“…Atrophie striae (Behrman & Goodman 1950;Epstein & Epstein 1963) have been reported after long-term corticosteroid therapy and have been attributed to loss of connec¬ tive tissue fibres.…”
The effects of systemic cortisol treatment on the biophysical and biochemical properties of skin were investigated. Rats were injected sc with cortisol for 14, 60 and 120 days and samples of lumbar skin were studied. Corticosteroids exert a biphasic effect on the strength of skin: 1) a relatively fast increase in the strength and stability, caused by an increased collagen cross-linking and 2) an inhibited collagen synthesis which ultimately results in a thinning of the skin and a decrease of collagen content consistent with clinical observations. The thermal stability is increased indicating an increased proportion of thermostable cross-links in skin collagen. No changes are observed in the percentage type III collagen with respect to type I collagen. Increased amounts of glucose attached to the \g=e\-amino group of lysine residues in the collagen are found after long-term treatments, an alteration which may play a role in hampering the tissue functions.
“…Atrophie striae (Behrman & Goodman 1950;Epstein & Epstein 1963) have been reported after long-term corticosteroid therapy and have been attributed to loss of connec¬ tive tissue fibres.…”
The effects of systemic cortisol treatment on the biophysical and biochemical properties of skin were investigated. Rats were injected sc with cortisol for 14, 60 and 120 days and samples of lumbar skin were studied. Corticosteroids exert a biphasic effect on the strength of skin: 1) a relatively fast increase in the strength and stability, caused by an increased collagen cross-linking and 2) an inhibited collagen synthesis which ultimately results in a thinning of the skin and a decrease of collagen content consistent with clinical observations. The thermal stability is increased indicating an increased proportion of thermostable cross-links in skin collagen. No changes are observed in the percentage type III collagen with respect to type I collagen. Increased amounts of glucose attached to the \g=e\-amino group of lysine residues in the collagen are found after long-term treatments, an alteration which may play a role in hampering the tissue functions.
“…26,37 This phenomenon is reflected in increased transparency and shininess of the skin, as well as the appearance of striae. 6,38 The factors that influence the degree of skin atrophy include age, body site, potency of topical corticosteroid, and the presence of occlusion. Atrophy from topical triamcinolone acetonide was first reported by Epstein et al 38 Atrophy has now been recognized as the most common adverse effect of topical corticosteroid therapy (Fig 2).…”
Section: Atrophymentioning
confidence: 99%
“…6,38 The factors that influence the degree of skin atrophy include age, body site, potency of topical corticosteroid, and the presence of occlusion. Atrophy from topical triamcinolone acetonide was first reported by Epstein et al 38 Atrophy has now been recognized as the most common adverse effect of topical corticosteroid therapy (Fig 2). 39 Topical application of corticosteroids can cause atrophy, not only because of the suppressive action on cell proliferation but also because of inhibition of collagen synthesis.…”
“…As the physiological agent proved to be of limited anti-inflammatory activity, halogenated glucocorticoids such as triamcinolone acetonide, betamethasone 17-valerate or clobetasol 17-propionate were synthesized [2,3]. The enhanced efficacy of these compounds was paralleled by an increased risk of local and systemic adverse effects [4]. Efforts in the development of safer derivatives [5] resulted in the introduction of the non-halogenated glucocorticoid C-17,21 double esters.…”
In this study, we investigated the effect of prednicarbate, mometasone furoate and betamethasone 17-valerate on total skin thickness over a treatment period of 6 weeks. The study was conducted as a double-blind, placebo-controlled randomized clinical trial with a confirmatory approach. The influence of these drugs on healthy human skin under non-occlusive conditions was assessed by measuring total skin thickness and epidermal thickness using 20 and 50 MHz sonography, respectively. Epidermal surface structure was evaluated using profilometry. Visual assessment addressed signs of atrophy and formation of telangiectasia. The reduction of total skin thickness induced by prednicarbate was clearly less than that caused by betamethasone 17-valerate and mometasone furoate. Prednicarbate led to a higher degree of skin thinning than vehicle. For technical reasons, epidermal thickness could not be reliably evaluated with 50 MHz sonography. Profilometry did not demonstrate any differences between treatments. Visible signs of atrophy or telangiectasia were detected in two subjects each upon betamethasone 17-valerate and mometasone furoate, but not upon prednicarbate or its vehicle. Prednicarbate is a topical glucocorticoid with an improved benefit/risk ratio, as it causes less skin atrophy than the equipotent betamethasone 17-valerate.
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