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iabetes is a disease that has a huge impact on our culture. It is estimated to account for 15% of all healthcare costs in the United States.¹ It has been implicated as the chief cause of nontraumatic lower extremity amputations, 35% of new cases of end-stage renal disease (ESRD), and a significant amount of cardiovascular disease. It has also been said that 100% of all diabetic patients have their skin affected in one way or another.² When you consider the elderly population, this effect is even greater.
       As many as 16 million people are affected with diabetes³; the tremendous impact of the cutaneous manifestations of diabetes is obvious. The pathogenesis of these skin diseases is becoming clearer as more research is conducted. Even without that knowledge, some disorders are characteristically associated with diabetes. For example, diabetic bullae, the syndrome of waxy skin and limited joint mobility, and diabetic dermopathy are virtually pathognomonic.

Diabetic dermopathy is one of the most common skin abnormalities affecting persons with diabetes.

       Disorders of the diabetic skin that contribute to its pathology include microangiopathy, infection, and metabolic disturbances of the tissue. These problems cause disease in other parts of the body as well. Consequently, it is important to understand the dermal manifestations of diabetes to effectively manage these common comorbidities.

Necrobiosis Lipoidica Diabeticorum

       Necrobiosis lipoidica diabeticorum (NLD) is not exclusive to diabetes. Actually, it is relatively rare and has an incidence of 0.7% in patients with diabetes.⁴ The disorder has a greater incidence in women and is 4 times more common in Caucasians. Although the average age of those affected is 34, there is a predominance of presentation in the young.⁵ One paper reports that at the time of diagnosis, two-thirds of patients will have diabetes, and all but 10% of the rest will develop it within 5 years; the rest will have an abnormal glucose-tolerance test or first-degree relative with diabetes.³
       Initially, NLD presents as an erythematous, nonscaly plaque on the pretibial and malleolar areas of the legs. Eventually, these areas enlarge and coalesce into larger plaques that then develop yellow, atrophic centers. The borders of NLD are irregular and enlarge slowly. The atrophy extends down into the dermis. Additionally, there are prominent telangiectasias, and approximately one-third of the lesions ulcerate. Slightly more than half of the patients diagnosed with NLD have associated retinopathy and/or other signs of microvascular compromise.⁶ The time required to see improvement varies from 3–4 years. Spontaneous resolution is sometimes noted. The mainstay of treatment is tight diabetic control. Topical and/or injected corticosteroids are also indicated. Intralesional injection of 0.1 ml triamcinolone 2.5–10mg/ml every 2–4 weeks has been found to be effective in severe cases.⁵

Granuloma Annulare

       The cause of granuloma annulare is unknown. It is a benign condition that has several clinical forms. The classic type is most common. The less common forms include generalized, multiple, perforating, and subcutaneous forms. This condition has lesions similar to NLD without the atrophic center. Lesions are common over trauma areas, such as the dorsum of the hand and elbows. It begins as papules and expands into annular borders with central areas of hyperpigmentation. In spite of its appearance, there are few other symptoms. There are several forms of treatment, including liquid nitrogen, to ablate the annular borders of the lesion.

Diabetic Dermopathy

       Diabetic dermopathy has been called one of the most common skin signs of diabetes, but it can be seen in non-diabetics as well. Prevalence is most noted in men with diabetes who are 60 years of age or above.⁵
       The exact cause of this disorder is unknown. Some theories about the pathogenesis include post-traumatic atrophy due to a thermal or mechanical insult or post-inflammatory hyperpigmentation in poorly vascularized skin.⁵ There is little evidence of angiopathy or its relationship to other diabetic angiopathies, but its incidence does correlate well with the severity of diabetes.⁶
       Diabetic dermopathy begins as pink patches approximately 0.5–1 cm in diameter on the pretibial and lateral leg areas. Eventually, they become hyperpigmented brown papules with a fine scale and surface atrophy. They are round, circumscribed, shallow, bilateral, and usually not symmetrical. They finally heal, forming scars. Treatment is episodic; these lesions often resolve spontaneously.

Acanthosis Nigricans

       Acanthosis nigricans is a disorder that can be found in disorders of insulin resistance, such as diabetes, obesity, and paraneoplastic syndromes. It has been reported to occur with an incidence approaching 74% in healthy obese adults, 66% in primary school children who weigh 200% of the ideal body weight, 28% of children weighing 120% of ideal body weight, and 71% in an unselected population of primary school children.^7-8 It has also been demonstrsted to occur with increased frequency in certain ethnic populations. American Indians have an incidence of acanthosis nigricans of 54%, and it occurs at an incidence of 40% in Hispanic populations.⁹
       Most authors have causally linked acanthosis nigricans to pathology related to the insulin growth factor (IGF) receptors found in the epidermis.¹⁰ The defect has been postulated as being related to defects in the receptor itself, postreceptor function, antibodies, or obesity.¹¹ Additionally, there are 3 lines of evidence that associate this disorder with high plasma levels of insulin. These include the finding of classic insulin receptors and IGF receptors in fibroblasts and keratanocytes in the epidermis. Second, acanthosis nigricans has also been found locally at the site of injection of insulin. Finally, as previously mentioned, most of the conditions associated with the disorder have a form of insulin resistance.
       Symptoms include velvety, hyperpigmented plaques. These are found on the flexural areas and the back of the neck. Additionally, there can be an associated papillomatosis. These lesions can range from shallow to deep. Histologically, the lesions show marked hyperkeratosis and papillomatosis, and they are mildly acanthotic.¹² Some also display atrophy and increased amounts of melanin in the basal epidermis.
       There are several ways to treat this disorder. One way is to use keratolytic agents like salicylic acid. Some success has also been found using omega-3 fatty acids and a diet rich in fish oils. Finally, good success has been found using weight control and exercise.¹ A combination of these, with good serum glucose control, is most likely to help.

Cutaneous Infections

       Cutaneous infection is the area of diabetic skin disease that is most often thought about. Actually, well-controlled patients with diabetes probably are no more susceptible to infection than the normal population. However, poor control (especially ketoacidosis) compromises resistance. The poorly controlled get more severe, protracted, and resistant infections. Once serum glucose control is reestablished, resistance usually returns to normal. Contrary to logic, hyperglycemia contributes little to the growth of most cutaneous organisms. In support of this, topically applied sugar and honey have actually been used in healing ulcers of the skin.¹³ A well-known exception involves Candida. It has been shown to have a direct correlation between growth and sugar concentration in the saliva.¹⁴

       Editor’s note: This article is adapted from a longer article originally published in the November 2000 issue of Skin & Aging, © HMP Communications, LLC.