No abstract

We report 5 cases of photocontact dermatitis due to suprofen, a nonsteroidal anti-inflammatory drug introduced to the Japanese market in 1989, and available as a 1% ointment. The patients developed pruritic eczematous lesions after applying the ointment for from 2 weeks to 3 months. All 5 patients reacted positively to photopatch testing with ultraviolet A (UVA) and suprofen down to 0.1-0.01% pet., and 3 patients showed positive reactions with ultraviolet B (UVB) and suprofen down to 1.0-0.1%. Moreover, all patients showed a cross-reaction with tiaprofenic acid, which has a very similar chemical structure to suprofen. However, there was no cross-reaction between suprofen and ketoprofen. Prescribers should be aware of the existence of photocontact sensitivity due to these drugs.

Chronic actinic dermatitis (CAD) has distinct clinical features different from polymoφhous light eruption (PLE). In order to clarify the difference between CAD and PLE, not only in clinical histories and findings but also in photobiological and histopathological reactions to phototests, we investigated 6 Japanese patients with CAD and performed provocative phototests which are our standardized methods in diagnosing PLE. On provocative phototests in CAD, pruritic papules were reproduced with smaller doses of UVB, at longer hours after irradiation (48-72 h) and they lasted for more days than in patients with PLE. Our study demonstrated that although milder cases of CAD and severe cases of PLE could not be distinguished clearly based on photobiological reactions alone, typical cases of CAD showed completely different provocative phototest results from those of PLE.

An infant boy born to a mother with systemic lupus erythematosus developed multiple morphea and annular erythematous lesions. The annular lesions appeared on his face, back, chest and extremities one month after birth and faded within 7 months. The sclerotic lesions progressed until the age of 6 months and remain on his back, chest, right cheek, the nape of the neck and left shoulder at the age of 3 years. Histological findings in the sclerotic lesions were consistent with scleroderma. Serological tests, performed at 14 months of age, were within normal limits. The mother developed acute SLE and died of cardio-renal failure 8 months after the delivery. It is highly probable that maternal factors transferred through the placenta caused the sclerotic lesions in the infant.

It is a well-known fact among clinicians that sunlight may exacerbate atopic dermatitis (AD), but little is known beyond that. In a preliminary study investigating this phenomenon, 19 patients with AD were selected for phototests. All of them had a normal minimal erythema dose (MED). However, 3 patients (15.7%) demonstrated abnormal cutaneous responses 24-72 h after provocation with ultraviolet light B (UVB). None of the patients had a positive response to pure ultraviolet light A (UVA) irradiation of up to 9 J/cm2. The photobiological results of this study confirm the existence of photosensitivity in AD and indicate that UVB wavelengths are responsible for it.