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Anetoderma

Anetoderma
Author:
Taraneh Paravar, MD
Section Editor:
Jeffrey Callen, MD, FACP, FAAD
Deputy Editor:
Abena O Ofori, MD
Literature review current through: Sep 2022. | This topic last updated: Dec 03, 2020.

INTRODUCTION — Anetoderma, also known as macular atrophy, is an uncommon disorder of elastic tissue that is clinically characterized by wrinkled and atrophic depressions or saccular outpouchings of the skin (picture 1A-C). The saccular outpouchings may herniate upon digital pressure. The primary histologic finding is the loss of elastic tissue in the dermis.

Anetoderma is divided into primary anetoderma and secondary anetoderma, with the former occurring in areas of previously normal skin and the latter developing in areas of prior skin pathology. Primary anetoderma may occur in association with underlying systemic conditions and warrants evaluation for associated disorders. There is no effective treatment for anetoderma.

The clinical manifestations, diagnosis, and management of anetoderma will be reviewed here. Anetoderma is distinct from atrophoderma of Pasini and Pierini, a disorder characterized by dermal atrophy and well-defined, hyperpigmented, depressed areas of skin. Atrophoderma of Pasini and Pierini is reviewed separately. (See "Atrophoderma of Pasini and Pierini".)

EPIDEMIOLOGY — Anetoderma is considered uncommon, and epidemiologic data are limited. The exact prevalence is not known.

Primary anetoderma tends to present between ages 20 to 40 but may occur at both younger and older ages. There seems to be a female predominance in primary anetoderma.

The epidemiology of secondary anetoderma reflects that of the causative skin pathology. Other subtypes of anetoderma, including iatrogenic anetoderma of prematurity, congenital anetoderma, and familial anetoderma, present in infancy or childhood [1-3]. (See 'Classification' below.)

CLINICAL MANIFESTATIONS — The clinical phenotype of anetoderma consists of well-circumscribed, round or oval, skin-colored or white macules or patches of wrinkled skin (picture 1A-C). Anetoderma may appear as atrophic, depressed patches or saccular outpouchings [1,4,5]. With digital palpation of saccular outpouchings, an inward herniation may be appreciated [1].

The macules and patches of anetoderma may be several millimeters to 1 to 2 centimeters in diameter [1]. There may be few lesions or hundreds. Common sites of involvement include the trunk and proximal extremities. The palms, soles, scalp, and mucosa are usually spared [6]. Anetoderma is generally asymptomatic but may be pruritic.

CLASSIFICATION — Anetoderma is subclassified into the following groups [1]:

Primary anetoderma

Secondary anetoderma  

Iatrogenic anetoderma of prematurity

Congenital anetoderma

Familial anetoderma

Drug-induced anetoderma

Primary anetoderma — Primary anetoderma occurs in areas of previously normal skin. Historically, primary anetoderma was divided into presentations with preceding inflammation (Jadassohn-Pellizzari type), including erythema and urticaria, and presentations without preceding inflammation (Schweninger-Buzzi type) [4,7]. Given that these two subtypes are histologically identical and have a similar prognosis, this classification scheme has mostly been abandoned [6,8].

Associated disorders — Primary anetoderma has occurred in patients with various systemic conditions and laboratory abnormalities (table 1). Some authors have classified such presentations as secondary anetoderma; however, we reserve the title of secondary anetoderma for anetoderma that develops in the site of preexisting skin disease (see 'Secondary anetoderma' below):

Antiphospholipid antibodies – The most consistently reported association of primary anetoderma is with antiphospholipid antibodies, including anticardiolipin antibodies, lupus anticoagulant antibodies, and anti-beta-2-glycoprotein antibodies [9]. Antiphospholipid antibodies in patients with anetoderma have occurred as an isolated finding or in association with other diseases. In a 2001 case report and review of 20 additional published cases of patients with both primary anetoderma and antiphospholipid antibodies, antiphospholipid antibodies occurred as an isolated finding in four patients; the remaining patients also had primary antiphospholipid syndrome, systemic lupus erythematosus (SLE), other autoimmune disorders, or HIV infection [9].

A retrospective chart review of patients with SLE provides support for an association between antiphospholipid antibodies and anetoderma. In the review, 5 of 33 patients (15 percent) with SLE and lupus anticoagulant antibodies had primary anetoderma, compared with none of 37 patients with SLE who were negative for lupus anticoagulant antibodies [10].

The prevalence of antiphospholipid antibodies in patients with primary anetoderma is not known. A retrospective study found primary anetoderma rare among patients with antiphospholipid syndrome; only 4 of 200 consecutive patients (2 percent) with antiphospholipid syndrome had primary anetoderma [11].

Other disorders – In addition to antiphospholipid antibodies, the occurrence of other conditions in association with anetoderma is documented in case reports or small studies (table 1). Additional data are necessary to clarify the relationship between anetoderma and these conditions.

Examples include autoimmune diseases (eg, SLE, Sjögren syndrome [12], Addison's disease [6], systemic sclerosis [13,14], vitiligo [6], alopecia areata [6,13]), prothrombotic states (protein C and S deficiency [15], antithrombin III deficiency [16]), cocaine use [17], multiple sclerosis [6], infections (HIV, tuberculosis, Lyme disease [18]), elevated homocysteine levels in the setting of anorexia [19], and subcutaneous injections during ovarian stimulation for in vitro fertilization [20].

There may be an association between the presence of antiphospholipid antibodies and the development of anetoderma in HIV-positive patients [9,21].

Laboratory abnormalities reported to associate with anetoderma include elevated antinuclear antibodies [22], rheumatoid factor and antithyroid antibodies [5,14], and decreased serum levels of alpha-1 antitrypsin [23].

Secondary anetoderma — Secondary anetoderma is typically defined as anetoderma occurring in areas affected by a prior skin eruption, such as acne, varicella, discoid lupus erythematosus, and papular eruption of HIV disease [21]. Information regarding associations between skin conditions and anetoderma are primarily derived from case reports. A list of associated skin disorders is provided in a table (table 2).

Iatrogenic anetoderma of prematurity — Iatrogenic anetoderma of prematurity has occurred in premature infants born between 24 and 32 weeks of pregnancy. Anetoderma appears weeks to months after birth [24]. The most common locations for lesion development are sites on the trunk and proximal extremities where monitoring leads, adhesive tape, or gel electrocardiographic electrodes previously were placed. In some cases, purpuric or erosive patches precede the lesions.

The etiology of iatrogenic anetoderma of prematurity is hypothesized to be either hypoxemia due to pressure on premature skin or traction on the skin during removal of devices. It has been suggested that low birth weight may be more predictive of this condition than gestational age [25]. Avoidance of lead placement at sites of increased pressure (dorsal body when infant is laying supine) may minimize the development of iatrogenic anetoderma of prematurity [7,24,26].

Other subtypes — Rare subtypes of anetoderma include congenital, familial, and drug-induced anetoderma:

Congenital anetoderma – Congenital anetoderma manifesting as anetoderma on the trunk of premature infants at the time of birth is documented in case reports [27,28].

Familial anetoderma – Familial anetoderma tends to develop in the first or second decade of life and may occur in association with ocular, neurologic, gastrointestinal, cardiovascular, or bony abnormalities [29]. Autosomal dominant and autosomal recessive patterns of inheritance have been noted [30,31]. Specific inherited syndromes in which anetoderma has been reported include terminal osseous dysplasia with pigmentary defects [32]; metaphyseal dysplasia, anetoderma, and optic atrophy [27]; exostoses with anetoderma and brachydactyly type E [27]; Reed syndrome [33]; and mutations in the citric acid cycle succinate dehydrogenase subunit B [34].

Drug-induced anetoderma – Medication-induced anetoderma has been reported to occur with penicillamine [6].

PATHOLOGY — The primary finding in anetoderma is a loss or significant reduction of elastic fibers in the dermis (papillary and/or upper- and mid-reticular dermis) as seen with an elastin stain, such as the Verhoeff-van Gieson stain. Fragmentation of the remaining elastic fibers may be seen, which can also be visualized on electron microscopy.

A perivascular inflammatory infiltrate composed of mostly lymphocytes, but also of histiocytes, plasma cells, eosinophils, and neutrophils, can occur. Of note, the presence or absence of histologic inflammation is not related to clinical findings [8,35]. Elastophagocytosis, or phagocytosis of elastic fibers by macrophages, may be seen [36]. Microthromboses have also been noted [10].

On immunohistochemistry, a greater loss of elastin has been noted in protruding lesions compared with indented lesions, possibly suggesting a more advanced stage in the former [37].

Direct immunofluorescence studies may demonstrate a granular or rarely linear band of immune reactants including immunoglobulins M (IgM) and G (IgG) as well as complement at the dermal-epidermal junction. A granular and fibrillar pattern of immune deposits can be seen between collagen fibers in the dermis. Fibrillar deposits of immune reactants, specifically C3, likely correlating with the location of elastic fibers, may be seen in the dermis. Immune reactants have also been noted around dermal blood vessels [38-40]. These direct immunofluorescence results are not specific to anetoderma.

PATHOGENESIS — The pathogenesis of anetoderma is not clearly understood. Available evidence suggests increased breakdown of elastic fibers may play a primary role. Potential mechanisms for this process include alterations in elastolytic enzyme activity, ischemia, phagocytosis of elastic fibers, and autoimmune and inflammatory processes [41]:

Upregulation or decreased inhibition of elastolytic enzyme activity – Increased elastic fiber breakdown may result from an increase in matrix metalloproteinase (MMP) elastolytic activity and a decrease in inhibition of this process. In support of this theory, increased production of proforms of gelatinase A (MMP-2) and gelatinase B (MMP-9) as well as increased activation of gelatinase A have been found in specimens of anetoderma [42]. Increased production of MMP-2 in lesional skin without an accompanying increase in the production of tissue inhibitors of MMP-2 also has been detected [43].

In addition, in three patients with pilomatricoma with anetoderma-like changes, MMP-9 staining of fibroblasts and inflammatory cells as well as MMP-12 staining of infiltrating cells in the dermis were noted [44]. These changes were not noted in three cases of ordinary pilomatricoma, supporting the role of MMP-9 and, possibly, MMP-12 in anetoderma.

A study that found high expression of tissue inhibitor of metalloproteinase (TIMP)-1 and variable expression of TIMP-2 suggests that increases in TIMP levels may be insufficient to suppress the increased MMP levels in anetoderma [37].

Ischemia – Ischemia may contribute to elastic fiber breakdown. The presence of microthromboses in biopsy specimens of anetoderma, both in patients with and without antiphospholipid antibodies, supports the theory that local ischemia may lead to activation of elastolytic enzymes and degradation of elastic tissue [23]. In iatrogenic anetoderma of prematurity, pressure may be a trigger for hypoxemia and may lead to the degeneration of elastic tissue [24].

Phagocytosis of elastic fibers – A role for phagocytosis of elastic fibers by macrophages has been suggested based upon the detection of this finding on electron microscopic examination of lesional tissue from a patient with clinical and histologic findings consistent with anetoderma [36].

Autoimmune and inflammatory processes – The association of anetoderma with antiphospholipid antibodies offers support to the theory that autoimmune and inflammatory processes contribute to anetoderma [15]. One theory is that anticardiolipin antibodies lead to endothelial damage or immune complex and complement activation [21,45]. Other theories include the possible cross-reaction between beta-2-glycoprotein and antigens on elastic fibers; this is supported by the presence of immune reactants on elastic fibers on immunofluorescence [38-40].

The presence of T lymphocytes in biopsy specimens of anetoderma lends support to an inflammatory component to this process [41].

In addition to elastic fiber breakdown, a decrease in the production of elastic fibers may contribute to anetoderma. The finding of reduced expression of fibulin-4, which aids in elastic fiber formation, in tissue specimens from anetoderma compared with specimens from healthy controls [46] suggests that there may be an impairment in elastic fiber assembly.

A link between citric acid cycle mutations and anetoderma has been proposed [34].

Theories to explain the development of secondary anetoderma include the release of elastolytic enzymes from the primary inflammatory skin disease [47]. Anetoderma occurring in sites of skin tumors may result from the destruction of elastic fibers by mechanical trauma [33]. (See 'Secondary anetoderma' above.)

DIAGNOSIS — The diagnosis of anetoderma usually can be made with physical examination alone. Examination of the skin demonstrates skin-colored or white, wrinkled and atrophic depressions or saccular outpouchings that may herniate on digital pressure. When the diagnosis is uncertain, a skin biopsy can be performed to confirm the diagnosis and to rule out other elastic tissue disorders. The biopsy must include the mid-dermis. A 4 mm punch biopsy is adequate. (See 'Clinical manifestations' above and "Skin biopsy techniques", section on 'Punch biopsy' and 'Pathology' above.)  

Once a diagnosis of anetoderma is made, the clinician should determine the subtype of anetoderma. The major distinction is between primary and secondary anetoderma. The patient history aids in differentiation. Secondary anetoderma develops in sites of preexisting skin disease. Therefore, if there was no preceding skin disorder or only mild erythema or urticarial-type lesions were noted at the sites of anetoderma, then the anetoderma is best categorized as primary anetoderma. Attention to the age of onset, family history, and penicillamine use is useful for identifying patients with other subtypes, including iatrogenic anetoderma of prematurity, congenital anetoderma, familial anetoderma, and drug-induced anetoderma. Unlike primary anetoderma, which usually occurs in adults, iatrogenic anetoderma of prematurity, congenital anetoderma, and familial anetoderma first appear in infancy or childhood. (See 'Classification' above.)

ADDITIONAL EVALUATION — Patients with primary anetoderma and familial anetoderma require evaluation for extracutaneous disorders:

Primary anetoderma – Patients with primary anetoderma require an evaluation for associated underlying disease (table 1). A review of systems and physical examination should be performed with particular attention to signs and symptoms of autoimmune disease. (See 'Associated disorders' above.)

In particular, given the association of primary anetoderma with antiphospholipid antibodies, patients with primary anetoderma should be asked about a history of thrombotic complications, including spontaneous abortions, strokes, deep vein thrombosis, and superficial phlebitis. The physical examination should assess for other findings seen in antiphospholipid syndrome, such as livedo reticularis, livedoid vasculopathy, vasculitis-like lesions, retiform purpura, cutaneous necrosis, superficial thrombophlebitis, and splinter hemorrhages [22,48].

Serologic testing for antiphospholipid antibodies is recommended in all patients with primary anetoderma, regardless of a history of thrombotic complications. Testing is typically performed at the time of diagnosis. Further study is necessary to determine the value of subsequent testing for patients who initially test negative; delayed development of antiphospholipid antibodies is documented in a case report [49]. Measures to minimize risk for thrombosis may be indicated for patients with antiphospholipid antibodies [50]. (See "Diagnosis of antiphospholipid syndrome" and "Management of antiphospholipid syndrome".)

The decision to perform tests for other underlying diseases is based upon a suspicion for specific disorders arising from the patient history, review of systems, or physical examination.

Familial anetoderma – Patients with a history that suggests familial anetoderma or with features that suggest an inherited syndrome should be evaluated for signs of ocular, neurologic, gastrointestinal, cardiovascular, and bony abnormalities. (See 'Other subtypes' above.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of anetoderma consists of elastic tissue disorders characterized by cutaneous atrophy:

Mid-dermal elastolysis – Mid-dermal elastolysis is an acquired disorder characterized by finely wrinkled skin seen in areas of sun exposure, such as the trunk, arms, and lateral neck (picture 2). Histologically, there is a loss of elastic fibers in the mid-dermis [4,51].

Papular elastorrhexis – Papular elastorrhexis presents with firm, white, nonfollicular papules that are several millimeters in diameter and located on the trunk. Histology demonstrates fragmentation and loss of elastic fibers in the reticular dermis [4,51].

Perifollicular elastolysis – Perifollicular elastolysis presents with small, gray or white, wrinkled perifollicular papules found on the neck, earlobes, upper trunk, and arms. Histologic examination demonstrates loss of perifollicular elastic fibers [4,51]. This is considered by some clinicians to be the same entity as papular acne scars [52,53].

Papular acne scars – Papular acne scars are found on the upper part of the trunk and are characterized by small, skin-colored to hypopigmented, noncompressible follicular papules seen in association with acne. Biopsy demonstrates decreased elastic fibers in the dermis and smaller collagen fibers [53].

Pseudoxanthoma elasticum-like papillary dermal elastolysis – This disorder presents with yellow to skin-colored papules symmetrically distributed over the lateral neck, supraclavicular area, flexural forearms, axilla, and lower abdomen. It is seen most commonly in older adult females. On biopsy there is a loss of elastic fibers in the papillary dermis [51].

Atrophoderma of Pasini and Pierini – Atrophoderma of Pasini and Pierini presents with large, hyperpigmented, and depressed areas of skin and most often occurs on the trunk or extremities (picture 3). (See "Atrophoderma of Pasini and Pierini".)

Cutis laxa – Cutis laxa includes both inherited and acquired forms and is characterized by loose sagging skin folds (picture 4). Pathology demonstrates reduced and fragmented elastic fibers in the dermis [4,51].

The differential diagnosis of iatrogenic anetoderma of prematurity and congenital anetoderma includes aplasia cutis congenita, focal dermal hypoplasia, and erosive and vesicular dermatosis. (See "Aplasia cutis congenita" and "Focal dermal hypoplasia (Goltz syndrome)".)

TREATMENT — Anetoderma is a benign, asymptomatic condition without a clear, effective treatment. Therefore, reassurance of the patient is our general course of action for existing lesions. In patients with secondary anetoderma, the primary skin disorder resulting in anetoderma should be treated whenever feasible to minimize risk for the development of new lesions (table 2). Surgical excision can successfully remove affected skin but is not routinely recommended given the resulting scar and the frequent existence of multiple lesions.

Although there are case reports describing improvement in the appearance of anetoderma with laser therapy, additional data are needed to confirm efficacy prior to a recommendation for routine use. In a case report of a patient who developed anetoderma secondary to Stevens-Johnson syndrome, sites of anetoderma on the lower back showed improved skin texture after treatment with a 10,600 nm carbon dioxide fractional laser system for three sessions at two-month intervals [54]. The mechanism of action may have involved regeneration of elastin fibers [54]. A pinhole carbon dioxide laser treatment also appeared beneficial in the treatment of a child with anetoderma secondary to juvenile xanthogranuloma [55]. In another case report, combination therapy for anetoderma with a 595 nm pulsed-dye laser and a 1550 nm nonablative fractionated laser demonstrated flattening of skin lesions and improved texture after three sessions at three-week intervals [56]. Of note, an increase in elastic fibers was detected after treatment compared with before treatment.

Medications have mostly been unsuccessful and include intralesional corticosteroids, oral penicillin G, aspirin, phenytoin, dapsone, vitamin E, and niacin [6]. Individual case reports of treatment with epsilon-aminocaproic acid (4 g every six hours) [57] as well as colchicine (1 mg per day) [58] have described benefit in patients with primary anetoderma with an inflammatory component. Given the paucity of positive efficacy data, we do not treat anetoderma with medication.

Other therapies with unclear efficacy include use of radiofrequency devices given the finding of increased elastin after radiofrequency treatment as well as rejuvenation procedures such as the use of fillers and chemical peels [4].

PROGNOSIS AND FOLLOW-UP — Lesions of anetoderma persist and do not resolve.

Given the association between primary anetoderma and antiphospholipid antibodies and autoimmune diseases, long-term, periodic follow-up of patients with anetoderma to assess for signs and symptoms of hypercoagulability and autoimmunity is prudent. Thrombotic complications in patients with both anetoderma and antiphospholipid antibodies include fetal loss, strokes, deep vein thrombosis, and superficial phlebitis [9,15]. Such complications may occur years after the diagnosis of primary anetoderma [13].

SUMMARY AND RECOMMENDATIONS

Anetoderma is an uncommon elastolytic disorder of the skin. The major subtypes of anetoderma are primary anetoderma and secondary anetoderma, with the former occurring in areas of previously normal skin and the latter developing in areas of prior skin pathology. Other subtypes include iatrogenic anetoderma of prematurity, congenital anetoderma, familial anetoderma, and drug-induced anetoderma. (See 'Classification' above.)

Primary anetoderma has been reported to occur in association with a variety of systemic conditions and laboratory abnormalities. The most consistently reported association is with antiphospholipid antibodies. (See 'Primary anetoderma' above.)

Anetoderma is characterized by wrinkled and atrophic depressions or saccular outpouchings of the skin (picture 1A-C). The saccular outpouchings may herniate upon digital pressure. (See 'Clinical manifestations' above.)

A diagnosis of anetoderma usually can be made based upon physical examination alone. If the diagnosis is uncertain, a skin biopsy can be performed to confirm the diagnosis. The primary pathologic finding is a loss or significant reduction of elastic fibers in the dermis. (See 'Diagnosis' above and 'Pathology' above.)

Once the diagnosis of anetoderma is made, the clinician should determine the subtype of anetoderma. Patients with primary anetoderma require an evaluation for associated underlying disease. (See 'Diagnosis' above and 'Additional evaluation' above.)

Data on medical and procedural interventions for anetoderma are primarily limited to case reports and are insufficient to confirm efficacy of any therapy. In general, we do not treat anetoderma. For patients with secondary anetoderma, we treat the primary skin disorder to minimize risk for development of new lesions. There are case reports describing cosmetic improvement in anetoderma with laser therapy; however, data are insufficient to recommend routine use of laser treatment. (See 'Treatment' above.)

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