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PubMed1987

Postgranulomatous anetoderma associated with Takayasu's arteritis in a child.

Takayasu's arteritis (TA) is a rare chronic inflammatory arteriopathy affecting mainly the aorta and its branches. Many skin manifestations have been reported in association with this disease. Pyoderma gangrenosum and subcutaneous inflammatory lesions of the leg are the most frequent. We studied a boy with TA in whom a papular rash of the trunk preceded the onset of vascular symptoms by many years. Histologically, the lesions were superficial and consisted of middermal noncaseating tuberculoid granulomas, which progressed to atrophy and anetoderma because of elastic network disruption. Granulomas were also found in synovial tissue but not in a temporal artery biopsy specimen, which showed only intimal hyperplasia. Our observations suggest that vascular and skin lesions with elastic tissue may both result from a common granulomatous hypersensitivity process.

Aortic Arch Syndromes↗
PubMed1998

Hamartomatous congenital melanocytic nevi showing secondary anetoderma-like changes.

A 47-year-old man had multiple large congenital melanocytic nevi associated with striking atrophic changes. Biopsy specimens showed a prominent reduction and fragmentation of elastic fibers in the papillary dermis. The anetoderma-like changes may have been secondary to a past inflammatory process but more likely represent a hamartoma.

Connective Tissue Diseases↗
PubMed2003

Familial anetoderma.

A 31-year-old Caucasian male presented with a history of erythematous, saccular outpouchings of the skin on his back, shoulders, and upper extremities (Fig. 1). The patient reported that his mother and aunt had a similar skin disorder, which initially began with inflammation, but healed leaving lax skin in its wake. He did not recall the name of the skin condition. Physical examination revealed large confluent zones of sac-like protrusions of erythematous skin on the back and shoulders. Histopathologic examination of the excisional biopsy revealed a relatively unremarkable epidermis. Perivascular lymphocytes were present in small numbers in the papillary dermis. Adnexal structures and deep dermis remained intact. The acid-orcein-Giemsa stain highlighted the absence of elastic fibers within the mid and lower reticular dermis (Fig. 2a,b), consistent with anetoderma.

Adult↗
PubMed2001

Anetoderma associated with antiphospholipid antibodies: case report and review of the literature.

The association of primary anetoderma (PA) with antiphospholipid antibodies (APAs; with or without criteria of primary antiphospholipid syndrome) has been observed repeatedly and a possible pathogenic significance of this asssociation has been hypothesized. We report the case of a 21-year-old-woman who developed anetodermic lesions on her upper trunk and arms. The presence of APAs was demonstrated, but no diagnostic criteria of systemic lupus erythematosus were present. A review of the literature disclosed 20 previously reported patients presenting this peculiar association. Thrombotic phenomena, represented by spontaneous abortions or venous thrombosis, are a frequent complication in this setting. Taking these observations into account a systematic search for APAs in patients with PA seems advisable.

Adult↗
PubMed2002

Anetoderma: an altered balance between metalloproteinases and tissue inhibitors of metalloproteinases.

The amount of elastic fibers from lesional and healthy skin areas of five patients with anetoderma was determined by automated image analysis. Dermal elastic fibers were almost completely absent in anetodermic skin and preelastic fibers were undetectable or extremely rare. Organ cultures were performed using explants from affected and unaffected skin areas of the same patient. We identified and quantified proteases in the culture media of explants: MMP-1 (collagenase 1), MMP-2 and MMP-9 (gelatinases A and B), MMP-3 (stromelysin 1), MMP-7 (matrilysin 1), and tissue inhibitors of metalloproteinases, TIMP-1 and TIMP-2. The data were compared with those of two healthy donors. For the five samples of anetodermic skin, MMP-1 levels were significantly higher compared with the uninvolved cultures and the two healthy samples. A significant increase of TIMP-1 expression was also observed in the affected cultures. We demonstrated a significant increase in the production of gelatinase A in lesional skin when compared with nonlesional skin and healthy donor samples. We found no significant production of TIMP-2 in the five samples of anetodermic skin compared with the samples from the two healthy donors. There was a significant decrease in TIMP-2 expression in the five nonlesional samples compared with the control samples. These data are in favor of an altered balance in anetodermic patients between MMP-2 and TIMP-2. Levels of MMP-9, MMP-3, and MMP-7 were significantly higher in the culture-conditioned media of the anetodermic skin samples than the nonlesional skin cultures. Because MMP-3, MMP-7, MMP-9 are known to degrade elastin, and MMP-3 can activate the latent forms of MMP-7 and MMP-9, we propose that these metalloproteinases also participate in the degradation of elastic fibers in anetodermic skin.

Adolescent↗
PubMed1997

Increased expression of gelatinases A and B by skin explants from patients with anetoderma.

The extent of alterations to the elastic fibre network in lesional skin areas of three patients with anetoderma was assessed by quantitative image analysis of tissue sections and compared with morphometric parameters from unaffected sites of the same individuals. In the anetodermic skins pre-elastic fibres were undetectable or extremely rare: the volume fraction (Vv%) occupied by these pre-elastic fibres was 0-0.3%, while in unaffected skins the Vv% occupied by pre-elastic fibres was 0.5-0.8%. A nearly complete absence of dermal elastic fibres in lesional skins from the three patients was evidenced (Vv% = 0.2-0.3%). Organ cultures were performed using explants from skin with or without anetodermic lesions to quantify the expressions of elastase-type proteinases. All tissues from anetodermic lesions expressed proforms of gelatinases A and B and the activated form of gelatinase A; their levels increased with the culture time. In comparison, enzymatic activities on oligopeptide substrates specific for leucocyte elastase and fibroblast plasma membrane-associated metalloelastase were not detected in the conditioned media of any explants at any time of culture from 1 to 5 days. Increased production of progelatinases A and B and activation of progelatinase A could be mainly responsible for the degradation of skin elastic fibres demonstrated in anetodermic skins.

Adult↗
PubMedDate not supplied

Anetoderma.

Anetoderma is a rare cutaneous condition with characteristic clinical features and histopathology. The condition is classified into idiopathic (Jadassohn or Pellizzari type) and atrophic (Schweinger-Buzzi type) concomitant with other diseases, and secondary to infection or drugs.

Atrophy↗
PubMed1977

Jadassohn-type anetoderma in association with keratoconus and cataract.

The unusual association of macular atrophy--Jadassohn type of anetoderma, bilateral subcapsular ocular cataracts and keratoconus--is described in an otherwise healthy adult male. This association has not, to the best of our knowledge, been previously described. The possibility that this is not a chance association is discussed.

Atrophy↗
PubMed2003

Primary anetoderma: a cutaneous sign of antiphospholipid antibodies.

Although a few reports in recent years have suggested that patients with antiphospholipid antibodies (aPL) are prone to developing primary anetoderma (PA), it is still unclear how often aPL are detected in unselected PA patients. We studied nine consecutive PA patients for the presence of autoimmune antibodies and disorders in general and the presence of aPL in particular. Six of the nine patients had clinical evidence of associated autoimmune disorders (Graves'disease and autoimmune haemolysis in one, systemic scleroderma in one, Hashimoto's thyroiditis in one, alopecia areata in one) and/or signs of hypercoagulability (recurrent fetal loss in two, recurrent stokes in one, recurrent deep vein thrombosis in one). In four ofthese six patients the onset of PA preceded these signs. Positive aPL was found in all: anticardiolipin (aCL) in six, anti-beta2-glycoprotein-I (a(beta)2GPI) in six and lupus anticoagulant (LAC) in four. The most frequent isotype was IgA. Among other autoantibodies found the most frequently was antinuclear antibodies. Four ofthe nine patients fulfilled the criteria for antiphospholipid syndrome (APS). It is concluded that PA is an important cutaneous sign for autoimmune disorders in general and the presence of aPL in particular. Hence, the work-up of these patients should include testing for LAC as well as for all different isotypes ofaCL and a(beta)2GPI. We recommend that PA be added to the list of the cutaneous manifestations of APS.

Adult↗
PubMed2003

[Post-traumatic arthritis in a patient with Jadassohn's anetoderma].

We describe the emergence of arthritis following a physical trauma, in a young man with clinical and histopathologic features of primary anetoderma (Jadassohn type) of 13 years' duration. Diagnosis of post-traumatic arthritis in a young patient with genetic predisposition was assumed. Indeed septic arthritis and other possible cause of arthritis were ruled out.

Adult↗
PubMed1990

[Post-varicella anetoderma. 3 cases].

We report three cases of typical macular atrophy which appeared during, or was noticed shortly after varicella. The three patients were children. These cases were particular in that anetoderma lesions occurred independently of the scarring varicella lesions and followed a prolonged course of their own afterwards. We were unable to classify these cases in the primary or secondary type of macular atrophy. The various dermatoses associated with macular atrophy and the numerous physiopathological hypotheses put forward concerning this entity are enumerated.

Atrophy↗
PubMed1986

[Jadassohn type anetoderma--case report].

A 19-year-old patient suffering from Jadassohn's anetoderma with progressive dermatrophia showed positive reaction to treatment with chloroquin diphosphate.

Actin Cytoskeleton↗
PubMed1986

[Anetoderma].

We report on a 17-year-old girl having suffered from Jadassohn's anetoderma since five years. Administration of Plaquenil resulted in marked improvement: The inflammation disappeared, and there did not occur any new symptoms. The presence of IgA in the capillary endothelium implies an immunological process.

Adolescent↗
PubMed1986

[A case report of Jadassohn anetoderma].

Itchy pink plaques have been developing on the trunk of a 29-year-old patient for two years. After a few weeks, these plaques usually change into atropic scars. Both types of efflorescence occur simultaneously. Histological examination of a fresh lesion showed leucocytoclastic vasculitis. These micromorphological changes are no longer visible in the atrophic scars. The clinical picture and histological findings are identical with those seen in Jadassohn's anetoderma. The histological changes correspond with the degenerative-inflammatory process first described by Cramer in 1963.

Adult↗
PubMed1985

Monoclonal antibody studies in the skin lesions of patients with anetoderma.

In all five patients studied, monoclonal antibody studies of cryostat sections of skin biopsy specimens of anetoderma lesions revealed inflammatory cells reacting with anti-Leu-1, pan-T-cell antibody, and anti-Leu-3a, the helper/inducer T-cell antibody. Small numbers of suppressor cells were present in only three biopsy specimens. Four specimens showed OKM1, antibody-reacting cells (monocytes). The age of the lesion was not correlated with inflammation or the T-cell subsets identified.

Adult↗
PubMed1981

[Mastocytosis evolving into anetoderma. Review of the literature (author's transl)].

The authors reviewed the literature of cases of mastocytosis with either anetoderma or pseudo-pelade. They studied the different substances in the secretions of mastocytes which could have an effect on collagen and elastic fibres. They supported the theory that there is a susceptible connective tissue. They stressed the underestimation of these associated features of mastocytosis.

Adolescent↗
PubMed1997

Transforming growth factor beta 1 and its latent form binding protein-1 associate with elastic fibres in human dermis: accumulation in actinic damage and absence in anetoderma.

Latent transforming growth factor-beta 1 (TGF-beta 1) and its binding protein-1 (LTBP-1) are components of the extracellular matrix microfibrils of cultured human fibroblasts. Using immunohistochemistry we have studied the localization of TGF-beta 1 and LTBP-1 and compared their distribution with that of elastic fibres in the interstitial connective tissue matrix of the human dermis. Prominent LTBP-1 specific fibrillar staining co-localized with the elastic fibres in normal human skin. Co-distribution was also observed in a number of pathological states of the elastic fibres such as solar elastosis, solar keratosis and pseudoxanthoma elasticum. TGF-beta 1 had a staining pattern similar to that of LTBP-1 in solar elastosis and solar keratosis. No staining for LTBP-1 or TGF-beta 1 was found in dermis devoid of elastic fibres, as in anetoderma. LTBP-1 is released from the extracellular matrix of cultured human fibroblasts, epithelial and endothelial cells by proteases. Analogously, the immunoreactivity for LTBP-1 and TGF-beta 1 were also lost from the skin sections by elastase, and by trypsin, a protease pretreatment commonly used in immunohistochemistry. These results indicate that LTBP-1 is a component of the elastin-associated microfibrils of the interstitial connective tissue matrix of human skin. Furthermore, the small latent form of TGF-beta 1 is likely to associate with the extracellular matrix of human dermis via LTBP-1. The release of latent TGF-beta 1 from the matrix, as a consequence of proteolytic cleavage of LTBP-1, is a plausible extracellular mechanism for the regulation of TGF-beta 1 activation.

Adolescent↗