The arylpropionic acid derivatives (APADs) ketoprofen and tiaprofenic acid can provoke photoallergic dermatitis. Possible cross-reactivity between APADs is of importance in patients using nonsteroidal anti-inflammatory drugs. Because of the similarities in chemical structures, we investigated patients with photoallergy to ketoprofen or tiaprofenic acid, in order to study cross-reactivity between APADs and a possible pattern of cross-reactivity between benzophenone-containing molecules, so as to determine the molecular basis of photoallergy to ketoprofen or tiaprofenic acid. 10 patients with photoallergy to topical ketoprofen, 2 with photoallergy to oral tiaprofenic acid, and 15 control subjects with no history of contact dermatitis from APADs, nor from benzophenone-containing molecules, were photopatch tested in triplicate with ketoprofen, tiaprofenic acid, other APADs (alminoprofen, fenoprofen, flurbiprofen, ibuprofen and naproxen), benzophenone-containing molecules (fenofibrate, oxybenzone, sulisobenzone), and unsubstituted benzophenone. 1 set was irradiated with UVA light, 1 with solar-simulated irradiation and 1 dark control. Tests were read at 2, 3 and 4 days. Patients reacted to both ketoprofen and tiaprofenic acid (12/12), fenofibrate (8/12), oxybenzone (3/12) and unsubstituted benzophenone (11/12), but not to other APADs, nor to sulisobenzone. Tests remained negative in control patients. Photoallergy is due to the benzophenone moiety of ketoprofen, or to the very similar thiophene-phenylketone of tiaprofenic acid, but not to their arylpropionic function. This induces cross-reactivity to fenofibrate and oxybenzone but not to APADs without a benzophenone moiety, which may therefore probably be used in such patients. Unsubstituted benzophenone should be added to standard phototesting series.

Congenital naevocellular naevi (CNN) have classical histological criteria that are thought to allow distinction from acquired naevi. These criteria are mainly the horizontal distribution of melanocytes, forming 'Indian files', and a prominent adnexotropism. In order to check whether the previously described criteria were reliable, we analysed 1349 unselected consecutive cases of naevocellular naevi excised in children under 16 years, during a 54-month period. The slides were analysed in order to determine by histological analysis only if they could be classified as CNN. These results were then compared with the clinical files, in which only the most reliable data from parental and/or medical observations were included. Of the 1349 naevi, 659 had the typical histological criteria of CNN, 32 of them being deep CNN, characterized by massive involvement of the lower dermis and hypodermis. The comparison with clinical data showed that 32 naevi with the histological criteria of congenital naevi were actually acquired, and that 179 naevi present at birth did not fulfil these criteria. This study shows that the classic histological criteria are not absolutely specific and are poorly sensitive as 36% of naevi present at birth lacked the classic criteria. The most specific criteria of true CNN were the involvement of eccrine glands and presence of melanocytes in the septae. In the case of deep CNN which corresponded to large or very large naevi, the clinicopathological correlation was 100%. Deep CNN could easily be distinguished from superficial CNN and often exhibited many histological changes consistent with a complex hamartoma, such as presence of brown fat tissue, abnormal vessels and numerous large terminal follicles. In conclusion, our study suggests that it is not possible to predict, by histological analysis alone, that a naevus was present at birth, except in deep CNN which are likely to be a separate entity among all congenital naevi. Studies dealing with congenital naevus-associated melanoma should take into account the lack of sensitivity of these criteria.

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