Abstract

Calmodulin (CaM) is an intracellular calcium binding protein which appears to have an essential modulatory role in a variety of intracellular processes. Levels of CaM in the epidermis in psoriasis have been shown to be elevated in both lesional and non-lesional skin (Van de Kerkhof & Van Erp, 1983; Tucker et al., 1984). We set out to determine whether successful treatment of psoriasis by standard methods would lead to a parallel reduction in epidermal CaM levels. Seven male and eight female in-patients, mean age 43 years, with active psoriasis covering between 10% and 75% of the skin surface area were studied. Six patients were treated by a modified Ingram regime, four with methotrexate, two with PUVA and one each with Tigason®, Tigason® plus PUVA, and topical steroids. Epidermal shave biopsies were taken from lesional (15 patients) and non-lesional (13 patients) forearm skin before commencing treatment and after clearance. The samples were homo genized, their protein content determined, and the CaM content measured using a CaM-sensitive phosphodiesterase assay. Following treatment there was no significant decrease in CaM levels in the non-lesional epidermis, the mean CaM levels ± SEM (n) being 0.96 ± 0.23 pre-treatment and 0.77 ± 0.56 (13) μg CaM per mg epidermal protein, which were only slightly higher than that present in the epidermis of normal volunteers (0.74 ±0.14 (13) μg CaM per mg protein). However, of the lesional samples, those which showed elevated Calmodulin pre-treatment (nine of the 15 patients) showed a significant decrease in CaM after treatment from 3.22 ± 0.90 to 1.25 ± 0.31 μg CaM per mg protein (P < 0.05). For the remaining six patients CaM levels were within the range for normal volunteers both pre- and post-treatment. These results suggest that elevated CaM levels fall towards the ‘normal’ range with treatment, while there is little change in those skins where the CaM levels are already low.

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