The guiding principle of
ulcer therapy for many years has been "No
acid, no
ulcer" and many still adhere to it. Nonsteroidal anti-inflammatory drugs (
NSAIDs) appear to cause
ulcers primarily through
prostaglandin depletion rather than through an
acid-based mechanism. These
ulcers affect a large number of patients and give few warning signs, often none, until it is too late. The profound relief offered to
arthritis patients by
NSAIDs, in the absence of equally effective remedies, means that rheumatologists must continue to deal with specific and quantifiable risks of
NSAID-related gastrointestinal (GI) ulceration and its associated complications. The
prostaglandin analog,
misoprostol, may address many of these concerns because it reverses the patient's
prostaglandin depleted condition. It is effective in preventing
NSAID-induced
ulcers, and does not interfere with the desired
analgesic or anti-inflammatory effects of
NSAIDs. The tools to assess the risk of
NSAID-related hospitalization or death due to GI complications are available and patients at greatest risk can be identified. Physicians whose patients are at risk may wish to consider
therapy with
misoprostol 400 to 800 micrograms/day in divided doses. It is recommended that
misoprostol be coadministered with the
NSAID after meals. The most common side effects that the patient may experience are some mild and transient
diarrhea and
cramps upon initiation of
misoprostol therapy and these can be minimized by taking
misoprostol with meals and avoiding
magnesium-containing
antacids. For
misoprostol's protective role to be demonstrated, it should be coprescribed with the
NSAID for the duration of the
NSAID therapy.(ABSTRACT TRUNCATED AT 250 WORDS)