对称性肢端角化病超微结构变化及角蛋白1的表达研究

Study on ultramicrostructure change and keratin1 expression in patients with symmetrical acral keratoderma

目的探讨对称性肢端角化病(SAK)皮损超微结构变化及角蛋白(KRT)1的表达。方法选取福建医科大学附属泉州第一医院及东莞市第六人民医院门诊SAK患者13例为研究对象,组织病理标本取材于手腕部位,皮损组织取材前2个月内均未外用维甲酸制剂或皮质类固醇制剂或中药制剂。健康对照皮肤为整形美容手术切除正常皮肤12例。采用透射电镜观察SAK患者皮损超微结构变化,免疫组化法检测13例SAK患者皮损及12例健康者皮肤组织中KRT1的表达。结果 SAK患者皮肤组织超微结构表现为角质化包膜连续性中断,角质层、棘层上部和颗粒层细胞核周围角蛋白丝显著聚集。KRT1在SAK皮损及正常皮肤组织中棘层、颗粒层及角质层均有表达,胞质及胞膜染色多见;KRT1在SAK皮损组织中表达明显高于正常皮肤(t=2.210,P=0.038)。结论 SAK皮损超微结构特点为表皮角蛋白丝分化异常,可能与KRT1过表达有关。

Objective To study the ultramicrostructure change and keartin（KRT1）expression in skin lesion of symmetrical acral keratoderma（SAK）.Methods Thirteen cases of SAK in the First Affiliated Hospital of Fujian Medical University and the outpatient department of the Dongguan Municipal Sixth People′s Hospital were selected as the study subjects.The histopathological samples were taken from the wrist site.The retinoic acid preparation or corticosteroid preparation or Chinese medicine preparation were not externally used within 2 months before taking skin lesion sample.The healthy control skin samples were the normal skin in12 cases by plastic surgical resection.The ultramicrostructural change were observed by the transmission electron microscopy.The KRT1 expression in skin lesion of 13 cases of SAK and healthy skin tissue of 12 cases were measured by immunohistochemistry method.Results The SAK ultramicrostructures manifested by the interruption of keratinizing envelope continuity in horny layer,and remarkable aggregation of keratin filament in upper stratum spinosum and surrounding nucleus of granular layer.KRT1 was expressed in the cells of SAK skin lesion and basal layer,spinous layer,granular layer and horny layer.The cytoplasm and cytomembrane staining was common.The KRT1 expression in skin lesion was significantly higher than that in normal skin（t=2.210,P=0.038）.Conclusion The ultramicrostructure features of SAK skin lesion are abnormal differentiation of epidermis keratin filaments,which might be related with overexpression of KRT1.