Severe gastric mucosal damage induced by NSAIDs in healthy subjects is associated withHelicobacter pylori infection and high levels of serum pepsinogens
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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 ofH. 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 ofH. pylori in subjects with and without NSAID-induced mucosal lesions. However, there was a positive association betweenH. pylori infection and the severity of mucosal damage: total mean endoscopic score was 2.9±0.3 inH. pylori-positive subjects versus 1.6±0.5 inH. 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. It is concluded thatH. pylori increases the severity of NSAID-induced gastrotoxicity and that pepsinogen A and C levels are valid markers of severe NSAID-induced mucosal lesions.
Key WordsNSAIDs H. pylori pepsinogen healthy volunteers endoscopy
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