Use of biologic or targeted-synthetic disease-modifying anti-rheumatic drugs and risk of diabetes treatment intensification in patients with rheumatoid arthritis and diabetes mellitus

被引:13
作者
Chen, Sarah K. [1 ,2 ]
Lee, Hemin [1 ]
Jin, Yinzhu [1 ]
Liu, Jun [1 ]
Kim, Seoyoung C. [1 ,2 ]
机构
[1] Harvard Med Sch, Brigham & Womens Hosp, Div Pharmacoepidemiol & Pharmacoecon, Boston, MA 02115 USA
[2] Harvard Med Sch, Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, Boston, MA 02115 USA
关键词
rheumatoid arthritis; biologic drug; diabetes; NECROSIS-FACTOR-ALPHA; PSORIATIC-ARTHRITIS; INSULIN-RESISTANCE; ABATACEPT; OBESITY; ASSOCIATION; TOFACITINIB; IMPROVEMENT; MODULATION; MORTALITY;
D O I
10.1093/rap/rkaa027
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objectives. Given that RA treatment might affect the severity of diabetes mellitus (DM), we compared the risk of DM treatment intensification in patients with both RA and DM newly initiating a biologic DMARD or tofacitinib. Methods. Using claims data from the IBM MarketScan database (2005-2016), we identified patients aged >= 18 years with RA who initiated abatacept, a TNF inhibitor (TNFi), rituximab, tocilizumab or tofacitinib. Patients were required to have type 1 or type 2 DM and to use at least one antidiabetic drug at baseline. We assessed DM treatment intensification (i.e. addition of a new insulin or non-insulin antidiabetic medication). We also assessed non-insulin antidiabetic medication switching events. Results. We included 10 019 patients with RA and DM initiating a biologic DMARD or tofacitinib. Baseline insulin use was the highest in rituximab initiators (44%) and lowest in tofacitinib initiators (35%). The incidence rate per 1000 person-years for DM treatment intensification ranged from 148.2 (tofacitinib) to 198.0 (rituximab). The risk of DM treatment intensification was similar between abatacept and TNFi [hazard ratio (HR) 0.97, 95% CI: 0.82, 1.15], rituximab (HR 0.99, 95% CI: 0.79, 1.23) and tocilizumab (HR 0.94, 95% CI: 0.74, 1.19), but lower for tofacitinib compared with abatacept (HR 0.67, 95% CI: 0.50, 0.90). The risk of non-insulin DM treatment switching was not different between abatacept and other biologic DMARDs. Conclusion. In patients with both RA and DM, we found no difference in the risk of DM treatment switching or intensification after initiating abatacept vs TNFi, rituximab and tocilizumab, whereas the risk appeared to be lower for tofacitinib.
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页码:1 / 11
页数:11
相关论文
共 36 条
[1]   Cytokines Tumor Necrosis Factor-α and Interferon-γ Induce Pancreatic β-Cell Apoptosis through STAT1-mediated Bim Protein Activation [J].
Barthson, Jenny ;
Germano, Carla M. ;
Moore, Fabrice ;
Maida, Adriano ;
Drucker, Daniel J. ;
Marchetti, Piero ;
Gysemans, Conny ;
Mathieu, Chantal ;
Nunez, Gabriel ;
Jurisicova, Andrea ;
Eizirik, Decio L. ;
Gurzov, Esteban N. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2011, 286 (45) :39632-39643
[2]   VALIDATION OF A COMBINED COMORBIDITY INDEX [J].
CHARLSON, M ;
SZATROWSKI, TP ;
PETERSON, J ;
GOLD, J .
JOURNAL OF CLINICAL EPIDEMIOLOGY, 1994, 47 (11) :1245-1251
[3]   Real-world comparative risks of herpes virus infections in tofacitinib and biologic-treated patients with rheumatoid arthritis [J].
Curtis, Jeffrey R. ;
Xie, Fenglong ;
Yun, Huifeng ;
Bernatsky, Sasha ;
Winthrop, Kevin L. .
ANNALS OF THE RHEUMATIC DISEASES, 2016, 75 (10) :1843-1847
[4]   Comparative Risk of Diabetes Mellitus in Patients With Rheumatoid Arthritis Treated With Biologic or Targeted Synthetic Disease-Modifying Drugs: A Cohort Study [J].
Desai, Rishi J. ;
Dejene, Sara ;
Jin, Yinzhu ;
Liu, Jun ;
Kim, Seoyoung C. .
ACR OPEN RHEUMATOLOGY, 2020, 2 (04) :222-231
[5]   Diabetes incidence in psoriatic arthritis, psoriasis and rheumatoid arthritis: a UK population-based cohort study [J].
Dubreuil, Maureen ;
Rho, Young Hee ;
Man, Ada ;
Zhu, Yanyan ;
Zhang, Yuqing ;
Love, Thorvardur Jon ;
Ogdie, Alexis ;
Gelfand, Joel M. ;
Choi, Hyon K. .
RHEUMATOLOGY, 2014, 53 (02) :346-352
[6]   A choice of death - the signal-transduction of immune-mediated beta-cell apoptosis [J].
Eizirik, DL ;
Mandrup-Poulsen, T .
DIABETOLOGIA, 2001, 44 (12) :2115-2133
[7]  
Fedele AL, 2016, CLIN EXP RHEUMATOL, V34, P315
[8]   CTLA-4Ig immunotherapy of obesity-induced insulin resistance by manipulation of macrophage polarization in adipose tissues [J].
Fujii, Masakazu ;
Inoguchi, Toyoshi ;
Batchuluun, Battsetseg ;
Sugiyama, Naonobu ;
Kobayashi, Kunihisa ;
Sonoda, Noriyuki ;
Takayanagi, Ryoichi .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2013, 438 (01) :103-109
[9]   The JAK/STAT pathway in obesity and diabetes [J].
Gurzov, Esteban N. ;
Stanley, William J. ;
Pappas, Evan G. ;
Thomas, Helen E. ;
Gough, Daniel J. .
FEBS JOURNAL, 2016, 283 (16) :3002-3015
[10]   ADIPOSE EXPRESSION OF TUMOR-NECROSIS-FACTOR-ALPHA - DIRECT ROLE IN OBESITY-LINKED INSULIN RESISTANCE [J].
HOTAMISLIGIL, GS ;
SHARGILL, NS ;
SPIEGELMAN, BM .
SCIENCE, 1993, 259 (5091) :87-91