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  • In this study we introduced a

    2018-10-25

    In this study, we introduced a special learning module “Faciocutaneous Clues to Systemic Diseases” for Chinese undergraduate medical students based on the following facts. Firstly, medical students will be confronted with skin conditions during their medical training and future careers, regardless of their specialty. The identification of skin clues is helpful for the early detection of a hidden internal disorder or malignancy, as described above. Secondly, there is no such specialized chapter in the textbook for undergraduate medical students in China (Supplementary Table 1). Thirdly, skin changes are often the initial complaint that makes patients seek medical attention. Unfortunately, a proportion of dermatologists in China pay more attention to local skin lesions and neglect the relationship between skin lesions and hidden systemic diseases, which results in increasing morbidity and mortality. Moreover, they teach this type of improper diagnostic mode to undergraduate medical students during their medical teaching. Fourthly, the face, in ikk inhibitor to other areas, is the most highly exposed organ and is also the first area seen by physicians when a patient visits. Increased awareness of faciocutaneous clues can guide physicians in the earlier screening of multisystem disorders.
    Conclusions
    Funding This work was supported by Teaching Innovation Project in Higher Education of Chongqing (No.132084, Zhu Shen).
    Introduction The treatment of metastatic melanoma is challenging. BRAF gene mutation is found in 40–60% of melanoma cases, the most common being the V600E mutation. Vemurafenib was approved by the Food and Drug Administration in 2011 as target therapy for the treatment with BRAF V600 mutation-positive metastatic melanoma. In this report, we present a case of metastatic amelanotic melanoma with unknown primary cancer as the initial presentation. The patient presented with neutrophilic septal panniculitis 1 week after vemurafenib treatment, which is a rare cutaneous toxicity of BRAF inhibitor (BRAFi). We also review the current literature on management of BRAFi-related adverse skin effects.
    Case Report The patient was a 75-year-old woman, a retired farmer, with a medical history of hypertension under regular control. She was diagnosed as having metastatic melanoma with unknown primary tumor, cTxNxM1, by excision of right axillary lymphadenopathy. Serum tumor marker surveys, including carcinoembryonic antigen, squamous cell carcinoma antigen, cancer antigen 153, cancer antigen 125, and alpha-fetoprotein, were all within normal limits. The pathology report of right axillary lymphadenopathy revealed infiltrating epithelioid malignancy with solid growth pattern, abundant cytoplasm, enlarged and vesicular nuclei, prominent nucleoli, and brisk mitotic activity (Figure 1A). The immunohistochemical studies showed negative reactivity for cytokeratin AE1/AE3, inhibin, calretinin, leukocyte common antigen, CD34, and CD30. Expressions of S-100 protein, HMB-45 (human melanoma black-45; Figure 1B and D), Melan-A (Figure 1C), and MiTF-1 (microphthalmia-associated transcription factor-1) were diffusely positive. The final diagnosis was metastatic malignant amelanotic epithelioid melanoma. On physical examination, no obvious primary skin tumor was noted. Whole-body positron emission tomography showed metastases to the right axillary area, right supraclavicular area, right shoulder, the mediastinum, and bilateral pulmonary hili (Figure 2B). She also had progressive dysphagia and dyspnea, which are probably related to the metastases with initial upper airway compression. The presence of a v-raf murine sarcoma viral oncogene homolog B1 (BRAF) gene point mutation at codon 600 from valine to glutamate was confirmed by the LightCycler HybProbe real-time polymerase chain reaction assay for the right axillary lymphadenopathy specimen (Figure 2A). Under a diagnosis of metastatic melanoma with BRAF V600E mutation, she received oral vemurafenib (720 mg daily), a specific inhibitor of mutant BRAF.