Twenty-two cutaneous primary melanomas in a patient with high genetic predisposition to melanoma receiving levodopa therapy for Parkinson’s disease
| Autor: | Isabelle Templier, Dominique Leroux, Julie Charles, Marie-Thérèse Leccia, Caroline Robert, Sylvie Lantuejoul, Dimitri Salameire |
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| Rok vydání: | 2009 |
| Předmět: | |
| Zdroj: | Pigment Cell & Melanoma Research. 22:851-853 |
| ISSN: | 1755-148X 1755-1471 |
| DOI: | 10.1111/j.1755-148x.2009.00624.x |
| Popis: | Dear Sir,We report the case of a man who developed 22 mel-anomas between 1999 and 2005. He had phototype IIskin by Fitzpatrick’s classification, and had beenexposed to high levels of solar radiation, working out-doors at a ski resort. He had no familial history of mela-noma. He had been diagnosed with Parkinson’s disease(PD) at the age of 50 yr. Levodopa therapy associatedwith a dopa-decarboxylase inhibitor was introducedfrom the age of 55 yr. His first dermatological examina-tion was performed in 1999 at the age of 58 yr,40 months after the introduction of levodopa, andshowed two atypical pigmented lesions, one located inthe upper part of the back and another on the left flank.Multiple nevi without clinical atypia were also found.Histopathological analysis of the two atypical lesionsrevealed superficial spreading melanomas (SSM). Themelanoma on the back had a 0.48 mm Breslow thick-ness, while the lesion on the left flank had a 2.1 mmBreslow thickness. By that time he had received acumulative dose of 638 g of levodopa. An attempt wasmade to discontinue the use of levodopa because acausal link between levodopa and melanoma inductionhas been hypothetized. However, the treatment waseventually resumed because of neurological deteriora-tion. Over the next 4 yr, he developed 20 additionalprimary melanomas with a Breslow thickness C; c.340C>T], [p.Leu113Leu;p.Pro114Ser]. This mutation leads to the synthesis of amutant p16 |
| Databáze: | OpenAIRE |
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