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• W2000100200 abstract "A lot has happened in the field of photodermatology over the last 125 years, during the existence of the BJD. In this period, good descriptions were published on several photodermatoses we now take for granted. An example is polymorphous light eruption, a term first used by Rasch in 1900,1 although the same condition was described earlier, before the BJD was established, by Willan as eczema solare and by Hutchinson as prurigo aestivalis. Another example is the first report on the induction of urticarial lesions by sunlight in 1904 by Merklen.2 In 1912, our colleague Meyer-Betz injected himself with haematoporphyrin and exposed his skin to the sun, thus demonstrating that the combination of a photosensitizing substance and sun exposure can induce a skin reaction that each of the two components separately would not induce, which is the definition of a drug-induced photosensitivity. He published this experiment in 1913.3 The first description of a phytophotodermatitis dates from 1928 by Oppenheim.4 In 1939, Epstein made the distinction between a dose-dependent phototoxic reaction and a nondose-dependent photoallergic reaction.5 The photopatch test was introduced in 1941 by Burckhardt.6 In the description of photodermatoses the U.K. played an important role. In 1961, Magnus, Jarrett, Prankerd and Rimington described a case of porphyria with a new type of light sensitivity, solar urticaria being the presenting symptom. In contrast with porphyria cutanea tarda there was prompt erythema and wealing instead of a delayed reaction. A diagnosis of porphyria was confirmed by the increased faecal coproporphyrin and protoporphyrin excretion. The urinary porphyrin was normal, which distinguished this condition from congenital porphyria. The red blood cells were found to contain grossly abnormal amounts of protoporphyrin and coproporphyrin. On phototesting with a quartz–xenon monochromator an abnormal wealing response was obtained between 360 and 450 nm. In view of the known increase of erythrocyte porphyrins in lead poisoning, lead in the patient's blood and urine was determined and these were within the normal range. The authors suggested the name ‘erythropoietic protoporphyria’ for this new condition.7 Also in 1961, Wilkinson published an article in the BJD describing photosensitivity in patients who developed contact and photocontact dermatitis due to soaps containing tetrachlorsalicylanilide as an antimicrobial agent.8 In the majority of the patients this photosensitivity to halogenated salicylanilides was transient, but in some it persisted for years, even after contact with the photoallergens was eliminated. The patients with persistent photosensitivity were called persistent light reactors. Later on, other patients were reported with the same clinical pattern and with a similar severe and persistent photosensitivity but without clinical photocontact dermatitis, although some of these patients had positive photopatch tests. These conditions were called photosensitive eczema by Ramsay and Kobza Black,9 or chronic photosensitivity dermatitis by Frain-Bell et al.10 Some of these patients evolved into a stage with more oedema and with extensive infiltration, which was difficult to differentiate histologically from mycosis fungoides and was called actinic reticuloid by Ive et al.11 Because the clinical picture is nearly the same for all of these conditions and because actinic reticuloid is only a histological variant, Hawk and Magnus in 1979 proposed the term ‘chronic actinic dermatitis’ to resolve the confusing terminology.12 Later on it turned out that these patients are not at an increased risk of developing lymphoreticular or other malignancies.13 Nearly all of these articles were published in the BJD. In the meantime, many other interesting articles on photodermatoses, such as erythropoietic protoporphyria,14 congenital erythropoietic porphyria15 and Smith–Lemli–Opitz syndrome,16 just to mention a few, have been published in the BJD. The evolution in photoprotection in the last 125 years has been at least as important as the evolution in the description of photodermatoses. Photoprotection became possible as soon as one realized what went wrong. In 1893 Bowles published an interesting article in the BJD suggesting that sunlight could be responsible for skin cancers: ‘If the sun's rays will produce sunburn, erythema, eczema solare, inflammation, and blistering, it is clearly capable of producing deep and intractable ulcerations of a low and chronic nature.’17 One year later, in 1894, Unna discovered the relationship between sun exposure and skin ageing, and he also associated the severe degenerative changes on the exposed areas of sailors’ skin with the development of skin cancer.18 In 1906–7, Dubreuilh was the first to establish a clear-cut relationship between skin cancer and solar exposure.19 Until then, photoprotection was always a question of avoiding sun exposure, looking for shade and wearing appropriate clothing, until Hausser and Vahle in 1922 carried out the first detailed action-spectrum studies for erythema and pigmentation in human skin.20 They showed that erythema and pigmentation depend on the wavelengths of the ultraviolet (UV) radiation and are due mainly to wavelengths shorter than 320 nm. It was soon realized that the skin could be protected by filtering out these specific wavelengths, which resulted in a growing interest in sunscreen agents. The first commercially available sunscreen appeared on the market in 1928 in the U.S.A.21 During the Second International Congress on Light in Copenhagen in 1932, Coblentz proposed to divide the ultraviolet spectrum into three spectral regions: UVA, UVB and UVC.22 At that time only ‘UVB’ filters were available, and this remained so for a long time. In 1956 Schulze proposed testing commercially available sunscreens by giving them a protection factor,23 and in 1974 Greiter popularized the concept of the sun protection factor.24 Real UVA filters became available only in 1979. The evolution in phototherapy was already explosive from the beginning of this 125-year period. In 1893 Finsen discovered that smallpox could be treated with red light with its heat rays filtered out. This was the start of his research into the treatment of lupus vulgaris using filtered sunlight. From 1897 on he also used a new carbon arc lamp in combination with quartz filters. Between 1895 and 1901, Finsen treated 804 patients and kept detailed records of his treatments. In 1901 he published his therapeutic results, and at the end of 1903 he received the Nobel Prize for Physiology or Medicine.25 It was the only Nobel Prize ever given for a dermatological project. Finsen, and also his coworkers, believed that the shorter UV rays were the most efficient wavelengths in the treatment of lupus vulgaris. A century later Møller, Kongshøj, Philipsen, Thomsen and Wulf from Copenhagen examined the equipment Finsen used and found a lack of shorter UV wavelengths. The therapeutic effect could, therefore, not be due to UVB, as Finsen thought, but had to be related to the longer UVA rays and was probably a photodynamic therapy effect, caused by the presence of coproporphyrin III in Mycobacterium tuberculosis.26 When in 1912 Kromayer constructed a quartz lamp with a high UV output and with a water cooling system, it became possible to treat different skin diseases.27 During World War I from 1914 to 1918 the soldiers’ traumatic ulcers were treated by exposure to natural sunlight or to quartz lamps, and this was done in Germany, the U.K., France and Italy.28 When in 1923 Rollier's textbook on heliotherapy was translated from French into English, the use of sun exposure in thermal stations in the treatment of tuberculosis became increasingly popular.29 In 1925 Goeckerman published his results using coal tar in combination with UV exposure from a high-pressure mercury lamp in the treatment of psoriasis,30 and for about half a century this was the most popular form of phototherapy in dermatology. In 1953, Ingram combined this treatment with the topical application of dithranol.31 Another major step forward in the history of phototherapy was the introduction of photochemotherapy and the use of total-body-irradiation cabins in 1970. Irradiation cabins had been described previously.32-34 Certain plant extracts in combination with sun exposure had also been used long before to treat vitiligo.35 After the isolation of the active ingredients of these plants as 8-methoxypsoralen and 5-methoxypsoralen, the first trials in patients with vitiligo with 8-methoxypsoralen and sun exposure started.36-38 Much later, topical 8-methoxypsoralen was used in combination with black light UVA tubes in the treatment of vitiligo.39 In the 1970s Mortazawi used the same type of UVA tubes in a total-body-irradiation cabin with topical 8-methoxypsoralen for the treatment of psoriasis.40, 41 In 1974 Parrish et al. reported the use of a new type of high-intensity UVA tube in combination with oral 8-methoxypsoralen in the treatment of psoriasis.42 This treatment was much more effective and was called photochemotherapy or PUVA treatment. It was a revolution in the treatment of psoriasis and stimulated interest in phototherapy in the same way as had Finsen's treatment of lupus vulgaris. In 1978 Wiskemann proposed an irradiation cabin with broadband UVB tubes as an alternative for PUVA in the treatment of psoriasis,43 but this was less efficient. Another breakthrough came in 1988 when the more efficient narrowband UVB phototherapy was introduced for the treatment of psoriasis by van Weelden et al.44 and Green et al.45 Both articles were published in the BJD. The last major step forward in phototherapy was the introduction of photodynamic therapy for actinic keratosis and superficial basal cell carcinoma in 1990 by Kennedy, Pottier and Pross.46 All this illustrates that in photodermatology the sun never sets. May the BJD also shine as never before in the next 125 years." @default.
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• W2000100200 date "2014-11-01" @default.
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• W2000100200 title "Photodermatology over the past 125 years" @default.
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