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Anetoderma is a benign but uncommon disorder that causes localized areas of flaccid or herniated sac-like skin due to a focal reduction of dermal Elastic fiber. Anetoderma is subclassified as primary anetoderma, secondary anetoderma, Iatrogenesis anetoderma of prematurity, congenital anetoderma, familial anetoderma, and drug-induced anetoderma.
Two forms of primary anetoderma have been identified, based on whether an inflammatory response took place prior to the atrophy's appearance, anetoderma of Jadassohn-Pellizzari, in which inflammation occurs before the atrophic lesions appear, and anetoderma of Schweninger-Buzzi, in which inflammation is not present. (2016). 9780323244756, Elsevier. ISBN 9780323244756
Lesions range widely in number from fewer than five to one hundred or more. The lesions do not change throughout a person's life, and new lesions frequently take years to appear. When the lesions combine, they create sizable atrophic regions that are identical to acquired cutis laxa. They could unite to encircle sizable regions, particularly along the neck and at the base of the limbs.
Secondary anetoderma is a skin disease that develops in areas where there has previously been or is currently skin pathology. It has been linked to a variety of conditions, such as acne, urticaria pigmentosa, syphilis, leprosy, granuloma annulare, insect bites, and antiphospholipid syndrome. Secondary anetoderma has been linked to infectious, inflammatory, and tumorous conditions.
Macular depressions or skin outpouchings linked to the loss of dermal elastic tissue that are observed in premature infants are referred to as anetoderma of prematurity. According to reports, the location of monitoring electrodes or leads, such as ECG electrodes, may be related to these cutaneous lesions.
Case reports have described instances of congenital anetoderma presenting as anetoderma on the trunk of premature infants at birth.
Penicillamine administration has been linked to drug-induced anetoderma, especially in Wilson disease patients.
Familial anetoderma is rare and is inherited autosomally. The familial form usually appears in the first ten years of life and may show up only as skin manifestations, but it can also be linked to ocular, neurological, and bony abnormalities.
In lesional skin, elastophagocytosis and tiny fragmented elastic fibrils can be seen in addition to the histopathology on electron microscopy. Desmosine has been used to quantify the amount of elastin in lesional skin, which is considerably lower in anetoderma, since it is a major amino acid in elastin.
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