GI Pharmacology: Drugs for Peptic Ulcer

Introduction / Overview

Peptic ulcer disease (PUD) remains a prevalent gastrointestinal disorder, affecting millions worldwide. The pathogenesis of PUD is multifactorial, involving an imbalance between aggressive factors such as gastric acid secretion, pepsin activity, and mucosal defensive mechanisms. Pharmacologic intervention targets this imbalance, aiming to reduce acid production, protect the mucosa, or eradicate Helicobacter pylori infection. The therapeutic landscape has evolved considerably over the past decades, with the introduction of proton pump inhibitors (PPIs), histamine‑2 receptor antagonists (H2RAs), misoprostol, and bismuth compounds. Understanding the pharmacodynamics, pharmacokinetics, and safety profiles of these agents is essential for effective clinical management and for anticipating drug–drug interactions, especially in patients with comorbidities or polypharmacy.

Learning objectives for this chapter include:

• Identify the major drug classes used in the treatment of peptic ulcer disease.
• Explain the mechanisms of action of proton pump inhibitors, H2 receptor antagonists, misoprostol, and bismuth preparations.
• Describe the pharmacokinetic properties and dosing considerations for each drug class.
• Recognize the therapeutic indications, off‑label uses, and contraindications associated with these agents.
• Summarize the common and serious adverse effect profiles and highlight key drug interactions.
• Apply relevant pharmacologic knowledge to special populations such as pregnant women, elderly patients, and those with hepatic or renal impairment.

Classification

Drug Classes and Categories

Therapeutic agents for peptic ulcer disease are broadly categorized into four main groups:

• Proton Pump Inhibitors (PPIs) – irreversible inhibitors of the H⁺/K⁺‑ATPase enzyme located on the gastric parietal cell canalicular membrane.
• Histamine‑2 Receptor Antagonists (H2RAs) – competitive antagonists of histamine H₂ receptors, thereby suppressing acid secretion.
• Prostaglandin Analogues (misoprostol) – synthetic prostaglandin E1 analogue with mucosal protective and anti‑secretory effects.
• Bismuth Compounds – agents such as bismuth subcitrate and subcitrate‑glycinate, which provide mucosal protection and possess antibacterial activity against H. pylori.

Some agents possess dual functions. For example, ranitidine is both an H₂RA and possesses mild antacid properties, while misoprostol also demonstrates anti‑ulcer effects in the esophagus and stomach.

Chemical Classification

From a chemical perspective, PPIs are small heterocyclic compounds containing a substituted 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Although the chemical nomenclature is complex, the pharmacologic activity of each class is primarily defined by its target interaction rather than by structural details.

Mechanism of Action

Proton Pump Inhibitors

PPIs bind covalently to the cysteine residues of the H⁺/K⁺‑ATPase enzyme, thereby irreversibly inhibiting acid secretion. The binding occurs after proton‑pump activation, which is mediated by gastrin, histamine, and acetylcholine. Because the inhibition is irreversible, new pumps must be synthesized to restore acid secretion, leading to a prolonged reduction in intragastric pH. PPIs are structurally heteroaryl‑propionic acids and are prodrugs that require activation within the acidic gastric environment. Upon oral administration, they remain largely unchanged in the bloodstream but are absorbed in the small intestine before reaching the stomach, where they are protonated and activated by pepsin in the acidic milieu.

Histamine‑2 Receptor Antagonists

H2RAs competitively inhibit histamine binding to the H₂ receptors on parietal cells, thereby reducing cyclic AMP production and subsequent proton secretion. They also inhibit acetylcholine‑mediated stimulation of acid secretion, although to a lesser extent than histamine. The blockade is reversible; therefore, acid secretion resumes gradually as the drug concentration falls. H2RAs display a shorter half‑life compared with PPIs, resulting in a less sustained acid suppression over 24 hours.

Misoprostol

Misoprostol is a synthetic analogue of prostaglandin E1 (PGE1). It activates EP2 and EP4 receptors on gastric mucosal cells, leading to increased mucous and bicarbonate secretion, enhanced mucosal blood flow, and delayed gastric emptying. Additionally, it suppresses acid secretion indirectly. The drug’s anti‑ulcer effect is mediated by mucosal protection rather than acid suppression. Misoprostol is notable for its anti‑nausea, anti‑emetic, and anti‑diarrheal properties, which may contribute to its tolerability profile in certain settings.

Bismuth Compounds

Bismuth salts act by forming a protective coating over ulcerated mucosa, thereby preventing further injury from gastric acid and pepsin. Bismuth also exhibits bacteriostatic activity against Helicobacter pylori, primarily through inhibition of urease and interference with bacterial adhesion. The dual role of bismuth in mucosal protection and bacterial inhibition makes it a valuable component of quadruple therapy regimens for H. pylori eradication.

Pharmacokinetics

Absorption

PPIs are weakly acidic prodrugs that are absorbed in the proximal small intestine. Their bioavailability is variable (approximately 20–40%) due to extensive first‑pass metabolism and pH‑dependent solubility. H2RAs exhibit high oral bioavailability (70–90%) and are primarily absorbed in the small intestine as well. Misoprostol is poorly absorbed (15–20%), with most of the dose reaching the colon, which may contribute to its gastrointestinal side effects. Bismuth salts are poorly absorbed (<1%) and remain largely in the gastrointestinal tract, where they exert their local effects.

Distribution

PPIs are highly protein‑bound (>95%) and distribute widely into tissues, including the gastric mucosa. H2RAs also demonstrate substantial protein binding, though less than PPIs. Misoprostol’s distribution is limited due to low absorption, but it can enter systemic circulation in small amounts. Bismuth compounds remain largely confined to the gastrointestinal lumen and have negligible systemic distribution.

Metabolism

PPIs undergo extensive hepatic metabolism via the cytochrome P450 system, particularly CYP2C19 and CYP3A4, leading to active and inactive metabolites. Genetic polymorphisms in CYP2C19 can influence PPI efficacy and drug levels. H2RAs are metabolized primarily by CYP1A2 and CYP2D6, with some hepatic glucuronidation. Misoprostol is metabolized by hepatic esterases and cytochrome P450 enzymes, resulting in inactive metabolites. Bismuth salts are not significantly metabolized; they are excreted unchanged.

Excretion

PPIs are excreted mainly through the kidneys as metabolites and in the bile as unchanged drug. H2RAs are eliminated via renal excretion of metabolites and unchanged drug. Misoprostol metabolites are excreted renally and via feces. Bismuth compounds are excreted unchanged in feces, with minimal renal elimination.

Half‑Life and Dosing Considerations

PPIs have a clinical half‑life of approximately 1–2 hours, but the pharmacodynamic effect persists for 24–48 hours due to irreversible pump inhibition. Standard dosing ranges from 20 mg to 40 mg once daily, typically taken 30–60 minutes before a meal. H2RAs exhibit a half‑life of 2–3 hours; dosing may be 50 mg twice daily or 100 mg once daily for ulcer prevention. Misoprostol is dosed at 200 μg four times daily for ulcer prophylaxis, although lower doses (200 μg) are used for gastro‑protective indications. Bismuth subcitrate or subcitrate‑glycinate is usually prescribed 500 mg four times daily in combination with antibiotics for H. pylori eradication.

Therapeutic Uses / Clinical Applications

Approved Indications

PPIs are indicated for the treatment of erosive esophagitis, peptic ulcer disease, Zollinger‑Ellison syndrome, and for the prevention of NSAID‑associated ulcers in high‑risk patients. H2RAs are employed for uncomplicated peptic ulcer disease, prevention of NSAID‑related gastric injury, and in combination therapy for H. pylori eradication. Misoprostol is approved for the prevention of NSAID‑induced gastric ulcers, particularly in patients with a history of ulceration or concurrent corticosteroid use. Bismuth compounds are primarily used as part of quadruple therapy for H. pylori eradication and for the treatment of duodenal ulcers refractory to PPI therapy.

Off‑Label Uses

PPIs are frequently prescribed off‑label for dyspepsia of unclear etiology, functional heartburn, and gastro‑esophageal reflux disease (GERD) refractory to lifestyle modifications. H2RAs have been applied in the management of gastric antral vascular ectasia (GAVE) and in certain cases of Zollinger‑Ellison syndrome when PPIs are insufficient. Misoprostol is occasionally used in the prevention of gastric bleeding in patients receiving long‑term anticoagulation or antiplatelet therapy, although the risk of diarrhea limits widespread adoption. Bismuth salts are also utilized in empiric treatment of chronic gastritis and in the management of peptic ulcer disease when H. pylori infection is uncertain.

Adverse Effects

Common Side Effects

PPIs can produce headache, abdominal pain, flatulence, diarrhea, nausea, and, with prolonged use, increased risk of Clostridioides difficile infection and fractures. H2RAs are associated with headache, dizziness, constipation, and, in older adults, confusion. Misoprostol’s most frequent adverse effects include abdominal cramps, diarrhea, nausea, and vomiting, reflecting its prostaglandin activity. Bismuth compounds commonly cause black discoloration of stool or tongue, metallic taste, and, rarely, neuropathy with chronic exposure.

Serious / Rare Adverse Reactions

PPIs have been linked to hypomagnesemia, vitamin B₁₂ deficiency, and potential increased susceptibility to pneumonia and upper respiratory tract infections. H2RAs may precipitate paradoxical acid breakthrough in some patients. Misoprostol’s severe GI toxicity includes severe diarrhea and dehydration, especially within the first 24–48 hours of therapy. Bismuth toxicity, though uncommon, can manifest as neurotoxicity, renal impairment, and, in extreme cases, acute liver failure.

Black Box Warnings

PPIs carry a black box warning regarding the potential for serious infections and bone fractures with long‑term use. Misoprostol carries a warning related to the risk of severe diarrhea and dehydration, particularly among the elderly and patients with renal insufficiency. Bismuth compounds have warnings about neurotoxicity with high cumulative doses.

Drug Interactions

Major Drug–Drug Interactions

PPIs inhibit CYP2C19, thereby increasing plasma concentrations of drugs metabolized by this enzyme, such as clopidogrel, diazepam, and certain antiepileptics. PPIs also reduce the absorption of drugs requiring an acidic environment, including ketoconazole, mycophenolate mofetil, and iron salts. H2RAs can potentiate the anticoagulant effect of warfarin by reducing stomach acidity and thus vitamin K absorption. Misoprostol may interact with antiplatelet agents, increasing the risk of bleeding. Bismuth compounds can interfere with the absorption of tetracyclines and fluoroquinolones, potentially reducing their antibacterial efficacy.

Contraindications

PPIs and H2RAs are contraindicated in patients with known hypersensitivity to the drug or its excipients. Misoprostol should not be used in patients with active peptic ulcer bleeding or with high risk of severe diarrhea. Bismuth compounds are contraindicated in patients with hypersensitivity to bismuth or in those with severe renal impairment due to the risk of accumulation.

Special Considerations

Use in Pregnancy / Lactation

PPIs are classified as category B in pregnancy, suggesting no evidence of risk in humans. Limited data exist for H2RAs, which are also category B. Misoprostol is contraindicated in pregnancy due to its uterotonic effects. Lactation: PPIs and H2RAs are excreted in breast milk at low levels; the risk appears minimal. Misoprostol is excreted in milk, and its use is discouraged during lactation. Bismuth compounds are excreted in milk; caution is advised.

Pediatric / Geriatric Considerations

In children, PPIs are used for GERD and H. pylori eradication, with dosing adjusted for weight. H2RAs are commonly prescribed for infantile reflux. Elderly patients exhibit altered pharmacokinetics and higher susceptibility to adverse effects, particularly hypomagnesemia and infections with PPIs. Dose adjustments and monitoring of renal function are recommended.

Renal / Hepatic Impairment

PPIs are metabolized hepatically; severe hepatic dysfunction may require dose reduction. Renal impairment can lead to accumulation of metabolites; however, most PPIs are cleared by the liver and can be used at standard doses. H2RAs may require dose modification in severe hepatic disease. Misoprostol is renally cleared; dosage reduction may be necessary in renal insufficiency. Bismuth compounds should be avoided in patients with severe renal failure due to the risk of systemic toxicity.

Summary / Key Points

• Proton pump inhibitors provide the most potent and sustained acid suppression, making them first‑line therapy for peptic ulcer disease and NSAID‑induced ulcer prophylaxis.
• Histamine‑2 receptor antagonists offer rapid onset but shorter duration, useful for breakthrough pain and as adjuncts in H. pylori regimens.
• Misoprostol protects gastric mucosa through prostaglandin‑mediated mechanisms but is limited by gastrointestinal intolerance.
• Bismuth compounds serve both as mucosal protectants and antibacterial agents, forming the cornerstone of quadruple therapy for H. pylori eradication.
• Drug interactions, particularly with PPIs and H2RAs, can alter the effectiveness and safety of concurrent medications; vigilant review of medication lists is recommended.
• Special populations—including pregnant women, lactating mothers, elderly patients, and those with hepatic or renal impairment—require careful dose adjustments and monitoring to mitigate adverse outcomes.

Mastery of the pharmacologic principles outlined above facilitates evidence‑based decision making in the management of peptic ulcer disease, enhancing patient outcomes while minimizing the risk of complications.

References

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