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 Table of Contents  
Year : 2022  |  Volume : 17  |  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 Submission04-Mar-2022
Date of Acceptance10-Mar-2022
Date of Web Publication21-May-2022

Correspondence Address:
Dr. Pallavi Patro
Department of Telemedicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226 014, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/injr.injr_41_22

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How to cite this article:
Patro P. Optimizing corticosteroid therapy in takayasu arteritis. Indian J Rheumatol 2022;17:199

How to cite this URL:
Patro P. Optimizing corticosteroid therapy in takayasu arteritis. Indian J Rheumatol [serial online] 2022 [cited 2022 Jul 4];17:199. Available from:

Dear Editor,

I read with great interest the recent paper on corticosteroid therapy in patients with Takayasu arteritis (TAK) published in the journal.[1] 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.[2] 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.[3] Recent studies have identified T-helper 17 (Th17) populations as potential culprits in the pathogenesis of TAK.[4],[5] Generally, Th17 cells in TAK are hyporesponsive to corticosteroids.[4],[5] Elevation of Th17.1 cells has been recently reported in TAK.[6] 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.[6],[7] 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.[6],[8],[9],[10]

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Conflicts of interest

There are no conflicts of interest.

  References Top

Shumy F, Anam AM, Choudhury MR, Shahin MA, Haq SA, Amin MZ, et al. Rate and predictors of response to glucocorticoid therapy in patients of takayasu arteritis at a tertiary level hospital of Bangladesh: A longitudinal study. Indian J Rheumatol 2021;16:375-80.  Back to cited text no. 1
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Goel R, Danda D, Joseph G, Ravindran R, Kumar S, Jayaseelan V, et al. Long-term outcome of 251 patients with Takayasu arteritis on combination immunosuppressant therapy: Single centre experience from a large tertiary care teaching hospital in Southern India. Semin Arthritis Rheum 2018;47:718-26.  Back to cited text no. 2
Misra DP, Rathore U, Patro P, Agarwal V, Sharma A. Corticosteroid monotherapy for the management of Takayasu arteritis – A systematic review and meta-analysis. Rheumatol Int 2021;41:1729-42.  Back to cited text no. 3
Saadoun D, Garrido M, Comarmond C, Desbois AC, Domont F, Savey L, et al. Th1 and Th17 cytokines drive inflammation in Takayasu arteritis. Arthritis Rheumatol 2015;67:1353-60.  Back to cited text no. 4
Misra DP, Chaurasia S, Misra R. Increased circulating Th17 cells, serum IL-17A, and IL-23 in Takayasu arteritis. Autoimmune Dis 2016;2016:7841718.  Back to cited text no. 5
Singh K, Rathore U, Rai MK, Behera MR, Jain N, Ora M, et al. Novel Th17 lymphocyte populations, Th17.1 and PD1+Th17, are increased in Takayasu arteritis, and both Th17 and Th17.1 sub-populations associate with active disease. J Inflamm Res 2022;15:1521-41.  Back to cited text no. 6
Ramesh R, Kozhaya L, McKevitt K, Djuretic IM, Carlson TJ, Quintero MA, et al. Pro-inflammatory human Th17 cells selectively express P-glycoprotein and are refractory to glucocorticoids. J Exp Med 2014;211:89-104.  Back to cited text no. 7
Ramstein J, Broos CE, Simpson LJ, Ansel KM, Sun SA, Ho ME, et al. IFN-γ-producing T-helper 17.1 cells are increased in sarcoidosis and are more prevalent than T-helper type 1 cells. Am J Respir Crit Care Med 2016;193:1281-91.  Back to cited text no. 8
van Langelaar J, van der Vuurst de Vries RM, Janssen M, Wierenga-Wolf AF, Spilt IM, Siepman TA, et al. T helper 17.1 cells associate with multiple sclerosis disease activity: Perspectives for early intervention. Brain 2018;141:1334-49.  Back to cited text no. 9
Lai JI, Tseng YJ, Chen MH, Huang CF, Chang PM. Clinical perspective of FDA approved drugs with P-glycoprotein inhibition activities for potential cancer therapeutics. Front Oncol 2020;10:561936.  Back to cited text no. 10


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