|LETTER TO EDITOR
|Year : 2022 | Volume
| Issue : 2 | Page : 199
Optimizing corticosteroid therapy in takayasu arteritis
Department of Telemedicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
|Date of Submission||04-Mar-2022|
|Date of Acceptance||10-Mar-2022|
|Date of Web Publication||21-May-2022|
Dr. Pallavi Patro
Department of Telemedicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226 014, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Patro P. Optimizing corticosteroid therapy in takayasu arteritis. Indian J Rheumatol 2022;17:199
I read with great interest the recent paper on corticosteroid therapy in patients with Takayasu arteritis (TAK) published in the journal. In this study, a majority of patients required addition of a disease-modifying antirheumatic drug along with corticosteroid at 6 months. I would like to highlight a couple of points in relation to this study. The authors of the study chose to uniformly treat their patients with prednisolone dose of 1 mg/kg/day at baseline. There is evidence from observations on a cohort of TAK from India that a dose of prednisolone of 0.5 mg/kg/day might be as effective as 1 mg/kg/day for induction of clinical remission as well as for future relapses of disease activity. This alternative regimen could also have been considered by the authors.
TAK inherently responds to corticosteroid therapy, however, disease activity relapses in a considerable proportion of patients when corticosteroids are tapered. Recent studies have identified T-helper 17 (Th17) populations as potential culprits in the pathogenesis of TAK., Generally, Th17 cells in TAK are hyporesponsive to corticosteroids., Elevation of Th17.1 cells has been recently reported in TAK. Th17.1 subset expresses drug efflux pump P-glycoprotein. It is food for thought whether corticosteroid resistance demonstrated by Th17.1 cells is a consequence of P-glycoprotein expression., In such a scenario, additional blockade of P-glycoprotein by agents known to have this property such as chlorpromazine, macrolide antibiotics, or phosphodiesterase inhibitors might suppress Th17.1 and T cells more effectively in TAK and in other diseases where they are implicated such as sarcoidosis and multiple sclerosis.,,,
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