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were obtained on-site. These were weighted using the SCUP-h

action spectrum,9 which is an estimate of the wavelength

dependency of human skin carcinogenesis. In order to place

the derived values in context, results were compared with

similar sunlight data. These have been reanalysed to derive the

relative exposure risk per minute (Fig. 1).

It can be seen that different tanning units carry different

risks. The sunbeds have approximately the same carcinogenicrisk, minute for minute, as local summer sunlight. It is of

signicance that the stand-up tanning units, which contain a

signicant UVB component, are equivalent to the greater risk

seen with Mediterranean sunlight. According to McGinley

et al.1 the relative UVB in sunbeds/Glasgow sunlight/

Mediterranean sunlight is 075 : 1 : 3. These ratios are similar

to the values in Figure 1.

These results show that all tanning units are potentially

harmful and that the stand-up type has a much greater risk

than has been generally appreciated. We have quantied the

risk per minute of exposure to an articial tanning unit using a

skin cancer model.9 The actual harm caused to sunbed

customers will depend on usage and may also be inuenced by

tanning efciency. Exposure time during each session is

usually much shorter in a stand-up unit than a traditional

sunbed. Public education programmes should be developed in

the light of these ndings.

Photobiology Unit, University of Dundee, H.MOSELEY

Ninewells Hospital and Medical School, M.DAVIDSON*

Dundee DD1 9SY, U.K. J.FERGUSON

*Public and Environmental Health Protection,

Perth and Kinross Council,

Perth, U.K.

E-mail: H.Moseley@dundee.ac.uk

References

1 McGinley J, Martin CJ, MacKie RM. Sunbeds in current use in

Scotland: a survey of their output and patterns of use. Br J Dermatol

1998; 139: 42838.

2 Moseley H, Davidson M, Ferguson J. A hazard assessment of

articial tanning units. Photodermatol Photoimmunol Photomed

1998; 14: 7987.

3 Swerdlow AJ, Weinstock MA. Do tanning lamps cause melanoma?

An epidemiological assessment. J Am Acad Dermatol 1998; 38:

8998.

4 Setlow RB, Grist E, Thomson K, Woodhead AD. Wavelengths

effective in induction of malignant melanoma. Proc Natl Acad Sci

USA 1993; 90: 666670.

5 Freeman SE, Gange RW, Sutherland JC. Production of pyrimidine

dimers in human skin exposed in situ to UVA irradiation. J InvestDermatol 1987; 88: 4303.

6 Peak MJ, Peak JG, Carne BA. Induction of direct and indirect single

strand breaks in human cell DNA by far and near ultraviolet

radiations: action spectrum and mechanisms. Photochem Photobiol

1987; 45: 3817.

7 Norris JFB. Local councils should remove sunbeds from leisure

centres. Br Med J1996; 313: 9412.

8 Health and Safety Executive. Controlling health risks from the use of

UV tanning equipment. IND (G) 209. Health and Safety Executive,

1995.

9 de Gruijl FR, van der Leun JC. Estimate of the wavelength

dependency of ultraviolet carcinogenesis in humans and its

relevance to the risk assessment of a stratospheric ozone depletion.

Health Phys 1994; 67: 31925.

Porphyria cutanea tarda presenting as solar urticaria

SIR, We describe an unusual presentation of porphyria cutaneatarda (PCT) in a 66-year-old man referred with two,

apparently separate, skin disorders. A retired joiner abruptly

became photosensitive in Spring 1997. On exposure to

sunlight, either direct or transmitted through window glass,

thin clothing or clouds, he experienced immediate `stinging'

redness with wealing on exposed sites. These features subsided

within 10 min following sunlight avoidance. Dark lm applied

to the side window of his car and the use of dark-coloured

gloves increased his sunlight tolerance.

On examination, his exposed skin (face, `v' of neck and back

of hands) was normal and bruising, scarring, blistering,

hyperpigmentation, hypertrichosis and milia were not present.

Five months prior to the onset of photosensitivity, he had

developed a pruritic, `eczematous' eruption with patches onhis limbs that persisted despite treatment with a potent topical

steroid and oral antibiotics. Examination of the arms and legs

revealed bilateral discoid pattern eczema.

He was known to have an alcohol-related peripheral

neuropathy as well as hypertension which was treated with

bendro uazide. This drug was stopped for 1 month without

apparent benet for either of his skin complaints. Overall, his

clinical features were suggestive of idiopathic solar urticaria

and coexistent discoid eczema.

Monochromator phototesting, as previously described,1

provoked urticaria at 400630 and 430630 nm wavebands

(Table 1). A porphyrin plasma scan showed an abnormal peak

at 615nm, suggestive of PCT.

2

His urinary uroporphyrinswere elevated at 824mg/24h (normal 041). Urinary

coproporphyrin excretion was within normal limits. A red

blood cell porphyrin scan and free erythrocyte porphyrin

concentration were normal. His aminotransferases were

elevated: alanine aminotransferase 60 U/L (normal 13 43)

and g-glutamyltransferase 161 U/L (normal 1170). Ferritin

was elevated at 526mg/L (normal 15300). Hepatitis B surface

antigen and hepatitis C antibody tests were negative. Anti-

nuclear factor and anti-Ro and La antibodies were not detectable

in his serum. As the porphyrin plasma scan was positive, tests

for a circulating photoallergen were not performed.

Abstinence from alcohol and fortnightly venesection

produced a rapid resolution of his solar urticaria and

normalization of phototesting and other indices (g-glutamyl-transferase, alanine aminotransferase and ferritin). A total of

75 L of blood was venesected over 8 months. Urinary

uroporphyrins remained marginally elevated. He has minimal

areas of residual discoid eczema.

On presentation, our patient had none of the classical

features of PCT. However, alerted by visible wavelength-

induced urticaria on phototesting, a porphyrin plasma scan

was requested and led to a diagnosis of PCT. Although an

urticarial response can often be induced on phototesting PCT

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patients, PCT presenting as solar urticaria is not described in

standard texts,35 and only one previous case has been

reported.6 Rimington et al. described two PCT patients with an

immediate swelling or urticarial response on sunlight

exposure and, in one, the initial working diagnosis was that

of idiopathic solar urticaria.6

In our patient, the resolution of photosensitivity follow-ing venesection is typical of PCT. Idiopathic solar urticaria

can occasionally respond to plasmapheresis when a

circulating photoallergen is demonstrated. If PCT and

idiopathic solar urticaria were to coexist in this case, the

resolution of the urticarial response might be related to the

removal of a circulating plasma factor rather than a

reduction in uroporphyrin. However, the response of solar

urticaria to plasmapheresis is variable, usually incomplete

and transient, and venesection has not been reported to be

effective.7

Although the coexistence of discoid eczema and PCT might

be coincidental, a dermatitic response has been described as a

prominent feature of PCT in some Egyptian patients.8

However, as both conditions can be associated with excessivealcohol consumption,9 this may have been the cause in our

patient. This man's presentation underlines the importance of

plasma porphyrin scan estimation in patients with solar

urticaria. Not all cases are idiopathic.

Photodermatology Unit, R.S.DAWE

Department of Dermatology, C.CLARK

Ninewells Hospital and Medical School, J.FERGUSON

Dundee DD1 9SY, U.K.

E-mail: c.clark@dundee.ac.uk

References

1 MacKenzie LA,Frain-Bell W. The construction and development of a

grating monochromator and its application to the study of the

reaction of the skin to light. Br J Dermatol 1973; 89: 25164.

2 Gibbs NK, Traynor N, Ferguson J. Biochemical diagnosis of the

cutaneous porphyrias: ve years experience of plasma spectro-

uorimetry. Br J Dermatol 1995; 133 (Suppl. 45): 18 (Abstr.).

3 Black MM, Gawkrodger DJ, Seymour CA et al. Porphyria cutanea

tarda. In: Textbook of Dermatology (Champion RH, Burton JL, Ebling

FJG, eds), 5th edn. Oxford: Blackwell, Scientic Publications, 1992:

23048.

4 Bickers DR, Pathak MA, Lim HW. The porphyrias. In: Dermatology in

General Medicine (Fitzpatrick TB, Eisen AZ, Wolff K et al., eds), 4th

edn. New York: McGraw-Hill Inc., 1993; 1854 93.

5 Braun-Falco O, Plewig G, Wolff HH et al. Porphyria cutanea tarda.

In: Dermatology (Braun-Falco O, Plewig G, Wolff HH, Winkelmann

RK, eds). Berlin: Springer-Verlag, 1991; 9069.

6 Rimington C, Magnus IA, Ryan EA et al. Porphyria and

photosensitivity. Q J Med1966; 141: 2957.7 Hudson-Peacock MJ, Farr PM, Diffey BL et al. Combined treatment of

solar urticaria with plasmapheresis and PUVA. Br J Dermatol 1993;

128: 4402.

8 El-Mofty AM. Cutaneous photosensitivity in Egyptians. Br J

Dermatol 1964; 76: 26877.

9 Higgins EN, du Vivier AWP. Cutaneous disease and alcohol misuse.

Br Med Bull 1994; 50: 8598.

Pseudoporphyria and propionic acid non-steroidal

anti-inammatory drugs

SIR, We were interested to read the recent report by Varma and

Lanigan1 of a patient with nabumetone-induced `pseudopor-

phyria'. We, too, have seen several patients with nabumetone-induced skin fragility, blistering and scarring occurring in

light-exposed sites. Porphyrin assays were normal in all cases

and the abnormal fragility slowly resolved on withdrawal of

the drug. The authors note that this phenomenon is well

documented with other non-steroidal anti-inammatory

drugs (NSAIDs). However, it appears that pseudoporphyria

has been reported only with ibuprofen,2 ketoprofen,3 oxapro-

zin,4 naproxen5 and nabumetone, all of which belong to the

phenylpropionic acid derivative group of NSAIDs. This

suggests that the phenylpropionate group may be acting as

a chromophore responsible for skin damage in the presence of

ultraviolet radiation or visible light. Of all subclasses of

NSAIDs, phenylpropionates have been shown to have the

greatest capacity for phototoxic reactions in vitro.6

Of the drugs reported to cause pseudoporphyria, naproxen is

the most frequently cited. The incidence of this side-effect is

not known, but may be relatively high: for example, in a

prospective study of 74 children with juvenile rheumatoid

arthritis treated with naproxen, 12% developed increased skin

fragility and blistering within 6 months of starting the drug.7

Naproxen and 6-methoxy-2-naphthylacetic acid, the active

metabolite of nabumetone, differ in chemical structure by a

single methyl group. As nabumetone is now widely prescribed

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q 1999 British Association of Dermatologists, British Journal of Dermatology, 141, 573609

Table 1. Results of monochromator

phototesting (doses expressed in mJ/cm2)Waveband Normal lowest MUD Delayed erythemal response

24-h MED (24-h MED)

30565 nm 27 No urticaria 039

335630 nm 1800 No urticaria >3900

365630 nm 8200 No urticaria 12,000

400630 nm 4700 3300 22,000

430630nm >82,000 2700 >39,000a

460630nm >82,000 No urticaria >82,000

MUD, minimal urticarial dose; MED, minimal erythema dose.aHigherdoses were nottestedbecause ofan immediate urticarial responseto doses of#2700mJ/cm2.

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