Anetoderma L90.1

Anetoderma (from the Greek aneto = flaccid) refers to a group of very rare, acquired, inflammatory or non-inflammatory (idiopathic) chronic connective tissue changes—primarily affecting the trunk—that lead to elastolysis, resulting in localized atrophy and characteristic hernia-like protrusions (or depressions) of the skin.   

In very rare cases, anetodermic lesions are observed to be photosensitive.

Mediodermal elastolysis can also be included in the spectrum of anetoderma, which is generally characterized by larger lesions but shows no significant etiological or pathogenetic differences from anetoderma.  

Unknown; pathogenetically, primary or post-inflammatory processes lead to the fragmentation and rarefaction of the skin’s elastic fiber network. Evidence of phagocytosis of elastic fiber fragments by macrophages. Deposition of IgM and C3 on the basement membrane, and of C3 on elastic fibers as well. Biochemical detection of desmosin (see underelastin) in affected skin.

The occurrence of anetoderma in association with HIV infections, syphilis, lichen planus, and other autoimmune diseases has been described on multiple occasions.

Note!Anetoderma is caused by a (predominantly) acquired (irreversible), circumscribed (probably inflammation-induced) elastolysis.

Note! Several cases of familial occurrence of the disease have been described (including in association with skeletal and ocular anomalies as well as neurological disorders).

Adolescents and adults (2nd-4th decade of life), female gender is preferentially affected.

Single or multiple, 0,2 cm to 1,0 cm large, sharply defined, roundish to oval flocks with often finely folded, thinned skin. Flocks partly sunken, partly hernia-like protrusion of the subcutaneous fatty tissue. The changes do not cause any complaints and are discovered rather by chance.

• Type Jadassohn: Anetodermia after inflammatory stage with redness and swelling.
• Type Pellizari: Urticarial preliminary stage.
• Type Alexander: After bullous initial stage.
• Type Schweninger-Buzzi: Without preliminary inflammatory stage.

Notice! There are legitimate doubts about the validity of the above-mentioned clinical (historical) classification; in most cases, post-inflammatory (secondary) elastolysis was involved, the causes of which remain mostly unknown!

Also a division into primary (idiopathic) and secondary (postinflammatory) anetoderms is not very satisfying from a clinical point of view, because inflammatory stages are rarely observed.

We understand anetodermia as atrophic-scarring end stage of different inflammatory processes of the skin.

Fragmentation, rarefaction, and phagocytosis of the elastic fibers; in some sections, elastic fibers are completely absent. Collagen fibers are thinned or fragmented, with larger spaces between the fiber bundles (assessed using Elastica-van Gieson staining). Reduced number of fibroblasts. Sparse perivascular round-cell infiltrates, depending on the severity.

In mid-dermal elastolysis, the loss of elastic fibers is confined to the mid-dermis in a band-like pattern!

• Superficial, scarring after pyoderma, acne vulgaris or zoster
• Cutis laxa (flaccid atrophy of the healthy skin, no wrinkled surface)
• Lupus erythematosus integumentalis (healed scar stage)
• Circumscribed scleroderma (confetti type)
• Peripheral neurofibromatosis(other signs of neurofibromaosis e.g. café au lait spots)
• Lichen sclerosus et atrophicus (tpyic glossy effect of lesions)
• Goltz-Gorlin syndrome (focal dermal hypoplasia)
• Adipose tissue herniations (e.g. piezogenic nodules, foot margins)
• Corticoid atrophies (after injections, ask for orthopedic history; localizations)
• Striae cutis distensae (tearing of connective tissue during rapid growth, during pregnancy)
• Atrophodermia idiopathica et progressiva (Pasini-Pierini) (extensive, brownish, sometimes marginal plaques, atrophy of the skin only very discretely developed)

Various treatments have been reported! None has proven effective for established lesions. Colchicine has been shown to prevent the development of new primary anetoderma lesions. In cases of secondary anetoderma, treating the underlying dermatoses should, in theory, prevent the development of new lesions (Kineston DP et al. 2008).

Other treatments whose efficacy has not been further investigated include cryotherapy, intralesional steroids, hydroxychloroquine, vitamin E, oral penicillin G, epsilon-aminocaproic acid, aspirin, niacin, dapsone, and phenytoin (Braun RP et al. 1998).

Established lesions can be excised as a definitive treatment; however, this leaves permanent scars.

Laser treatment can improve the appearance of the lesion, as shown in several case reports (Cho S et al. 2012; Nechat C et al. 2026)

1. Bilen N et al. (2003) Anetoderma associated with antiphospholipid syndrome and systemic lupus erythematosus. Lupus 12: 714-716
2. Braun RP et al. (1998) Treatment of primary anetoderma with colchicine. J Am Acad Dermatol 38:1002–1003.
3. Cho S et al. (2012) Treatment of anetoderma occurring after resolution of Stevens-Johnson syndrome using an ablative 10,600-nm carbon dioxide fractional laser. Dermatol Surg 38:677–679.
4. Dikarinen AI, Palatsie R, Adomian GE et al. (1984) Anetoderma: Biochemical and ultrastructural demonstration of an elastin defect in the skin of three patients. J Am Acad Dermatol 11: 66–72
5. Emer J et al. (2013) Generalized anetoderma following intravenous penicillin therapy for secondary syphilis in an HIV-positive patient. J Clin Aesthet Dermatol 6:23–28
6. Fujioka M et al. (2003) Secondary anetoderma overlying pilomatrixomas. Dermatology 207: 316–318

7. Fukayama M et al. (2018) Japanese familial anetoderma: A report of two cases and a review of the published literature. J Dermatol 45:1459–1462.

8. Ghomrasseni S et al. (2002) Anetoderma: an altered balance between metalloproteinases and tissue inhibitors of metalloproteinases. Am J Dermatopathol 24: 118–129
9. Hodak E et al. (2003) Primary anetoderma: a cutaneous sign of antiphospholipid antibodies. Lupus 12: 564–568
10. Hunt R (2011) Circumscribed lenticular anetoderma in an HIV-infected man with a history of syphilis and lichen planus. Dermatol Online J 17: 2
11. Jadassohn J (1892) On a peculiar form of atrophia maculosa cutis. Arch Dermatol Syphilol (Berlin) 1: 342–358
12. Kasper RC et al. (2001) Anetoderma arising in cutaneous B-cell lymphoproliferative disease. Am J Dermatopathol 23: 124-132
13. Kineston DP et al. (2008) Anetoderma: a case report and review of the literature. Cutis 81:501–506.
14. Patrizi A et al. (2011) Familial anetoderma: a report of two families. Eur J Dermatol 21:680–685
15. Pellizari C (1884) Atrophic urticarial erythema: idiopathic partial atrophy of the skin. Gior Ital Mal Ven 19: 230
16. Schweninger E, Buzzi F (1881) Multiple benign tumor-like new growths of the skin. In: International Atlas of Rare Skin Diseases, Part 5, Plate 15. L. Voss, Leipzig
17. Nechat C et al. (2026) “Fractional CO₂ Laser Treatment of Anetoderma: Clinical Outcomes in a Sequentially Documented Case,” J Cosmt Dermatol 25, no. 7 (2026): e71062, https://doi.org/10.1111/jocd.71062.