Anetoderma. Anetoderma, the primary type.
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Adult↗
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Increased anticardiolipin antibodies associated with the development of anetoderma in HIV-1 disease. Military Medical Consortium for the Advancement of Retroviral research (MMCARR).
BACKGROUND AND OBJECTIVE: Anetoderma has been reported in patients with HIV-1 disease. In patients with autoimmune disease, anetoderma has been associated with increased levels of antiphospholipid antibodies (APL) that include anticardiolipin antibodies (ACA) and lupus anticoagulant (LA). This has led to speculation that the autoimmune phenomena seen in HIV-1 disease and the immune dysregulation induced by HIV-1 disease may play a role in the development of these lesions. We have seen both primary and secondary lesions of anetoderma in patients followed for HIV-1 disease. In this study, we wanted to determine whether there was an association in the development of anetoderma and elevated anticardiolipin antibodies (ACA) in HIV-1 patients. METHODS: Quantitative ACA levels were measured in eight HIV-1-infected patients with anetoderma and four HIV-1-infected patients without anetoderma. RESULTS: Anticardiolipin antibodies were moderately elevated in seven of eight patients with lesions and were borderline in the four HIV-1-positive patients without lesions of anetoderma. CONCLUSIONS: There appears to be a correlation between increased ACA and the development of cutaneous lesions of anetoderma in HIV-1 disease. Patterns of immune dysregulation, including APL, may predispose to the development of lesions of anetoderma in HIV-1-positive patients. Although some of the lesions appear to represent primary anetoderma, the majority of our patients develop lesions in areas secondary to well characterized eruptions.
Adult↗
Antiphospholipid antibodies and anetoderma: are they associated?
BACKGROUND: Macular atrophy or anetoderma is a rare skin disease of unknown pathogenesis, characterised by wrinkled or flaccid skin. OBJECTIVE: The finding of anetoderma in 5 patients followed up because of false-positive seroreactions of syphilis prompted us to study the occurrence of antiphospholipid (aPL) antibodies in anetoderma. METHODS: 14 unselected patients with primary anetoderma (PA) were collected from hospital records and clinical, immunological and histological findings were compared in the two patient groups. RESULTS: Of the 5 patients, 3 fulfilled the criteria for antiphospholipid syndrome. In two cases, it was secondary to systemic lupus erythematosus (SLE). Of the 14 PA patients 1 had aPL antibodies and 4 had borrelia antibodies. Two patients had thyroid antibodies; 1 of them developed SLE. In several biopsy specimens, microthromboses were seen in both patient groups. CONCLUSION: On the basis of this study and our previous findings, it seems that anetoderma is more often associated with aPL-positive SLE or lupus-like disease than with aPL-negative disease. Immunological mechanisms play an important role in both primary and secondary anetoderma. The meaning of false-positive serological tests for syphilis or borrelia and aPL antibodies is not clear, but they may be reacting to some still unidentified antigen. Probably, various systemic as well as local inflammatory and non-inflammatory processes, e.g. microthromboses, can trigger anetoderma via still unknown pathomechanisms.
Adolescent↗
Anetoderma and its prothrombotic abnormalities.
BACKGROUND: Anetoderma is characterized by circumscribed areas of flaccid skin due to the loss of elastic tissue in the dermis. It may be primary or secondary to various dermatoses. The primary form has been reported in association with autoimmune diseases and recently with antiphospholipid antibodies. Its etiology remains unknown. OBJECTIVES: To analyze clinical and laboratory data from a series of patients with anetoderma referred in our university reference center for connective tissue disorders. PATIENTS AND METHODS: All the consecutive patients with histologically confirmed anetoderma followed in our clinic from 1996 to 2001 were enrolled in this study. Laboratory investigations included the screening for prothrombotic abnormalities and classical immunological investigations for systemic lupus erythematosus. Clinical and laboratory data were analyzed retrospectively. RESULTS: Anetoderma was primary in 9 cases and secondary to lupus profundus in 2 cases. Prothrombotic abnormalities were detected in 10 patients (9/9 with primary and 1/2 with secondary anetoderma). Antiphospholipid antibodies were detected in 9 patients. Only 4 patients fulfilled criteria for definite antiphospholipid syndrome which was primary for 3 and associated with systemic lupus erythematosus in the other. CONCLUSION: Patients with anetoderma should be evaluated for the possible presence of a prothrombotic state and warned of its potential risks when present.
Adolescent↗
Anetoderma arising in cutaneous B-cell lymphoproliferative disease.
Anetoderma is circumscribed atrophy of the skin due to a localized deficiency in elastic tissue. It can follow inflammatory skin diseases of several types, and occasionally is present in the skin around neoplasms. There are a few reports of anetoderma in the lesional skin of cutaneous lymphoma. We report on two patients who presented with multiple lesions of anetoderma and who later proved to have low-grade cutaneous B-cell lymphomas. One patient (Patient 1) is a 39-year-old man and the other patient is a 26-year-old woman who is a renal transplant recipient (Patient 2). Some biopsy specimens from the anetodermic skin of Patient 1 appeared to show an urticarial reaction, although plasma cells were present. A large nodule showed lymphoid follicles surrounded by plasmacytoid lymphocytes, with loss of elastic tissue in the adjacent dermis. The plasmacytoid cells stained overwhelmingly for lambda light chain, and staining of the urticarial lesions from this patient also showed a marked majority of lambda positive cells. Immunoglobulin heavy chain gene (IgH) rearrangements showed a dominant clonal pattern in the nodular lesion. We classified the disease in Patient 1 as marginal zone lymphoma and the disease in Patient 2 as a post-transplant lymphoproliferative disorder. Because of the intimate association of anetoderma and cutaneous B-cell lymphoproliferative disorders in these two patients, it seems possible that anetoderma could result from either a local effect of the neoplastic cells or associated inflammatory cells, especially neutrophils as in Case 1. The infiltrates of Case 1 had many interstitial neutrophils and only a few clonal plasmacytoid lymphocytes, indicating that this presentation of B-cell lymphoma can be a diagnostic pitfall. Given these two cases and similar ones in the literature, biopsy of lesional skin in anetoderma should be performed to ensure that lymphomatous infiltrates are not present. Even if plasma cells are sparse, studies to detect clonality are appropriate. Cutaneous B-cell lymphoma can be added to the list of associations of elastolysis and cutaneous lymphoma, which includes granulomatous slack skin (T-cell lymphoma) and cutis laxa (myeloma).
Adult↗
Morphometric analysis of elastic skin fibres from patients with: cutis laxa, anetoderma, pseudoxanthoma elasticum, and Buschke-Ollendorff and Williams-Beuren syndromes.
Computed morphometric analysis of elastic skin fibres in patients with cutis laxa, anetoderma, Williams-Beuren syndrome, pseudoxanthoma elasticum (PXE), and Buschke-Ollendorff syndrome, all clinically ascertained, was performed and compared with data obtained from healthy individuals of the same age. The diameters, area fractions (AA%) and volume fractions (VV%) occupied by pre-elastic fibres and dermal elastic fibres were determined. Irrespective of age the diameter of dermal elastic fibres followed a Gaussian distribution for all groups studied. These diameters were taken into consideration for VV% determinations. Compared with data from skin of healthy subjects of similar age range, VV% of pre-elastic fibres was significantly decreased in patients with cutis laxa, anetoderma, Williams-Beuren syndrome, and PXE and undetectable in Buschke-Ollendorff patients. VV% of dermal elastic fibres was four- to fivefold increased in Buschke-Ollendorff syndrome, two- to threefold increased in PXE skin, four- to fivefold decreased in cutis laxa and anetoderma skin and about twofold decreased in Williams-Beuren skin. The diameter of oxytalan fibres was decreased in anetoderma and Williams-Beuren syndrome while oxytalan fibre diameter was unchanged in PXE and cutis laxa. The diameter of dermal elastic fibres was increased in PXE and Buschke-Ollendorff syndrome, but was decreased in anetoderma and Williams-Beuren syndrome and unchanged in cutis laxa. We demonstrated that cutis laxa, anetoderma, Williams-Beuren syndrome, PXE, and Buschke-Ollendorff syndrome could be easily differentiated by morphometric analysis of elastic skin fibres. Thus we propose that morphometric analyses together with skin biopsies are a valuable tool for distinguishing between inherited and/or acquired skin diseases known to display alterations of elastic fibres.
Adolescent↗
Anetoderma: another facet of Lyme disease?
Lyme disease has been suspected to be one cause of secondary anetoderma. We present a 25-year-old male patient with multiple lesions of anetoderma with a diameter of up to 2 cm that developed within the last 4 weeks without subjective symptoms. The histopathologic pattern was similar to the inflammatory stage of acrodermatitis chronica atrophicans. Polymerase chain reaction analysis out of the paraffin-embedded tissue, confirmed by sequencing of the obtained nucleotide product, revealed a part of the 23 S ribosomal RNA gene of Borrelia burgdorferi sensu lato. Enzyme-linked immunosorbent assay showed an increased serum IgG titer against B burgdorferi corroborated by Western blot analysis. After a treatment with oral doxycycline (100 mg twice a day) for 30 days the anti-B burgdorferi titer decreased significantly and no new lesions appeared. Some cases of anetoderma might be caused by Borrelia and patients with anetoderma should be examined for borreliosis including serology and polymerase chain reaction of lesional skin. In cases of Borrelia-induced anetoderma, early antibiotic treatment could prevent further progression of the disfiguring skin lesions and the underlying disease.
Adult↗
Spontaneous atrophic patches in extremely premature infants. Anetoderma of prematurity.
BACKGROUND: Anetoderma, characterized clinically by macular depressions or outpouchings of skin, is associated with loss of dermal elastic tissue as noted on histopathologic findings. We report on 9 extremely premature infants who developed patches of anetoderma during their course in the neonatal intensive care unit. OBSERVATIONS: All 9 patients were born between the ages of 24 and 29 weeks of gestation and had numerous complications associated with prematurity. Eight of the 9 infants were noted to have developed anetoderma on the trunk and proximal extremities while in the neonatal intensive care unit. The locations of the lesions on the skin were not explained by previous trauma, although many areas corresponded with placement of monitoring leads or with adhesive for a monitoring device. Reduction or absence of elastic tissue supported the diagnosis of anetoderma in 4 of 5 biopsy specimens. CONCLUSION: We report a previously unrecognized type of anetoderma associated with extreme prematurity. The exact cause is uncertain, although reactions to cutaneous monitoring leads or adhesives is suspected.
Atrophy↗
[Anetoderma during antiphospholipid syndrome. 3 cases].
INTRODUCTION: Anetoderma is a skin disease of unknown etiology sometimes encountered in patients with a lupus syndrome. We report a clinical and pathology analysis of 3 selected cases of anetoderma associated with systemic lupus erythematosus and/or antiphospholipid syndrome. CASE REPORTS: Three patients had skin lesions typical of anetoderma. Antiphospholipid antibodies were present in all three (anticardiolipin in 3, circulating lupus anticoagulants in 3, anti-beta 2GP1 in 2). One patient with systemic lupus erythematosus had signs of antiphospholipid syndrome, the two others had primary antiphospholipid syndrome. DISCUSSION: The analysis of our cases and a review of the literature suggest that anetoderma is a disease which develops in the immunological environment of lupus, and is apparently more related to the presence of antiphospholipids than lupus itself. Thus anetoderma could be another cutaneous sign of the antiphospholipid syndrome.
Adult↗
Anetoderma. Clinical findings, associations, and long-term follow-up evaluations.
In 16 patients with anetoderma, a clinicohistologic entity related to a local dermal defect of elastic tissue, old lesions did not heal, and new lesions often continued to form for many years, despite various forms of treatment. Systemic lupus erythematosus, which occurred in one patient, must be ruled out in patients with anetoderma. Discoid lupus erythematosus occurred later in one patient. Other associated findings, noted in one patient each, included cataract, congenital hip dislocation, congenital fusion of the vertebrae at C2-3, diverticulum of the midesophagus, Addison's disease (before the onset of anetoderma), and mitral valve prolapse. Our results and a review of the literature indicate that patients with anetoderma must be examined for associated eye, bone, heart, pulmonary, digestive tract, and endocrine abnormalities for a better assessment of their skin disorders.
Adolescent↗
Primary anetoderma associated with a wide spectrum of autoimmune abnormalities.
Although the underlying pathologic mechanisms of primary anetoderma have not yet been identified, data suggest the participation of an immunologic mechanism in some cases. In a woman with clinical and histopathologic features of primary anetoderma (Jadassohn-Pellizzari type) of 30 years' duration, laboratory investigation disclosed positive antinuclear factor, hypocomplementemia, hypergammaglobulinemia, granular deposits of immunoreactants along the dermoepidermal junction, and fibrillar deposits in the papillary dermis. In addition, she was found to have autoimmune hemolysis and circulating lupus anticoagulant associated with recurrent deep-vein thrombosis and a history of Graves' disease (starting 5 years after onset of primary anetoderma). To our knowledge, none of the latter three autoimmune conditions has been previously associated with primary anetoderma.
Antibodies, Antinuclear↗
Anetoderma in systemic lupus erythematosus: relationship to antiphospholipid antibodies.
Anetoderma is an elastolytic disorder where multiple patches of slack skin are formed. Twelve patients with anetoderma associated with systemic lupus erythematous have been described, all in the dermatological literature. Recently, a role for antiphospholipid antibodies has been proposed with microthromboses as its pathogenic mechanism. We present herein a 20-year-old female patient who developed anetoderma soon after sun exposure. She was found to have a false positive VDRL and gradually developed other manifestations of SLE, including interstitial cystitis. She has had repeatedly positive antiphospholipid antibodies. Although there are patients who may have a primary form, diagnosis of anetoderma should trigger a search for SLE and/or antiphospholipid antibodies.
Adult↗
Anetoderma and borreliosis: is there a pathogenetic relationship?
A 32-year-old man simultaneously developed anetoderma and acrodermatitis chronica atrophicans on his left arm and showed a positive serology for borreliosis with ELISA and Western Blot tests. In addition, a 45 year-old man is presented with anetoderma without any associated systemic or cutaneous diseases, with B. afzelii confirmed as a singular causality through serology (ELISA, Western Blot) and amplification of B. afzelii-specific DNA from the skin by PCR. These two observations highly suggest that anetoderma can be the result of an infection with B. afzelii. We conclude that in patients with anetoderma a serological investigation for Borreliosis should be performed.
Adult↗
[Anetoderma Schwenninger-Buzzi in a dark-skinned patient].
A 10-year-old boy in Uganda developed primary anetoderma (Schwenninger-Buzzi). It is important not to confuse anetoderma with BL leprosy in spite of some superficial resemblance of the two diseases. Primary anetoderma is probably extremely rare in patients with dark skin although this may partly be due to a lack of dermatologists in Africa who could diagnose the disease.
Atrophy↗
Anetoderma secondary to generalized granuloma annulare.
Anetoderma is a rare disorder of cutaneous atrophy with loss of dermal elastic tissue. Secondary anetoderma is seen after a variety of dermatoses. We describe a 33-year-old woman with secondary anetoderma after generalized granuloma annulare lesions that were most pronounced on sun-exposed areas.
Adult↗
Familial anetoderma.
Two families with anetoderma are described. Unlike previous reports of familial anetoderma, the disease process seemed to be limited to the skin, and there were no associated ocular, gastrointestinal, or orthopedic anomalies in the affected patients or in any other family members. Although infrequently reported, anetoderma may occur in families, and patients must be examined for associated systemic abnormalities for a thorough assessment of their skin disorder.
Adult↗
Anetoderma of prematurity in association with electrocardiographic electrodes.
Anetoderma in premature infants is an uncommon lesion that may be associated with the use of various types of monitoring leads. In 2 infants multiple papules of anetoderma occurred on the forehead in association with the use of gel electrocardiographic electrodes. It is postulated that the cause of these papules was a local hypoxemia caused by pressure from the electrodes. Growth-restricted infants may be particularly predisposed to iatrogenic anetoderma.
Biopsy, Needle↗
Systemic lupus erythematosus-associated anetoderma and anti-phospholipid antibodies.
Anetoderma is characterized by a loss of normal elastic tissue that presents clinically as localized areas of wrinkled or flaccid skin. We describe the case of a 30-year-old woman with systemic lupus erythematosus-associated anetoderma and positive anti-phospholipid antibodies. We discuss the possible role of these antibodies in the pathogenesis of anetoderma, and, when detected, the need to check for an associated anti-phospholipid syndrome in such patients.
Adult↗