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What Is Discoid Lupus Erythematosus (DLE)? — an article on the Smart Living Network
July 28, 2008 at 8:29 PMComments: 0 Faves: 0

What Is Discoid Lupus Erythematosus (DLE)?


Of the three major kinds of lupus, Discoid Lupus Erythematosus (DLE) accounts for about 10% of lupus cases. DLE is usually much less serious than the far more common Systemic Lupus Erythematosus as it affects only the skin. Despite this limit in organs affected, DLE can still be difficult to live with.


The "discoid" part of DLE refers to its most common symptom; a disc-shaped rash. Some rash lesions can be about 5 to 10 mm in diameter with a darker red circle around a lighter pink scaly circular lesion. Discoid lesions are rarely painful or itchy. As these lesions heal, the skin often becomes hardened and scaly through a process called keratosis. There may also be scarring or pigmentation changes as the lesions disappear. Those with DLE tend to be sensitive to ultraviolet light and must dress and apply sunscreen accordingly. In addition to excess sun-exposure, lesion development may be triggered by trauma, exposure to cold or even mental stress. About 10% of those with DLE will go on to develop the more serious Systemic Lupus Erythematosus (SLE). There are other, less common variants of DLE, usually the result of complications. DLE lesions which develop a particularly thick scale (hyperkeratosis) are considered verrucous (wart-like) or hypertrophic (thickened) lesions. A mucosal variant of DLE exists where lesions appear on the mucosal membranes of the nose, eyes, or mouth. Lesions on the hands or feet are considered Palmar and Plantar DLE, respectively.


Despite the characteristic DLE rash, a skin biopsy is usually required for a definitive diagnosis. During this test, a small piece of lesion is removed and later prepared and examined under a microscope. The damage caused by the autoimmunity of DLE is usually recognizable at such magnification. Blood work may also be done to examine ANA levels (autoantibody associated with lupus), sedimentation rate, and complement levels. Often these tests are done to eliminate an SLE diagnosis.


The exact cause of DLE is unknown. Scientists believe it must be some sort of autoimmune disorder as it exhibits similar immune activity to other autoimmune diseases (such as SLE and rheumatoid arthritis). DLE most likely has a genetic basis since it tends to run in families. Ultraviolet light is the most common trigger for the development of DLE lesions, however it unlikely to cause the actual disease.


The most effective treatment for DLE patients is the avoidance of sunlight and other sources of ultraviolet light (some fluorescent and halogen bulbs emit small amounts). This can be accomplished by wearing protective clothing as well as diligently applying sunscreen. Lesions are usually treated with anti-inflammatory creams, aloes, and ointments. It is important to keep lesions clean to reduce the chance of a secondary skin infection. Living with DLE is by no means a fun experience, but can be made more bearable by avoiding unprotected sun exposure as well as taking care of lesions.

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