The dermatosis can precede, coincide or occur after the diagnosis of diabetes [3]. The cause of NL remains unknown. It has been reported in patients with various diseases. Many theories have been proposed to try to explain the pathogenic mechanisms of the NL and current theories postulate the following: a. Appears to be the most important in pathogenesis.
The vascular damage is preferentially localized in the basement membrane of small vessels, which is due to the combination of multiple factors. We found elevated levels of fibronectin, alpha macroglobulin, ceruloplasmin in LN patients and granuloma annulare and diabetes mellitus and elevated haptoglobin, in patients without diabetes mellitus NL.
These protein abnormalities could be responsible for angiopathy. In agreement with previous reports of HLA patterns in diabetic patients, it is suggested that genetic factors do not play an important role in NL. Immunological mechanisms. For some authors, the trigger factor for NL can be mediated by immune vasculitis due to evidence of immunoglobulin deposits IgM, IgA and C3 in the walls of the affected vessels, plus IgM, C3 or fibrinogen in the dermo-epidermal junction in some patients.
An increase of dendritic cells S positive has been detected in the epidermis [3,17]. Alterations of collagen. It is accepted that the granulomatous response may be due to alterations of collagen. It is postulated that hyperglycemia causes increased activity of the aldolase -reducing enzyme, resulting in retention of water in the tissues, and destruction of collagen hyperhydration.
Other studies reveal decreased concentration of hydroxyproline in the affected skin, with decreased collagen content and decreased number of fibroblasts. However, this hypothesis does not explain the cases where no hyperglycemia is detected [3,17]. Sweat and neural abnormalities. The functioning of sweat glands is altered and the number of nerve endings in biopsies is found to be decreased. However, these changes appear to be the result of the local destruction of these structures by a primary inflammatory process [3,17].
Clinically it is characterized as a chronic disfiguring process. Most lesions are located in the legs, especially in the pretibial region, although lesions on the face, scalp, arms, and trunk may also occur. The lesions are unique but may be multiple. Initially presents as erythematous papules that increase in size and become plaques with a brownish yellow atrophic center with telangiectasias on the surface.
The lesions may resolve spontaneously or become chronic with occasional ulceration.
The occurrence of squamous cell carcinoma has been reported as a rare complication [13,16,17,19]. Cases with atypical features are outlined, considering both these lesions are located outside of the legs face, scalp , fingers, penis, nipples, postsurgical scars , as different morphology injuries that may occur as papules, nodules, morphoeic plaques, or ulcerated lesions and piercing injuries. Histopathology found that the epidermis may be normal, ulcerated or atrophic.
There are necrobiotic granulomas in the dermis. The necrobiotic pattern is more common in diabetics and those located in the legs [3]. The granulomatous process in NL extends from the deep dermis to the top of the septum of the subcutaneous tissue, resulting in a septal panniculitis. Necrobiosis in reaction areas of degeneration of collagen is observed. Collagen bundles may be thickened, chipped, or hyalinized amorphous anuclear and extend in different directions. Predominately in the lower third of the dermis and can reach the subcutaneous fat.
Necrobiotic areas around lymphocytes, plasma cells, fibroblasts and epithelial cells are observed. In some areas, the inflammatory infiltrate is arranged in palisades surrounding areas of necrobiosis [3].
In the granulomatous reaction, collagen degeneration is moderate. Granulomas composed of histiocytes, epithelioid cells and multinucleated giant cells were observed. Around these granulomas there is no lymphocytic infiltrate. In older lesions, areas of hyalinization of collagen is observed. Yen Shan et al reported three cases with atypical histopathological features such as prominent tuberculoid granulomas, and the perineural inflammatory infiltrate predominantly lobular panniculitis [20].
Direct immunofluorescence of NL demonstrated in IgM, IgA and fibrinogen in the walls of venous vessels, causing vascular thinning. In nondiabetic vascular changes are not prominent. Treatment can be divided into 6 categories: 1. Cutaneous blood flow enhancers: In this group the combination of high doses of aspirin with dipyridamole, stanozolol, ticlopidine, perilesional injections of heparin, pentoxifylline and prostagland E1 are cited all with varying results in different studies. Corticosteroids: Topical and intralesional corticosteroids may reduce inflammation in active lesions or lesions on the edges of growth, but has little benefit in stable atrophic lesions, which could worsen atrophy thereof.
Intralesional triamcinolone was reported as beneficial in active lesions. In two case reportsthe benefit of clobetasol propionate under occlusion was demonstrated and in two other studies the use of systemic corticosteroids in short pulses was suggested to be beneficial. Surgery: NL tends to exhibit the phenomenon of Koebner so curative surgery can not be guaranteed. Cutaneous healing enhancers: Various reports of efficacy of various topical preparations that act to promote cutaneous healing for ulcerated NL.
One case report has described the efficacy of recombinant granulocyte macrophage colony stimulating factor topically to ulcerated NL in young patients with diabetes. Physical modifications of wound background is also beneficial in promoting wound repair. Promogran, a new protease modulating matrix, has been reported to be effective in wound healing. This preparation inactives metalloprotease and other enzymes found in large quantities to have a negative effect on wound healing.
The bovine collagen gel applied in a non-diabetic patient under occlusion for 6 weeks, resulted in healing at 24 weeks with no recurrence after 5 months. In two diabetic women with ulcerated NL HBO achieved healing of the lesion after 98 and sessions, this could be related to the correction of tissue hypoxia.
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Immunomodulators: Within immunomodulatory efficacy in several studies of cyclosporine, mycophenolate mofetil, thalidomide, infliximab and tacrolimus are cited. Miscellaneous: This group includes nicotinamide, clofazimine, chloroquine and topical tretinoin. A study of nicotinamide showed improvement in the lesions of NL in 8 of 15 patients. In two studies with topic tretinoin has reported an improvement of the atrophic component NL. Application NL benzoyl peroxide has been reported to ulcerated beneficial [15,18]. The main findings of this condition are shown in Table V.
Rare process. More frequently in women. Associated with Diabetes mellitus and impaired glucose tolerance. Unknown etiology. Erythematous plaques with atrophic center on shins. Necrobiotic dermal granulomas.
Poor therapeutic response. Table V. Necrobiosis lipoidica. The limited variety of benign cutaneous polyarteritis nodosa was individualized by Lindberg in [23] Both cutaneous and systemic PAN polyarteritis histologically characterized by necrotizing vasculitis of medium-sized arteries, but cutaneous PAN may be clinically differentiated from systemic polyarteritis because they involve organs. The largest series of cutaneous PAN not demonstrate development of systemic disease in a mean follow up of 7 years [21].
The etiology is so far unknown , although the demonstration of deposits of immune IgM and C3 in lesions of some vessels as well as the detection of circulating immune complexes in others, suggesting immune complex mediation. In some cases there is a high titer of antistreptolysin O ASO. On the other hand, cutaneous polyarteritis nodosa designates the exclusive skin involvement deep dermis and panniculus , with a benignchronic course. Skin lesions were distributed especially in the legs, but can occur in the upper limbs, face, scalp and mucous membranes [22].
Are erythematous and painful nodular lesions, the size will vary between 0.
It is commonly found in some patients, lesions and other recent developments, injuries later stages.