Drug-induced, Ro/SSA-positive cutaneous lupus erythematosus.
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.
Srivastava
Monika
M
Department of Dermatology, Johns Hopkins Medical Institutions, Baltimore, MD, USA.
Rencic
Adrienne
A
Diglio
Gerardine
G
Santana
Helen
H
Bonitz
Paula
P
Watson
Rosemarie
R
Ha
Esther
E
Anhalt
Grant J
GJ
Provost
Thomas T
TT
Nousari
Carlos H
CH
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
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