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A02BX comprises other drugs used for peptic ulcer disease and gastro‑oesophageal reflux disease (GORD), including mucosal protectants, bismuth salts, antireflux alginates and several less commonly used antisecretory or cytoprotective agents.

Pharmacological overview

Subgroup A02BX belongs to ATC group A02 “Drugs for acid related disorders” within the alimentary tract and metabolism system.
It is defined as “Other drugs for peptic ulcer and gastro‑oesophageal reflux disease (GORD)” and contains heterogeneous agents that do not fit the main H2‑blocker (A02BA) or proton pump inhibitor (A02BC) classes.

Key active substances include carbenoxolone, sucralfate, pirenzepine, bismuth subcitrate/subnitrate, proglumide, gefarnate, sulglicotide, alginic acid, rebamipide, teprenone and irsogladine, as well as certain combinations (e.g. carbenoxolone with psycholeptics).
Clinically these medicines are used for treatment and prophylaxis of gastric and duodenal ulcers, erosive gastritis, GORD, and in some cases as part of Helicobacter pylori eradication regimens or for symptom control in reflux disease.

Mechanisms of action

• Carbenoxolone and acetoxolone are synthetic derivatives of glycyrrhetinic acid that enhance mucosal defensiveness and may influence prostaglandin synthesis and mucus secretion.
• Sucralfate acts as a local mucosal protectant forming a viscous, adhesive barrier over ulcer craters in acid environments and binding bile salts and pepsin.
• Bismuth subcitrate and subnitrate combine mucosal protective effects with direct anti‑Helicobacter pylori activity and toxin binding.
• Pirenzepine is a selective M1 muscarinic antagonist that reduces gastric acid secretion while relatively sparing other cholinergic functions.
• Proglumide and related agents (e.g. some glutamic acid derivatives) act as gastrin receptor antagonists or modulators of gastric secretory responses.
• Gefarnate, sulglicotide, rebamipide, teprenone and irsogladine are cytoprotective agents that enhance endogenous prostaglandins, mucus and microcirculation, thereby improving mucosal resistance to injury.
• Alginic acid preparations for GORD form a low‑density, viscous “raft” that floats on the gastric contents, reducing reflux of acid into the oesophagus and providing mechanical protection; many marketed suspensions combine alginate with antacids such as aluminium hydroxide and calcium carbonate.

General toxicological profile

Overall, A02BX medicines have a relatively favourable systemic toxicological profile when used at recommended doses, but some class‑specific risks are clinically important.

• Carbenoxolone can cause sodium and water retention, hypertension, hypokalaemia and oedema, reflecting mineralocorticoid‑like effects similar to liquorice; these effects are dose‑related and more pronounced in older patients or those with cardiovascular/renal disease.
• Bismuth salts may cause darkening of stool and tongue; with prolonged high‑dose use, bismuth accumulation can rarely lead to neurotoxicity (encephalopathy).
• Sucralfate has minimal systemic absorption but can contribute to aluminium load, particularly in patients with chronic kidney disease, where accumulation of aluminium is undesirable.
• Pirenzepine and proglumide may cause anticholinergic or gastrointestinal adverse effects, including dry mouth, blurred vision, constipation or diarrhoea, and rarely CNS symptoms.
• Cytoprotective agents such as rebamipide, teprenone, gefarnate and irsogladine are generally well tolerated; reported adverse reactions are usually mild (e.g. gastrointestinal discomfort, headache, rash).
• Alginate‑based GORD products have low systemic toxicity; adverse effects are mainly gastrointestinal (bloating, nausea, constipation or diarrhoea) and hypersensitivity to excipients.

From a reproductive toxicology perspective, long‑term mucosal inflammation due to chronic Helicobacter pylori infection carries its own risk profile, including development of intestinal metaplasia and eventual gastric carcinoma if left untreated, which must be balanced against the toxicological risks of pharmacotherapy.

Lactation safety considerations (group level)

For most A02BX medicines, high‑quality controlled data in breastfeeding are limited, and risk assessment relies on pharmacokinetic properties, systemic bioavailability, maternal adverse‑effect profiles and long clinical experience.

• Sucralfate and alginate‑antacid combinations have negligible systemic absorption; transfer into breast milk is expected to be minimal, and clinically relevant exposure of the breastfed infant is unlikely at therapeutic doses.
• Bismuth salts show low oral bioavailability, and bismuth does not appear to accumulate in breast milk at significant levels during short‑term standard dosing, though prolonged or high‑dose use warrants caution because of theoretical neurotoxicity.
• Carbenoxolone’s systemic actions and potential for electrolyte disturbances and mineralocorticoid‑like effects suggest careful use in breastfeeding, especially in mothers with hypertension, cardiac disease or renal impairment; infant exposure via milk is expected to be low but has not been extensively quantified.
• Pirenzepine, proglumide and some cytoprotective agents may pass into milk to a limited extent depending on lipophilicity and protein binding, but clinically significant infant effects have not been clearly documented; however, anticholinergic or CNS‑active properties justify a precautionary approach, particularly in neonates and premature infants.

Given the heterogeneity of A02BX, lactation decisions should be individualised: agents with minimal systemic absorption (sucralfate, alginates) are generally preferred when an A02BX medicine is needed in a breastfeeding mother, while systemic antisecretory and bismuth agents call for a more detailed benefit‑risk evaluation.
In all cases, monitoring of the infant for poor weight gain, gastrointestinal intolerance, changes in stool colour or unusual behaviour represents a pragmatic safety measure in clinical practice.

Example table: selected A02BX agents

Clinical positioning in pregnancy and lactation

During pregnancy, the choice of agent for peptic ulcer and GORD must consider both maternal disease severity and fetal safety; guidelines typically prioritise lifestyle measures, antacids, alginates and H2‑blockers before less established A02BX options.
In breastfeeding, the need for acid control or mucosal protection should be weighed against the drug’s systemic bioavailability and toxicology profile, favouring locally acting or minimally absorbed medicines whenever possible.

For women with chronic Helicobacter pylori infection, eradication therapy (often combining bismuth, antibiotics and a PPI) may be indicated to prevent long‑term complications such as gastric carcinoma; the timing of eradication relative to pregnancy and lactation requires individualised assessment and, ideally, specialist consultation.
By actively identifying and treating H. pylori infection, clinicians can reduce the burden of peptic ulcer disease and the downstream need for chronic antisecretory therapy, aligning with the broader goal of lowering toxic exposures for mothers and infants.