[Possibilities of endocavitary therapy with cold ultraviolet rays].
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Tanning and thickening of the epidermis are cardinal defensive responses of human skin to ultraviolet (UV) radiation that lead to increased photoprotection. Earlier studies have shown that skin pigmentation can be used to predict minimal erythema dose and minimal phototoxic dose. In this study it was calculated how much of the increase in photoprotection after 4 weeks of repeated exposure to suberythemogenic doses of either UVA or UVB radiation sources or psoralen plus UVA (PUVA) therapy that was attributable to melanogenesis. The backs of 12 volunteers were exposed to 6 different UVA and UVB radiation sources 9 times during 4 weeks. Skin pigmentation was assessed by skin reflectance measuring. Photoprotection was determined from the minimal erythema dose. Melanogenesis accounted for 63-95% of the increase in photoprotection after 4 weeks of exposure to UVA radiation. Exposure to two UVB sources induced a significant increase in photoprotection but not in pigmentation. Melanogenesis accounted only for 6-11% of the increase in photoprotection after 4 weeks of UVB exposure. The pigmentary and photoprotective responses to PUVA therapy were followed in 14 patients. After 2 weeks of exposure, the increase in photoprotection was significantly higher than predicted from the increase in skin pigmentation. After 4 weeks, melanogenesis accounted for only 36% of the increase in photoprotection. This study shows that melanogenesis accounts for the increased photoprotection after 2 weeks of exposure to UVA radiation, but after 4 weeks other protective mechanisms occur. During suberythemal UVB exposure and during PUVA therapy the importance of skin pigmentation in the overall photoprotection gradually decreases during a 4-week irradiation period.
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Although light therapy has been shown to be effective in the treatment of seasonal affective disorder (SAD), little research has been done to determine which light wavelengths affect treatment outcome. In this triple crossover study the authors compared 1 week of light therapy in which bright (2500 lux), full-spectrum fluorescent light, with and without blockade of the ultraviolet (UV) spectrum, was used with a dim (500 lux) light control in 11 SAD patients. The dim light condition had no significant antidepressant effects as measured by the Hamilton Rating Scale for Depression (HAM-D), the Beck Depression Inventory (BDI), and an atypical depressive symptom (ATYP) score. The UV-light condition significantly reduced HAM-D, BDI, and ATYP scores, whereas the UV-blocked condition significantly reduced only the ATYP score. These results suggest that the UV-spectrum in light therapy may have a differential effect on typical and atypical symptoms in SAD.
Pityriasis versicolor alba is a hypopigmented or depigmented variant of pityriasis versicolor characterized by maculous, partly pityriasiform, scaly depigmented lesions occurring particularly in seborrhoeic areas. Long-persisting hypopigmentation after healing of the pityriasis versicolor was first described by Gudden in 1853. Hypopigmentation and depigmentation were later differentiated as an independent variant of the disease. In 1848, Eichstedt recognized the pathogen-related character of pityriasis versicolor in its hyperpigmented form. Today it is generally accepted that the disease is caused by yeasts of the genus Malassezia, of which nine species are differentiated. It is controversial whether a single species is responsible for the disease. The pathogenesis of depigmentation has not been established. A screening effect by the scale layer as well as toxic effects on pigment synthesis by fungal metabolites have been discussed. With regard to the second mechanism, the newly discovered tryptophan-derived metabolites of M. furfur might be significant. Evidence-based data concerning the therapy of pityriasis versicolor alba do not exist. According to current recommendations, pityriasis versicolor should be rapidly treated with antimycotics, followed by ultraviolet therapy to induce maturation of existent melanosomes and accelerate repigmentation. However, depigmented lesions are difficult to improve by ultraviolet therapy.
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BACKGROUND: Encouraging results of previous uncontrolled trials suggest that calcipotriol may potentiate the efficacy of psoralen plus ultraviolet (UV) A (PUVA) therapy in patients with vitiligo. OBJECTIVES: We performed a placebo-controlled double-blind study to investigate whether the effectiveness of PUVA treatment could be enhanced by combination with topical calcipotriol in the treatment of vitiligo. METHODS: Thirty-five patients with generalized vitiligo enrolled in the study. Symmetrical lesions of similar dimensions and with no spontaneous repigmentation on arms, legs or trunk were selected as reference lesions. In this randomized left-right comparison study, calcipotriol 0.05 mg g(-1) cream or placebo was applied to the reference lesions 1 h before PUVA treatment (oral 8-methoxypsoralen and conventional UVA units) twice weekly. Patients were examined at weekly intervals. The mean number of sessions and the cumulative UVA dosage for initial and complete repigmentation were calculated. RESULTS: Twenty-seven patients (nine women, 18 men; mean +/- SEM age 29.8 +/- 13.5 years) were evaluated. The mean +/- SEM cumulative UVA dose and number of UVA exposures for initial repigmentation were 52.52 +/- 6.10 J cm(-2) and 9.33 +/- 0.65 on the calcipotriol side, and 78.20 +/- 7.88 J cm(-2) and 12.00 +/- 0.81 on the placebo side, respectively (P < 0.001). For complete repigmentation, respective values were 232.79 +/- 14.97 J cm(-2) and 27.40 +/- 1.47 on the calcipotriol side and 259.93 +/- 13.71 J cm(-2) and 30.07 +/- 1.34 on the placebo side (P = 0.001). Treatment with calcipotriol and PUVA resulted in significantly higher percentages of repigmentation for both initial (81%) and complete pigmentation (63%), compared with placebo and PUVA (7% and 15%, respectively). CONCLUSIONS: Our results have shown that concurrent topical calcipotriol potentiates the efficacy of PUVA in the treatment of vitiligo, and that this combination achieves earlier pigmentation with a lower total UVA dosage.
An elderly white man with a long history of psoriasis, previously treated with topical steroids and ultraviolet B (UVB), developed bullous pemphigoid shortly after starting psoralen plus UVA (PUVA) therapy. The eruption spread from the forearms to the arms and neck after phototherapy was discontinued. The clinical features of the 12 reported cases of PUVA-induced bullous pemphigoid are reviewed.
BACKGROUND: St John's wort (SJW) is widely used as a treatment for depression. A phototoxic reaction, due to its content of hypericin, can occur in animals and in cell culture, and has been reported in humans. Hypericin displays absorption within the ultraviolet (UV) A1 spectrum and there may therefore be a potential for phototoxicity if taken during high-dose UVA1 therapy. OBJECTIVES: To assess the phototoxicity risk of SJW ingestion. METHODS: Eleven adult volunteers of skin types I and II were exposed to a geometric dose series of UVA1 irradiation from a high-output source (Dermalight Ultra 1; Dr Hönle, Martinsreid, Germany; irradiance 70-77 mW cm(-2)) on the photoprotected lower back skin at eight 1.5-cm(2) test areas. Irradiation was carried out at baseline and after 10 days of SJW extract 1020 mg (equivalent to 3000 microg of hypericin) daily. Four, 8, 24 and 48 h after each exposure, the minimal erythema dose (MED) and the presence or absence of pigmentation were recorded visually and erythema was assessed objectively with an erythema meter. RESULTS: The median MED and D(0.025), an objective measure of MED, were lower at all time-points after SJW ingestion. The visual erythemal peak (lowest median MED), which was seen at 8 h postirradiation, was lower after SJW (median 14 J cm(-2), range 10-56) than at baseline (median 20 J cm(-2), range 14-56) (P = 0.047). Similarly, the median D(0.025) at 8 h postirradiation was lower after SJW (median 22.0 J cm(-2), range 15.2-53.9) than at baseline (median 33.7 J cm(-2), range 22.9-136.0) (P = 0.014). The MED and D(0.025) were also significantly different at the 48-h and 4-h time-points, respectively. Significance was not reached at the 24-h time-point. Median intensity of postirradiation erythema increased at all time-points after ingestion of SJW. Despite these differences, the maximum slope of the dose-response curve was not increased after SJW ingestion. CONCLUSIONS: These data suggest that SJW extract has the potential to lower the erythemal threshold to UVA1 irradiation in a significant proportion of individuals and highlight the importance of ascertaining a full drug history, including herbal remedies, before initiating UVA1 phototherapy.
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The potentially beneficial effect of 8-methoxypsoralen and ultraviolet A (PUVA) irradiation for treatment of drug-resistant cutaneous manifestations of graft-versus-host disease led us to investigate the effect of this therapy in a larger series of patients with GvHD. To date, 11 patients with histologically demonstrated cutaneous GvHD (acute GvHD grade III-IV in 4 patients, extensive lichenoid chronic GvHD in 6 patients, sclerodermatous chronic GvHD in 1 patient) have received PUVA treatment for 2-24 weeks. All patients have been on CsA for GvH prophylaxis; 5 with mismatched grafts had additionally received methotrexate or monoclonal antibody campath-1 after bone marrow transplantation. Seven patients were on CsA and prednisolone; 2 patients on CsA, prednisolone, and azathioprine; 1 patient on azathioprine and prednisolone; and 1 patient had no immunosuppressive treatment for the duration of PUVA treatment. The 8-methoxypsoralen (0.6 mg/kg bw) was given as photosensitizer before each ultraviolet A irradiation (0.3-8.5 joules/cm2). The only observed adverse reaction was mild nausea. In all patients improvement of cutaneous lesions could be observed with complete response in 5 patients and partial response in 6 patients. Immunosuppressive drugs could be withdrawn in 2 patients and reduced in 8 patients after initiation of PUVA treatment. These findings suggest that PUVA therapy may be a useful adjunct to conventional therapy for cutaneous GvHD.
The ability of photochemotherapy with 8-methoxypsoralen in conjunction with high-intensity long-wave ultraviolet light (PUVA) to stimulate melanogenesis is well known. This effect on the pigmentary system is evidenced by the diffuse tanning of clinically normal skin in PUVA-treated patients with psoriasis and other disorders, as well as by the repigmentation of lesions in vitiligo. It is now recognized that there may be additional pigmentary effects, resulting in clinical lesions such as PUVA mottling, PUVA lentigines, and localized hypopigmentation. We have documented the occurrence of yet another association with PUVA therapy--the paradoxical appearance of widespread hypopigmentation consistent with vitiligo in three PUVA-treated patients, one with psoriasis and two with mycosis fungoides. Histologic and ultrastructural findings are presented.
BACKGROUND: Treatment modalities for granuloma annulare (GA) often remain unsatisfactory or can be accompanied by potentially hazardous side-effects. Psoralen plus ultraviolet (UV) A (PUVA) bath photochemotherapy has been reported to be highly effective in the treatment of GA. Another form of topical PUVA therapy, using 8-methoxypsoralen-containing cream or gel preparations, has been proven to be as effective as bath PUVA therapy in the treatment of palmoplantar dermatoses. OBJECTIVES: To assess the efficacy of cream PUVA photochemotherapy in patients with GA. METHODS: Five patients with GA were treated. The diagnosis was confirmed by pretreatment skin biopsies. Cream PUVA therapy was performed four times a week: the mean number of treatments was 26 (range 17-40) and mean cumulative UVA dose was 55.9 J cm-2 (range 18.2-109.2). RESULTS: Cream PUVA photochemotherapy induced significant clinical improvement (one patient) or clearance (four patients) of GA in all patients. Clearance was documented clinically and histopathologically. CONCLUSIONS: Cream PUVA phototherapy can be highly effective in patients affected by localized forms of GA.
Vitiligo vulgaris is a common disease throughout the world although its pathogenesis is not yet known. The most frequent treatment used for vitiligo is PUVA (psoralen plus ultraviolet A) and topical steroids but against stable refractory vitiligo, various other surgical techniques have been developed such as autografting, epidermal grafting with suction blisters, epithelial sheet grafting, and transplantation of cultured melanocytes. We have discovered a new method using ultrasonic abrasion, seed-grafting and PUVA therapy. The ultrasonic surgical aspirator abrades only the epidermis of recipient sites. This easily and safely removes only the epidermis, even on spotty lesions or intricate regions which are difficult to remove using a conventional motor-driven grinder or liquid nitrogen. Epidermal seed-grafting can cover more area than sheet-grafting, and subsequent PUVA treatment can enlarge the area of pigmentation with coalescence of adjacent grafts. In this article, we provide a general overview of the current surgical therapies including our method for treating stable refractory vitiligo.
Two alternate oral formulations of 8-methoxypsoralen, one liquid and the other crystalline, were evaluated in a double-blind trial for their comparative efficacy in combination with ultraviolet A (UVA) light in the treatment of severe psoriasis. With the liquid formulation a greater proportion of patients achieved a good clinical result within the 20 treatment sessions than patients receiving the crystalline formulation. This difference is even more striking using a more rigorous criterion of clearance. Among all patients who achieved clearance, no significant differences were seen in either the number of treatments required or in the total UVA energy employed between the two groups. The preceding clinical results are discussed in light of published pharmacokinetic data.
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Reflectance spectrophotometry was used to obtain indices of the hemoglobin and melanin content of psoriatic lesions and adjacent clinically normal skin in thirteen patients undergoing photochemotherapy. The pretreatment lesional hemoglobin index was 2.8 times greater than that of adjacent uninvolved skin. With therapy, this index decreased rapidly initially, and during the second or third week approached that of the uninvolved skin. The ratio of lesional and uninvolved skin hemoglobin indices decreased to approximately 1.3, and continuation of PUVA treatment failed to reduce it further. Termination of treatment at this stage, which occurs before clinical resolution, resulted in subsequent clearance of psoriasis. The decrease in the lesional hemoglobin index and the clearance time appeared to be dose-dependent, and, indeed, a more aggressive regimen resulted in approximately 50% reduction in both the number of treatments and the cumulative dose required to achieve a stable hemoglobin index ratio and subsequent clinical clearance.