Photo-dermatology最新文献

Sib patients with xeroderma pigmentosum (XP), XP90TO (42 years old, male) and XP92TO (40 years old, female, were assigned to group F by the complementation analysis in hybridized heterodikaryons. The XP90TO and XP92TO fibroblasts exhibited the typical XPF characteristics of a threefold higher sensitivity to the lethal effect of 254 nm UV and a reduced level of 12% unscheduled DNA synthesis (UDS) compared with normal cells. Clinically, both patients manifested moderate to severe acute sun sensitivity by age 8, pigmented freckles by age 10 and skin malignancies at higher ages (6 basaliomas at 42 years in XP90TO; 1 basalioma at 41 years in XP92TO). Despite the still currently sun-sensitive state, the patients showed normal minimal erythema dose (MED) at monochromatic wavelengths of 290, 300 and 305 nm but abnormally delayed peaking of erythema reaction at 48 h after exposure. After irradiation with more than 3 MED, XP92TO showed a long persistence of induced erythema for at least 7 days. A review of the 16 reported XPF patients indicated mild skin manifestations, no neurological abnormalities, and more delayed skin carcinogenesis at a lower frequency than that in XPA patients. In addition, we have collected clinical information from Japanese XP patients in rare complementation groups D and E and reviewed their clinical and photobiological characteristics.

Systemic intradermal and topical inhibitors of eicosanoid synthesis have been shown to decrease the intensity delay the onset of erythema produced with a single exposure to ultraviolet (UV) light. We studied the effect of single and multiple doses of meclofenomate on erythema induced by single and multiple doses of UV light. Thirty Caucasian subjects took either meclofenomate 100 mg t.i.d. or matching placebo for 5 days, crossing over to the alternative for 5 more days after a 2-day washout period. A statistical analysis was made of erythema response immediately prior to the study and then on 8 successive days during the study. Analysis of single and multiple exposure data revealed a statistically significant inhibition of erythema from meclofenomate therapy as compared with placebo.

Human keratinocytes (NCTC 2544) in culture were labeled with either 14C-arachidonic acid or 14C-stearic acid and then exposed to UVB irradiation (9 or 90 mJ/cm2). Exposure of the keratinocytes to UVB irradiation resulted in considerable rearrangement of the membrane fatty acids. Following UVB irradiation the percentage amounts of 14C-arachidonic acid and 14C-stearic acid were significantly decreased in phospholipids, in phosphatidylethanolamine and in phosphatidylcholine. The liberation of stearic acid from phospholipids was accompanied by accumulation of radiolabel into the culture medium, but in 14C-arachidonic acid-labeled cells the amount of radiolabel in the culture medium was not changed following UVB irradiation despite liberation of arachidonic acid from phospholipids. It seems evident that, following UVB irradiation, the rate of reincorporation of liberated 14C-arachidonic acid, a polyunsaturated fatty acid, is higher and thus different from that of a saturated fatty acid, 14C-stearic acid. The present study suggests that exposure of keratinocytes to UVB irradiation is followed by liberation of both saturated and unsaturated fatty acids and also considerable reacylation of the unsaturated fatty acids.

Thirty patients suffering from polymorphous light eruption (PLE), selected by criteria pointing to UVB sensitivity, were phototested for reproduction of skin lesions. Twenty-seven patients (90.0%) had symptoms compatible with or very similar to papulovesicular light eruption (PVLE). Of the 30 patients, 56.7% developed typical lesion of PLE at the test site by provocative phototesting with UVB. Eruptions of the immediate onset type were apt to be reproduced by multiple repeated irradiation, but those of the delayed onset type were reproduced by a single high-dose exposure. In addition, pruritus at the test site seen in all patients was thought to be an important diagnostic symptom. It was obvious that UVB played an etiological role in PLE, including PVLE.

A human sunburn cell (SBC) count is used to evaluate the reduction in UV-induced skin damage achieved by a highly protective sunscreen formulation containing 3 filters and reflective pigments (sun protection factor 34). Results indicate that, for the same minimal erythema level, SBC counts do not significantly differ between protected and unprotected skin, showing that the very high efficacy demonstrated against actinic erythema also extends to UV-induced skin damage.

Literature on the biological (mutagenesis) and molecular (DNA lesions and their cellular processing) events resulting from exposure of cells to solar ultraviolet and visible radiations is discussed. The problems encountered with research in this area are presented. Our sparse understanding of the complex mixture of events caused in cells by solar radiation and the mechanisms subserving these events is outlined.

Five females with nickel contact allergy and longstanding hand dermatitis were treated with oral methoxsalen and a series of whole-body UVA irradiations with a cumulative UVA dose of 30 to 58 J/cm2. Lymphocyte stimulation to nickel sulphate was determined prior to PUVA therapy, and monitored during the treatment and at 1 year after treatment. In 4 patients the cutaneous threshold to nickel sulphate patch testing was determined immediately post-PUVA and at 1 year. In all cases, the dermatosis cleared during the PUVA treatment. In 2 patients the immediate post-PUVA skin nickel reactivity was low compared with the 1-year follow-up value, while in 2 patients a progressive diminution of the skin reactivity was noticed. One patient was in clinical remission and had negative skin test at 1-year follow-up. In spite of diminished cutaneous sensitivity and/or clinical remission, the sensitivity of blood lymphocytes to nickel was approximately the same or increased, as determined by the lymphocyte transformation test. Thus no evidence was found to indicate that systemic, nickel-specific suppressive immune regulative mechanisms would have been activated by the treatment.