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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 tissue.[3] Anetoderma is subclassified as primary anetoderma, secondary anetoderma, iatrogenic anetoderma of prematurity, congenital anetoderma, familial anetoderma, and drug-induced anetoderma.[4]
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.[5]
Signs and symptoms
Typically pink macules that are round or oval and have a diameter of 0.5 to 1 centimeters grow on the trunk, thighs, and upper arms. They are less frequently found on the neck, face, and other areas. Usually, the soles, palms, and scalp are unaffected. Every macule grows for one or two weeks until it reaches a size of 2-3 centimeters.[6] Larger erythematous plaques can occasionally be seen, and nodules have also been identified as the main lesion.[3]
Lesions range widely in number from fewer than five to one hundred or more.[6] The lesions do not change throughout a person's life, and new lesions frequently take years to appear.[3] 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.[6]
Causes
Primary anetoderma is an idiopathic development of atrophic lesions in skin areas that appeared normal prior to the onset of atrophy.[7]
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.[14]
Case reports have described instances of congenital anetoderma presenting as anetoderma on the trunk of premature infants at birth.[15][16]
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.[17]
Diagnosis
Anetoderma can be diagnosed clinically. But if the diagnosis proves to be difficult, a skin biopsy—ideally a punch biopsy—can be carried out to include the mid dermis.[18] Under a microscope, the epidermis of anetoderma exhibits a nearly total loss of elastic fibers in the reticular and papillary dermal layers. A dermal periadnexal and perivascular infiltrate containing histiocytes and plasma cells can also be seen in the histopathology of the lesion.[19]
In lesional skin, elastophagocytosis and tiny fragmented elastic fibrils can be seen in addition to the histopathology on electron microscopy.[20][21]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.[22]
Classification
There are five subtypes of anetoderma: drug-induced anetoderma, familial anetoderma, prematurity-associated anetoderma, primary (idiopathic) anetoderma, and secondary anetoderma from a previous dermatosis. The Jadassohn-Pellizzari type and the Schweninger-Buzzi type are the historical subtypes of the primary type, which is found in areas of previously normal skin. While the Schweninger-Buzzi type of anetoderma develops in skin that appears normal with no predisposition skin changes, the Jadassohn-Pellizzari type occurs following the occurrence of inflammatory or urticarial lesions. These terms are now obsolete because the two primary types are identical histologically as well as having a similar disease course.[4]
^ abKineston, Donald P; Xia, Yang; Turiansky, George W (June 2008). "Anetoderma: a case report and review of the literature". Cutis. 81 (6): 501–506. PMID18666393.
^ abThivolet, J; Cambazard, F; Souteyrand, P; Pierini, A M (1981). "Mastocytosis evolving into anetoderma. Review of the literature". Annales de dermatologie et de venereologie. 108 (3): 259–266. PMID7020556.
^zkan, ebnem; Fetil, Emel; zler, Fatih; Pabucuolu, Uur; Yalin, Nagihan; Gne, Ali Tahsin (2000). "Anetoderma secondary to generalized granuloma annulare". Journal of the American Academy of Dermatology. 42 (2). Elsevier BV: 335–338. doi:10.1016/s0190-9622(00)90106-3. ISSN0190-9622. PMID10640927.
^Shames, Bruce S.; Nassif, Aude; Bailey, Cynthia S.; Saltzstein, Sidney L. (1994). "Secondary Anetoderma Involving a Pilomatricoma". The American Journal of Dermatopathology. 16 (5). Ovid Technologies (Wolters Kluwer Health): 557–566. doi:10.1097/00000372-199410000-00020. ISSN0193-1091. PMID7802171.
^Disdier, Patrick; Harlé, Jean-Robert; Andrac, Lucille; Verrot, Denis; Bolla, Gilles; Marco, Marielle San; Weiller, Pierre-Jean (1994). "Primary anetoderma associated with the antiphospholipid syndrome". Journal of the American Academy of Dermatology. 30 (1). Elsevier BV: 133–134. doi:10.1016/s0190-9622(08)81902-0. ISSN0190-9622. PMID8277016.
^Colditz, Paul B.; Dunster, Kimble R.; Joy, Gloria J.; Robertson, Ivan M. (1999). "Anetoderma of prematurity in association with electrocardiographic electrodes". Journal of the American Academy of Dermatology. 41 (3). Elsevier BV: 479–481. doi:10.1016/s0190-9622(99)70126-x. ISSN0190-9622. PMID10459128.
^ZAKI, I.; SCERRI, L.; NELSON, H. (1994). "Primary anetoderma: phagocytosis of elastic fibres by macrophages". Clinical and Experimental Dermatology. 19 (5). Oxford University Press (OUP): 388–390. doi:10.1111/j.1365-2230.1994.tb02688.x. ISSN0307-6938. PMID7955494.
^Oikarinen, Aarne I.; Palatsi, Riitta; Adomian, Gerald E.; Oikarinen, Heljä; Clark, Joan G.; Uitto, Jouni (1984). "Anetoderma: Biochemical and ultrastructural demonstration of an elastin defect in the skin of three patients". Journal of the American Academy of Dermatology. 11 (1). Elsevier BV: 64–72. doi:10.1016/s0190-9622(84)70136-8. ISSN0190-9622. PMID6736354.
Further reading
Olivo, M. P. (January 1, 1993). "Anetoderma. Anetoderma, the primary type". Archives of Dermatology. 129 (1). American Medical Association (AMA): 106–107. doi:10.1001/archderm.129.1.106. ISSN0003-987X. PMID8420480.
Ghomrasseni, Sabah; Dridi, Myriam; Gogly, Bruno; Bonnefoix, Mireille; Vabres, Pierre; Venencie, Pierre Yves; Pellat, Bernard; Godeau, Gaston (2002). "Anetoderma". The American Journal of Dermatopathology. 24 (2). Ovid Technologies (Wolters Kluwer Health): 118–129. doi:10.1097/00000372-200204000-00003. ISSN0193-1091. PMID11979071. S2CID40039865.