Ulcerated lower leg lesion

The patient’s atrophic plaques with a violaceous rim, indurated borders, and ulceration on the anterior pretibial surface were consistent with ulcerated necrobiosis lipoidica (NL).

NL typically manifests on the bilateral pretibial region as small papules or nodules that expand into yellow-brown atrophic, telangiectatic plaques with an elevated violaceous rim.^1,2 Most lesions are asymptomatic due to nerve damage, but up to 35% of patients may experience pruritus and tenderness.² Close monitoring of lesions is recommended due to risk of ulceration and potential for malignancy.² Rare reports show development of squamous cell carcinoma within NL lesions.¹

Women are 3 times more likely than men to have NL, with an average age of onset between 30 and 40 years.¹ The exact pathogenesis of NL is unknown.² Theories include vascular abnormalities (immunoglobulin deposition or microangiopathic changes leading to collagen degradation), abnormalities of collagen synthesis, neutrophil migration, and elevated tumor necrosis factor-alpha levels.^1,3

While NL can be diagnosed clinically, a skin biopsy may be necessary in atypical lesions. The biopsy will reveal palisading granulomatous inflammation in the dermis, with multinucleated histiocytes palisading around degenerated collagen bundles.²

No treatment has proven to be effective for NL. Glucose control in patients with diabetes does not have a significant effect on the NL lesions.^1-3 Corticosteroids (topical, intralesional, and systemic—depending on the severity) are considered first-line therapy.^1-3 Lifestyle modifications, such as smoking cessation and trauma avoidance, are recommended to promote healing; proper wound care is important when there is ulceration.^1,3 Other treatment options include oral pentoxifylline, topical retinoids or calcineurin inhibitors, and systemic immune system modulators (eg, tumor necrosis factor inhibitors and cyclosporine).

Since this patient did not respond to the topical betamethasone, she was started on oral pentoxifylline 400 mg tid. Unfortunately, she had to discontinue the medication because of gastrointestinal upset and was then started on doxycycline 100 mg orally bid. She was lost to follow-up.

‌

Photo courtesy of Cyrelle F. Finan, MD. Text courtesy of Harika Echuri, MD, Tulane University School of Medicine, New Orleans, LA, Cyrelle F. Finan, MD, Department of Dermatology, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

The patient’s atrophic plaques with a violaceous rim, indurated borders, and ulceration on the anterior pretibial surface were consistent with ulcerated necrobiosis lipoidica (NL).

NL typically manifests on the bilateral pretibial region as small papules or nodules that expand into yellow-brown atrophic, telangiectatic plaques with an elevated violaceous rim.^1,2 Most lesions are asymptomatic due to nerve damage, but up to 35% of patients may experience pruritus and tenderness.² Close monitoring of lesions is recommended due to risk of ulceration and potential for malignancy.² Rare reports show development of squamous cell carcinoma within NL lesions.¹

Women are 3 times more likely than men to have NL, with an average age of onset between 30 and 40 years.¹ The exact pathogenesis of NL is unknown.² Theories include vascular abnormalities (immunoglobulin deposition or microangiopathic changes leading to collagen degradation), abnormalities of collagen synthesis, neutrophil migration, and elevated tumor necrosis factor-alpha levels.^1,3

While NL can be diagnosed clinically, a skin biopsy may be necessary in atypical lesions. The biopsy will reveal palisading granulomatous inflammation in the dermis, with multinucleated histiocytes palisading around degenerated collagen bundles.²

No treatment has proven to be effective for NL. Glucose control in patients with diabetes does not have a significant effect on the NL lesions.^1-3 Corticosteroids (topical, intralesional, and systemic—depending on the severity) are considered first-line therapy.^1-3 Lifestyle modifications, such as smoking cessation and trauma avoidance, are recommended to promote healing; proper wound care is important when there is ulceration.^1,3 Other treatment options include oral pentoxifylline, topical retinoids or calcineurin inhibitors, and systemic immune system modulators (eg, tumor necrosis factor inhibitors and cyclosporine).

Since this patient did not respond to the topical betamethasone, she was started on oral pentoxifylline 400 mg tid. Unfortunately, she had to discontinue the medication because of gastrointestinal upset and was then started on doxycycline 100 mg orally bid. She was lost to follow-up.

‌

Photo courtesy of Cyrelle F. Finan, MD. Text courtesy of Harika Echuri, MD, Tulane University School of Medicine, New Orleans, LA, Cyrelle F. Finan, MD, Department of Dermatology, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

The patient’s atrophic plaques with a violaceous rim, indurated borders, and ulceration on the anterior pretibial surface were consistent with ulcerated necrobiosis lipoidica (NL).

NL typically manifests on the bilateral pretibial region as small papules or nodules that expand into yellow-brown atrophic, telangiectatic plaques with an elevated violaceous rim.^1,2 Most lesions are asymptomatic due to nerve damage, but up to 35% of patients may experience pruritus and tenderness.² Close monitoring of lesions is recommended due to risk of ulceration and potential for malignancy.² Rare reports show development of squamous cell carcinoma within NL lesions.¹

Women are 3 times more likely than men to have NL, with an average age of onset between 30 and 40 years.¹ The exact pathogenesis of NL is unknown.² Theories include vascular abnormalities (immunoglobulin deposition or microangiopathic changes leading to collagen degradation), abnormalities of collagen synthesis, neutrophil migration, and elevated tumor necrosis factor-alpha levels.^1,3

While NL can be diagnosed clinically, a skin biopsy may be necessary in atypical lesions. The biopsy will reveal palisading granulomatous inflammation in the dermis, with multinucleated histiocytes palisading around degenerated collagen bundles.²

No treatment has proven to be effective for NL. Glucose control in patients with diabetes does not have a significant effect on the NL lesions.^1-3 Corticosteroids (topical, intralesional, and systemic—depending on the severity) are considered first-line therapy.^1-3 Lifestyle modifications, such as smoking cessation and trauma avoidance, are recommended to promote healing; proper wound care is important when there is ulceration.^1,3 Other treatment options include oral pentoxifylline, topical retinoids or calcineurin inhibitors, and systemic immune system modulators (eg, tumor necrosis factor inhibitors and cyclosporine).

Since this patient did not respond to the topical betamethasone, she was started on oral pentoxifylline 400 mg tid. Unfortunately, she had to discontinue the medication because of gastrointestinal upset and was then started on doxycycline 100 mg orally bid. She was lost to follow-up.

‌

Photo courtesy of Cyrelle F. Finan, MD. Text courtesy of Harika Echuri, MD, Tulane University School of Medicine, New Orleans, LA, Cyrelle F. Finan, MD, Department of Dermatology, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.