What are the causes of fatty progressive necrosis?

summary

Lipoid progressive necrosis, also known as diabetic lipoid progressive necrosis, is characterized by the presence of large scleroderma like plaques in front of the tibia, often accompanied by diabetes. What are the causes of fat progressive necrosis?

What are the causes of fatty progressive necrosis?

The etiology is not clear, there are two possibilities. 2 / 3-3 / 4 of the patients have diabetes, so it is considered to be related to diabetes, accompanied by diabetic microangiopathy, resulting in glycoprotein deposition in the wall of small blood vessels, gradually causing vascular occlusion and tissue necrosis. The other thought that it had nothing to do with diabetes, only 0.3% of all diabetic patients had the disease, and the course of the disease had nothing to do with the severity, duration and controlled condition of diabetes.

The average age of onset is 30-40 years old. It is rare in children and newborns. The onset age of patients with diabetes is earlier than that of patients without diabetes. The gender difference is obvious, and the ratio of male to female is about 1:4. The lesions are mainly located on the side of the leg. At the beginning, they are round, hard, dark red, asymptomatic papules or plaques, one or several of which are different. They develop slowly and fuse with each other to form stoloning, oval or irregular hard plaques with clear and irregular edges. It is usually brownish red or purple, flat or concave in the center, smooth and glassy on the surface, with obvious telangiectasia and fibrosis. Its appearance is like scleroderma, and about 1 / 3 of the lesions may be ulcerated. The surrounding skin is normal. The lesions located in the deep part were usually nodular, and the surface skin was mostly unchanged. About 15% of the lesions occurred in the arm, trunk and scalp, and the lower limbs were not involved in some cases. In the scalp, it can cause alopecia due to atrophy and scar like lesions, and there is often hypopigmentation at the hair margin. The course of the disease is chronic, often develops slowly for several years, can also be in a static state for a long time or scar formation after healing.

Examination showed that the main histopathological changes occurred in the dermis, with unclear progressive necrosis and fibrosis, mixed with lamellar lymphocytes and granulomatous infiltration. The histiocytes arranged in palisade shape at the edge of the progressive necrosis area, but not as obvious as granuloma annulare or rheumatoid nodules. The aggregation of epithelioid cells may be tuberculosis like or sarcoidosis like, with foreign body giant cells and Langhans giant cells. The intima of small vessels in necrotic area was thickened and fibrotic. The epidermis becomes thin or ulcerated, and the skin appendages can also be destroyed.

matters needing attention

The patients with diabetes should be treated actively. However, the rash may not subside immediately after diabetes control. We can try to inject corticosteroids into skin lesions, especially triamcinolone acetonide and betamethasone dipropionate. Intractable or ulcerative lesions can be treated by skin grafting after resection, but there are still reports of recurrence after skin grafting. Topical use of tretinoin may contribute to the recovery of atrophic skin lesions.