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The effect of local application of 8-methoxypsoralen (8-MOP) and subsequent UVA irradiation on palmoplantar pustulosis (PPP) was studied in 10 patients. In 8 patients 8-MOP baths were used, and in 5 patients an 8-MOP ointment was applied, 3 patients receiving both forms of treatment. The number of treatment sessions varied from 15 to 128, with maximal UVA doses of 1.2 to 12 J/cm2, and total cumulative doses of 8 to 348 J/cm2. Two patients experienced a brisk phototoxic erythema and one patient developed a bullous reaction. Only 3 patients responded favourably to the treatment, 2 with moderate and 1 with good clearing of the lesions. In the remaining 7 patients either no effect (5 patients) or an exacerbation of the disease (2 patients) was seen.

Twenty-six patients with long-standing, recurrent polymorphous light eruptions were treated with psoralen photochemotherapy. Thirteen patients received oral methoxsalen, while 13 were photosensitized by trioxsalen baths. After an average of 20 PUVA exposures, a good or excellent therapeutic result was achieved in 12 of the orally treated and 10 of the topically treated patients. In most of the cases, clinical desensitization lasted throughout the summer season, without further PUVA exposures. When the polymorphic phototest reaction (PPR) was registered 72 h after skin testing with a medium pressure mercury lamp, a remarkable reduction or total abolition of the reaction was seen in tests made on PUVA-exposed skin, as compared with tests made on a comparable skin site, shielded from UVA exposure during the treatments. A concomitant decrease in the erythemal reactivity (MED) of the skin was usually--though not invariably--seen. It is concluded that in addition to including an increase in the shielding properties of stratum corneum, PUVA treatment may induce non-responsiveness in PMLE skin by other, possibly anti-inflammatory or immunological mechanisms.

The effect of local application of 8-methoxypsoralen (8-MOP) and subsequent UVA irradiation on palmoplantar pustulosis (PPP) was studied in 10 patients. In 8 patients 8-MOP baths were used, and in 5 patients an 8-MOP ointment was applied, 3 patients receiving both forms of treatment. The number of treatment sessions varied from 15 to 128, with maximal UVA doses of 1.2 to 12 J/cm2, and total cumulative doses of 8 to 348 J/cm2. Two patients experienced a brisk phototoxic erythema and one patient developed a bullous reaction. Only 3 patients responded favourably to the treatment, 2 with moderate and 1 with good clearing of the lesions. In the remaining 7 patients either no effect (5 patients) or an exacerbation of the disease (2 patients) was seen.

Serum total an unbound testosterone (T) and sex hormone binding globulin (SHBG) levels were studied in fifty-four female acne patients before treatment and during the treatment by two different oral contraceptives, the other containing 0.150 mg desogestrel plus 0.03 mg EE and the other 0.150 mg levonorgestrel plus 0.03 mg EE. Pretreatment values were abnormal in 57% of the patients. A borderline significant correlation between the severity of acne and SHBG was found. Ater six months' treatment a 250% increase in SHBG was seen in desogestrel/EE group and no significant change in SHBG in levonorgestrel/EE group. However, at the same time serum free testosterone fell 60% in both treatment groups. SHBG cannot be the only regulator of serum free testosterone. Acne improved significantly in both treatment groups. It is likely that the improvement was in connection with the free testosterone decrease and the improvement was better in the desogestrel/EE group where also SHBG elevation was seen.Serum total and unbound testosterone (T) and sex hormone binding globulin (SHBG) levels were studied in 54 female acne patients before and during the treatment by 2 different oral contraceptives, 1 containing 0.150 mg desogestrel + 0.03 mg ethinyl estradiol (EE) and the other 0.150 mg levonorgestrel + 0.03 mg EE. Pretreatment values were abnormal in 57% of the patients. A borderline significant correlation between the severity of acne and SHBG was found. After 6 months of treatment, a 250% increase in SHBG was seen in the desogestrel/EE group and no significant change in SHBG level in the levonorgestrel/EE group. However, at the time same, serum free testosterone fell 60% in both treatment groups. SHBG cannot be the only regulator of serum free testosterone. Acne improved significantly in both treatment groups. It is likely that the improvement was the result of the free testosterone decrease and the imnprovement was greater in the desogsertel/EE group where SHBG elevation was also seen.

The vascular permeability increasing effect of several trypsin-like enzymes purified from the rat submandibular gland was studied. The size of the lesion caused by an intradermal injection of small amounts of the enzymes in blued rabbits was used as the measure of the permeability increasing effect. Salivain and four isozymic forms of a kallikrein-like peptidase caused a very marked increase in the vascular permeability. A clearly weaker response was obtained with glandulain and Depot-Padutin®, and a very weak response with trypsin. These lesions as well as that caused by bradykinin could not be prevented by prometazine, as was the lesion caused by histamine. The response to the enzymes was lowered to about one half by prior injections of phenylbutazone. It was concluded that the enzymes effect the vascular permeability by liberating vasoactive kinins.