I I I I Detection of anti-basement membrane zone antibodies in bullous systemic lupus erythematosus Camila Krysicka Janniger, MD, a Cezary Kowalewski, MD, PhD, c Tariq Mahmood, MD, b W. Clark Lambert, MD, PhD, a and Robert A. Schwartz, MD, MPH a Newark, New Jersey, and Warsaw, Poland We describe a 42-year-old black woman with long-standing systemic lupus erythematosus in whom vesiculobullous lesions developed.Routine histologic and immunologic studies fulfilled the criteria for the diagnosis of bullous systemic lupus erythematosus. Indirect immunoflu- orescence showed antinuclear antibodies without basement membrane zone fluorescence. We destroyed the nuclear antigens of the indirect immunofluorescence substrate with 2 mol/L sodium chloride, which unmasked basement membrane zone linear IgG staining. We also confirmed anti-basement membrane zone antibodies by employing a new technique of direct immunofluorescence on sodium chloride--split skin. Our findings prove that a thorough search for anti-basement membrane zone antibodies can be revealing. Our results support the idea that a subset of bullous systemic lupus erythematosus has the staining characteristics of epi- dermolysis acquisita, with the dermal side of the split skin showing linear immunoglobulin deposition. (J AM ACADDE~MATOL1991;24:643-7.) Bullous systemic lupus erythematosus (SLE) is a recently recognized distinct subset of lupus erythe- matosus, t-8 The original criteria for its diagnosis by Camisa and Sharma 5 specifically excluded the pres- ence of epidermolysis bullosa acquisita (EBA) anti- bodies. This point was subsequently questioned,9. 10 because patients with bullous SLE and EBA anti- bodies were reported. 914 Later, Camisa revised the criteria so that the presence or absence of EBA antibodies had no bearing on the diagnosis of bullous SLE. We describe an additional patient with bullous SLE and the presence of EBA antibodies. CASE REPORT A 40-year-old black woman had a 9-year history of SLE. A renal biopsy specimen in 1981 showed prolifer- ative nephritis. The patient was treated with corticoster- oids and antimalarial agents. Prednisone was discontin- ued in April 1985 because of clinically inactive disease. The patient was seen in March I986 with increased From the Deparlments of Dermatology a and Rheumatology, b New Jersey Medical School, and the Department of Dermatology, Med- ical Academy of Warsaw. c Reprint requcsts: Camila Krysicka Janniger, MD, Department of Der- matology, New Jcrsey Medical School, 185 S. Orange Ave., Newark, NJ 07103-2714. 16/4/19379 Fig. 1. Vesiculobullous lesions on forearm. 643