Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement
Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.
Celecoxib, a Selective COX-2 Inhibitor Improved Upper Gastrointestinal (GI) Adverse Lesions in Patients with Rheumatoid Arthritis on Long-Term NSAID Therapy with Endoscopic Evaluation.
Tsuji1, Shigeyoshi, Miyoshi2, Hirofumi, Tomita3, Tetsuya, Nakase2, Takanobu, Hamada2, Masayuki, Oomae2, Takahiro, Tsumoto2, Chikako
Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for pain relief in patients with rheumatoid arthritis (RA); however, gastrointestinal (GI) adverse events are one of the serious problems of NSAIDs. Selective cyclooxygenase (COX)-2 inhibitors have been proven to be less associated with GI complications than traditional NSAIDs. However, their effects on the GI tract have not been well studied in patients with preexisting NSAIDs-induced GI complications. Here, we prospectively investigated the effects of celecoxib (CEL) after switching from NSAIDs on the GI tract in RA patients with endoscopically identified GI mucosal injury.
We conducted upper GI endoscopy to examine GI tract injury in RA patients who had been treated with NSAIDs for 3 or more months with informed consent. GI mucosal injury was evaluated according to the modified LANZA score. Patients with mucosal injury without ulcers were switched from NSAIDs to CEL, while those with ulcers were switched to CEL with famotidine (FAM) on complete ulcer healing with therapy. At 16 week, the extent of GI mucosal injury was endoscopically reevaluated. Disease activity score (DAS28), joint symptoms, and visual analogue scale (VAS; global improvement and pain) were evaluated before and at 8 and 16 weeks after switching to CEL. Wilcoxon signed rank test was used and significance level was set at 0.05.
Eighty-two patients were eligible for the study (69 females), and the average age and affected period were 62.2 (3083) and 17.5 (150) years, respectively. The most prevalently-used NSAID was loxoprofen sodium (49.4%), followed by diclofenac sodium (25.9%), meloxicam (13.6%), and etodolac (11.1%). Endoscopic analysis revealed GI mucosal injury, including 6 ulcers, in 45 of 82 patients (54.9%). LANZA scores were 1, 2, 3, and 4, for 11, 12, 16, and 6 patients, respectively, and the mean score was 2.4 ± 1.0. The incidence ratio of GI mucosal injury was significantly higher in patients using diclofenac sodium (p<0.05) compared with those using other NSAIDs. At 16 week, LANZA score and the total number of GI erosions/redness were significantly reduced to 1.6 ± 1.3 and 6.5 ± 6.1, from respective pre-treatment values of 2.1 ± 0.8 and 10.6 ± 8.6, respectively (p<0.01). Of the 6 patients achieving complete remission of GI ulcers, 1 exhibited recurrent ulcers at week 16, and was diagnosed as having an H. pylori infection. At 16 week, DAS28 (ESR4) and DAS28 (CRP4) were significantly improved to 3.6 ± 1.3 (p<0.05) and 3.0 ± 1.1 (p<0.01), compared with each pre-treatment value of 3.9 ± 1.3 and 3.3 ± 1.1, and the number of tender and swollen joints were significantly reduced to 2.4 ± 3.7 (p<0.05) and 0.8 ± 1.2 (p<0.01), compared with each pre-treatment value of 3.1 ± 3.2 and 1.8 ± 2.2, respectively. VAS score was not changed after switching to CEL, suggesting its comparable analgesic effects to other NSAIDs.
In RA patients receiving long-term NSAIDs therapy, we demonstrated for the first time that preexisting NSAID-induced upper GI injury is improved after switching to CEL. Further, Its GI safety profile was accompanied by analgesic effects, suggesting the usefulness of switching to CEL for these patients.
To cite this abstract, please use the following information:
Tsuji, Shigeyoshi, Miyoshi, Hirofumi, Tomita, Tetsuya, Nakase, Takanobu, Hamada, Masayuki, Oomae, Takahiro, et al; Celecoxib, a Selective COX-2 Inhibitor Improved Upper Gastrointestinal (GI) Adverse Lesions in Patients with Rheumatoid Arthritis on Long-Term NSAID Therapy with Endoscopic Evaluation. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :298