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| LETTER TO EDITOR |
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| Year : 2022 | Volume
: 17
| Issue : 2 | Page : 199 |
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Optimizing corticosteroid therapy in takayasu arteritis
Pallavi Patro
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 |
Correspondence Address:
Dr. Pallavi Patro
Department of Telemedicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226 014, Uttar Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/injr.injr_41_22
How to cite this article:
Patro P. Optimizing corticosteroid therapy in takayasu arteritis. Indian J Rheumatol 2022;17:199 |
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]
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
| 1. | 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.  [Full text] |
| 2. | 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. |
| 3. | 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. |
| 4. | 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. |
| 5. | Misra DP, Chaurasia S, Misra R. Increased circulating Th17 cells, serum IL-17A, and IL-23 in Takayasu arteritis. Autoimmune Dis 2016;2016:7841718. |
| 6. | 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. |
| 7. | 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. |
| 8. | 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. |
| 9. | 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. |
| 10. | 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. |
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