You, me, and H. Pylori

"My wife gave me ulcers!" the patient said, quite angrily. He stood motionless at the pharmacy counter, clenching the over-the-counter products ...

Apr 1st, 2013


"My wife gave me ulcers!" the patient said, quite angrily. He stood motionless at the pharmacy counter, clenching the over-the-counter products he was holding so tightly that I was reasonably sure I would be the victim of an imminent package-ripping, tablet-flying, bottle-popping explosion. I found myself hoping that he had selected the cherry-cream-flavored antacid, my personal favorite.

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"How can you be so sure?" I responded, softly, and somewhat tongue-in-cheek.

"She has ulcers, and my doctor told me now I have them too!" he said, defiantly.

"I don't know," I said, with a smile. "Maybe you should review the list of suspects again. My coworkers here give me agita all the time." I could feel the playful glares of my coworkers coming at me from every corner of the pharmacy.

He stood there staring at me for a few moments and then, finally, he relaxed and smiled.

"I'm serious," he said. "My doctor said that our ulcers are caused by some kind of infection and that I may have caught the infection from her. Is that true?"

Peptic ulcer disease occurs when there is a disruption of the fragile balance between factors that are protective of the gastric mucosa (such as secretions of mucus and bicarbonate) and factors that are destructive to it (such as secretions of hydrochloric acid and pepsin). Ulcers are defined as "breaks" in the gastrointestinal mucosa, which may occur in the stomach, duodenum, or small intestine.

Under normal conditions, the presence of food stimulates the parietal cells in the stomach wall to secrete hydrochloric acid. However, physical and emotional stress, psychological illness, and certain medical conditions can increase the risk of ulcers, since they may also stimulate secretion of hydrochloric acid.

Key to the overall health of the gastric mucosa is the presence of cytoprotective prostaglandins. Prostaglandins enhance the gastric mucosal cells' resistance to injury by maintaining mucosal blood flow (which removes any infiltrating acid) and by stimulating the secretion of mucus and bicarbonate. So, patients who use nonsteroidal anti-inflammatory agents (NSAIAs) on a regular basis are at high risk for the formation of ulcers, since these drugs inhibit prostaglandin production. At the same time, patients who eat diets rich in vegetable oils may be at lower risk for the formation of ulcers, since these oils are a rich source of the building blocks for prostaglandin production.

Most ulcers are related to the presence of the organism H. pylori, which causes inflammation of the mucosa. H. pylori is usually acquired as a result of poor sanitation, contaminated food, shared eating and drinking utensils, and, yes, even kissing. At first, the organism colonizes the mouth and then it descends to colonize the gastric mucosa, where it can persist indefinitely.

Patients with peptic ulcer disease endure pain that is sometimes described as a "burning" or "gnawing" and which may or may not be relieved by the ingestion of food. Symptoms may disappear for weeks or months only to reappear again. Increased intensity or frequency of pain may indicate a worsening of the disease, including deeper tissue involvement and complications such as bleeding and perforation.

The treatment of peptic ulcer disease begins with the elimination, if possible, of all factors that contribute to the incidence of the disease. The patient's medication therapy is changed to avoid the use of ulcerogenic medications, such as aspirin, NSAIAs, and corticosteroids. Lifestyle changes such as smoking and alcohol cessation, avoidance of foods that aggravate symptoms, and reduction of stress are encouraged.

Patients with peptic ulcer disease are initially treated with drug regimens aimed at eradicating H. pylori. These regimens include proton pump inhibitors, antimicrobials, and/or bismuth subsalicylate (Pepto-Bismol) and are taken for up to 14 days for eradication of the infection. Histamine-2 receptor antagonists and proton pump inhibitors are the mainstay of therapy of peptic ulcer disease, aimed at reducing acid secretion in the stomach.

Histamine-2 receptor antagonists inhibit gastric acid secretion by competitively inhibiting the action of histamine at its receptors on the parietal cells. Tagamet (cimetidine) was the first histamine-2 receptor antagonist introduced, but it has been replaced by famotidine (Pepcid), ranitidine (Zantac), and nizatidine (Axid), since they cause fewer adverse effects and drug interactions.

Adverse reactions of histamine-2 receptor antagonists include CNS effects (such as delusions, confusion, and headache) and oral manifestations (such as xerostomia, taste alterations, and halitosis). Over the course of therapy, tolerance develops to the effect of the histamine-2 receptor antagonists as gastric histamine release increases to compensate for their effects.

Proton pump inhibitors (PPIs) inhibit gastric acid secretion by binding to the "proton pump" of the parietal cells, inhibiting the secretion of hydrogen ions or "protons" (the basis of acid in our physiology). Proton pump inhibitors such as Prilosec (omeprazole), Nexium (esomeprazole), Prevacid (lansoprazole), Protonix (pantoprazole), and Aciphex (rabeprazole) effectively heal ulcers more rapidly than other agents and tolerance to their effects does not occur.

Adverse effects of the proton pump inhibitors include headache and abdominal pain. Long-term use of the proton pump inhibitors, especially at high doses, has been associated with an increased risk of osteoporotic fractures and possible tooth demineralization (due to impaired acid secretion and, thus, calcium absorption). Oral manifestations of these agents include xerostomia and mucosal atrophy of the tongue.

Antacids contain various magnesium, aluminum, and calcium salts. They are quite effective in promoting the healing of ulcers due to their ability to neutralize available stomach acid on contact. However, they are so effective in neutralizing stomach acid, they sometimes cause rebound hyperacidity.

Adverse effects of antacids include hypercalcemia (calcium salts), which is problematic for patients with renal disease or patients at high risk for kidney stones, constipation (aluminum salts), and diarrhea (magnesium salts). The latter two adverse effects are often ameliorated by combining aluminum and magnesium salts in the same preparation.

All of the antacids, all of the histamine-2 receptor antagonists, and two of the proton-pump inhibitors (Prilosec and Prevacid) are available over-the-counter. As a result, patients often self-medicate their condition with these agents, with or without medical supervision, and may not disclose the use of these agents and the existence of their symptoms during a review of their medical history. In addition, self-medicating patients often fail to make lifestyle changes necessary for successful therapy.

Self-medicating patients may also fail to recognize and address adverse reactions and drug interactions. Many patients combine two or three agents in an attempt to maximize their beneficial effects. Unfortunately, this often compounds mutual adverse effects and drug interactions.

Histamine-2 receptor antagonists (especially Tagamet) and proton pump inhibitors (especially Prilosec) inhibit the hepatic metabolism of many drugs, including warfarin, metronidazole, lidocaine, phenytoin, diazepam, carbamazepine, benzodiazepines, and antidepressants. This may result in decreased metabolism of these drugs, enhanced duration of action (including adverse reactions), and possibly toxic blood levels.

Proton pump inhibitors and antacids are so effective in preventing stomach acid secretion, the resulting high gastric pH interferes with the absorption and efficacy of other drugs, vitamins, and minerals. This is one mechanism by which Prilosec may interfere with the cardioprotective effects of Plavix (clopidogrel).

Antacids may bind to the surface of some drugs and reduce their overall efficacy, including, ironically, histamine-2 receptor antagonists and proton pump inhibitors. Antacids also alter urinary pH and interfere with the renal excretion of some drugs.

Overall, it is possible to minimize the adverse effects and numerous drug interactions associated with these medications by adjusting doses and administration times. However, while these dosing adjustments are often required, they may not be made in patients who self-medicate.

So, what is the best way to manage your patient if they have peptic ulcer disease? The first step is to assess the severity of the condition and the degree to which it is being controlled. Are they self-medicating? Is medical consultation necessary? Many patients with ulcers continue to smoke and drink alcohol. They should be encouraged at every visit to quit smoking and avoid alcohol.

Patients with ulcers may have underlying emotional stress and psychological conditions, which may warrant stress-reduction techniques. Medications used in dentistry that are ulcerogenic (such as NSAIAs) should be avoided in favor of medications that are benign to the gastric mucosa, (such as acetaminophen). Since antacids, histamine-2 receptor antagonists, and proton-pump inhibitors may interact with medications used in dentistry (such as metronidazole, lidocaine, and benzodiazepines), as well as medications that may have an impact on dentistry (such as warfarin), a complete medical history and possible medication dosage adjustments may be required. Proper patient positioning in the dental chair (semi-supine position) may increase patient comfort.

I spent a few minutes counseling my patient on the treatment of his peptic ulcer disease and the over-the-counter products he was purchasing. As he was leaving, he mentioned that he was meeting his wife for dinner. I couldn't help but wonder about his dinner choice … and the topic of conversation. RDH

THOMAS A. VIOLA, RPH, CCP, In addition to his daily practice of the profession of pharmacy, Thomas A. Viola, RPh, CCP, also serves the professions of dentistry, dental hygiene, and dental assisting as an educator, published writer, and professional speaker. As an educator, Viola is a member of the faculty of seven dental hygiene and dental assisting programs, as well as several national board exam review courses. Visit Viola’s website:

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