[ACUTE DISSEMINATED LUPUS ERYTHEMATOSUS IN A FAMILY].
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Five cases of chilblain lupus erythematosus were retrospectively reviewed regarding their clinical, histopathologic, serologic, and immunofluorescence findings. Ages at onset of chilblain lupus erythematosus varied from 26 to 73 years, with a female-to-male ratio of 3:2. Since other entities can be confused with this disorder, we propose the following diagnostic criteria. The two major criteria are skin lesions in acral locations induced by exposure to cold or a drop in temperature, and evidence of lupus erythematosus in the skin lesions by results of histopathologic examination or direct immunofluorescence study. The three minor criteria are coexistence of systemic lupus erythematosus or other skin lesions of discoid lupus erythematosus, response to anti-lupus erythematosus therapy, and negative results of cryoglobulin and cold agglutinin studies. We conclude that chilblain lupus erythematosus can be diagnosed and treated. Discoid lupus erythematosus lesions respond more quickly to treatment than chilblain lupus erythematosus lesions. Treatment with antimalarial agents, prednisone, pentoxifylline, or dapsone was of benefit to our patients.
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A patient previously reported to have discoid lupus erythematosus as a neonate eventually developed systemic lupus erythematosus (SLE) at age 19 years. This case illustrates that although neonatal lupus erythematosus is usually self-limited, SLE may develop in selected patients in future years.
Thirty four sera from: 12 patients with Systemic Lupus Erythematosus (SLE), 9 with Subacute Cutaneous Lupus Erythematosus (SCLE) and 13 with Discoid Lupus Erythematosus (DLE) (disseminatus 3, localised 10) were tested for the presence of: (a) anti-thyroglobulin and anti-microsomal autoantibodies (b) anti-Sm/RNP, anti-doublestranded. DNA (anti-ds. DNA), anti-single-Stranded. DNA (anti-ss. DNA), anti-cardiolipin (anti-Cl), anti-SSA, anti-SSB, Antinuclear Antibodies (ANA). T3, T4, TSH levels were also determined. Five patients with SLE (41.6%), 4 with SCLE (44.4%), and 2 with DLE (15.3%) had thyroid autoantibodies and only three of the 41 controls (7.3%). Five patients (14.7%), especially from SLE and SCLE groups, had biochemical hypothyroidism whereas only one had hyperthyroidism. Statistical evaluation for the possible coexistence of thyroid autoantibodies with a panel of lupus characteristic autoantibodies, revealed highly significant correlations with anti-Sm/RNP, IgG (p = 0.003) and anti-ds. DNA, IgM (p = 0.012). It may be concluded, that not only SLE but also SCLE predisposes to autoimmune thyroid disease and the prevalence of the latter is related to a great extent to the subset of the LE spectrum. From these results and from the inhibition experiments, it seems that some of the specific mono- or polyclonal autoantibodies may be multiple organ reactive.