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目的：研究１例地方性慢性砷中毒（ＥＣＡ）患者１６份砷角化症皮损活检标本及其Ｓ１００＋细胞的变化。方法：石蜡切片，ＨＥ染色，抗Ｓ１００蛋白抗体为一抗，ＬＢＡＢ法显示Ｓ１００＋细胞在皮损内的变化。结果：病理所见有良性角化症标本３份，癌前角化症标本（光线性角化）５份，恶性角化症标本（鲍温病，鳞癌）８份。表皮Ｓ１００＋郎格罕氏细胞（ＬＣ）在良性角化和癌前角化时增多，在恶性角化时减少，并有形态学改变。癌前病变者真皮Ｓ１００＋细胞数目多于良性角化，鲍温病真皮浸润区Ｓ１００＋细胞与鳞癌相比显著增多。结论：展示了砷角化症癌变成鳞癌的各期皮损，Ｓ１００＋ＬＣ在ＥＣＡ皮损的变化符合临床非砷性相同病变时ＯＫＴ＋６ＬＣ的变化，砷可使Ｓ１００＋ＬＣ受损，并导致多发性皮肤恶性肿瘤。
Objective: To study the changes of 16 arsenic keratosis lesions and S100 + cells in 1 case of endemic chronic arsenism (ECA). Methods: Paraffin sections, HE staining, anti-S 100 protein antibody as a primary antibody, LB 100 B cells showed changes in the lesions. Results: There were 3 specimens of benign keratosis, 5 specimens of precancerous keratosis (light keratosis) and 8 specimens of malignant keratosis (Bowen’s disease and squamous cell carcinoma). Epidermal S 100 + Langerhans cells (LC) increased in benign keratosis and precancerous keratosis, decreased in malignant keratosis, and morphologically altered. Precancerous lesion dermis S 100 + cell number than benign keratosis, Bowen’s disease dermal infiltration area S 100 + cells compared with squamous cell carcinoma was significantly increased. CONCLUSIONS: The various stages of carcinogenesis of squamous cell carcinomas of arsenite were demonstrated. The changes of S100 + LC in ECA lesions were in accordance with the changes of OKT + 6LC in the same clinical non-arsenic lesions. A100 + LC was impaired and Causes multiple skin cancer.