug 2025

Last updated: 19 Aug 2025

Achlorhydria indicates the complete lack of production of gastric acid by the gastric parietal cells. Hypochlorhydria is a reduction in the production of gastric acid.

Both achlorhydria and hypochlorhydria are commonly the consequence of chronic atrophic gastritis, which is usually caused by autoimmune or Helicobacter pylori related destruction of acid producing gastric parietal cells.

Patients are usually asymptomatic but may present with signs and/or symptoms of iron, cobalamin (vitamin B12), or calcium deficiency. Patients with hypochlorhydria and achlorhydria are predisposed to enteric infection with organisms such as Clostridium difficile, Salmonella, and Campylobacter.

There is no specific treatment. It is reasonable to test for H pylori and, if present, eradicate it. Other treatments aim to prevent or treat complications arising from achlorhydria.

Although the prognosis is excellent, it carries a small increased risk for the development of gastric adenocarcinoma and gastric neuroendocrine tumors from enterochromaffin cell hyperplasia.

Definition

Achlorhydria indicates the complete lack of production of gastric acid (i.e., hydrochloric acid), 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).[1][2][3][4] Hypochlorhydria is a reduction in the production of gastric acid.

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). This is characterized histopathologically by the loss of oxyntic glands that contain acid-producing parietal cells in the fundus and body of the stomach.[5][6][7] Chronic atrophic gastritis typically occurs from chronic inflammation, predominantly from chronic Helicobacter pylori infection or from autoimmune gastritis.[8]

History and exam

Other diagnostic factors

age >60 years
female sex
autoimmune disorders
weakness
lethargy
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
koilonychia

Full details

Risk factors

autoimmune disorders
age >60 years
Helicobacter pylori infection
prior gastric surgery
hypergastrinemia
gastric carcinoid

Full details

Diagnostic investigations

1st investigations to order

hemoglobin
biopsy of corpus and/or fundus of stomach
intragastric pH

Full details

Investigations to consider

serum gastrin
gastric acid secretory test (gastric analysis)
parietal cell antibodies
intrinsic factor antibodies
diagnostic tests for Helicobacter pylori infection
serum pepsinogen I and II (PGI and PGII)

Full details

Treatment algorithm

ACUTE

all patients

Contributors

Authors

C. Prakash Gyawali, MD, FRCP

Professor of Medicine

Division of Gastroenterology

WashU Medicine

St. Louis

Disclosures

CPG declares that he has no competing interests.

Acknowledgements

Dr C. Prakash Gyawali would like to gratefully acknowledge Dr Joseph Spataro, Dr Hamzeh Saraireh, Dr Mitchell L. Schubert, and Dr Juan Diego Baltodano, previous contributors to this topic.

Disclosures

JS declares that he has no competing interests. HS is the author of one study referenced in this topic. MLS is an author of several studies referenced in this topic. JDB declares that he has no competing interests.

Peer reviewers

George Triadafilopoulos, MD

Professor of Medicine

Department of Gastroenterology, Hepatology & Nutrition

Division of Internal Medicine

The University of Texas MD Anderson Cancer Center

Houston

Disclosures

GT declares that he has no competing interests.

Peter J. Kahrilas, MD

Gilbert H. Marquardt Professor of Medicine

Professor of Medicine (Gastroenterology and Hepatology)

Feinberg School of Medicine

Northwestern University

Evanston

Disclosures

PJK declares that he has no competing interests.

Heinz F. Hammer, MD

Associate Professor of Gastroenterology and Internal Medicine

Medical University of Graz

Attending Gastroenterologist

University Hospitals Graz

Austria

Disclosures

HFH has been reimbursed by AstraZeneca, Nycomed, and Janssen, the manufacturers of proton-pump inhibitors, for attending several conferences and speaking, and has been paid by AstraZeneca for running educational programs.

Peer reviewer acknowledgements

BMJ Best Practice topics are updated on a rolling basis in line with developments in evidence and guidance. The peer reviewers listed here have reviewed the content at least once during the history of the topic.

Disclosures

Peer reviewer affiliations and disclosures pertain to the time of the review.

References

Our in-house evidence and editorial teams collaborate with international expert contributors and peer reviewers to ensure that we provide access to the most clinically relevant information possible.

Key articles

Gupta S, Li D, El Serag HB, et al. AGA clinical practice guidelines on management of gastric intestinal metaplasia. Gastroenterology. 2020 Feb;158(3):693-702.Full text Abstract

Malfertheiner P, Megraud F, Rokkas T, et al. Management of Helicobacter pylori infection: the Maastricht VI/Florence consensus report. Gut. 2022 Aug 8.Full text Abstract

Chey WD, Howden CW, Moss SF, et al. ACG clinical guideline: treatment of Helicobacter pylori infection. Am J Gastroenterol. 2024 Sep 1;119(9):1730-53.Full text Abstract

Reference articles

A full list of sources referenced in this topic is available to users with access to all of BMJ Best Practice.

Differentials
- Antisecretory drug-induced hypochlorhydria and hypergastrinemia
More Differentials
Guidelines
- Treatment of Helicobacter pylori infection
- Management of Helicobacter pylori infection: the Maastricht VI/Florence consensus report
More Guidelines
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Achlorhydria

Summary

Definition

History and exam

Other diagnostic factors

Risk factors

Diagnostic investigations

1st investigations to order

Investigations to consider

Treatment algorithm

all patients

Contributors

Authors

C. Prakash Gyawali, MD, FRCP

Disclosures

Acknowledgements

Disclosures

Peer reviewers

George Triadafilopoulos, MD

Disclosures

Peter J. Kahrilas, MD

Disclosures

Heinz F. Hammer, MD

Disclosures

Peer reviewer acknowledgements

Disclosures

References

Key articles

Reference articles

A full list of sources referenced in this topic is available to users with access to all of BMJ Best Practice.

Differentials

Guidelines

Log in or subscribe to access all of BMJ Best Practice

Log in or subscribe to access all of BMJ Best Practice

Log in to access all of BMJ Best Practice