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Subacute cutaneous lupus erythematosus in the course of rheumatoid arthritis: a relationship with TNF-α antagonists and rituximab therapy?
Immunopharmacol Immunotoxicol. 2013 Jun; 35(3):443-6.II

Abstract

INTRODUCTION

Drug-induced subacute cutaneous lupus erythematosus (DI-SCLE) is caused by different medicines, first of all: calcium channel blockers, angiotensin converting enzyme inhibitors, thiazides, terbinafine, statins and antagonists of tumor necrosis factor-α (TNF-α). DI-SCLE does not distinguish from idiopathic form of the disease, clinically, histopathologically and immunologically. However, receding of symptoms is observed after recapture of the provoking drug.

AIM

To present a patient with rheumatoid arthritis (RA), who developed SCLE after treatment with TNF-α antagonists and rituximab.

CASE REPORT

In a 31-year-old woman with RA leucopenia due to treatment with etanercept and adalimumab was observed. Therefore, the treatment was changed to rituximab, but after starting the therapy, erythematous and oedematous skin lesions of an oval or annular shape appeared on the cheeks, auricles, lips and the decolette. Histopathological evaluation of the skin lesions revealed SCLE. Ro/SS-A and La/SS-B antibodies were detected in serum. Regression of skin lesions and hematologic disturbances was achieved after starting corticosteroid therapy.

CONCLUSIONS

Co-existence of SCLE with RA should be considered in some patients. The role of TNF-α antagonists and rituximab therapy in induction of idiopathic form of SCLE requires further investigations.

Authors+Show Affiliations

Department of Dermatology, Silesian Medical University, Katowice, Poland. annadlis@neostrada.plNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Case Reports
Journal Article

Language

eng

PubMed ID

23537059

Citation

Lis-Święty, Anna, et al. "Subacute Cutaneous Lupus Erythematosus in the Course of Rheumatoid Arthritis: a Relationship With TNF-α Antagonists and Rituximab Therapy?" Immunopharmacology and Immunotoxicology, vol. 35, no. 3, 2013, pp. 443-6.
Lis-Święty A, Brzezińska-Wcisło L, Widuchowska M, et al. Subacute cutaneous lupus erythematosus in the course of rheumatoid arthritis: a relationship with TNF-α antagonists and rituximab therapy? Immunopharmacol Immunotoxicol. 2013;35(3):443-6.
Lis-Święty, A., Brzezińska-Wcisło, L., Widuchowska, M., & Kucharz, E. (2013). Subacute cutaneous lupus erythematosus in the course of rheumatoid arthritis: a relationship with TNF-α antagonists and rituximab therapy? Immunopharmacology and Immunotoxicology, 35(3), 443-6. https://doi.org/10.3109/08923973.2013.780077
Lis-Święty A, et al. Subacute Cutaneous Lupus Erythematosus in the Course of Rheumatoid Arthritis: a Relationship With TNF-α Antagonists and Rituximab Therapy. Immunopharmacol Immunotoxicol. 2013;35(3):443-6. PubMed PMID: 23537059.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Subacute cutaneous lupus erythematosus in the course of rheumatoid arthritis: a relationship with TNF-α antagonists and rituximab therapy? AU - Lis-Święty,Anna, AU - Brzezińska-Wcisło,Ligia, AU - Widuchowska,Małgorzata, AU - Kucharz,Eugeniusz, Y1 - 2013/03/28/ PY - 2013/3/30/entrez PY - 2013/3/30/pubmed PY - 2013/12/18/medline SP - 443 EP - 6 JF - Immunopharmacology and immunotoxicology JO - Immunopharmacol Immunotoxicol VL - 35 IS - 3 N2 - INTRODUCTION: Drug-induced subacute cutaneous lupus erythematosus (DI-SCLE) is caused by different medicines, first of all: calcium channel blockers, angiotensin converting enzyme inhibitors, thiazides, terbinafine, statins and antagonists of tumor necrosis factor-α (TNF-α). DI-SCLE does not distinguish from idiopathic form of the disease, clinically, histopathologically and immunologically. However, receding of symptoms is observed after recapture of the provoking drug. AIM: To present a patient with rheumatoid arthritis (RA), who developed SCLE after treatment with TNF-α antagonists and rituximab. CASE REPORT: In a 31-year-old woman with RA leucopenia due to treatment with etanercept and adalimumab was observed. Therefore, the treatment was changed to rituximab, but after starting the therapy, erythematous and oedematous skin lesions of an oval or annular shape appeared on the cheeks, auricles, lips and the decolette. Histopathological evaluation of the skin lesions revealed SCLE. Ro/SS-A and La/SS-B antibodies were detected in serum. Regression of skin lesions and hematologic disturbances was achieved after starting corticosteroid therapy. CONCLUSIONS: Co-existence of SCLE with RA should be considered in some patients. The role of TNF-α antagonists and rituximab therapy in induction of idiopathic form of SCLE requires further investigations. SN - 1532-2513 UR - https://www.unboundmedicine.com/medline/citation/23537059/Subacute_cutaneous_lupus_erythematosus_in_the_course_of_rheumatoid_arthritis:_a_relationship_with_TNF_α_antagonists_and_rituximab_therapy L2 - https://www.tandfonline.com/doi/full/10.3109/08923973.2013.780077 DB - PRIME DP - Unbound Medicine ER -