Pantoprazole selectively accumulates in the acidic environment of gastric parietal cells and acts at the final step of
acid secretion by binding 2 key
cysteine residues of the
proton pump involved in gastric acid production. The bioavailability of
pantoprazole is not altered by concomitant administration of food or
antacids or with repeated dosing. Both oral and IV formulations of
pantoprazole exhibit linear pharmacokinetics. Several clinical trials have proved
pantoprazole superior to histamine-2-receptor antagonists (H2RAs) in reducing
acid secretion and elevating gastric pH levels.
Pantoprazole has been shown to be more effective than
ranitidine (P < 0.05),
famotidine (P < 0.001), and
nizatidine (P < 0.05), and at least as effective as
omeprazole, in healing erosive
esophagitis and relieving associated symptoms of
GERD, including regurgitation.
Pantoprazole is also more effective than the H2RA
nizatidine for the treatment of nighttime
heartburn (P < 0.05). Studies have shown
pantoprazole to be well tolerated; adverse events, including
headache,
diarrhea,
flatulence,
abdominal pain,
eructation,
nausea, and
rash, occurred in < or = 6% of patients. The oral and IV formulations of
pantoprazole are equally potent in inhibiting gastric acid secretion; thus, switching between formulations requires no dosage adjustments. Special patient populations, including the elderly and patients with renal or mild to moderate hepatic impairment, can take
pantoprazole without an adjustment in dosage.
CONCLUSIONS: Because of its unique pharmacokinetic properties, mechanism of action, and reduced potential for producing
cytochrome P-450-based drug interactions,
pantoprazole in both oral and IV formulations is effective over a full 24 hours and is well tolerated in a variety of patient types.