Anetoderma is a rare skin condition in which patches of skin lose their underlying elastic tissue and become soft, slack, and often pouch-like. The name itself comes from the Greek word “anetos,” meaning relaxed or slack, and was coined in 1891. The hallmark feature is circumscribed areas where you can press a finger into the skin and feel it give way or herniate outward, because the structural scaffolding that normally keeps skin taut has been destroyed. While the lesions themselves are typically harmless and painless, anetoderma sometimes signals an underlying autoimmune or clotting disorder that deserves attention.
What Anetoderma Looks and Feels Like
The lesions tend to be round or oval patches, usually a few centimeters across, scattered over the trunk, upper arms, and thighs. They come in two basic forms. In the protruding type, the skin bulges outward like a small, soft pouch that you can push inward with a fingertip. In the indented type, the skin sinks in, leaving a shallow depression. Some people have both types at once. The surface of the patch often looks wrinkled or slightly atrophic, and it may be skin-colored, whitish, or slightly pink. One research group has proposed that the protruding form may represent a more advanced stage of the same process, with greater elastic fiber destruction than the indented form.1PubMed Central. A Clinicoimmunohistopathologic Study of Anetoderma: Is Protruding Type More Advanced in Stage Than Indented Type?
The patches rarely itch or hurt, which is part of why people sometimes live with them for years before seeking a diagnosis. They can appear gradually over months to years, and new lesions may continue forming while old ones persist unchanged. The cosmetic impact tends to bother people more than any physical symptom, especially when lesions are numerous or appear on visible areas like the neck or upper chest.
What Is Happening Under the Skin
Under a microscope, the defining feature is the focal loss of elastic fibers in the dermis. A study examining 15 biopsy-confirmed cases found that every single one showed this loss, though some retained fine, irregular, or twisted remnants of elastic fibers rather than a complete wipeout.2JAMA Dermatology. Histopathologic Findings in Anetoderma The collagen framework usually stays relatively intact, which is why the skin does not ulcerate or scar in the usual sense. It just loses its snap.
The elastic fibers are not simply absent from birth. In most cases, they are actively broken down. Research points to a family of enzymes called matrix metalloproteinases, specifically MMP-2 and MMP-9 (also known as gelatinases A and B). Skin explants taken from anetoderma lesions show significantly higher levels of these enzymes compared to normal skin.3PubMed Central. A Clinicoimmunohistopathologic Study of Anetoderma: Is Protruding Type More Advanced in Stage Than Indented Type? A separate study confirmed that skin from anetoderma patients produced both the inactive and activated forms of these gelatinases at increasing levels over time in culture, while other elastase-type enzymes were not detected, suggesting that MMP-2 and MMP-9 are the main culprits.4British Journal of Dermatology. Increased expression of gelatinases A and B by skin explants from patients with anetoderma
Researchers have also found that a growth factor called TGF-β1 and its binding protein, which normally associate closely with elastic fibers in healthy skin, are absent in the elastic-fiber-depleted zones of anetoderma.5British Journal of Dermatology. Transforming growht factor β1 and its latent form binding protein‐1 associate with elastic fibres in human dermis: accumulation in actinic damage and absence in anetoderma Whether this absence is a cause of the fiber loss or a consequence of it remains unclear, but it suggests that the normal repair and maintenance signals for elastic tissue are disrupted.
Primary Versus Secondary Forms
Dermatologists divide anetoderma into two broad categories. Primary anetoderma appears on previously normal-looking skin with no identifiable prior skin disease at that site. Secondary anetoderma develops at sites where another skin condition came first, such as acne, varicella (chickenpox), or another inflammatory dermatosis. In secondary cases, the original condition presumably triggered the inflammatory process that chewed through the elastic fibers.
The distinction matters clinically because primary anetoderma carries a stronger association with systemic autoimmune conditions, while secondary anetoderma is more often an isolated aftermath of a prior skin problem. That said, the boundary between the two is not always clean. Some patients classified as having primary anetoderma may have had a subtle inflammatory phase that went unnoticed before the characteristic laxity appeared.
Autoimmune Connections
The link between anetoderma and autoimmune disease is one of the most clinically important things to understand about this condition. Systemic lupus erythematosus and antiphospholipid syndrome show up repeatedly in case reports alongside anetoderma, to the point where some researchers argue that anetoderma should be considered a potential cutaneous sign of antiphospholipid antibodies.6PubMed. Primary anetoderma: a cutaneous sign of antiphospholipid antibodies
Antiphospholipid syndrome is a clotting disorder driven by antibodies that increase the risk of blood clots in veins and arteries. One proposed explanation for why it might cause anetoderma is that tiny blood vessel clots in the skin lead to localized ischemia, damaging the elastic fibers in the affected area. A case report described a patient whose anetoderma was confirmed by biopsy showing ruptured elastic fibers, and who also had a history of deep vein thrombosis. Laboratory testing revealed antiphospholipid antibodies, confirming the suspected connection.7PubMed Central. Anetoderma: an alert for antiphospholipid antibody syndrome
Other reports have described patients in whom anetoderma coexisted with both lupus and antiphospholipid syndrome simultaneously.8PubMed. Anetoderma associated with antiphospholipid syndrome and systemic lupus erythematosus This overlap makes sense given that lupus itself predisposes people to antiphospholipid antibodies. The practical takeaway is that a diagnosis of anetoderma, particularly the primary form, should prompt testing for lupus and antiphospholipid antibodies.9PubMed. Anetoderma in systemic lupus erythematosus: relationship to antiphospholipid antibodies Detecting a prothrombotic state early means you can take steps to reduce the risk of serious clotting events like stroke or pulmonary embolism.10PubMed. Anetoderma and its prothrombotic abnormalities
Sjögren syndrome, another autoimmune condition that primarily affects moisture-producing glands, has also appeared alongside primary anetoderma in case reports. In one such case, the patient tested positive for anticardiolipin antibodies as well, reinforcing the pattern of anetoderma clustering with autoimmune and prothrombotic conditions.11Actas Dermo-Sifiliográficas. Primary Anetoderma Associated With Primary Sjögren Syndrome and Anticardiolipin Antibodies
Infections That Can Trigger It
Anetoderma is not exclusively an autoimmune story. Certain infections have been linked to it as well, most likely because the inflammatory response to the infection damages elastic fibers as collateral.
Syphilis is one notable example. A reported case of generalized anetoderma occurred in the setting of secondary syphilis, with the skin changes developing during the active infectious phase. In that case, the patient was treated with benzathine penicillin for the syphilis itself.12PubMed Central. Generalized anetoderma: An unusual manifestation of secondary syphilis treated with injection penicillin Whether the anetoderma patches themselves resolved after treatment of the infection is a separate question; once elastic fibers are destroyed, the damage is often permanent even if the underlying trigger is eliminated.
Lyme disease has also been implicated. In one case, researchers used molecular testing on a biopsy from an anetoderma lesion and detected DNA from the Lyme-causing bacterium Borrelia burgdorferi directly within the affected skin tissue. The patient’s blood also showed elevated antibodies against Borrelia. The authors suggested that patients with anetoderma should be tested for Lyme disease, particularly in areas where the infection is common.13PubMed. Anetoderma: another facet of Lyme disease?
HIV and hepatitis B have also been mentioned in the broader literature as possible triggers, though these associations rest on smaller numbers of cases. The common thread across all infectious triggers seems to be that a sustained inflammatory or immune response in the skin creates the conditions for elastic fiber breakdown.
What a Diagnostic Workup Typically Involves
If your dermatologist suspects anetoderma based on the appearance and feel of the lesions, a punch biopsy is the standard next step. The biopsy specimen is stained with a special elastic tissue stain (such as Verhoeff-van Gieson) to confirm the characteristic loss of elastic fibers. Without this stain, the diagnosis can be missed because the rest of the dermal architecture may look relatively normal on routine staining.
Beyond confirming the skin diagnosis, the workup should include blood tests to look for underlying systemic conditions. Testing for antiphospholipid antibodies, including lupus anticoagulant, anticardiolipin antibodies, and anti-β2-glycoprotein I antibodies across all isotypes, is recommended.14PubMed. Primary anetoderma: a cutaneous sign of antiphospholipid antibodies An antinuclear antibody test and basic lupus screening are also reasonable, given the well-documented overlap. If you are in a region endemic for Lyme disease, or if the clinical picture suggests a possible infectious trigger, testing for Borrelia or syphilis may be appropriate as well.
Patients with anetoderma should also be examined for associated abnormalities beyond the skin. A long-term follow-up study noted associated findings including cataracts, congenital hip dislocation, vertebral fusion, esophageal diverticulum, Addison’s disease, and mitral valve prolapse among individual patients. The authors concluded that patients with anetoderma warrant evaluation for eye, bone, heart, pulmonary, digestive, and endocrine abnormalities.15JAMA Dermatology. Anetoderma: Clinical Findings, Associations, and Long-term Follow-up Evaluations This is especially relevant in familial cases, where extracutaneous features have historically been more prominent.
Familial and Genetic Cases
Most anetoderma is sporadic, meaning it shows up without any family history. But rare familial forms do exist. As of one review, familial anetoderma had been reported in only about ten families worldwide. In the first four families described, the condition was always accompanied by extracutaneous abnormalities involving bones, the nervous system, or the eyes. In the six families described more recently, anetoderma was limited to the skin.16PubMed. Familial anetoderma: a report of two families
The inheritance pattern has proven hard to pin down. A review of published cases concluded that the mode of inheritance is not straightforward, meaning it does not follow a simple dominant or recessive pattern, and suggested that family members of anyone diagnosed with anetoderma should be examined.17PubMed. Japanese familial anetoderma: A report of two cases and review of the published work Whether the familial cases share the same underlying mechanism as sporadic anetoderma, or represent a distinct genetic disorder that happens to destroy elastic fibers through a different pathway, remains an open question.
Treatment Options and Their Limits
This is where the honest picture gets frustrating. There is no established, reliably effective treatment for anetoderma. Once the elastic fibers in a patch of skin are destroyed, the body does not regenerate them in a clinically meaningful way. The laxity tends to be permanent. Treatment efforts have therefore focused on two fronts: trying to halt the progression of new lesions, and trying to improve the cosmetic appearance of existing ones.
On the systemic side, some case reports have suggested possible benefit from drugs that inhibit neutrophil activity, specifically dapsone and colchicine. The rationale is strongest in cases where biopsy shows an inflammatory infiltrate containing granulocytes, since these white blood cells release enzymes that can damage elastic tissue. One report of primary anetoderma associated with Sjögren syndrome noted the presence of granulocytes in the lesions and suggested that such patients might benefit from dapsone or colchicine.18Actas Dermo-Sifiliográficas. Primary Anetoderma Associated With Primary Sjögren Syndrome and Anticardiolipin Antibodies But “might benefit” is a far cry from “proven effective.” No controlled trials exist, and the evidence consists entirely of scattered case reports.
When anetoderma is secondary to an identifiable trigger like syphilis, Lyme disease, or an autoimmune flare, treating the underlying condition can stop new lesions from forming. But the patches that have already developed typically remain.
Laser and Procedural Approaches
Several types of laser treatment have been tried for anetoderma with mixed results, reflecting the challenge of restoring tissue that the body does not readily rebuild. The idea behind ablative fractional lasers is that creating controlled micro-injuries in the skin stimulates a wound-healing response, which can remodel collagen and potentially encourage some elastic fiber deposition.
A documented case treated with fractional CO2 laser over multiple sessions showed progressive improvement. The wrinkled, sunken appearance of lesions on the back and chin area became visibly tighter, with less noticeable skin laxity. Blinded scoring by two dermatologists rated the final improvement as moderate to marked, and the patient reported satisfaction with no complications.19PubMed Central. Fractional CO 2 Laser Treatment of Anetoderma: Clinical Outcomes in a Sequentially Documented Case
That said, laser treatment does not work for everyone. A case of extensive primary anetoderma treated with an erbium YAG fractionally ablative laser showed no meaningful improvement, and the authors observed that patients with secondary anetoderma and those with limited body surface involvement may respond better than patients with widespread disease.20SKIN: The Journal of Cutaneous Medicine. Extensive Primary Anetoderma Refractory to Erbium YAG Fractionally Ablative Laser The extent of elastic fiber loss likely determines whether the remaining tissue has enough structural integrity to remodel in a useful way.
For patients with a small number of lesions in cosmetically sensitive areas, surgical excision is sometimes an option. The affected skin is removed and the wound is closed, replacing the lax patch with a scar. This trades one cosmetic issue for another, so it is generally reserved for cases where the lesions are particularly bothersome and few in number.
How Anetoderma Differs From Similar-Looking Conditions
Several other skin conditions can produce areas of thin, lax, or wrinkled skin, and distinguishing them from anetoderma matters because the workup and implications differ. Mid-dermal elastolysis, for example, produces widespread fine wrinkling on the trunk and arms, often in young to middle-aged women after sun exposure. Unlike anetoderma, it does not produce the characteristic sac-like herniation when you press the skin, and the elastic fiber loss is confined to the mid-dermis rather than being full-thickness.
Cutis laxa is a broader condition involving widespread skin laxity due to elastic fiber abnormalities, but it tends to affect large areas of the body rather than producing discrete, circumscribed patches. It can be inherited or acquired, and the inherited forms often come with serious systemic involvement including lung and vascular problems.
Atrophoderma of Pasini and Pierini presents as depressed, brownish patches on the back that can superficially resemble indented anetoderma. But histologically it involves changes in collagen rather than selective elastic fiber loss, and it does not produce the characteristic “buttonhole” sign where the skin pops inward under pressure.
The biopsy with elastic fiber staining is the definitive way to sort these apart. If the stain shows focal loss of elastic fibers in the dermis with relatively preserved collagen, anetoderma is the diagnosis. If the elastic fibers are intact but the collagen is abnormal, something else is going on.
Anetoderma in Premature Infants
An unusual context in which anetoderma appears is in premature babies who have spent time in neonatal intensive care units. These infants sometimes develop anetoderma-like lesions at sites where monitoring electrodes, adhesive tape, or other medical devices were applied to their fragile skin. The combination of immature skin, prolonged contact with adhesives, and the inflammatory response to skin trauma likely conspires to damage elastic fibers that are not yet fully developed.
This form of anetoderma is considered secondary, since there is a clear precipitating event. Whether the lesions persist into childhood and adulthood or gradually improve as the child grows and the skin matures is variable, and long-term follow-up data in this population are limited. Awareness of this possibility has led some neonatal units to use gentler adhesives and minimize unnecessary skin contact with monitoring equipment.
Primary anetoderma occurring in infants without a clear trigger is extremely rare but has been documented, including in the first year of life.21Journal of Skin and Stem Cell. Primary Anetoderma in an Infant: A Case Report From Southeast Asia These cases can be particularly challenging diagnostically because the differential diagnosis in a young child also includes inherited connective tissue disorders.