Morphea is a medical phrase for localized scleroderma. The disease involves isolated patches of hardened skin there usually is no internal organ involvement. Morphea, also known as contained scleroderma, is a thickening and hardening of the skin and subcutaneous tissues from excessive collagen deposition. Morphea includes exact conditions ranging from very small plaques only connecting the skin to widespread disease causing functional and cosmetic deformities. Morphea discriminates from systemic sclerosis by its supposed require of internal organ involvement. Morphea is an uncommon situation that is thought to affect 1 in 1,000 people. Adequate studies on the incidence and prevalence have not been performed.
Morphea also may be under-reported as physicians may be unaware of this disorder and smaller morphea plaques may be less often referred to a dermatologist or rheumatologist. As in many other connective tissue or autoimmune disorders, morphea mainly involves women with a W:M ratio of 3:1. Physicians and scientists don’t know what causes morphea. Case reports and observational studies suggest there is a higher occurrence of family history of autoimmune diseases in patients with morphea. Tests for autoantibodies associated with morphea have shown results in higher frequencies of anti-histone and anti-topoisomerase IIa antibodies.
Case information of morphea co-existing with other systemic autoimmune diseases such as primary biliary cirrhosis, vitiligo, and systemic lupus erythematosus lend support to morphea as an autoimmune disease. Throughout the years, several different treatments have been tried for morphea including topical, intra-lesional, and systemic corticosteroids. Antimalarials such as hydroxychloroquine or chloroquine had been used. Other immunomodulators such as methotrexate, topical tacrolimus, and penicillamine has been tried. Ultraviolet A (UVA) light, with or without psoralens have also been tried. UVA-1, a more exact wavelength of UVA light, is able to penetrate the deeper portions of the skin.
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Morphea also may be under-reported as physicians may be unaware of this disorder and smaller morphea plaques may be less often referred to a dermatologist or rheumatologist. As in many other connective tissue or autoimmune disorders, morphea mainly involves women with a W:M ratio of 3:1. Physicians and scientists don’t know what causes morphea. Case reports and observational studies suggest there is a higher occurrence of family history of autoimmune diseases in patients with morphea. Tests for autoantibodies associated with morphea have shown results in higher frequencies of anti-histone and anti-topoisomerase IIa antibodies.
Case information of morphea co-existing with other systemic autoimmune diseases such as primary biliary cirrhosis, vitiligo, and systemic lupus erythematosus lend support to morphea as an autoimmune disease. Throughout the years, several different treatments have been tried for morphea including topical, intra-lesional, and systemic corticosteroids. Antimalarials such as hydroxychloroquine or chloroquine had been used. Other immunomodulators such as methotrexate, topical tacrolimus, and penicillamine has been tried. Ultraviolet A (UVA) light, with or without psoralens have also been tried. UVA-1, a more exact wavelength of UVA light, is able to penetrate the deeper portions of the skin.
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