Isoniazid treatment for latent tuberculosis infection is tolerable for rheumatoid arthritis patients receiving tumor necrosis factor inhibitor therapy.
- Author:
Yoon Kyoung SUNG
1
;
Soo Kyung CHO
;
Dam KIM
;
Soyoung WON
;
Chan Bum CHOI
;
Tae Hwan KIM
;
Jae Bum JUN
;
Dae Hyun YOO
;
Sang Cheol BAE
Author Information
- Publication Type:Original Article
- Keywords: Latent tuberculosis; Isoniazid; Arthritis; Rheumatoid; Tumor necrosis factor inhibitor
- MeSH: Arthritis; Arthritis, Rheumatoid*; Follow-Up Studies; Humans; Isoniazid*; Latent Tuberculosis*; Liver Function Tests; Logistic Models; Methotrexate; Proportional Hazards Models; Retrospective Studies; Risk Factors; Tumor Necrosis Factor-alpha*
- From:The Korean Journal of Internal Medicine 2018;33(5):1016-1024
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/AIMS: To evaluate the impact of isoniazid (INH) treatment for latent tuberculosis infection (LTBI) on the development of liver function test (LFT) abnormality and the persistence of tumor necrosis factor (TNF) inhibitors in rheumatoid arthritis (RA) patients. METHODS: We retrospectively enrolled patients with RA who were treated with TNF inhibitors at a university hospital between December 2000 and November 2011. After dividing the patients into two groups based on the occurrence of LFT abnormality during follow-up, we compared demographic and clinical features between the two groups. A multivariable logistic regression analysis was performed to identify the impact of INH treatment on LFT abnormality. The impact of INH treatment on the persistence of TNF inhibitors was also evaluated with the log-rank test and the Cox-proportional hazards model. RESULTS: A total of 312 RA patients including 96 patients (30.9%) who took INH for LTBI were included in this analysis. Thirty-nine patients (12.5%) experienced LFT abnormalities while using TNF inhibitors. The use of INH was associated with LFT abnormalities (odds ratio, 3.01; 95% confidence interval [CI], 1.39 to 6.48) after adjusting for covariates, including methotrexate use. However, the persistence of TNF inhibitors over 5 years did not differ between patients receiving or not receiving INH treatment (49.4 vs. 54.6%, p = 0.79). INH treatment was not a risk factor for discontinuation of TNF inhibitors (hazard ratio, 1.01; 95% CI, 0.66 to 1.57). CONCLUSION: INH treatment for LTBI in RA patients who started TNF inhibitors is associated with the occurrence of LFT abnormality; however, it does not lead to discontinuation of TNF inhibitors.
