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. 2013:2013:641416.
doi: 10.1155/2013/641416. Epub 2013 Oct 1.

Pruritic vesicular eruption on the lower legs in a diabetic female

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Pruritic vesicular eruption on the lower legs in a diabetic female

Hassan Riad et al. Case Rep Dermatol Med. 2013.

Abstract

A 50-year-old diabetic female presented with highly pruritic vesicles and excoriated lesions over the anterior aspect of both lower legs. The lesions were recurrent over the last two years. She received a lot of medications with partial response. Hb A1c was 10.8% (normal up to 7%). CBC showed microcytic, hypochromic anemia. Serum zinc, folate, IgE, TSH and T4 were all within normal ranges. Biopsy showed epidermal separation secondary to keratinocyte necrosis and minimal monocytic, perivascular infiltrate. Direct immunofluorescence was negative for intraepidermal and subepidremal deposition of immunoglobulin. The dermis was positive for mucin deposition stainable by both PAS and Alcian blue while it was negative for Congo red and APC immunoperoxidase staining for amyloid material. In conclusion, the case was diagnosed as bullosis diabeticorum by distinctive clinical and pathological features and after exclusion of other possible differentials. Pruritus was partially controlled by topical potent steroid and the case was resolved spontaneously after eight months.

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Figures

Figure 1
Figure 1
(a) The distribution of the lesions, bilateral and almost symmetrical, on both lower limbs. (b) Higher magnification showing the vesicular lesions lying on erythematous base and the fine white scars in healed lesions. (c) A close-up view of the vesicular lesions showing tense blistering with central crustations, on the right side of the photo a superficial white scar of healed lesion.
Figure 2
Figure 2
(a) H&E section, ×100 magnification showing an acute totally intraepidermal blister. At both angles of the blister, the separation is entirely intraepidermal. Stratum corneum is intact which attests the acute onset of the lesion, and no signs of regeneration can be seen. No evidence of common pathological changes that induce intraepidermal blister as acantholysis or ballooning degeneration. No inflammatory cells in or around the lesion. (b) H&E section, ×200 magnification showing epidermal separation at the level of the spinous layer. Necrotic individual keratinocytes can be seen intravesicular and at the roof of the blister (no acantholysis, no ballooning or multinuclear cells). (c) H&E section, ×400 magnification showed sparse perivascular infiltrate, and collagen bundles in the papillary dermis are separated by scanty mucin deposition.

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