NLD is a reflection of the degenerative changes observed in the dermis histologi-cally and the yellow color of mature lesions (presumably caused by the granulomatous inflammation in the dermis allowing the visualization of subcutaneous fat). An estimated 0.3% of patients with diabetes develop NLD and the lesions most commonly (approx 85%) appear on the extensor surfaces of the distal lower extremities (i.e., the shins) (12) (see Fig. 2). Additional locations include the distal upper extremities and the face and scalp. Initially, the lesions are red-brown in color and then over time acquire a yellow color centrally. In mature lesions, there is associated epidermal atrophy and deep dermal/subcutaneous blood vessels are easily visualized.
There is some disagreement as to the proportion of patients with NLD who have frank diabetes. The range that is usually cited is 40-65%, based primarily on clinical series from the 1950s and 1960s (19). In a more recent retrospective study of consecutive patients seen over a period of 25 yr, only 7 (11%) of 65 patients with classic biopsy-proven NLD had diabetes mellitus at presentation (20). However, the lesions are not pathognomic, as the diagnosis of NLD can predate the onset of diabetes and additional patients with NLD have equivocal glucose tolerance tests as well as family histories of diabetes. In patients with type 1 and 2 diabetes, the presumed underlying
etiology, as in the case of diabetic dermopathy, is microangiopathy. A higher incidence of both diabetic nephropathy and retinopathy was observed in children and adolescents with NLD in comparison to those without NLD, suggesting an association with poor metabolic control (21). Histologically, granulomatous inflammation surrounds degenerated collagen and elastin (necrobiosis).
Clinical improvement of NLD lesions has been reported following the use of topical corticosteroids (including class I) with or without occlusion, intralesional corticosteroids, oral clofazamine, oral pentoxifylline, and oral acetylsalicylic acid (ASA) plus dipyridamole (22-26). The reported therapeutic success of topical and intralesional corticosteroids as well as clofazamine and pentoxifylline is based on case reports and small series of patients. Clinical trials involving antithrombotic agents were based in part on the presence of microangiopathy and the observation that platelets in diabetics may have an increased tendency to aggregate. However, a double-blind, placebo-controlled trial of ASA plus dipyridamole in 14 patients with NLD failed to demonstrate any differences between the treatment and control groups (27). Similar negative findings were observed in a randomized, double-blind 6-mo trial of low-dose ASA (28).
Up to one-third of patients with NLD of the lower extremities can develop ulcerations within the lesions. In addition to the above-outlined therapies, single or small series of patients with ulcerative NLD have been treated with topical granulocyte-macrophage colony-stimulating factor (GM-CSF), tretinoin or collagen, hyperbaric oxygen, oral nicotinamide, oral corticosteroids, and oral cyclosporine (29-35). Treatment of the ulcers also includes local care and elevation of the legs (24). Glucose levels in patients receiving nicotinamide should be monitored because the dosage of insulin may need to be adjusted. The use of potent immunosuppressives is reserved for those individuals with significant morbidity.
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