Ultraviolet A sunbed used for the treatment of scleroderma.
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Adult↗
Biomedical subjects
A Oikarinen
Publications and source records attributed to A Oikarinen.
Steroid-induced dermal atrophy: effects of glucocorticosteroids on collagen metabolism in human skin fibroblast cultures.
Collagen production by human skin fibroblast cultures was studied by incubation with [3H] proline and several glucocorticosteroids known to produce dermal atrophy in vivo. Collagen production was measured as formation of [3H]hydroxyproline or collagenase-digestible 3H-polypeptides, and the values were corrected for changes in cell number in the same cultures. The steroids, in a wide concentration range, failed to elicit any consistent alterations in collagen production. Review of the literature dealing with corticosteroid-induced changes in collagen production by human skin fibroblasts indicate conflicting results even under apparently similar incubation conditions. Consequently, no unifying hypothesis for steroid-induced dermal atrophy can be developed presently based on the in vitro data.
Cell Count↗
Effects of PUVA and UVB treatments on restoration of epidermal barrier function and vascular response after suction blister injury in human skin in vivo.
PUVA and UVB phototherapies are used in the treatment of psoriasis and other inflammatory skin diseases. Ultraviolet radiation causes inflammation and modulates cell kinetics in the skin. PUVA also has an inhibitory effect on skin DNA synthesis. In this study, the effects of PUVA and UVB treatments on epidermal would healing were examined using the suction blister wound model. The healing of the wound was studied indirectly by measuring water evaporation and blood flow in the wound area. On the fourth day, water evaporation was more abundant in PUVA-treated patients (42 +/- 5 g/m2h) than in UVB treated (36 +/- 4 g/m2h) or control patients (27 +/- 3 g/m2h) (analysis of variance, the least significant difference test at a level of 0.05). The P value for the difference of means between the PUVA and control groups was 0.014. Blood flow was also more abundant during the fourth (PUVA 162 +/- 11 arbitrary units, UVB 122 +/- 10, controls 115 +/- 15) and sixth (PUVA 108 +/- 18, UVB 73 +/- 17, controls 57 +/- 13) day in PUVA treated patients (analysis of variance, the least significant difference test at a level of 0.05). The results suggest that PUVA treatment decreases the restoration of the epidermal barrier function. The PUVA-treated patients also showed a more intense and prolonged vascular response that may be due to PUVA-related inflammation.
Adult↗
Differential modulation of transforming growth factor-beta by betamethasone-17- valerate and isotretinoin: corticosteroid decreases and isotretinoin increases the level of transforming growth factor-beta in suction blister fluid.
Retinoids and glucocorticoids are known to have a potential to modulate the expression of transforming growth factor-beta (TGF-beta). We investigated the effect of oral isotretinoin (13-cis-retinoic acid) on the expression of two distinct isoforms of TGF-beta, TGF-beta1 and TGF-beta2, in suction blister fluid and serum in acne patients. We also investigated the effect of topical glucocorticoid (betamethasone-17-valerate) and age on suction blister fluid TGF-beta1 in healthy volunteers. Six weeks of isotretinoin treatment caused a statistically significant 19% increase in suction blister fluid TGF-beta1. The suction blister fluid TGF-beta2 level remained below the sensitivity level of the immunoassay in many cases. Isotretinoin did not affect the serum TGF-beta1 or TGF-beta2 level. Betamethasone-17-valerate pretreatment for 3 days twice a day caused a statistically significant 17% decrease in suction blister fluid TGF-beta1. The active form of TGF-beta1 represented 5% of the total TGF-beta1 in suction blister fluid. Our diffusion calculations suggest that all TGF-beta1 and TGF-beta2 detected in suction blister fluid have diffused from systemic circulation. The increase in suction blister fluid TGF-beta1 after isotretinoin treatment seems to be of local origin, while the decrease in suction blister fluid TGF-beta1 after glucocorticoid pretreatment seems to be due to glucocorticoid-induced vasoconstriction resulting in decreased diffusion of TGF-beta1 from the circulation. Modulation of local interstitial fluid TGF-beta1 concentration may be one mechanism by which isotretinoin and glucocorticoids mediate their effects in skin.
Acne Vulgaris↗