Treatment of nevus of Ota by Q-switched ruby laser.

BACKGROUND: There are few reports on therapy for nevus of Ota. Moreover, traditional treatments are largely palliative or risk permanent pigmentary changes and/or scarring. OBJECTIVE: The efficacy of the Q-switched ruby laser (694 nm, 40 nsec) as a therapy for nevus of Ota was investigated. METHODS: Nine nevi or portions thereof were irradiated up to six times with 4.5 and/or 7.5 J/cm2 at a mean exposure interval of 3 weeks. Sequential skin biopsy specimens were processed for light microscopy, immunohistochemistry, and electron microscopy. RESULTS: Cosmetic improvement occurred at both doses in the irradiated parts of the six nevi available for follow-up. No appreciable difference was noted between single and multiple treatments. There was no gross scarring. Light microscopy revealed dose-related immediate injury with more melanophages and fewer dermal melanocytes after irradiation in comparison with control areas. Electron microscopic distinction between dermal melanocytes and melanin-laden macrophages was difficult. A monoclonal antibody to human melanosome-specific antigen type 1 (HMSA-1) was used to distinguish between the two cell populations. CONCLUSION: Our findings suggest that the Q-switched ruby laser is useful for treating nevus of Ota.

Effect of hypoxia on sunburn cell formation and inflammation induced by ultraviolet radiation.

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.

Effect of temperature on the cutaneous phototoxic reaction to 8-methoxypsoralen in human skin.

Phototoxic erythema in human skin resulting from topical 8-methoxypsoralen (8-MOP) + UVA exposure was examined at different skin temperatures. Increased skin temperature resulting from radiant or conductive heating during UVA exposure decreased the ensuing phototoxic response. Preheating the skin for 30 min prior to UVA exposure caused a greater decrease in phototoxicity.

Effect of cutaneous hypoxia upon erythema and pigment responses to UVA, UVB, and PUVA (8-MOP + UVA) in human skin.

The effect of oxygen deprivation upon UVA-, UVB-, and PUVA-induced pigment and erythema responses in normal human skin was examined. Before exposure, varying degrees of hypoxia in the skin of the forearm were achieved by inflating a sphygmomanometer cuff applied to the upper arm. After the transcutaneously measured pO2 had stabilized, sites on the inner forearm were exposed to UVA, UVB, or 8-MOP + UVA radiation, to determine dose thresholds for the induction of erythema and pigmentation at different cuff pressures. Inflation of the cuff to greater than systolic pressure completely inhibited immediate and delayed pigment responses (IPD, DT) to UVA doses greater than 10 times the normal pigmentation threshold dose. UVA-induced delayed erythema responses were partially inhibited by cuff inflation: 2.7 times the minimal erythema dose of UVA was necessary to cause an erythema response when exposure occurred during vascular occlusion. In contrast, erythema and pigment responses to UVB and PUVA were unaltered by cuff pressures exceeding systolic pressure during exposure. Inhibition of UVA-induced erythema and pigment responses by vascular occlusion were reversed by the transcutaneous diffusion of 100% O2. These findings indicate that the cutaneous responses to UVA and UVB occur by separate pathways differing with respect to O2 dependence. Our findings agree with those of other studies which indicate that PUVA-induced phototoxicity and melanogenesis are not O2-dependent.

Contribution of topical tar oil to ultraviolet B phototherapy for psoriasis.

A bilateral comparison study of twenty-two outpatients with psoriasis assessed clearing experience and remission time on halves of the body to which tar oil and oil vehicle (an emollient) were applied twice daily. In addition, both sides were treated three times a week with suberythemogenic doses of ultraviolet B radiation. Of the eighteen patients who complied with the protocol, fourteen (78%) had clearing. There was no significant difference between body halves with regard to the number of treatments to clearing, the dose of ultraviolet B to clearing, or the remission time (p greater than 0.2, all comparisons). Our data indicate with 95% confidence that using tar oil in conjunction with ultraviolet B phototherapy reduces the average total ultraviolet B dose required for clearing by a maximum of 9%, in comparison with using oil vehicle and ultraviolet B. These findings suggest that there is insufficient evidence for substantial clinical benefit to recommend tar oil use in conjunction with outpatient ultraviolet B phototherapy for psoriasis.

Tanning.

Cutaneous pigment responses to ultraviolet radiation are outlined in this article. The responses induced by different wavebands are compared, and the protection against further exposure that is conferred by different types of tanning is discussed. The term "tanning" is used here to denote the spectrum of adaptive changes in the skin resulting from ultraviolet exposure and is not applied exclusively to increased melanin pigmentation.

Cutaneous phototoxicity due to psoralens.

Psoralen phototoxicity has several features which distinguish it from other cutaneous responses to UV radiation, with or without an exogenous photosensitizing agent. Erythema resulting from psoralen phototoxicity shows a longer latent period between irradiation and onset, during which no visible cutaneous changes are present. The dose-response curve is steeper, with blistering reactions occurring in some subjects after as little as three to four times the minimum phototoxic dose of UV radiation at 320-400 nm (UVA). The acute phase of psoralen phototoxicity is followed by a more marked increase in epidermal pigmentation than is seen after most other phototoxic reactions or following UV irradiation alone. The pathways leading to the development of cutaneous phototoxicity have not been identified. The importance of the cross-linking of DNA as the initiating event is suggested but not proved by comparative data on different psoralen compounds with different cross-linking abilities and by wavelength-dependent selective photochemistry. The subsequent pathways leading to erythema and the mediators which are liberated have not been identified. In contrast to erythema induced by UVA and UV at 290-320 and at 220-290 nm (UVB and UVC, respectively), no evidence for the involvement of prostaglandins has been demonstrable. Histopathologic studies show changes in the epidermis and dermis, with damage to keratinocytes and an inflammatory infiltrate in the dermis, both of which occur later and are of longer duration than the damage induced by UVA, UVB, or UVC alone. Despite the widespread application of psoralen phototoxicity in humans in the form of PUVA treatment, much work remains to be done before we can elucidate the important mechanisms and pathways leading to the inflammatory and therapeutic responses which are induced in the skin. Improvement of our knowledge in this area is central to the evolution of safer and more effective forms of photochemotherapy.

Prolonged skin photosensitization induced by methoxsalen and subphototoxic UVA irradiation.

Topical 8-methoxypsoralen (8-MOP) was used to briefly provide free psoralen sufficient for marked cutaneous photosensitization, but only a small dose of UVA was delivered initially, in an effort to produce many monoadducts but few crosslinks. After ample time for clearance of the remaining free psoralen a second UVA exposure was delivered. The second exposure should not have generated any additional monoadducts in the absence of free psoralen, but the remaining monoadducts could be converted to crosslinks. The observation of a prolonged persistent UVA-photosensitive state caused by prior, very small doses of UVA given while free 8-MOP was present strongly suggests that psoralen-DNA crosslinks per se initiate much of the phototoxic effect of 8-MOP on skin, and that monoadducts induce much less acute inflammatory response. Because erythema was studied as the end point, the data say nothing about relative contributions of monoadducts vs crosslinks in causing mutagenesis, hyperpigmentation, therapeutic or other cutaneous responses. Other explanations for the induced persistent photosensitive state are also possible, but less tenable or entirely hypothetical.

Sunscreens block the induction of epidermal ornithine decarboxylase by ultraviolet-B radiation: a new way of evaluating sunscreen efficacy in vivo.

Two proprietary sunscreen preparations containing para-aminobenzoic acid and sulisobenzone, respectively, were tested for their ability to block the induction of ornithine decarboxylase by medium wavelength ultraviolet radiation (UV-B) in the epidermis of the hairless mouse. Both preparations were effective, the sunscreen treated animals requiring more radiation for ornithine decarboxylase induction. The UV dose-dependent gradients were reduced by a mean factor of 7.35 (sulisobenzone) and 15 (PABA). These figures correlate well with other in vivo sunscreen assays. This new method provides a simple and reproducible way of evaluating sunscreens in vivo.

Epidermal ornithine decarboxylase activity and thymidine incorporation following treatment with ultraviolet A combined with topical 8-methoxy-psoralen or anthracene in the hairless mouse.

Epidermal thymidine incorporation, as a measure of DNA synthesis, and ornithine decarboxylase activity were estimated in hairless albino mice following phototoxic reactions induced by topical anthracene + UV-A, and topical 8-methoxypsoralen (8-MOP) + UV-A. Both treatments caused depression of epidermal thymidine incorporation to 26% of control values at 4 h; this depression persisted through 24 h following 8-MOP + UV-A. Animals treated with anthracene + UV-A showed a fourfold increase in thymidine incorporation at 48 h, declining at 72 and 96 h; after 8-MOP + UV-A increased thymidine incorporation was observed between 4 and 10 days, when a plateau of 96 h duration was observed. After treatment with anthracene + UV-A, epidermal ornithine decarboxylase activity (ODC) was maximal at 4 h, and exhibited a rapid decline, with normal levels at 48 h. Following 8-MOP, UV-A dose-dependent ODC induction occurred: this was later than that induced by anthracene + UV-A with no detectable activity at 4 or 12 h, and maximum activity at 24 h, the elevation persisting through 96 h. The relationship between ODC induction and epidermal hyperproliferation following these treatments is discussed.