Post by Max on Jul 13, 2005 5:50:45 GMT -5
(Ro)accutane induced aging skin due to hormonal deficits
Intrinsic skin aging is determined primarily by genetic factors and hormonal status. It reflects the same degenerative process seen in other organs. Skin function is one of the parameters most influenced by aging. The hormonal influences include reduced pituitary, adrenal and gonadal secretion. The hormonal changes of aging lead to the development of a specific body and skin phenotype. Individuals in developed lands spend up to a third of their life (women-post-menopausal) or perhaps 20 years (men-partial androgen deficiency of the aging man, PADAM) with oestrogen or androgen deficiency. Other hormones whose levels decrease with aging include melatonin, growth hormone (GH), dehydroepiandrosterone und insulin-like growth factor-I (IGF-I). Since the skin not only fulfils a protective function for the organism but is also an active peripheral endocrine organ, which even releases effective hormones in the circulation, local hormone substitution could become interesting in the future [1].
(Ro)accutane induced skin fragility
The origin and frequency of skin fragility, a frequent side effect of oral synthetic retinoids, was studied in ten patients receiving isotretinoin (13-cis-retinoic acid) for disorders of keratinization and in hairless mice treated with isotretinoin and the aromatic retinoid, etretinate (RO 10-9359). Clinical skin fragility occurred in eight of ten patients, and experimental friction blisters could be induced by pencil eraser abrasion in nine of nine patients and in the hairless mice. Light and electron microscopy of friction blisters showed fraying or loss of the stratum corneum and outer layers of the viable epidermis, loss of desmosomes and tonofilaments, and intracellular and intercellular deposits of amorphous material that did not stain with stains for mucin. The skin fragility produced by oral synthetic retinoids is epidermal in origin, since retinoids induce profound disruption of epidermal morphologic appearance [2].
Intrinsic skin aging is determined primarily by genetic factors and hormonal status. It reflects the same degenerative process seen in other organs. Skin function is one of the parameters most influenced by aging. The hormonal influences include reduced pituitary, adrenal and gonadal secretion. The hormonal changes of aging lead to the development of a specific body and skin phenotype. Individuals in developed lands spend up to a third of their life (women-post-menopausal) or perhaps 20 years (men-partial androgen deficiency of the aging man, PADAM) with oestrogen or androgen deficiency. Other hormones whose levels decrease with aging include melatonin, growth hormone (GH), dehydroepiandrosterone und insulin-like growth factor-I (IGF-I). Since the skin not only fulfils a protective function for the organism but is also an active peripheral endocrine organ, which even releases effective hormones in the circulation, local hormone substitution could become interesting in the future [1].
(Ro)accutane induced skin fragility
The origin and frequency of skin fragility, a frequent side effect of oral synthetic retinoids, was studied in ten patients receiving isotretinoin (13-cis-retinoic acid) for disorders of keratinization and in hairless mice treated with isotretinoin and the aromatic retinoid, etretinate (RO 10-9359). Clinical skin fragility occurred in eight of ten patients, and experimental friction blisters could be induced by pencil eraser abrasion in nine of nine patients and in the hairless mice. Light and electron microscopy of friction blisters showed fraying or loss of the stratum corneum and outer layers of the viable epidermis, loss of desmosomes and tonofilaments, and intracellular and intercellular deposits of amorphous material that did not stain with stains for mucin. The skin fragility produced by oral synthetic retinoids is epidermal in origin, since retinoids induce profound disruption of epidermal morphologic appearance [2].
