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1.
Chinese Journal of General Practitioners ; (6): 483-484, 2014.
Article in Chinese | WPRIM | ID: wpr-451278

ABSTRACT

The clinical data of 186 patients with acute gout attack during upper gastrointestinal bleeding were analyzed retrospectively.The ratio of male to female was 1.7∶1, smokers and alcohol drinkers accounted for 66.1% ( 123/186 ) and 62.4% ( 116/186 ) of patients were had underlying diseases.All patients had different degree of joint painful and fever , the blood uric acid levels were higher.Gastroscopic examinations were performed in 166 patients , of whom 88 cases received endoscopic intervention.The symptoms of gout were improved after treatment with dexamethasone and celecoxib ; and the medication did not induce or increase gastrointestinal bleeding.

2.
Clinical Medicine of China ; (12): 358-360, 2013.
Article in Chinese | WPRIM | ID: wpr-432053

ABSTRACT

Objective To study the expression of Vascular Endothelial Growth Factor (VEGF),Malondialdehyde (MDA),Hypoxia Inducible Factor-1 α (HIF-1 α) in the Non-Steroidal Anti-Inflammatory Drug (NSAID)-associated gastric mucosa injury tissue,and to understand the mechanism of NSAID induced gastric mucosa injury.Methods We collected 114 biopsy specimen of gastric mucosa under endoscope from patients admitted to our hospital,including 70 cases with NSAID-associated chronic erosive gastritis or gastric ulcer (NSAID group) and 44 cases with chronic superficial gastritis who never take NSAID as controls (the control group).Immunohistochemistry technique was used to detect the positive expressions of VEGF,MDA,HIF-1α in patients.Results The positive rate of VEGF expression in the NSADI group was significantly lower than that in the normal control group (25.7% (18/70) vs.54.5% (24/44),x2 =9.70,P < 0.05).The positive rates of MDA and HIF-1α in the NSADI group were significantly higher than these in the normal control group (MDA:62.9% (44/70) vs.27.3% (12/44),x2 =13.70,P <0.05; HIF-1α:45.7% (32/70) vs.13.6% (6/44),x2 =12.50,P < 0.05).Conclusion NSAID drugs may induce gastric mucosa injury by decreasing the expression of VEGF and increase the levels of MDA and HIF1-α in gastric mucosa tissue.

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