title: Subacute cutaneous lupus erythematosus in the course of rheumatoid arthritis: a relationship with TNF-α antagonists and rituximab therapy?
abstract: BACKGROUND
  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.
  
  
  OBJECTIVE
  To present a patient with rheumatoid arthritis (RA), who developed SCLE after treatment with TNF-α antagonists and rituximab.
  
  
  METHODS
  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.affiliation: Department of Dermatology, Silesian Medical University, Katowice, Poland. annadlis@neostrada.pl
authors.forename: Anna
authors.initials: A
authors.lastname: Lis-Święty
authors.forename: Ligia
authors.initials: L
authors.lastname: Brzezińska-Wcisło
authors.forename: Małgorzata
authors.initials: M
authors.lastname: Widuchowska
authors.forename: Eugeniusz
authors.initials: E
authors.lastname: Kucharz
mesh_terms: D000305:Adrenal Cortex Hormones / Q000008:administration & dosage / Q000627:therapeutic use; D000328:Adult; D000974:Antibodies, Antinuclear / Q000276:immunology; D058846:Antibodies, Monoclonal, Murine-Derived / Q000008:administration & dosage / Q000009:adverse effects* / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000008:administration & dosage / Q000009:adverse effects* / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000276:immunology; D005260:Female; D006801:Humans; D008178:Lupus Erythematosus, Cutaneous / Q000139:chemically induced* / Q000175:diagnosis / Q000188:drug therapy / Q000276:immunology; D000069283:Rituximab; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000305:Adrenal Cortex Hormones; D000974:Antibodies, Antinuclear; D058846:Antibodies, Monoclonal, Murine-Derived; D018501:Antirheumatic Agents; C035356:SS-A antibodies; D014409:Tumor Necrosis Factor-alpha; D000069283:Rituximab