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Acid-suppressing therapy


Proton pump inhibitors (PPIs) such as omeprazole (Prilosec), esomeprazole (Nexium), and patoprazole (Protonix) have become some of the most widely used drugs in the country, in large part because of aggressive marketing to both doctors and patients. The drugs suppress stomach acid production almost completely, and as such are useful in patients with severe gastroesophageal reflux disease (GERD) or peptic ulcer. However, when taken p.r.n. (as many patients take them), they can require up to 24 hours to produce full symptom relief. Regular use can result in painful rebound hyperacidity when the drug is stopped if it is not tapered properly.

PPIs are often used unnecessarily in patients who do not require total suppression of acid production. This is of particular concern in light of the following considerations.

  • The Journal of the American Medical Association reported in December 2005 that PPI use triples the risk of potentially dangerous Clostridium difficile diarrhea in primary care patients.1
  • In the same month, the federal Agency for Healthcare Research and Quality released an exhaustive overview of treatments for GERD. It concluded that while PPIs are the most effective medication for patients who actually have this condition, they caused more side effects than the H2 blockers.2
  • Because these drugs are so costly, they can have important adverse effects on patients' budgets, as well as on fiscally-strapped public programs that help patients pay for their prescriptions.
  • The more prescriptions a patient has to juggle, the greater the likelihood of reduced compliance with essential drugs, as well as increased risk of medication errors and adverse drug reactions.3-5

For acute use, "PPI p.r.n." may not spell "relief." PPIs do not work well p.r.n. because they can take over 24 hours to suppress acid to clinically useful levels.6

PPIs are rarely required as first-line therapy.7 PPIs should be used as initial treatment only in patients with severe GERD, peptic ulcer disease, or Zollinger-Ellison syndrome, as well as those being given a regimen to eradicate H. pylori.

Alternative initial choices exist for indications other than those above.

  • GERD: H2 blockers and antacids should be used as first-line therapy, and will provide a 60-70% rate of symptom relief.7
  • Non-ulcer ("functional") dyspepsia (NUD): There is little difference between the effectiveness of H2 blockers vs. PPIs,8 and many patients benefit from promotility drugs rather than acid suppression.9

Non-prescription alternatives work well for many patients.

  • Avoid NSAIDs, alcohol, tobacco, nicotine, caffeine, and chocolate.
  • Avoid large meals right before bedtime.
  • Elevate the head of the bed.
  • Replace tight clothing that restricts the abdomen.
  • Don't recline within 2-3 hours after a meal.
  • Lose weight.

If the clinical picture suggests peptic ulcer disease, eradicate H. pylori.10 The regimen of choice is triple therapy with a PPI, amoxicillin, and clarithromycin.11

If first-line treatment fails, it doesn't matter which PPI you use, as they all have similar efficacy.12-19

If patients are on PPIs, they can be tapered in several common conditions:

  • GERD, when patient is symptom-free.
  • Peptic ulcer disease, after 8 weeks of therapy and H. pylori eradication.
  • NUD, when patient is symptom-free.

PPIs can lead to hypergastrinemia, which can result in hypersecretion of acid when the PPI is stopped. This can make it difficult for some patients to discontinue use.20 For this reason, the following tapering regimen is recommended.

  • Reduce PPI dose by half the first two weeks. Reduce by half again if the patient was taking high-dose PPI.
  • Stop PPI and prescribe rescue therapy (antacids and H2 blockers) for the next two weeks.
  • Slowly decrease use of H2 blockers and antacids as symptoms improve.

These are general recommendations only; specific clinical decisions should be made by the treating physician based on an individual patient's clinical condition.

References:

  1. Dial S, Delaney JA, Barkun AN, Suissa S. Use of gastric acid-suppressive agents and the risk of community-acquired Clostridium difficile-associated disease. Journal of the American Medical Association. 2005:294(23):2989-95.
  2. Comparative effectiveness of management strategies for gastroesophageal reflux disease. AHRQ Pub No. 06-CH003. December 1, 2005. Available at: http://effectivehealthcare.ahrq.gov/repFiles/GERD%20Final%20Report.pdf.
  3. Chapman RH, Benner JS, Petrilla AA, Tierce JC, Collins SR, Battleman DS, Schwartz JS. Predictors of adherence with antihypertensive and lipid-lowering therapy. Archives of Internal Medicine. 2005;165:1147-52.
  4. Atkin PA, Veitch PC, Veitch EM, Ogle SJ. The epidemiology of serious adverse drug reactions among the elderly. Drugs & Aging. 1999;14:141-52.
  5. Schneeweiss S, Hasfor J, Gottler M, Hoffmann A, Riethling AK, Avorn J. Admissions caused by adverse drug events to internal medicine and emergency departments in hospitals: A longitudinal population-based study. European Journal of Clinical Pharmacology. 2002;58:285-91.
  6. Spechler S, Peikin S, El-Serag H. Medication strategies for heartburn. American Gastroenterological Association. September 16, 2002.
  7. Peterson WL. Improving the management of GERD. Evidence-based therapeutic strategies. Consensus Opinion in Gastroenterology, American Gastroenterology Association. 2004.
  8. Blum AL, Arnold R, Stolte M, Fischer M, Koelz HR. Short course acid suppressive treatment for patients with functional dyspepsia: Results depend on Helicopter pylori status. The Rosch Study Group. Gut. 2000;47:473-80.
  9. Allescher HD, Bockenhoff A, Knapp G, Wienbeck M, Hartung J. Treatment of non-ulcer dyspepsia: A meta-analysis of placebo-controlled prospective studies. Scandinavian Journal of Gastroenterology. 2001;36:934-41.
  10. Gisbert JP, Khorrami S, Carballo F, Calvet X, Gene E, Dominguez-Munoz JE. H. pylori eradication therapy vs. antisecretory non-eradication therapy (with or without long-term maintenance antisecretory therapy) for the prevention of recurrent bleeding from peptic ulcer. Cochrane Database Syst Rev. 2003;(4):CD004062.
  11. Talley NJ, Vakil N. Practice Parameters Committee of the American College of Gastroenterology. Guidelines for the management of dyspepsia. American Journal of Gastroenterology. 2005;100(10):2324-37.
  12. McDonagh MS, Carson S, for the Oregon Evidence-based Practice Center. Drug class review on proton pump inhibitors. April 2004.
  13. Langman MJ. Which PPI? Gut. 2001;49:309-10.
  14. Stedman CA, Barclay ML. Review article: Comparison of the pharmacokinetics, acid suppression and efficacy of proton pump inhibitors. Alimentary Pharmacology & Therapeutics. 2000;14:963-78.
  15. Vanderhoff BT, Tahboub RM. Proton pump inhibitors: An update. American Family Physician. 2002;66:273-80.
  16. Welage LS, Berardi RR. Evaluation of omeprazole, lansoprazole, pantoprazole, and rabeprazole in the treatment of acid-related disorders. Journal of the American Pharmaceutical Association. 2000;40:52-62; quiz:121-3.
  17. Carswell CI, Goa KL. Rabeprazole: An update of its use in acid-related disorders. Drugs. 2001;61:2327-56.
  18. Hutchinson TA, Shahan DR, eds. Drugdex system. Vol.116. Greenwood Village, CO. Micromedex; edition expires 2003.06.
  19. Chan J. Acid-peptic therapy. In: Anderson PO, Knoben JE, Troutman WG, eds. Handbook of clinical drug data. 10th ed. Toronto: McGraw-Hill;2002:528-52.
  20. Qvigstad G, Waldum H. rebound hypersecretion after inhibition of gastric acid secretion. Basic & Clinical Pharmacology & Toxicology. 2004;94:202-8.