[Development and regression of dermal corticosteroid atrophy. 2. Changes in compression rate]

In the 1st comm. results on development and remission of steroid-induced dermal atrophy were presented. Measurements were carried out with an instrument we constructed ourselves. This device enabled calculation of the rate of compression (CR) of a skin fold as well as determination of skin fold thickness (SFT). CR is specified in mm/log t. It is postulated that the CR depends on the viscosity of the basic substance and on the density of the collagen fiber skeletons led to an increase of SFT and CR. Loss of basic substance in quantitatively unchanged collagen skeletons led to a reduction of SFT and CR. In skin areas treated with corticosteroids, CR was reduced at roughly the same time as SFT. With the exception of hydrocortisone, the reduction was observed from about the 5th to the 10th d onwards in all products tested and became most pronounced after the 12th d. Following the end of steroid treatment (17th d), CR normalized within 6 to 10 d. It is concluded from the results that early steroid-induced dermal atrophy is caused by a lowering of the water/basic substance system. A steroid-specific inhibition of hyaluronic acid and glycosamine synthesis by the fibroblasts is assumed to be the cause of thickness loss. Skin areas treated with control ointments free of active substance displayed signs of increased hydratation.