title: Drug-induced, Ro/SSA-positive cutaneous lupus erythematosus.
abstract: OBJECTIVE
  To study the clinical and immunopathologic findings of drug-induced, Ro/SSA-positive cutaneous lupus erythematosus (CLE).
  
  
  METHODS
  Retrospective medical and laboratory record review.
  
  
  METHODS
  Immunodermatology Division of Johns Hopkins Hospital (Baltimore, Md).
  
  
  METHODS
  Of 120 patients found to have anti-Ro/SSA antibodies by hemagglutination and/or double immunodiffusion, 70 had clinical and immunopathologic confirmation of CLE. Fifteen of these 70 patients had a history of new drug exposure, defined as less than 6 months, associated with disease development.
  
  
  RESULTS
  The disease-associated drugs included hydrochlorothiazide (5 patients), angiotensin-converting enzyme inhibitors (3 patients), calcium channel blockers (3 patients), interferons (2 patients), and statins (2 patients). The most common presentations were photodistributed diffuse erythema and subacute CLE-type lesions without evidence of significant systemic disease. All specimens revealed interface dermatitis and fine granular IgG deposition along the basement membrane zone and throughout the epidermis. Most patients experienced improvement or resolution of clinical lesions within 8 weeks and decrease of Ro/SSA titers within 8 months after discontinuation of drug treatment.
  
  
  CONCLUSIONS
  Antihypertensive drugs are the most commonly associated with Ro-positive CLE. Clinical and immunopathologic features of this drug-induced variant do not seem to differ from the idiopathic disease. In most cases, the disease improves or resolves on discontinuation of the offending drug treatment. It is not known if these drugs precipitate disease in patients who have subclinical disease. Drug-induced Ro/SSA-positive CLE should be included on the differential diagnosis in patients presenting with photosensitive or subacute CLE-type eruptions.
authors.affiliation: Department of Dermatology, Johns Hopkins Medical Institutions, Baltimore, MD, USA.
authors.forename: Monika
authors.initials: M
authors.lastname: Srivastava
authors.forename: Adrienne
authors.initials: A
authors.lastname: Rencic
authors.forename: Gerardine
authors.initials: G
authors.lastname: Diglio
authors.forename: Helen
authors.initials: H
authors.lastname: Santana
authors.forename: Paula
authors.initials: P
authors.lastname: Bonitz
authors.forename: Rosemarie
authors.initials: R
authors.lastname: Watson
authors.forename: Esther
authors.initials: E
authors.lastname: Ha
authors.forename: Grant J
authors.initials: GJ
authors.lastname: Anhalt
authors.forename: Thomas T
authors.initials: TT
authors.lastname: Provost
authors.forename: Carlos H
authors.initials: CH
authors.lastname: Nousari
mesh_terms: D000328:Adult; D000368:Aged; D000974:Antibodies, Antinuclear / Q000032:analysis; D000924:Anticholesteremic Agents / Q000009:adverse effects; D001323:Autoantibodies / Q000032:analysis*; D001324:Autoantigens; D005260:Female; D019085:Fluorescent Antibody Technique, Direct; D006386:Hemagglutination Tests; D006801:Humans; D008178:Lupus Erythematosus, Cutaneous / Q000139:chemically induced* / Q000175:diagnosis / Q000276:immunology; D008297:Male; D008875:Middle Aged; D017035:Pravastatin / Q000009:adverse effects; D020733:RNA, Small Cytoplasmic; D012189:Retrospective Studies; D012261:Ribonucleoproteins / Q000276:immunology*; D012867:Skin / Q000276:immunology; D000099207:SS-A Antigen
chemical_list: D000974:Antibodies, Antinuclear; D000924:Anticholesteremic Agents; D001323:Autoantibodies; D001324:Autoantigens; D017035:Pravastatin; D020733:RNA, Small Cytoplasmic; D012261:Ribonucleoproteins; D000099207:SS-A Antigen; C116006:RO60 protein, human