Search

Zusammenfassung.Der vorliegende Beitrag hat zum Ziel, den praktisch tätigen Ärzten und Ärztinnen einen Überblick über die im Rahmen der physiologischen Hautalterung (Turgorverlust, Klimakterium) bzw. beschleunigter Hautalterungsprozesse (Photoaging, Rosazea etc.) auftretenden dermatologischen Probleme zu geben. Im Zusammenhang mit der Lichtalterung ist bei neu auftretenden Veränderungen ein besonderes Augenmerk auf die Abgrenzung benigner Läsionen wie Lentigines von malignen Tumoren zu richten. Die nachfolgenden Ausführungen sollen es den primär versorgenden Ärzten und Ärztinnen ermöglichen, den kosmetologischen Bedürfnissen ihrer Patienten bei nicht-malignen aktinischen Hautschäden gerecht zu werden und abgestufte Behandlungsvorschläge zu machen. Zudem sollen die Angaben als Wegleitung dienen, um die Patienten in Zusammenarbeit mit dem Dermatologen hinsichtlich ästhetisch-dermatologischer Methoden zu beraten bzw. die richtigen Massnahmen bei Verdacht auf Hautmalignom ergreifen zu können.

Treatment of melanoma remains a challenge in advanced disease. Recently, the molecular differentiation in BRAF-mutated, NRAS-mutated and c-kit-mutated melanomas led to new treatment strategies. Different trials show that imatinib or nilotinib lead to meaningful responses in c-kit-mutated melanoma patients. There are little published data on sequential inhibition using these two drugs in melanoma. We describe the sequential use of imatinib after nilotinib in a c-kit-mutated melanoma patient, who progressed on interferon, Allovectin, dacarbazine, nilotinib and ipilimumab, and was finally treated with the c-kit inhibitor imatinib. From July 2011 to September 2011, the patient received ipilimumab (four doses with 3 mg/kg). Clinical assessment after immunotherapy showed disease progression. Therefore, a treatment change to imatinib 800 mg daily was made from February 2012 to May 2013. Under this treatment, the patient showed a partial response as per the RECIST criteria. The present lesions continued responding (computed tomography scans: May 2012–March 2013). Unfortunately, in October 2012, new brain metastases developed. Nevertheless, the use of c-kit inhibitors in c-kit-mutated melanoma patients seems to be a promising treatment option. Furthermore, a delayed response to ipilimumab after 6 months could also have led to or supported the partial response in this case. However, when two biologically similar compounds are administered in a melanoma patient and the tumour mass shows progressive disease upon administration of the first agent, an additional progression with no effect may be expected when the second one is used. This case shows, in contrast, that the use of imatinib after progression upon nilotinib can be beneficial.

Melanoma today is considered as a spectrum of melanocytic malignancies characterised by clinical and molecular features, including targetable mutations in several kinases such as BRAF or c-KIT. The successful development of therapies targeting these mutations has resulted in new specific treatment options. These include vemurafenib, dabrafenib, trametinib, imatinib and other kinase inhibitors that are selected when the respective mutation is present.