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| Necrobiosis lipoidica | |
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| Other names | Necrobiosis lipoidica diabeticorum |
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Necrobiosis lipoidica is a rare, chronic skin condition predominantly associated with diabetes mellitus (known as necrobiosis lipoidica diabeticorum or NLD).[1] It can also occur in individuals with rheumatoid arthritis or without any underlying conditions (idiopathic)[2] and can also be displayed in patients with obesity, hypertension, celiac disease, and metabolic syndrome. About a quarter of necrobiosis lipoidica is associated with diabetes mellitus.
The broader overarching definition of necrobiosis is a gradual physiological death of a cell. It can be caused by basophilia, erythema or a tumor. As a derma pathology term, it means altered collagen or altered dermal connective tissue. Necrobiosis lipoidica is linked to microvascular damage and collagen degeneration.
It is characterized by hardened, raised areas of the skin, often appearing on the shins, with a yellowish center and a surrounding dark pink area. The lesions are generally asymptomatic but can become tender and ulcerate when injured. Histological features and skin changes are caused by thickening of blood vessel wall, collagen deterioration, granuloma (clustered white blood cells in tissues) formation and fat deposit. Necrobiosis lipoidica has many possible contributing factors and research for treatment and causes is an ongoing process.
The exact cause of this condition is not known, but it involves collagen degeneration and a granulomatous response in the layer of the skin called the dermis, often affecting the deeper fat layer and thickening dermal blood vessels.
A clinical examination is required to diagnose. It usually occurs on the shins, in an oval or irregular shape. The color is usually yellow-brown with a atrophic surface, visible with blood vessels. Diagnosis is further confirmed through a skin biopsy showing inflammatory cell infiltrate and necrotising vasculitis. Treatments like PUVA therapy, photodynamic therapy, low dose aspirin, and corticosteroids are used to manage symptoms, as there is no cure.
Etiology
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It affects approximately 0.3%- 1.2% of diabetics, showing a higher prevalence in women (3:1 female-to-male ratio). (Sibbald C, Reid S, Alavi A. Necrobiosis Lipoidica. Dermatol Clin. 2015 Jul;33(3):343-60.) There are many factors involving Necrobiosis Lipoidica, a theory for why it is commonly associated with diabetes is a result of "vacsular disturbance involving immune complex deposition or microangiopathic changes that lead to collagen degeneration". The core pathologies of diabetes including thickening of basement membrane, loss of perictes, endothelial dysfunction and capillary occlusion all relate to this.
Signs and symptoms
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NL/NLD most frequently appears on the patient's shins, often on both legs,[1] although it may also occur on forearms, hands, trunk, and, rarely, nipple, penis, and surgical sites. The lesions are often asymptomatic but may become tender and ulcerate when injured. The first symptom of NL is often a "bruised" appearance (erythema) that is not necessarily associated with a known injury. The extent to which NL is inherited is unknown.[citation needed]
NLD appears as a hardened, raised area of the skin. The center of the affected area usually has a yellowish tint while the area surrounding it is a dark pink. It is possible for the affected area to spread or turn into an open sore. When this happens the patient is at greater risk of developing ulcers. If an injury to the skin occurs on the affected area, it may not heal properly or it will leave a dark scar.[citation needed]
Pathophysiology
[edit]Although the exact cause of this condition is not known, it is an inflammatory disorder characterised by collagen degeneration, combined with a granulomatous response. It always involves the dermis diffusely, and sometimes also involves the deeper fat layer. Commonly, dermal blood vessels are thickened (microangiopathy).[3]
It can be precipitated by local trauma, though it often occurs without any injury.[4]
Diagnosis
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NL is diagnosed by a skin biopsy, demonstrating superficial and deep perivascular and interstitial mixed inflammatory cell infiltrate (including lymphocytes, plasma cells, mononucleated and multinucleated histiocytes, and eosinophils) in the dermis and subcutis, as well as necrotising vasculitis with adjacent necrobiosis and necrosis of adnexal structures. Areas of necrobiosis are often more extensive and less well defined than in granuloma annulare. Presence of lipid in necrobiotic areas may be demonstrated by Sudan stains. Cholesterol clefts, fibrin, and mucin may also be present in areas of necrobiosis. Depending on the severity of the necrobiosis, certain cell types may be more predominant. When a lesion is in its early stages, neutrophils may be present, whereas in later stages of development lymphocytes and histiocytes may be more predominant.[citation needed]
Treatment
[edit] | This section relies largely or entirely on a single source. (August 2024) |
There is no clearly defined cure for necrobiosis.[5] NLD may be treated with PUVA therapy, Photodynamic therapy and improved therapeutic control.[medical citation needed]
Although there are some techniques that can be used to diminish the signs of necrobiosis such as low dose aspirin orally, a steroid cream or injection into the affected area, this process may be effective for only a small percentage of those treated.
See also
[edit]References
[edit]- ^ a b James, William D.; Elston, Dirk; Treat, James R.; Rosenbach, Misha A.; Neuhaus, Isaac (2020). "26. Errors in metabolism". Andrews' Diseases of the Skin: Clinical Dermatology (13th ed.). Edinburgh: Elsevier. pp. 538–539. ISBN 978-0-323-54753-6.
- ^ Lepe, Kenia; Riley, Christopher A.; Hashmi, Muhammad F.; Salazar, Francisco J. (2024). "Necrobiosis Lipoidica". StatPearls. StatPearls Publishing. PMID 29083569.
- ^ Klaus J. Busam (15 January 2009). Dermatopathology. Elsevier Health Sciences. p. 54. ISBN 978-0-443-06654-2. Retrieved 22 August 2011.
- ^ Michael I. Greenberg (2005). Greenberg's text-atlas of emergency medicine. Lippincott Williams & Wilkins. p. 416. ISBN 978-0-7817-4586-4. Retrieved 22 August 2011.
- ^ AOCD Website
External links
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