OBJECTIVE: To evaluate the side effects of non-steroidal anti-inflammatory drugs (NSAID) on gastric mucosa, and to study the preventive effects of teprenone in patients. METHODS:108 patients taking NSAID for more than 3 months with no infection of helicobacter pylori (Hp) were collected. All patients were screened by endoscopy and their upper gastrointestinal symptoms were evaluated. Then, 16 patients with ulcers were excluded and 92 patients were randomly divided into intervention group with teprenone and control group. After follow-up for 3 months, patients were screened again by endoscopy and their upper gastrointestinal symptoms were also evaluated. Specimens of gastric mucosa were studied by PAS dyeing, and Cyclooxygenase (COX) level were evaluated by immunohistochemical technique. RESULTS: Of patients taking NSAIDs, the erosion was found in 48 (44.4%) patients while 16 (14.8%) were found with peptic ulcers. The damages were improved significantly (Z = -4.96, P = 0.000) in the intervention group with teprenone (n = 45) as compared with control group (n = 47) after follow-up for 3 months. Both the cox-1 level [31.1% (14/45) vs 6.7% (3/45), P = 0.003] and mucus thickness [66.7% (30/45) vs 13.3% (6/45), P= 0.000] also increased in the intervention group as compared with control group. No significant difference was found on COX-2 level between these two groups [28.9% (13/45) vs 31.1% (14/45), P = 0.82]. CONCLUSION: Long-term use of NSAID caused severe damages on gastric and duodenal mucosa; teprenone improved NSAID-related gastric side effects and increased the COX-1 level and mucus thickness.
RCT Entities:
OBJECTIVE: To evaluate the side effects of non-steroidal anti-inflammatory drugs (NSAID) on gastric mucosa, and to study the preventive effects of teprenone in patients. METHODS: 108 patients taking NSAID for more than 3 months with no infection of helicobacter pylori (Hp) were collected. All patients were screened by endoscopy and their upper gastrointestinal symptoms were evaluated. Then, 16 patients with ulcers were excluded and 92 patients were randomly divided into intervention group with teprenone and control group. After follow-up for 3 months, patients were screened again by endoscopy and their upper gastrointestinal symptoms were also evaluated. Specimens of gastric mucosa were studied by PAS dyeing, and Cyclooxygenase (COX) level were evaluated by immunohistochemical technique. RESULTS: Of patients taking NSAIDs, the erosion was found in 48 (44.4%) patients while 16 (14.8%) were found with peptic ulcers. The damages were improved significantly (Z = -4.96, P = 0.000) in the intervention group with teprenone (n = 45) as compared with control group (n = 47) after follow-up for 3 months. Both the cox-1 level [31.1% (14/45) vs 6.7% (3/45), P = 0.003] and mucus thickness [66.7% (30/45) vs 13.3% (6/45), P= 0.000] also increased in the intervention group as compared with control group. No significant difference was found on COX-2 level between these two groups [28.9% (13/45) vs 31.1% (14/45), P = 0.82]. CONCLUSION: Long-term use of NSAID caused severe damages on gastric and duodenal mucosa; teprenone improved NSAID-related gastric side effects and increased the COX-1 level and mucus thickness.