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• Prevalence, levels, and immunoglobulin classes of anti— single-stranded DNA antibodies were determined by an enzyme-linked immunosorbent assay in 52 patients with localized scleroderma (33 with morphea, four with generalized morphea, and 15 with linear scleroderma), in 60 healthy controls, and, for comparison, in 31 patients with systemic lupus erythematosus. Localized scleroderma revealed a significant prevalence of anti—single-stranded DNA antibodies, mainly characterized by high levels and IgM and IgA isotypes. Comparison of antibody characteristics in different clinical forms of localized scleroderma showed some significant differences (levels and immunoglobulin isotypes). Comparison with systemic lupus erythematosus showed that frequency, high levels, and IgG isotype of anti—single-stranded DNA antibodies significantly prevailed in systemic lupus erythematosus, while the IgM isotype significantly prevailed in localized scleroderma. However, generalized morphea and linear scleroderma did not significantly differ from systemic lupus erythematosus as regards antibody frequency and prevalence of high antibody levels.(Arch Dermatol. 1991;127:1180-1183)

TO THE EDITOR.— Many authors have reported the association of alopecia areata (AA) with one or more autoimmune diseases, such as Addison disease,1-3 pernicious anemia,2,3,5,8 idiopathic hypoparathyroidism,1-5 premature ovarian failure,3,5 ulcerative colitis,6,7 hypothyroidism,3,8 some cases of diabetes mellitus,8 and moniliasis.1-5No notable incidence of thyroid antibodies was found by Cunliffe et al9 in 71 patients with isolated AA. On the contrary, Kern et al10 reported a high incidence of thyroid, adrenal, and parietal cell antibodies.We performed an immunological study of 52 patients with isolated AA to clarify the possible relationship between AA and autoimmunity. SUBJECTS AND METHODS.— Fifty patients with typical cases of AA and two with alopecia totalis were examined. None of them had previously received corticosteroid therapy. Of the 52 patients, who ranged from 3 to 63 years in age, 33 were men and 19 were women.

Nail matrix melanocytic nevi are considered rare and only a few histologically proven melanocytic nevi of the nail matrix have been reported in the literature.1-5 Most of these cases have occurred in children.1-3,5 Clinical evidence that nevoid nail area melanosis in children may spontaneously regress over the years has recently been reported.1 However, all these cases lacked pathologic study. We describe the progressive fading of longitudinal melanonychia due to a nail matrix melanocytic nevus in a child.Figure 1.Longitudinal melanonychia of the third right finger in June 1990. Note evident fading of the band in January 1991. REPORT OF A CASE. A 1-year-old boy was first referred to our department in June 1990 because of a band of longitudinal melanonychia of the third right fingernail. His parents said that they had first noticed a gradually enlarging pigmented band 4 months before, when the child was 8

TO THE EDITOR.— Complement-fixing activity to melanin-producing cells (CFA-MPC),1 also known as melanin-producing cell autoantibody,2-4 has been reported in serum samples from nine patients using the indirect immunofluorescent complement-fixation technique on normal human skin. Six patients2-4 had vitiligo associated with type 1 polyglandular autoimmune disease,5 including hypoparathyroidism, Addison's disease, and chronic candidiasis. The remaining three patients did not present with vitiligo but had candidiasis with or without hypoparathyroidism.1 On the basis of these latter three cases Nordlund,1 cited by Peserico et al,3 suggested that CFA-MPC should not be considered the cause of vitiligo, as this factor was always associated with candidiasis but seldom with vitiligo. Until now, no follow-up studies were conducted on cases with CFA-MPC without vitiligo. REPORT OF CASES.— Since 1980, we have conducted follow-up studies on nine patients with type 1 polyglandular autoimmune disease and chronic candidiasis. They

TO THE EDITOR.— In their article in the Archives (111:1024-1026, 1975), Weedon and Barnett reported a particularly large variant of keratoacanthoma centrifugum marginatum. We have recently observed a strikingly similar case. REPORT OF A CASE.— A 64-year-old woman was first treated by a country physician in January 1974 for a 2-cm keratotic noduleFig 1.—Lesion right calf showing central healing. Inset shows advancing edge in greater detail.Fig 2.—Advancing edge with distinctive epithelial infolding (hematoxylin eosin, original magnification × 10). on the front of her right calf. The patient was first examined in, and subsequently admitted to, our clinic in February 1975, when she had an extensive lesion, 20 × 15 cm, on the front of her right calf extending to both the medial and the lateral sides (Fig 1). It had a "serpiginous outline with an elevated rolled advancing edge, and there was central healing present." A biopsy confirmed

TO THE EDITOR.— The association of vitiligo with a number of organspecific autoimmune disorders, such as pernicious anemia,1 hyperthyroidism and hypothyroidism,2 Addison disease,3 and diabetes mellitus4 is well known. An increased incidence of organ-specific antibodies was reported in patients with vitiligo,5,6 but, more recently, no statistically significant incidence of autoantibodies was found in vitiligo patients.7One of the difficulties in accepting an autoimmune form of vitiligo has been the absence of circulating antimelanocyte antibodies; only Von Langhof et al8 found an "antimelanin antibody" in serum samples from patients with vitiligo, but their report was not confirmed.7 Antibodies against the cytoplasm of malignant melanoma cells have been found in cases of vitiligo associated with resolving halo nevus, but not in isolated vitiligo.9We here report our attempts to demonstrate a specific antimelanocyte antibody in sera of patients with vitiligo. PATIENTS AND METHODS.—

Most studies have failed to identify a specific antimelanocyte antibody in the serum of patients with vitiligo.1-3 Only recently, Hertz et al4 described two patients with vitiligo and polyendocrine deficiencies who had evidence for an autoantibody that binds to melanin-producing cells (MPC) in human skin, nevi, and melanomas. They stated that other investigators1,2 probably failed to identify this antibody because patients who were known antibody-formers were not selected, and only a conventional indirect immunofluorescence technique (IIT) was used.We have retested the serum of two patients with vitiligo and "autoimmune polyendocrine diseases" who had been described previously.2 PATIENTS AND METHODS Patient 1 is a 25-year-old woman with vitiligo, chronic idiopathic hypoparathyroidism, Addison's disease, chronic candidiasis, and atrophic gastritis with thyroid microsomal, gastric parietal cells, adrenal cortex, pancreatic islet cell, and prolactinsecreting cell autoantibodies.Patient 2 is a 57-year-old man with vitiligo, Hashimoto's thyroiditis, atrophic gastritis, and