The incidence of diabetes in America is increasing steadily with the epidemic of obesity.
Fourteen percent of health care expenditures in America are diabetes related.
Metabolic abnormalities in glucose and insulin relate directly to diabetic thick skin, limited joint mobility, eruptive xanthomas, and acanthosis nigricans.
Neuropathy, vasculopathy, and immune dysfunction associated with diabetes contribute directly to lower-extremity ulcers and certain cutaneous infections.
Diabetes-associated skin conditions without a known pathogenesis include: necrobiosis lipoidica, granuloma annulare, diabetic dermopathy, acquired perforating dermatosis, and bullosis diabeticorum.
Diabetes mellitus (DM) is a major cause of morbidity and mortality in the United States; 2017 estimates suggest 23.4 million Americans have known diabetes.1 Approximately 14% of all health care expenditures in the United States are directly attributable to the medical care of diabetes. Men and women diagnosed with diabetes at age 40 years are expected to lose 12 and 14 life-years, respectively.2 Major studies show that tight glycemic control decreases microvascular disease (ie, retinopathy, neuropathy, nephropathy), but that coronary vascular disease, the major contributor to morbidity and mortality in patients with diabetes, receives no benefit from intensive glycemic control in patients with longstanding diabetes. In one large, randomized, controlled trial with approximately a third of patients having known coronary artery disease, intensive glycemic control was, in fact, associated with an increase in mortality. Newly diagnosed Type 2 diabetes appears to have long-term benefit from similar degrees of tight control.3 New guidelines for glycemic control (glycosylated hemoglobin [HbA1c] <7%) attempt to balance this body of evidence.4 Tight glycemic control may have a beneficial effect on a subset of skin-related, diabetes-associated disorders, but evidence is generally lacking.
Diabetes is characterized by a state of relative or complete insulin deficiency, leading to defects in glucose, fat, and protein metabolism. In Type 1 diabetes (formerly insulin-dependent DM), an insufficiency of insulin occurs through a gradual, immune-mediated destruction of β islet cells in the pancreas, marked by autoantibodies. In Type 2 diabetes (formerly noninsulin-dependent DM), chronic hyperglycemia occurs mainly through end-organ insulin resistance followed by a progressive decrease in pancreatic insulin release associated with aging. Diabetes can be diagnosed by a fasting blood glucose level of 126 mg/dL or higher, a random value of 200 mg/dL or higher, or an HbA1c level of 6.5% or above. A genetic predisposition and a strong association with obesity exist in Type 2 diabetes. In both types of diabetes, abnormalities of insulin and elevated blood glucose levels lead to metabolic, vascular, neuropathic, and immunologic abnormalities. Affected organs include the cardiovascular, renal, and nervous systems, the eyes, and the skin.
Nearly all patients with diabetes have cutaneous findings related to their condition, including those listed in Table 137-1. Some diabetes-associated skin conditions are a direct result of the related metabolic changes such as hyperglycemia and hyperlipidemia. Progressive damage to ...