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  • Acanthosis nigricans (see Section 5) and lipodystrophy.

    Associated with insulin resistance in diabetes mellitus. Insulin-like epidermal growth factors may cause epidermal hyperplasia.

  • Adverse cutaneous drug reactions in diabetes (see Section 23).

    Insulin: Local reactions—lipodystrophy with decreased adipose tissue at the sites of subcutaneous injection; Arthus-like reaction with urticarial lesion at site of injection.

    Systemic insulin allergy: Urticaria, serum sickness–like reactions.

    Oral hypoglycemic agents: Exanthematous eruptions, urticaria, erythema multiforme, and photosensitivity.

  • Calciphylaxis (see Section 18).

  • Cutaneous perforating disorders.

    Rare conditions in which horny plugs perforate into the dermis or dermal debris is eliminated through the epidermis. Not always associated with diabetes (see Section 18).

  • Diabetic bullae (bullosis diabeticorum).

  • Diabetic dermopathy.

  • Eruptive xanthomas.

  • Granuloma annulare (see Section 14).

  • Infections (see Sections 25 and 26).

    Poorly controlled diabetes associated with increased incidence of primary and secondary Staphylococcus aureus infections, cellulitis (S. aureus, group A streptococcus), erythrasma, dermatophytoses, candidiasis, and mucormycosis with necrotizing nasopharyngeal infections.

  • Necrobiosis lipoidica.

  • Peripheral neuropathy (diabetic foot).

  • Peripheral vascular disease (see Section 17).

    Small-vessel vasculopathy (microangiopathy): Involves arterioles, venules, and capillaries. Characterized by basement membrane thickening and endothelial cell proliferation. Presents clinically as acral erysipelas-like erythema, and ± ulceration.

    Large-vessel vasculopathy: Incidence greatly increased in diabetes. Ischemia is most often symptomatic on lower legs and feet with gangrene and ulceration. Predisposes to infections.

  • Scleredema diabeticorum.

    Synonym: Scleredema adultorum of Buschke. Need not be associated with diabetes. Onset correlates with duration of diabetes and with the presence of microangiopathy. Skin findings: Poorly demarcated scleroderma-like induration of the skin and subcutaneous tissue of the upper back, neck, and proximal extremities. Rapid onset and progression.

  • Scleroderma-like syndrome. Scleroderma-like thickening of skin and limited joint mobility (“prayer sign”).


  • Large, intact bullae arise spontaneously on the lower legs, feet, dorsa of the hands, and fingers on noninflamed bases (Fig. 15-1).

  • Neither trauma nor an immunologic mechanism has been implicated. Histologically, bullae show intra- or subepidermal clefting without acantholysis.


Diabetic bulla A large, intact bulla is seen on the pretibial skin on the right lower leg. The patient had many of the vascular complications of diabetes mellitus, i.e., renal failure, retinopathy, and atherosclerosis obliterans resulting in amputation of the left big toe. (Used with permission of Dr. Kenneth Greer.)


  • Peripheral neuropathy is responsible for the “diabetic foot.”

  • Other factors are angiopathy, atherosclerosis, and infection; most often they are combined.

  • Diabetic neuropathy is combined: motor and sensory. Motor neuropathy leads to weakness and muscle wasting distally.

  • Autonomic neuropathy accompanies sensory neuropathy and leads to anhidrosis, which may not be confined to the distal extremities.

  • Sensory neuropathy predisposes to neurotropic ulcers ...

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