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Vitiligo treatment.
... The total number of treatments required is between 50 and 300. Darker skin types show maximal responses to PUVA and repigmented areas can remain stable during decades, but if therapy is stopped, partial repigmentation may reverse (17,30). In all patients on oral PUVA, the recommendation is to wear protective sunglasses for 12-24 h after the treatment. ...
Vitiligo is a skin disease having an impact on the quality of life. Phototherapy or photochemotherapy are the first-line treatment choices in generalized vitiligo and are among the most effective treatment modalities either alone or in combination with other therapies. Treatment methods with ultraviolet include oral / topical psoralen plus UVA (PUVA), psoralen plus sunlight (PUVAsol), UVA, broadband UVB, narrowband UVB, excimer laser, monochromatic excimer light and sunlight. This review focuses on the modalities, principals and studies of UV treatment in vitiligo.
Ultraviolet radiation-based therapies of vitiligo are the most potent options for its treatment. This chapter shall provide detailed information about the role and application of phototherapeutic regimens. Initially, the disease will be defined and compared to other conditions in the differential diagnosis. The main portion of this chapter will concentrate on ultraviolet phototherapy and photochemotherapy. Adjunctive and combined therapeutic modalities are discussed, as well as alternative treatment options.
Dieses Kapitel beschäftigt sich mit der Anwendung von Photochemotherapie und Phototherapie bei Vitiligo. Zunächst wird die Krankheit definiert und werden Differentialdiagnosen und assoziierte Phänomene beschrieben. Allgemeine therapeutische Maßnahmen und Alternativen zu phototherapeutischen Verfahren folgen. Den Hauptteil bildet die Beschreibung der praktischen Durchführung und Wirkung der Bestrahlungsbehandlung mit oder ohne Photosensibilisator sowie von kombinierten Therapieformen.
Photochemotherapy (PUVA) combines the use of pso-ralens with long-length (320-400 nm) ultraviolet radiation (UVA), producing a beneficial effect that cannot be reached by the two components separately. Psoralens can be administered orally or topically (solutions, creams, or bath) with posterior exposition to UVA.
Photosensitization can be defined as a process in which a reaction to normally harmless radiation is induced by the introduction of a specific radiation-absorbing substance (photosensitizer) that causes another component (substrate) to be changed by the radiation. Photosensitivity is characterized by phototoxic and photoallergic effects. Drugs and chemicals may interact with UV to induce photosensitivity. Photosensitive disorders may be classified as those entirely caused by solar exposure and the photoaggravated disorders. Those in the former category include polymorphic light eruption, hydroa vacciniforme, actinic prurigo, solar urticaria and chronic actinic dermatitis. Photosensitivity can be diagnosed by photo test, photo patch test and photo drug test. Recently the photodynamic therapy (PDT) is used for the treatment of cancers. There are various photosensitizers such as photofrin, foscan, 5-Aminolevulinic acid (5-ALA) etc which used in photodynamic therapy. Photosensitizers are also used to treat vitiligo, microbial infections and acne.
Vitiligo is a common skin disease characterized by loss of normal melanin pigments in the skin and its pathogenesis is still unclear. Treatment modalities include psoralen plus ultraviolet A, narrow-band ultraviolet B (NB UVB) phototherapy, topical and systemic steroids, topical calcineurin inhibitors, topical vitamin D analogues in monotherapy or in association with phototherapy, and surgical treatment. NB UVB (310-315 nm) radiation is now considered as the 'gold standard' for the treatment of diffuse vitiligo, and treatment with two recently introduced UVB sources that emit 308 nm wavelengths, the 308 nm xenon chloride (XeCl) excimer laser and the 308 nm XeCl excimer light, has also been reported to be effective and might be the treatment of choice for localized disease: this treatment modality has been defined as 'targeted phototherapy.'
There is good evidence that 8-methoxypsoralen is photocarcinogenic in psoriatic patients undergoing long-term photochemotherapy (PUVA) in the U.S.A. However, this conclusion has not been supported by two major European studies which have indicated that PUVA is a tumour promoter of damage initiated by other agents. Variation in PUVA treatment protocols in the U.S.A. and Europe may partly account for the different conclusions. There is much interest in the therapeutic potential of monofunctional psoralens. It is hoped that these may reduce long-term risk. Monofunctional and cross-linking psoralens have been shown to be photocarcinogenic in mouse skin. The relative risk of different compounds may be assessed in the mouse, but it is important to base comparisons on dose protocols that have been shown to be therapeutically effective.
Psoralens and sunlight have been used by the Egyptians and Indians for hundreds of years for the treatment of vitiligo. The combination of oral psoralens and artificial ultraviolet A (PUVA) therapy was approved for the management of severe psoriasis by the Food and Drug Administration in 1982. Since then PUVA therapy has been found to be an effective modality in the treatment of many cutaneous conditions. When properly administered, the major short-term side effects are minimal. The long-term side effects may include an increased risk of squamous cell carcinoma, atypical cutaneous pigmentation, accelerated skin aging, and ophthalmologic abnormalities. By careful patient selection and limiting the cumulative UVA dosage and frequency by using combinations or alternative therapies, these side effects may be reduced. Continued reporting of carefully carried out long-term prospective studies will provide us with more knowledge of the long-term side effects of PUVA. In the meantime, for each patient on PUVA therapy the risk/benefit ratio should be carefully considered.
8-Methoxypsoralen in combination with long wavelength ultraviolet light is employed for the treatment of several cutaneous disorders, such as psoriasis, vitiligo and mycosis fungoides. It is common to attribute the efficacy of the photochemotherapy to the formation of psoralen DNA photoadducts. Thus, the main research effort has been directed towards the elucidation of nucleic acid photochemistry and related subsequent events (mutagenicity, toxicity). However, psoralens have been shown to undergo photoaddition reactions with other cellular components. In this review the status of psoralen-DNA photobiology is briefly summarized. The main focus, however, is on a survey of psoralen photochemical modification of proteins and the ways by which these additional photobiological events can impact the antigenicity and potentially immunogenicity of treated cells. Some preliminary results show the extent of psoralen-amino acid photoadduct formation and their impact on enzymatic processing.
A rapid gas chromatographic assay has been developed for the separation and determination of khellin in human serum. Using a DB-17 capillary column and a simple chloroform extraction, khellin and an internal standard, trioxsalen, were separated from endogenous substances without further clean-up. Spiked serum samples in the range 0.11-1.1 micrograms/ml were assayed and a linear calibration curve obtained.
Vitiligo is a common idiopathic acquired or inherited disease with loss of normal melanin pigments and functioning melanocytes from otherwise healthy looking skin. Clinically, vitiligo can be grouped into several unique types (Figs. 1, 2). The localized type includes focal and segmental vitiligo. Generalized types are vitiligo vulgaris, acrofacial vitiligo, and universal vitiligo. A genetic predisposition is considered.13 and 46
The leukoderma of vitiligo does not contain any functioning melanocytes.35 Pathogenesis of vitiligo leukoderma is still unknown, but currently three major theories have been proposed.11 One is the neural theory, that presupposes that there is a chemical mediator liberated at the nerve endings that destroys the melanocytes or inhibits the production of melanin pigments. A second theory proposes that melanocytes are destroyed either by themselves through generation of melanin precursors (or metabolites) or by surrounding keratinocytes that liberate chemicals that cause oxidative stresses. In normal melanocytes there is some defense or scavenging mechanism against these cytotoxic melanin precursors or chemicals generating oxidative stresses, but there is a defect in this defense process (mechanism) in vitiligo melanocytes (Fig. 3).26 The third theory is the autoimmune hypothesis, which speculates that vitiligo is an autoimmune disease. Vitiligo patients develop autoantibodies against melanocytes.9 and 39 In metastatic melanoma patients, depigmented macules similar or identical to vitiligo leukoderma can be developed by destruction of melanocytes through the interaction with cytolytic T-lymphocytes, which are activated by tyrosinase gene family proteins7 and 56 and other melanogenesis-associated proteins.4
Photochemotherapy has been the most successful treatment of vitiligo to date. In this study we tried to evaluate the efficacy, safety and patient acceptability of photochemotherapy (PUVA, or psoralen and ultraviolet A, therapy) for vitiligo patients treated in King Khalid University Hospital over the period of 1987-1994. The treatment success strongly depended on the number of treatments. More than 75% repigmentation was achieved in 42% of the patients who received 100 to more than 200 treatments. Unfortunately, however, only 27% of the patients received this number of treatments. Reasons for the failure of our patients to continue treatment to successful repigmentation, and recommendations for correction of this failure, are discussed.
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