Purpose Patients with carcinomas often share symptoms of vision deterioration as part of paraneoplastic retinopathy (PNR), based on a cross-reaction between antigens expressed by the underlying tumor and retinal proteins. However, some of the underlying symptoms may be explained by a drug-induced toxicity. The application of new therapeutic strategies with mitogen-activated protein kinase (MEK) and fibroblast growth factor receptor (FGFR) inhibitors in advanced cancers are still under evaluation for safety and tolerability, but also for dose-limiting toxicities. In the presented data, we identified a drug-induced pseudo-central serous chorioretinopathy (pCSC) to be the reason for central vision deterioration. Methods A retrospective, observational, case-controlled study included seven patients receiving MEK and six patients receiving FGFR inhibitor treatment for bronchopulmonal cancer. We compared the clinical and diagnostic pictures of pCSC patients with that of 50 CSC patients (100 eyes) and 7 patients (14 eyes) with PNR. The activity of pCSC was assessed by clinical examination, supported by multimodal imaging. The relationships between clinical symptomatology and systemic disease activity were evaluated. Results Three out of thirteen patients (23.1%) showed signs of pCSC (one FGFR and two MEK inhibitor patients). All three pCSC patients showed central bilateral detachment of the neurosensory retina on OCT imaging, but also paracentral multifocal lesions in the second subject. Compared to our CSC and PNR patients, the lesions in pCSC patients showed no lipofuscin irregularities on FAF. With reduction of the MEK treatment, the lesions on one MEK subject disappeared and BCVA restored to 0.8. In one MEK- and the FGFR subject, the lesions reduced in size without therapy discontinuation. Conclusion Based on our data, MEK and FGFR inhibitor-associated pCSC is a mild, self-limited retinopathy that seems to disappear simultaneously or shortly after discontinuation of medication, with subsequent restoration of the central visual function.

We describe a remarkable case of probably vemurafenib-related sterile abscess. This adverse event is of substantial clinical relevance, as it mimicks metastatic melanoma and requires careful diagnostic evaluation and proper treatment to allow a favorable patient outcome.

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INTRODUCTION Immunotherapy, especially with immune checkpoint inhibitors (ICPI), has increasingly become an attractive treatment modality for various types of cancers. However, many patients develop ICPI-associated autoimmune adverse events such as pneumonitis, colitis or rarely neurological syndromes. Large and medium vessel vasculitis haS only occasionally been reported. Here we report the first case of ICPI-associated mononeuritis multiplex in a patient with malignant mesothelioma, caused by a histological proven small vessel vasculitis. CASE REPORT A 61-year old female developed subacute progressive painful and asymmetric sensorimotor deficits on distal extremities. Electrophysiologically, signs of a severe axonal neuropathy of both legs and the right arm were found, and swellings of the corresponding nerves were seen upon nerve ultrasound exam. The clinical and electrophysiological findings were reminiscent of mononeuritis multiplex. Laboratory work up including CSF examination was normal. More than two years prior to developing peripheral nerve deficits, the patient had been diagnosed with malignant pleural mesothelioma and treated with the anti-PD1 monoclonal antibody pembrolizumab on progression after chemotherapy. Biopsy of the right sural nerve revealed a small vessel vasculitis with a lymphocyte predominance of CD8+ T cells over CD4+ T as well as B lymphocytes. Despite discontinuation of pembrolizumab and immunosuppressive treatment (high dose methylprednisone, cyclophosphamide) complemented by opioid therapy, painful allodynia persisted. CONCLUSION ICPI-associated autoimmune disorders also include small vessel vasculitis with rare phenotypes such as mononeuritis multiplex. Further studies are required to improve our understanding of the link between ICPIs, and the pathogenic process leading to vasculitis, as well as to optimize treatment options for those rare diseases.

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