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• W2023444405 abstract "The clinical and histomorphological picture of linear focal elastosis (LFE; elastotic striae) was first described in 1989 by Burket, Zelickson and Padilla, who reported three caucasian men aged 69–75 with yellow, palpable, symmetrical lines on both sides of the lumbosacral segments of the vertebral column.1 Mid- and lower dermal elastosis was a prominent feature on histopathology. Only 20 cases of LFE have since been described in the literature, although this is an underestimation of the real occurrence of the disease. The originally reported cases suggested that LFE occurs predominantly in elderly men. Analysis of the reports currently available confirm this male predominance, with only four female patients reported among 20 published cases.2-5 The age preference is less clear because six out of 20 patients were less than 20 years old, and the youngest patient was aged 7 at the time of disease onset.6 Nine out of 20 patients were of Asian descent, two reported men were black.7, 8 Analysis of the available case reports does not necessarily reflect the true epidemiological and demographic proportions of the disease. A distinct clinical picture of the affection is marked by the occurrence of several asymptomatic, yellow, palpable, irregularly indurated, striae-like bands or lines extending horizontally across the middle and lower back. In a few cases, the location was noted outside this area, on the legs only in two cases,4, 5 and on the shoulders besides a typical location on the back in another two;8, 9 in one case the lesion migrated from the lumbar to shoulder area.10 The lesions may first impress like striae distensae, but they are palpable rather than depressed, and yellow in colour, making them different from purplish striae rubrae distensae. No concomitant morbidity or significant associated findings with putative relevance to LFE were noted in any reported case. Moiin and Hashimoto reported the case of a 29-year-old black man with LFE onset in early childhood whose father had had similar lesions since childhood, which raised the suspicion of a genetically conditioned abnormality.7 A focal increase in elastic fibres is a hallmark of the disease as seen from biopsy specimens under optic or electron microscopy. Using a haematoxylin–eosin stain, the epidermis looks unaffected, collagen bundles in the dermis appear normal or hypertrophic but they are separated by fine fibrillar, weakly basophilic material, especially in the subpapillary and reticular dermis.11 Occasionally, aggregated, lumpy elastic fibres have been observed embedded within hypertrophic collagen masses.8 Mild perivascular lymphocytic infiltrate was also noted in some cases; calcium was always negative in von Kossa staining.12 Special elastin staining, such as Verhoeff–van Gieson or Weigert, reveals increased amounts of fairly thin, wavy, elongated and fragmented elastic fibres separating the dermal collagen bundles. In biopsy specimens from their 13-year-old patient, Breier et al. used an image analysis procedure and found 110% focal increase in elastic fibres compared to healthy adjacent skin.5 These authors also noted a split in the ends of the elastic fibres into a paintbrush formation. Few cellular components are associated with the bundles. The elastic fibres in the papillary dermis and dermoepidermal junction are of normal appearance. A comparison of the microscopic appearance of LFE in young patients led Chang et al. to the idea of a continuum of elastolysis prevailing in the earlier stages of the affection with elastosis setting in later on.6 Initial fragmentation of the elastic fibres is followed by reactive regeneration according to this paradigm, although only a few authors have had the opportunity to compare the various stages of lesion development. In electron microscopy, no apparent degeneration is visible, the fragmented elastic fibres are aggregated with abundant interposed electron-dense material that partially attains a fibrous appearance. Hashimoto noted excessive amount of dense material in contrast to somewhat deficient skeleton fibrils of elastic fibres.8 Hagari et al. discerned changes in elastic fibres in early and late stages of their maturation.13 The latter show granular depositions of electron-dense material in the elastin-rich matrix that are remnants of microfibrillar components of outer fibre structures, and matrix production is thought to proceed along them. The immature fibres are composed mainly of microfibrils that are contiguous to intracellular filaments of fibroblasts, their content of elastin is initially low but increases proportionally to their progressing sequential maturation. These findings support the conclusion that active elastogenesis is ongoing in the lesions.13, 14 Despite our incomplete knowledge of the causes and mechanisms of increased production of dermal elastic tissue, the clinical entity of LFE uniquely complements the variation in span of elastopathies currently delineated.15, 16 Initial observations of the disease onset in elderly men in a typical location indicated that hormonal, age-related factors play a causative role together with typical repetitive mechanical stress exerted upon the lower back skin. The horizontal striae-like appearance of the affection supported this view, and the synonym elastotic striae already coined by Burket et al. should better reflect the notion of elastotic variant of striae distensae. The hallmarks of common striae distensae are epidermal atrophy, rarefaction of dermis due to rupturing collagen bundles and dilation of dermal vessels. Indeed, following the period of diminished elastic content, there is a regenerative phase of increased de novo synthesis of elastic fibres found in older striae distensae. In some of the published cases, there was a concomitant finding of LFE and striae distensae that were present at different locations, or were adjacent to LFE.8, 9 The opinion prevailed that LFE represents an excessive regenerative process of elastic fibres and is analogous to keloidal repair of striae distensae.6, 8 However, the factors known to play a precipitating role in pathogenesis of striae distensae, such as glucocorticoids, rapid loss of weight and diabetes, were conspicuously absent in patients with LFE. In addition, the unique anatomical site of LFE is very different from striae distensae, preferentially occurring at abdomen, thighs, arms and breasts.17 The histopathological picture closely resembling LFE, especially with regard to excessive accumulation of otherwise normally appearing elastic fibres in the mid-dermis, is seen with late-onset focal dermal elastosis Tojima. This entity is usually recognized in elderly people by their papular appearance and consistent preference for the neck and flexural creases.18 The innocuous nature of both affections explains the low reporting rate in the literature. Akagi et al. described a patient with the concomitant presence of pseudoxanthoma elasticum-like papillary dermal elastolysis Rongioletti–Rebora and LFE with distinct clinical features.19 Complete loss of oxytalan fibres in the papillary dermis was seen together with elastogenic changes in the subpapillary dermis, and the elastolytic–elastotic stratification was also confirmed by direct immunofluorescence using antibodies against fibrillin and other constituents of the elastic fibres. The authors surmised that the elastolytic component is common for both conditions and is the primary event in LFE.19 According to recent studies, elastolysis may result from the release of matrix metalloproteinases as might be the case in actinic dermal elastosis, or as proved in mid-dermal elastolysis Shelley–Wood, both of these being precipitated by excessive UV exposure.20, 21 Because of the increasing number of reported LFE cases with the disease onset below the age of 20, there is a compelling need to reconsider the pathogenetic scenario. These cases seem to dispute the view that premature ageing, androgenic changes or cumulative mechanic trauma alone can explain all cases of LFE. There is emerging evidence that the intrinsic anomaly of elastic fibre metabolism and degradation, or the hamartomatous/nevoid degenerative (regenerative) process, or even an extrinsic toxic influence creates the necessary conditions for this peculiar disorder to be initiated.11, 18, 22" @default.
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• W2023444405 title "Linear focal elastosis: what's new?" @default.
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