Palmoplantar Keratoderma Like Drug Eruption Due to Sorafenib
Author(s) -
Nuran Allı,
Sibel Doğan,
Burcu Hazar Tantoğlu
Publication year - 2018
Publication title -
turkish journal of dermatology
Language(s) - English
Resource type - Journals
eISSN - 1308-5255
pISSN - 1307-7635
DOI - 10.4274/tdd.2395
Subject(s) - drug eruption , palmoplantar keratoderma , keratoderma , dermatology , sorafenib , medicine , drug , hyperkeratosis , pharmacology , cancer research , hepatocellular carcinoma
A 69 year-old female patient was admitted to our outpatient clinic for the tenderness of palms and soles and the thickening of the skin under the feet. These complaints lasted for three months and the pain of her feet started to cause difficulty when walking. Medical history revealed that she was on follow-up for a hepatic tumor of unknown origin for three years at oncology department. A malignant transformation was suspected and she was diagnosed hepatocellular adenocarcinoma after a liver needle biopsy 9 months ago. She was given adriamycin chemotherapy for three months. After finishing this treatment, sorafenib therapy was commenced for the last three months. Soon after the initiation of sorafenib therapy, tenderness of palms and soles started. On dermatologic examination, mild palmar erythema and hyperkeratosis along with superficial fissuring on palmar sides of the fingers were noted. Severe hyperkeratotic plaques and nodosities were found especially on lateral plantar surfaces of bilateral feet and on plantar surfaces and pulpas of the third, fourth and fifth toes (Figure 1 and 2). The epidermal changes and sudden onset of painful keratoderma was related to sorafenib use as the complaints correlated with the commence of this treatment. A biopsy was suggested but not accepted by the patient. She was prescribed topical keratolytics and put on follow-up with a slight symptomatic relief after this therapy. Sorafenib is a multi-target tyrosine kinase inhibitor used for unresectable hepatocellular carcinoma and advanced renal carcinoma which decreases cell proliferation by inhibiting intracellular (c-RAF, b-RAF; V600E mutant BRAF) and cell surface kinases [KIT, FMS-like tyrosine kinase-3, RET, vascular endothelial growth factor receptor (VEGFR)-1, VEGFR-2, VEGFR-3, and platelet-derived growth factor receptor-ß] that are involved in
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