๐Ÿ—‚ ็ธฝ็›ฎ้Œ„ ๏ฝœ ๐Ÿ“– ่‹ฑๆ–‡ๅŽŸๆ–‡๏ผˆๆœฌ็ฏ‡๏ผ‰ ๏ฝœ ๐Ÿ“ ๅฎŒๆ•ด็ฟป่ญฏ ๏ฝœ โญ ็ฒพ่ฏ็ญ†่จ˜

Acquired symmetrical acrokeratoderma

Acquired symmetrical acrokeratoderma

dermis contains a mild perivascular lymphocytic infiltrate or dense mixed lichenoid infiltrate.4 Follicular plugging is commonly present and occasionally the orifices of the eccrine ducts are similarly affected.27 Eccrine sweat glands may be diminished in number and atrophic, with thickened, hyalinized basement membranes. Absent or atrophic hair follicles are seen in the areas of alopecia.1,4,25

At the ultrastructural level, keratinocytes in KID syndrome show reduction of tonofibrils and abnormal membrane-bound granules containing mucous material that is discharged into the intercellular spaces.28

Histology of PAON is characterized by ortho- or parakeratotic plaques or filiform keratosis protruding from dilated ostia of hyperplastic sweat glands and hair follicles (Fig. 3.81A). The underlying epithelium reveals vacuolated cells with pyknotic nuclei and lacks keratohyalin granules (Fig. 3.81B). In contrast to true porokeratosis of any type, dysmaturation and signs of interface dermatitis are absent. In the papillary dermis a sparse or lichenoid

In China a series of patients were described that developed brown to black hyperkeratotic plaques over acral regions. The lesions were symmetrically distributed particularly on the wrists and dorsum of hands, fingers, and feet, but without involvement of palms and soles. A whitish discoloration of the skin after contact with water or sweating and worsening of the symptoms during the summer has been observed.1,2 Genetic studies have not been reported. Histopathology reveals epidermal hyperkeratosis, acanthosis, and a papillary dermal perivascular lymphohistiocytic infiltrate.2 Ultrastructural features of a biopsy taken after immersion consist of epidermal hyperkeratosis and spongiosis with partial split of the desmosomes.1