Page 8 - 53-Peptic ulcer diseases (Loét dạ dày)

812 PART VI Stomach and Duodenum

NSAID Ulcers • Is there Hp infection? If antibiotic therapy had already been
H2RAs prescribed, the patient should be tested to confirm that the
infection has indeed been eradicated. If no attempt had been
Conventional doses of H2RAs are more effective in healing made to diagnose and treat Hp infection, it should be made
NSAID-related DUs than GUs. There are limited data on the now. False-negative test results for Hp should be considered
efficacy of H2RAs in healing peptic ulcers if patients continue to (see Chapter 52).
receive NSAIDs. Therefore, H2RAs are not preferred agents in • Is the patient still taking an NSAID? NSAID use may be sur-
patients with ulcers who require uninterrupted NSAID therapy. reptitious. A careful history regarding the use of over-the-
counter NSAIDs (including low-dose aspirin) should be ob-
PPIs tained, and NSAIDs should be stopped if possible.
• Does the patient smoke cigarettes? If so, he or she should be
Current evidence 76-78 indicates that PPIs are superior to stan- counseled strongly to discontinue cigarettes.
dard-dose H2RAs in healing NSAID-induced peptic ulcers. In a • Has the duration of ulcer treatment been adequate? Large ul-
randomized comparison of esomeprazole (20 or 40 mg/day) and cers require a longer duration of therapy than small ulcers to
ranitidine (150 mg twice daily) in ulcer patients who continued to heal. A large ulcer (e.g., >2 cm) probably should not be con-
take NSAIDs, ulcer healing at 8 weeks occurred in 85% and 86% sidered refractory until it has persisted beyond 12 weeks of
of patients given esomeprazole and in 76% of those given raniti- antisecretory therapy.
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dine. In another study of patients with NSAID-associated GUs • Is there evidence of a hyper-secretory condition? A family his-
who continued to use NSAIDs, ulcer healing at 8 weeks occurred tory of gastrinoma or MEN type I or a personal history of
in 69% and 73% of patients given lansoprazole (15 or 30 mg/day) chronic diarrhea, hypercalcemia caused by hyperparathyroid-
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but in only 53% of those given ranitidine (150 mg twice daily). ism, or ulcers involving the postbulbar duodenum or proximal
jejunum suggest a diagnosis of ZES (see Chapter 34).
Misoprostol • Finally, is the ulcer indeed peptic? Primary or metastatic neo-
plasms, infections (e.g., cytomegalovirus), cocaine use, eosino-
In ulcer patients who continued their NSAID, misoprostol healed philic gastroenteritis, and Crohn disease can cause ulcerations of
the ulcers in 67% of patients at 8 weeks, compared with only 26% the stomach and duodenum that can mimic peptic ulcers. These
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of patients treated with placebo. However, misoprostol is not disorders should be considered and excluded appropriately.
as effective as PPI therapy in healing NSAID-associated ulcers.
One randomized trial compared full-dose misoprostol (200 μg 4 Treatment options for truly refractory peptic ulcers include
times daily) with omeprazole (20 or 40 mg daily) in DU or GU a more prolonged course of antisecretory therapy, often at dou-
patients who continued NSAID treatment. After 8 weeks, DUs ble the prior PPI dose. Although uncommon nowadays, elective
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had healed in 89% of patients receiving either dose of omeprazole ulcer surgery may be necessary to attempt to heal a symptomatic
and in 77% of those receiving misoprostol. Similarly, GUs had refractory or penetrating ulcer. Surgical options are discussed
healed in 87% of those receiving 20 mg of omeprazole, 80% of later in this chapter.
those receiving 40 mg of omeprazole, and 73% of those receiv-
ing misoprostol. Although misoprostol is seldom used for treat- PREVENTION OF ULCER DISEASE
ment or prevention of peptic ulcer nowadays, 2 randomized trials
have shown that misoprostol is effective for the healing of small Most studies of ulcer prophylaxis have used endoscopy endpoints
bowel ulcers and erosions in patients with obscure bleeding taking (rather than clinical endpoints) to assess the effectiveness of various
NSAIDs and low-dose aspirin. 81,82 regimens. An “endoscopic ulcer” has been arbitrarily defined as a
circumscribed mucosal defect having a diameter of 5 mm or more
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Other Causes of Ulcers and Idiopathic Ulcers with a perceivable depth. However, many studies have loosened
this criterion to include flat mucosal breaks with a diameter of 3
When the cause of a peptic ulcer can be identified as other than Hp mm or more as ulcers. The distinction between small ulcers and
or NSAID use (e.g., gastrinoma), the underlying disorder should erosions is arbitrary and is prone to interobserver bias. The clini-
be treated (see Chapter 34).The treatment of idiopathic, non-Hp, cal relevance of these minor endoscopic lesions is uncertain. It is
non-NSAID ulcers relies on acid antisecretory therapy, usually a assumed that endoscopic findings roughly correlate with clinical
PPI, which is often given long term (maintenance therapy), much outcomes in subjects at low-to-average risk for ulcer complications.
as antisecretory therapy is used long term to prevent NSAID- It is unclear if results of endoscopic studies can be generalized to
induced ulcers in moderate- and high-risk patients (see later). high-risk patients. Because there are few prospective outcome tri-
als to evaluate the true clinical efficacy of ulcer prophylactic agents,
REFRACTORY ULCERS clinical judgment relies on data largely using endoscopic endpoints.
Hp ulcers do not require ulcer prophylaxis if the organism can
Most peptic ulcers heal within 8 weeks of initiation of antisecre- be eradicated from the stomach (see earlier and Chapter 52). Most
tory therapy. Nevertheless, in a small but considerable minor- use of ulcer prophylaxis regimens is, therefore, related to preven-
ity of patients, the ulcers persist despite conventional treatment. tion of NSAID ulcers in patients at moderate-to-high ulcer risk.
Such ulcers can be considered refractory. There is no standardized The risk factors for NSAID-induced ulcers are listed in Table
definition for refractory peptic ulcer, making comparisons among 53.1. Pharmaceutical agents that may reduce the development of
studies difficult. In some patients with refractory ulcers, symptoms NSAID-induced ulcers are discussed later. Ulcer prophylaxis is
of ulcer disease persist and may be severe. In others, the refrac- also frequently used in patients with idiopathic ulcers. Among the
tory ulcer becomes asymptomatic and is only detected at endoscopy agents listed, only the antisecretory agents are commonly used in
(e.g., at the 8-week follow-up endoscopy to assess healing of a GU). the prevention of idiopathic ulcers.
For the patient whose ulcer does not heal despite a trial of
conventional therapy, the clinician should ask the following ques- Antacids
tions:

Many clinicians prescribe antacids as co-therapy for patients tak-
• Has the patient complied with the prescribed treatment? ing NSAIDs, both to relieve dyspeptic symptoms and to (hope-
• Is the ulcer penetrating the pancreas, liver, or other organ? fully) prevent ulcers; however, antacids have no proved efficacy