Nothing is ever simple in this complex world of ours. Even ulceration of our gastrointestinal tracts goes beyond elementary caustic erosion to something far more involved, with one plus one surpassing two. Helicobacter pylori, a major protagonist in this drama, is an uninvited bacterial guest in 80% of the developing world and 20–50% of the industrialized world’s stomachs. Nonsteroidal anti-inflammatory drugs (NSAIDs) costar, with their more than 30 billion over-the-counter tablets and 70 million prescriptions sold yearly in the United States. H. pylori plus or minus a widespread pill-popping mentality can add up to gastritis, peptic ulcer disease (PUD), gastric lymphoma, or gastric cancer. Isn’t it high time we ganged up on gastritis and his big brother, uncompromising ulcer?
While multiple factors such as cigarette smoking, genetic predisposition (in first-degree relatives), psychological stress (neuroticism), diet, beverages containing alcohol and caffeine, and specific disorders (chronic pulmonary disease, chronic renal failure, liver cirrhosis, kidney stones, hyperparathyroidism, coronary artery disease, chronic pancreatitis) may play a role in the pathogenesis of gastritis and PUD, the main culprits are still our pesky bacteria and our friendly, neighborhood pharmacies. When the aggressive factors mentioned, along with defects in gastrointestinal protection/repair and an unhealthy dose of gastric acid, have their way with us, we are left with no choice but to submit and then call on a gang of our own for support against these chronic thugs.
When do we sound the alarm, however? Abdominal pain, in the form of a burning or gnawing discomfort 90 minutes to 3 hours after a meal and relieved by food or antacids, is suspect. Should the pain disturb our nightly slumber and creep upon us with two accomplices, namely nausea and vomiting, it becomes necessary to call in the professionals, before something far more sinister transpires. Left to its own devices or benevolently ignored, PUD can progress from simple misdemeanor to complicated capital crime of gastrointestinal bleeding, perforation, or gastric outlet obstruction. Like thieves in the night, as many as 20% of ulcer-related hemorrhages drain their unwary victims without as much as a single warning sign or symptom.
Our stalwart clinical investigators are left with two tools at their disposal, radiographic (barium studies) and endoscopic procedures. Before making “CSI” proud, however, trial therapy in individuals who are otherwise healthy and younger than 45 years is the name of the game. Barium studies can then be employed as a first test, to localize a duodenal or a gastric ulcer, the latter unfortunately representing a malignancy in many cases, and both ulcer types not without an evident link to chronic active gastritis. It does not end there, however, as up to 8% of malignant gastric ulcers appear benign to radiography, requiring the bigger guns of endoscopy and biopsy to settle the issue, as well as to identify lesions too small to detect by radiographic examination.
Once apprehended, placing an ulcer behind bars requires a three-step approach. While acid neutralizing and inhibitory drugs are still useful adjuncts, the mainstay of therapy entails eradication of H. pylori and elimination or prevention of NSAID-induced disease. Antacids like Maalox and Mylanta, which are not without side effects, have gone the route of the horse and buggy, ceding the turf to exotically named remedies like H2 receptor antagonists (cimetidine, ranitidine, famotidine, nizatidine) and proton pump inhibitors (omeprazole, esomeprazole, lansoprazole, rabeprazole, pantoprazole), all effective in reducing stomach acid through a myriad of mechanisms, and none without an unpleasant side that can border on the downright dangerous. As is always the case, health care professionals must be questioned in that light, and drug brochures and inserts combed with a magnifying glass.
Firepower in our medical armory continues to grow, as we add sucralfate and bismuth-containing preparations (Pepto-Bismol) to coat and blanket intruders who have “dug in.” Triple therapy for 14 days with Pepto-Bismol, metronidazole, and tetracycline (known as Helidac) is effective against H. pylori, but not without drawbacks such as poor patient compliance to a long treatment regimen and side effects such as black stools, constipation, darkening of the tongue, and worse to further blacken already gloomy days. The mere mention of quadruple therapy at that point may be just enough to warrant our raising the white flag.
As we top off our bag of tricks by cutting our reliance on NSAIDs for daily aches and pains and adding a prostaglandin, called misoprostol, to prevent NSAID-induced ulceration, the grim realization that surgery may be the only option left open to us looms heavily on the horizon. Outgunning ulcer-related complications in patients unresponsive to medical and endoscopic therapy may mandate a call to the knife, but only as a last resort.
Ganging up on gastritis before it transforms itself into uncompromising ulcer is an exercise in weekly vigilance for those not weak of heart.
© 2007, Albert M. Balesh, M.D. All rights reserved.
