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We report the third case of prolonged photosensitivity secondary to contact photoallergy to topical ketoprofen, a 2-arylpropionic acid derivative. The patient suffered from persistent photosensitivity for more than 1 year after the withdrawal of ketoprofen with recurrent eruptions on sun-exposed skin areas. This photosensitivity was associated with a persistent decrease in polychromatic and UVA minimal erythemal doses. Photobiological testing revealed cross-reactivity with fenofibrate and benzophenones. Photoallergy to ketoprofen is due to the benzophenone structure or to the very similar thiophene phenylketone of tiaprofenic acid, but not to the arylpropionic function. Thus, fenofibrate, tiaprofenic acid and benzophenones should be avoided by patients with a positive history of photocontact dermatitis to ketoprofen.

This study explores the role played by TGF alpha in estrogen-induced renal tumors. Tumors were induced in male Syrian hamster by chronic administration of diethylstilbestrol (DES). Six experimental groups (n = 5-9) were chronically exposed to DES and sacrificed after 1, 2, 4, 6, 9 and 11 months, respectively. In the course of treatment, the nephrons were the site of an important increase of cell turnover, which was characterized by a process of hyperplasia/dysplasia in proximal tubules preceding the neoplastic transformation. In treated animals and in controls, the analysis of renal tissue by Western blot revealed the presence of a 6 kDa polypeptide crossreacting with anti-TGF alpha antibody. In controls, TGF alpha immunoreactivity was localized in proximal and in distal tubules. Before tumor development (1-4 months), TGF alpha RIA showed an increase of TGF alpha concentration in renal tissue, in parallel with the increased cell proliferation observed in proximal tubules. In addition, Western blot analysis also demonstrated in kidney tissue the presence of a 165 kDa protein displaying the immunoreactivity of EGF/TGF alpha receptor. The receptor immunoreactivity was localized in proximal tubular cells suggesting an involvement of TGF alpha in tubular epithelial growth through autocrine or paracrine pathways. In large neoplasms, immunocytochemistry revealed only clusters of transformed cells intensely stained by the anti-TGF alpha antibody. These cells displayed the appearance of stellate or polyhedric cells infiltrating adjacent neoplastic tissues. Antisera raised against intra- or extracytoplasmic domains of the EGF/TGF alpha receptor were assayed to localize this receptor in the tumors. In contrast with tubular structures, immunoreactivity to EGF/TGF alpha receptor was never detected in tumoral tissue. The apparent absence of EGF/ TGF alpha receptor immunoreactivity in malignant cells seems to exclude an involvement of this growth factor in the tumorigenic process, although it could be involved in tumor neovascularization.

Fixed solar urticaria (FSU) represents an uncommon form of urticaria related mostly to radiation from the ultraviolet (UVB, UVA) and visible spectrum. The exact pathomechanism has so far remained unknown. A 52‐year‐old woman with a 3‐year history of urticated eruptions limited to certain skin areas is presented. Photobiological testing revealed positive reactions limited to the visible light range. The induced lesions appeared only in originally affected skin sites. The particular distribution of whealing supports the concept of specific alteration of mast cells in well defined areas. The clinical findings and the results of phototesting lead to the diagnosis of FSU to visible light. It is recommended to carry out phototesting in patients with FSU in the originally affected skin areas, usually covered and protected by the patient, to avoid false‐negative results. Fexofenadine given in the conventional dosage can prevent recurrences and represents a successful treatment measure when dealing with this peculiar form of solar urticaria.