Cost precludes routine post-treatment testing in all pa-tients. Instead, cure of infection should only be sought in se-lected patients: complicated peptic ulcer disease (i. e. , bleed-ing, perforation or obstruction). MALT lymphoma, or after resection of early gastric cancer. Because antibiotic treatment suppresses the organism even if it is not eradicated, confirma-tion of cure should only be done 4 weeks after completion of therapy.

Initial Treatment of Peptic Ulcer Disease A number of excellent treatment options are available for the healing of pep-tic ulcers. Antacids are highly effective agents for healing ulcers and controlling symptoms. However, from a practical perspec-tive, the inconvenient dosing frequency and adverse effects of therapy limit the use of antacids to symptom control only. Antacids neutralize acid that is already secreted. This increases intragastric pH, which also inactivates pepsin. The greatest buffering capacity is achieved when antacids are given 1 hour after eating(Table 21).
TABLE 21 Diagnostic Tests for Helicobacter Pylori

H2-receptor antagonists remain a mainstay of ulcer thera-py. Acid secretion is decreased by competitively and selectively inhibiting the H2 receptor of the parietal cell. There are four different H2receptor antagonists: cimetidine, ranitidine, famo-tidine, and nizatidine, All of these compounds act by the same mechanism but have different relative potencies for inhibiting gastric acid secretion; cimetidine is the least potent, whereas famotidine is the most potent. As a consequence of inhibiting gastric acid secretion, gastric pH rises and pepsin activity de-creases. This class of drugs is uniformly safe and well tolerat-ed, although the risk of adverse effects is slightly increased with cimetidine because of binding to cytochrome P450 and hence increased drug interactions. H2 receptor antagonists heal 90% to 95% of duodenal ulcers and 88% of gastric ulcers at 8 weeks. Given as a single full dose at bedtime, each of the avail-able compounds (cimetidine, 800 mg; ranitidine, 300 mg; famotidine, 40 mg;and nizatidine, 300 mg) has a comparable efficacy for ulcer healing.

The proton pump inhibitors omeprazole and lansoprazo1e are substituted benzimidazoles that bind irreversibly to the H+, K+-ATPase enzyme of the gastric parietal cell, thereby blocking the final step of gastric acid secretion in response to any type of stimulation, resulting in long-lasting inhibition of gastric acid secretion. For gastric secretory activity to be re-stored, new enzyme needs to be resynthesized, which normally takes 2 to 5 days. The proton pump inhibitors are remarkably well tolerated. Adverse effects are uncommon and are typically no more common than those experienced with placebo. The proton pump inhibitors achieve duodenal ulcer healing rates at 4 weeks that typically are noted at 8 weeks with H2-receptor antagonists. Omeprazole, 20 mg once daily, and lansoprazole, 15 mg daily, result in healing rates of 90% to 100% at 4 weeks. In addition to accelerating duodenal ulcer healing, the proton pump inhibitors typically relieve symptoms more rapidly than H2-receptor antagonists. In contrast to the dramatic accel-eration of healing of duodenal ulcers with proton pump in-hibitors, gastric ulcer healing is essentially comparable to that from H2 receptor antagonists at 8 weeks, Furthermore, dou-bling of the dosage used for duodenal ulcer therapy (ornepra-zole, 40 mg daily; lansoprazole, 30 mg daily) is required to achieve comparable healing rates, which results in higher costs to the patient.

Sucralfate is a complex salt of sucrose sulfate and alu-minum hydroxide that is as effective as H2 receptor antagonists in the treatment of duodenal ulcer disease. It is insoluble in water; and in the acid milieu of the stomach, sucralfate is bro-ken down into sucrose sulfate and an aluminum salt. There, it becomes a gel-like substance that binds to both defective and normal mucosa in the stomach and the duodenum. Sucralfate has little or no effect on acid secretion and acts through several different mucosal protective mechanisms. It binds to mucosal surfaces and acts as a physical barrier to the diffusion of acid, pepsin, and bile acids. Sucraifate is as effective as Ha receptor antagonists in the treatment of duodenal ulcer disease. The drug is well tolerated with few adverse effects. The evidence for efficacy in gastric ulcer disease is less compelling. The cor-rect dose is lg four times a day, which makes it less convenient than other agents for treating peptic ulcer disease.

Treatment of H.Pylori Infection Eradication of H. py-lori accelerates the rate of duodenal and gastric ulcer healing to approximate that of omeprazole at 4 weeks. Eradication of H. pylori essentially cures both duodenal and gastric ulcers and should be attempted in all patients with current or past docu-mented peptic ulcer disease and evidence of infection.

However, treatment of H. pylori infection is confusing and rapidly evolving. Despite in vitro sensitivity to a variety of antibiotics, in vivo activity of these same drugs against H. py-lori is disappointing. As such, eradication of the organism is difficult. Combinations of two antibiotics plus either a proton pump inhibitor or ranitidine bismuth are used to maximize the chance of eradication. Factors such as compliance and antibiot-ic resistance, especially to clarithromycin and metronidazole, influence treatment efficacy. Compliance is essential for treat-ment success, and all of these regimens offer simpler dosing than earlier options. Nevertheless, antibiotic resistance remains a problem in the treatment of H. pylori. Resistance to metron-idazole is approximately 50% and that to clarithromycin is 10% (Table 22).

Given the fact that prophylactic medications are expensive and NSAID use is common, ulcer prophylaxis should be con-sidered only in high-risk individuals: age older than 60 years, history of prior peptic ulcer disease or ulcer hemorrhage, co-administration of anticoagulants or corticosteroids, and high dose of NSAIDS (Table 23). Misoprostol is a prostaglandin E1 analogue that is effective for the prophylaxis of NSAID-in-duced ulcers in patients and decreases the incidence of serious gastrointestinal complications such as bleeding, perforation, and gastric outlet obstruction. It acts by prostaglandin-depen-dent pathways to decrease gastric acid secretion and enhance mucosal defenses. Lower doses of misoprostol (200 ug bid or tid) are just as effective as four times a day dosing for preven-tion of duodenal and gastric ulcers. Adverse effects with miso-prostol are diarrhea and abdominal cramps, especially in pa-tients treated with full doses (200 ug qid). Data suggest that omeprazole at a dose of 20 mg daily is more effective than ei-ther H2 receptor antagonists or misoprostol for the prophylaxis of NSAID ulcers. Furthermore, omeprazole is typically better tolerated than misoprostol. High-dose famotidine, 40 mg twice daily, is more effective than placebo in preventing both duode-nal and gastric ulcers in patients receiving long-term NSAII) therapy. Conventional doses of famotidine and the other H2 re-ceptor antagonists are effective for the prophylaxis of duodenal ulcers but not gastric ulcers.

Maintenance Therapy Maintenance therapy with a chronic low dose (half strength)of any of the H2 blockers is now an obsolete concept. Maintenance therapy is now indicat-ed only for patients with H. pylori-positive peptic ulcer disease if eradication is unsuccessful.

Surgery Once central to the management of peptic ulcer disease, surgery now has a negligible role in the management of uncomplicated peptic ulcer disease, with the recognition that ulcers can be cured by elimination of H. pylori and NSAIDs. However, complications of peptic ulcer disease have not de-creased and surgery continues to play an important role in the management of complications.

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