primary local cutaneous amyloidosis examination and diagnosis of primary local cutaneous amyloidosis
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Common examination of primary localized cutaneous amyloidosis
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Histopathology: The deposits of macula and mossy cutaneous amyloidosis are confined to dermal papilla, which are hemispherical, conical or lumpy, with cracks between them and epidermis. HE staining showed eosinous red and homogeneous, with a small amount of blue-stained cell fragments. Hyperkeratosis of epidermis, irregular thickening of granular layer and spinous cell layer, and atrophy of epidermis above amyloid protein. Basal cells are liquefied and degenerated, especially in plaque type. Amyloid protein is deposited around the blood vessels of cutaneous heterochromic amyloidosis, and irregular hyperplasia of epidermis and lengthening of epidermal process can be seen. Amyloid deposition around hair follicles is sheath-like. The epidermis of nodular cutaneous amyloidosis shrinks and thinns, and the epidermal process disappears. Large subepidermal amyloid expands from dermis to subcutaneous. Vascular wall may be thickened by amyloid deposition, sweat glands and adipocytes may also be involved, and chronic inflammatory cells infiltrate in dermis. Stained with methyl violet or crystal violet, amyloid protein has metachromatic phenomenon and can be dyed into bright purplish red; Congo red staining showed green and birefringence by polarizing microscope. PAS staining showed amyloid protein resistant to amylase. Immunofluorescence examination showed the deposition of immunoglobulin around amyloid protein, which has been confirmed as antikeratin autoantibody (AK auto Ab). DACM staining showed disulfide bond bands, which also indicated that amyloid protein originated from keratin.
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