A Guide To Cutaneous Manifestations Of Diabetes
As the diabetic population continues to swell worldwide, there has also been an increased occurrence of various cutaneous manifestations associated with the disease. Researchers have reported a greater than 30 percent incidence of these disorders and they have been found in up to 70 percent of all patients with diabetes at some point during the course of their illness.1-5 Another problematic statistic for the diabetic population is the fact that 15 percent of all people with diabetes will experience at least one ulceration during their lifetime.6
Although those with type 1 diabetes are more highly associated with developing autoimmune type cutaneous lesions, non-insulin dependent diabetic patients can also be afflicted by these lesions.7,8 One common cause of these cutaneous lesions appears to be poor glycemic control. Other typical findings associated with uncontrolled diabetes that contribute to the various cutaneous manifestations include neuropathy, immunopathy, angiopathy and nephropathy among others. While insulin-dependent diabetic patients are more predisposed to these cutaneous lesions, patients with type 2 are at an increased risk to develop skin infections, which one may see in 50 percent of these patients.9,10
Accordingly, let us take a closer look at the more common diabetic cutaneous afflictions and their proposed etiologies. Diabetic ulcerations and various associated infections have been covered in depth in previous articles in this publication. Therefore, we will direct our focus toward the more autoimmune cutaneous presentations.
What The Research Reveals About Cutaneous Disorders In Patients With Diabetes
There have been theories about an array of etiologies that may account for various diabetic cutaneous symptomatologies. However, alterations in metabolism and microangiopathy may help explain the predisposition for development.11 Microangiopathic changes are associated with abnormalities of local skin perfusion and the loss of capillary reserve.11 The failure of the microcirculatory system to meet the metabolic requirements of skin results in a variety of presentations. Further, it also serves as one of the main culprits in the development of diabetic foot ulcerations. The combination of small vessel disease, decreased large vessel run-off, neuropathy, susceptibility to infection and altered biomechanics all play a part in diabetic wound formation and cutaneous manifestations.11
Vascular endothelial cells are susceptible to hyperglycemic damage.12,13 Abnormalities in the aldose reductase pathway lead to an increase in sorbitol and other biochemical changes that directly contribute to endothelial damage.14,15 Hyperglycemic states of patients with poorly controlled diabetes also lead to glycylated end-products, which become deposited in the basement membrane in vascular endothelial cells.16 This process interferes with endothelial receptors and ultimately has negative effects on adhesions to the endothelium.6
Hyperglycemia also causes stress on antioxidants by creating a surplus of oxygen radicals. Excess radicals, which suppress nitric oxide production and release, contribute to the endothelial damage as well.17 Prolonged hyperglycemic states lead to activation of protein kinase C, which up-regulates several growth factors, leading to production of oxygen species and glycation end products.11 Although large vessel disease, which is common among those with diabetes, limits blood flow getting to the skin, it is the impairment in the capillary beds that impairs skin perfusion.18-20 Decreased microcirculation ultimately leads to tissue death due to the reduced supply of oxygen, nutrients and mediators that facilitate the repair process during injury. The tissue death results in local functional ischemia of the skin.21,22