Higher doses of methotrexate associated with discontinuation of oral glucocorticoids after initiation of biological DMARDs: A retrospective observational study based on data from a Japanese multicenter registry study

Abstract

Objective

Glucocorticoids are important drugs used to treat rheumatoid arthritis. We recommend glucocorticoid discontinuation as soon as possible given the associated side-effects, but many patients continue to take oral glucocorticoids long-term. The present study aimed to explore factors associated with glucocorticoid discontinuation at 52 weeks after initiating biological disease-modifying antirheumatic drugs (bDMARDs).

Methods

Subjects were 564 patients from a Japanese multicenter registry who were administered glucocorticoids and methotrexate (MTX) followed by initiation of the first bDMARD. We examined the status of oral glucocorticoid use at 52 weeks after initiating the first bDMARD.

Results

By 52 weeks after bDMARD initiation, 164 patients (29.1%) discontinued glucocorticoids. Multivariable analysis identified age, MTX dose, and glucocorticoid dose as factors independently associated with glucocorticoid discontinuation. After adjusting for baseline characteristics using propensity score matching, among patient groups administered MTX ≤ 8 mg/week and MTX > 8 mg/week, 105 pairs remained. A significantly higher rate of glucocorticoid discontinuation (41.0%) was noted for patients administered MTX > 8 mg/week.

Conclusion

Our findings suggest that glucocorticoids may be discontinued after initiating bDMARDs. Moreover, higher MTX doses (>8 mg/week) at the time of bDMARD initiation were associated with glucocorticoid discontinuation among patients treated with bDMARDs.

Keywords:

• Glucocorticoids
• rheumatoid arthritis
• biological disease-modifying antirheumatic drugs
• methotrexate

Acknowledgment

The authors thank all investigators for their contributions to this study.

Conflict of interest

MS has received speakers’ fees from Bristol-Myers Squibb, Eisai, and Asahi Kasei. TK has received grant/research support and/or speakers’ fees from AbbVie, Astellas, Bristol-Myers Squibb, Chugai, Daiichi-Sankyo, Eli Lilly, Janssen, Mitsubishi Tanabe, Novartis, Pfizer, and Takeda. NT has received speakers’ fees from AbbVie, Bristol-Myers Squibb, Chugai, Eisai, Mitsubishi Tanabe, and Pfizer. SA has received speakers’ fees from AbbVie, Astellas, Bristol-Myers Squibb, Chugai, Daiichi-Sankyo, Eisai, Janssen, Takeda, and UCB Japan. AK received a research grant and/or speaker fee from Abbvie, Asahi-Kasei, Astellas, Bristol-Myers Squibb, Chugai, Eisai, Eli Lily, Mitsubishi-Tanabe, Pfizer, and UCB Japan. YH has received speakers’ fees from AbbVie, Asahi Kasei, Astellas, Ayumi, Bristol-Myers Squibb, Chugai, Daiichi-Sankyo, Eisai, Eli Lilly, Janssen, Mitsubishi Tanabe, Nippon Kayaku, Pfizer, and UCB Japan. TF has received speakers’ fees from AbbVie, Astellas, Bristol-Myers Squibb, Chugai, and Mitsubishi Tanabe. YS has received speakers’ fees from Astellas, Bristol-Myers Squibb, and Ono. NI has received grant/research support, consulting fees, and/or speakers’ fees from AbbVie, Asahi Kasei, Astellas, Bristol-Myers Squibb, Chugai, Daiichi-Sankyo, Eisai, Eli Lilly, Kaken, Medical Corporation Sanjinkai, Medical Corporation Toukoukai, Mitsubishi Tanabe, Ono, Otsuka, Pfizer, Taisho Toyama, Takeda, and Zimmer Biomet. The other authors declare no conflicts of interest.