The frequency of occurrence of Helicobacter pylori in the antral mucosa was investigated prospectively in a group of 66 patients (17 men, 49 women, mean age 58 ± 8,4 years) who had been treated with nonsteroidal antirheumatic drugs and 33 controls (14 men, 19 women, mean age ± years) who had not received these drugs. In the first group the indication for gastroscopy was ingestion of nonsteroidal antirheumatic drugs for at least 8 weeks, irrespective of dyspeptic symptoms (present in 25 patients), while in the second group the reason for endoscopy was either clinical symptoms (n = 18) or the presence of blood in the faeces. Helicobacter pylori was demonstrated by culture in 36 out of the 66 patients who had received nonsteroidal antirheumatics ( %); these comprised 24 out of 46 patients ( %) with chronic inactive gastritis and 12 out of 15 patients (80 %) with chronic active gastritis. In the control group H. pylori was detected by culture in 22 out of 33 patients ( %); these included 11 out of 19 patients ( %) with chronic inactive gastritis and 11 out of 12 patients ( %) with chronic active gastritis. H. pylori was not demonstrated in any of the seven patients who had histologically normal gastric mucosa. In both groups there was significant correlation between demonstration of the microorganism and severity of inflammation. There is hence no evidence that nonsteroidal antirheumatic drugs have any influence on the colonisation of the antral mucosa by Helicobacter pylori.
Non-steroidal anti-inflammatory drugs (NSAIDs) are used successfully to alleviate pain and inflammation in somatic musculoskeletal pain disorders. To this end, they inhibit the paracrine synthesis of prostaglandins (PGs), which induce pain while also having “house-keeping” effects. The COX-1 isoenzymes and the inducible COX-2 enzyme are available for PG synthesis in an organism. Inhibition of COX-1, followed by decreasing PG levels, leads to gastrointestinal side-effects affecting the GI mucosa. Unlike traditional NSAIDs, coxibs selectively inhibit COX-2, thereby causing fewer gastrointestinal problems. Co-medication with proton-pump inhibitors or a synthetic PG analogue also leads to a lower ulcer rate. Other non-PG-dependent mechanisms protect the mucosa. They also may be disrupted by NSAIDs.
Nicht-steroidale Antirheumatika werden, wie der Name besagt, bei Rheuma und entzündlich-rheumatischen Erkrankungen eingesetzt. Nicht-steroidale Antirheumatika sind aber auch gegen Beschwerden wie Schmerzen, Fieber und Entzündungen wirksam. Der Namensteil "nicht-steroidal" besagt, dass diese Gruppe von Wirkstoffen keine Steroide sind, also nicht das typische chemische Grundgerüst der Kortison-Verbindungen und Sexualhormone haben. Dadurch ergibt sich eine Abgrenzung zu den Glukokortikoiden , einer weiteren wichtigen Gruppe entzündungshemmender Wirkstoffe, die ebenfalls bei entzündlich-rheumatischen Erkrankungen eingesetzt werden.