Photo-dermatology最新文献

Because solar ultraviolet (UV) exposure is ubiquitous, it is difficult to quantify in human populations. We developed a method to index cumulative UV damage, based upon visual manifestations of facial actinic elastosis. Four photographic slides were taken of each subject's facial skin. These slides were projected on a screen and graded by consensus of 2 raters using a 5-point relative severity scale. Rating disagreements were resolved by a skilled dermatologist who acted as adjudicator. High photographic quality was maintained by standardization of camera settings, lighting, and photographic techniques. Inter- and intrarater variability in grading was minimized by training using standard slides and by practice. This index has been tested in 2 large epidemiologic studies. The method proved highly reliable and, within categories of age and tanning ability, a valid measure of cumulative UV exposure. In addition, this method appeared superior to others in speed, ease of use and cost.

At 16 different dermatology clinics in Scandinavia from 1980-1985, photopatch testing was performed on 1993 patients with suspected photodermatosis. The collective results are presented in this article. The most common cause of sun-related dermatosis was polymorphic light eruption (PLE) (38%), while secondary aggravation of pre-existing skin diseases was established in 16% of the patient group. Photocontact dermatitis (11%) and contact dermatitis (10%) were responsible for 274 and 369 positive test reactions (respectively) on photopatch testing using the SPDRG standard series. Musk ambrette and para-aminobenzoic acid were the leading photosensitizers, while perfume mixture, balsam of Peru and lichen mixture were the most frequent causes of contact sensitivity. The principal photoallergens and contact allergens in the PLE, persistent light reaction and actinic reticuloid groups are discussed, together with the problems, risks and possible mechanisms of induction of photosensitization in these patients. The incidence, causes and diagnostic and therapeutic implications of secondary sunscreen sensitivity in these groups are also addressed.

Oxygen intermediates are responsible for a number of ultraviolet (UV) radiation effects. To test the hypothesis that UV-induced formation of sunburn cells and skin edema (ear swelling) result from oxidative damage, we examined the effect of hypoxia tissue responses to UV in the mouse ear. Hypoxia resulting from vascular occlusion by ear clamping, either before or after UVB exposure, decreased formation of sunburn cells. Ear clamping alone caused significant ear swelling, which was enhanced when combined with UVB exposure. Using topical 8-methoxypsoralen + UVA (PUVA), increased sunburn cells were observed when ears were clamped for 10 min prior to UVA exposure, but not following exposure. Ear swelling caused by PUVA was also enhanced when ears were clamped during exposure. These results suggest that induction of sunburn cells by UVB is dependent on oxygen, and that UVB and PUVA induce sunburn cell formation by distinct mechanisms.

Exposure of normal skin to visible light (400-700 nm) resulted in the induction of immediate pigment darkening (IPD), immediate erythema and a persistent (delayed) tanning reaction. The intensity of pigmentation and time course of the reaction were monitored by measuring chromaticity coordinates. Both IPD and immediate erythema faded over a 24-h period but, unlike erythema, the pigmentation did not totally disappear and the residual tanning response remained unchanged for the rest of the 10-day observation period. The threshold dose for IPD with visible light was between 40 and 80 J/cm2, while the threshold dose for "persistent" pigmentation was greater than or equal to 80 J/cm2.

A 58-year-old man developed a lichenoid reaction on light-exposed areas and subacute prurigo separate from the sun-exposed areas after receiving 200 mg of carbamazepine daily for one year. The difference action spectrum for erythema with or without ingesting the drug ranged from 250 to 390 nm with peaks at 260 and 290 nm. A positive photoingestion test was obtained after administering 2 mg of carbamazepine orally in one dose. Patch test with carbamazepine was negative, while photopatch test with carbamazepine was positive. Positive intracutaneous test was obtained with an irradiated mixture of human serum albumin and carbamazepine at 24 h and 48 h after injection. This patient appeared to be a case of photosensitive lichenoid reaction accompanied by nonphotosensitive subacute prurigo caused by carbamazepine.