mobic and Helicobacter-Infections

Rheumatological conditions often give rise to gastrointestinal (GI) symptoms and vice versa, but the greatest point of contact between rheumatologists and gastroenterologists arises through gastrointestinal toxicity resulting from the use of nonsteroidal antiinflammatory drugs (NSAIDs). Standard NSAIDs are toxic to the entire GI tract. The point prevalence of ulcers in patients on long-term NSAID treatment is about 20% and the annual incidence of complications in these patients is 1% to 4%; 1,200 patients in the United Kingdom die each year as a result. Withdrawing NSAID treatment, or reducing the dose, is not always possible, and approximately 25% of patients require continued long-term antiinflammatory treatment. Misoprostol and acid-suppressing drugs such as ranitidine and omeprazole are helpful as prophylactic treatment in high risk patients, and in healing established ulcers, especially in patients carrying Helicobacter pylori, but there is a pressing need for new, safer antiinflammatory drugs toease the burden of NSAID gastropathy. Selective inhibition of the COX-2 isoform of cyclooxygenase has been proposed as a new and safer therapeutic option. Clinical studies with meloxican, a selective COX-2 inhibitor, support this view. Meloxicam has been extensively studied in arthritis patients and combines antiinflammatory efficacy with a lower incidence of GI toxicity than currently available NSAIDs.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Rheumatoid; Cyclooxygenase Inhibitors; Digestive System; Gastrointestinal Diseases; Helicobacter Infections; Helicobacter pylori; Humans; Meloxicam; Rats; Stomach Ulcer; Thiazines; Thiazoles

Helicobacter pylori infection and NSAIDs are considered the two most important exogenous factors in ulcer disease. The interrelation between the two factors is not, however, clear. Moreover, serum pepsinogen has been suggested as a risk marker for the development of NSAID-induced gastrointestinal lesions. Fifty-one healthy volunteers, enrolled in a prospective, double-blind study carried out to evaluate gastrointestinal side effects of meloxicam and piroxicam, were analyzed to determine whether: (1) the prevalence of H. pylori correlates with the occurrence and severity of NSAID-induced gastrointestinal lesions, and (2) serum pepsinogen A and C levels could be used as markers of NSAID-induced mucosal damage. Upper endoscopy was performed by the same investigator before and after 28 days of treatment with placebo, meloxicam (7.5 mg/day and 15 mg/day), or piroxicam (20 mg/day). NSAID-induced damage was graded separately for hemorrhages and erosion ulcers according to Lanza's scale. There were no statistically significant differences in the prevalence of H. pylori in subjects with and without NSAID-induced mucosal lesions. However, there was a positive association between H. pylori infection and the severity of mucosal damage: total mean endoscopic score was 2.9 +/- 0.3 in H. pylori-positive subjects versus 1.6 +/- 0.5 in H. pylori-negative subjects (P < 0.05). Pepsinogen A and C levels increased from 55.3 +/- 3 to 149.4 +/- 15 and from 6.3 +/- 0.5 to 11.5 +/- 2.2, respectively (P < 0.05) in subjects who developed severe endoscopic injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Causality; Double-Blind Method; Gastric Mucosa; Gastrointestinal Diseases; Helicobacter Infections; Helicobacter pylori; Humans; Male; Meloxicam; Pepsinogens; Piroxicam; Prospective Studies; Thiazines; Thiazoles