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A case of anetoderma is described in which progressive protrusion of the anterior teeth was a concomitant finding. A possible interrelationship between these two conditions is suggested, based upon the anatomy and physiology of the oxytalan fibers of the periodontal ligament.
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.
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.
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.
A 40-year-old male patient with primary anetoderma is presented in whom antiphospholipid antibodies were detected while not fulfilling diagnostic criteria for antiphospholipid syndrome. The possible pathogenic role of antiphospholipid antibodies in the disease development is postulated.
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.
A 19-year-old patient suffering from Jadassohn's anetoderma with progressive dermatrophia showed positive reaction to treatment with chloroquin diphosphate.
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.
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.
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.
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.
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.
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