Medications for the Treatment of Gastric Acidity

These medications are potent inhibitors of H⁺,K⁺-ATPase. This enzyme, located in the apical secretory membrane of the parietal cell, plays a key role in the secretion of H+ (protons). These medications can completely inhibit acid secretion and have a long duration of action. They promote ulcer healing and are also key components of H. pylori eradication regimens. Proton pump inhibitors have replaced H2 blockers in most clinical situations because of efficacy.

Proton Pump Inhibitors

duodenal ulcers (ie, multiple ulcers, bleeding ulcers, those >Gastritis and GERD require 8 to 12 weeks of therapy; GERD additionally often requires long-term maintenance.

Long-term proton pump inhibitor therapy produces elevated gastrin levels, which lead to enterochromaffin-like cell hyperplasia. However, there is no evidence of dysplasia or malignant transformation in patients receiving this treatment. Micronutrient deficiencies (eg, vitamin B12 and magnesium) have been reported in a small number of patients. The absolute excess risk is 0.3 to 0.4% per patient per year. Some studies suggest that the risk of enteric infections such as Clostridioides difficile may be higher in patients receiving long-term therapy, but other studies do not support this observation. The absolute excess risk varies from 0 to 0.09% per patient. Carefully conducted studies have shown no effect on bone health or the risk of dementia, Parkinson disease, heart disease, and pneumonia.

H2 blockers are well absorbed from the gastrointestinal tract, with onset of action 30 to 60 minutes after ingestion and peak effects at 1 to 2 hours. IV administration produces a more rapid onset of action. Duration of action is proportional to dose and ranges from 6 to 20 hours. Doses should often be reduced in older patients.

For duodenal ulcers≥Gastritis

N

Cimetidine has minor antiandrogen effects expressed as reversible gynecomastia and, less commonly, erectile dysfunction with prolonged use. Mental status changes, diarrhea, rash, drug fever, myalgias, thrombocytopenia, and sinus bradycardia and hypotension after rapid IV administration have been reported with all H2 blockers, generally in < 1% of treated patients but more commonly in older patients.

Cimetidine

These agents neutralize gastric acid and reduce pepsin activity (which diminishes as gastric pH rises to >

Antacids relieve symptoms, promote ulcer healing, and reduce recurrence. They are relatively inexpensive but must be taken 5 to 7 times/day. The optimal antacid regimen for ulcer healing seems to be 15 to 30 mL of liquid or 2 to 4 tablets 1 and 3 hours after each meal and at bedtime. The total daily dosage of antacids should provide 200 to 400 mEq of neutralizing capacity. However, antacids have been superseded by acid-suppressive therapy in the treatment of peptic ulcer and are used only for short-term symptom relief.

In general, there are 2 types of antacids:

• Absorbable

• Nonabsorbable

Absorbable antacids

Nonabsorbable antacids (eg, aluminum or magnesium hydroxide) have fewer systemic adverse effects and are preferred.

Aluminum hydroxide causes constipation.

Certain prostaglandins (especially misoprostolmisoprostol are abdominal cramping and diarrhea, which occur in 30% of patients. Misoprostol is a powerful abortifacient and is absolutely contraindicated in women of childbearing age who are not using contraception.

sucralfate is negligible. Constipation occurs in 3 to 5% of patients. Sucralfate may bind to other medications and interfere with their absorption.

Potassium-competitive acid inhibitors (PCABs) work by competing for potassium on the luminal side of the parietal cell, causing rapid and reversible inhibition of proton pumps and therefore acid secretion (1).

H. pylori eradication (2, 3).