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Summary Objective Our aims were to investigate the motivation for therapy, the understanding and valuation of potential treatment toxicities in melanoma patients offered adjuvant therapies. Methods Between September 2018 and September 2019 49 adjuvant patients with stage III and IV melanoma received a self‐created, pre‐treatment questionnaire. Furthermore, the patients were handed out the REPERES‐G, EQ‐5D‐3L and EORTC QLQ C‐30 questionnaires. Results Eight patients (18.3 %) decided against adjuvant therapy (mean age 71.6 years). Four of these had stage IIIA melanoma. The majority of patients (73.4 %) decided for adjuvant treatment with PD1‐inhibitors despite their potential high grade, persistent, irreversible or even fatal toxicities. About a third of patients with BRAF V600 mutated melanoma who decided for therapy chose targeted therapy (31.3 %). These patients were younger (mean age 49 years), still working and had families with children. The REPERES‐G questionnaire showed that our patients were generally satisfied with medical care. The average scores in the EQ‐5D‐3L and EORTC QLQ C‐30 questionnaires indicated good subjective general health. Conclusions Despite the associated toxicities as well as the required time and effort for a one‐year treatment the majority of patients decided for adjuvant treatments.

Background Schizophrenia spectrum disorders (SSDs) are presumed to be associated with retinal thinning. However, evidence is lacking as to whether these retinal alterations reflect a disease-specific process or are rather a consequence of comorbid diseases or concomitant microvascular impairment. Methods The study included 126 eyes of 65 patients with SSDs and 143 eyes of 72 healthy controls. We examined macula and optic disc measures by optical coherence tomography (OCT) and OCT angiography (OCT-A). Additive mixed models were used to assess the impact of SSDs on retinal thickness and perfusion and to explore the association of retinal and clinical disease-related parameters by controlling for several ocular and systemic covariates (age, sex, spherical equivalent, intraocular pressure, body mass index, diabetes, hypertension, smoking status, and OCT signal strength). Results OCT revealed significantly lower parafoveal macular, macular ganglion cell–inner plexiform layer (GCIPL), and macular retinal nerve fiber layer (RNFL) thickness and thinner mean and superior peripapillary RNFL in SSDs. In contrast, the applied OCT-A investigations, which included macular and peripapillary perfusion density, macular vessel density, and size of the foveal avascular zone, did not reveal any significant between-group differences. Finally, a longer duration of illness and higher chlorpromazine equivalent doses were associated with lower parafoveal macular and macular RNFL thickness. Conclusions This study strengthens the evidence for disease-related retinal thinning in SSDs.

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e18007 Background: Progressive multifocal leukencaphalopathy (PML) is a rare demyelinating infection of the central nervous system caused by viruses (CMV, JC, BK). It is almost exclusively described in profound immunocompromised patients developed as a primary infection or by reactivation of the virus after a latent infection. PML is typically observed among patients with severe immunodeficiency like HIV or in the setting of autologous or allogenic transplantation. Methods: Our patient was a 64-year-old woman with B-CLL diagnosed in 2000 in state B of Binet treated with 12 cycles of fludarabin until July 2007 in a B-cell and lymphoma-reducing manner. For the reason of progressive disease 3 cycles of rituximab, fludarabin, mitoxantrone, and cyclophosphamide were added (dose reduced causing hematologic toxicity) until October 2007 continuing rituximab once a month up to Mai 2008. Results: In a CT scan mixed response was observed with progressive disease infradiafragmatic and regression supradiafragmatic. Corticosteroids could stop B-symptoms and leads to a distinct shrinkage of the lymphomas within 2 weeks. Later on she presented with confusion and disorientation. An MRI of the brain showed subcortical and periventricular lesions with increased signal on T2-weighted and fluid attentuated inversion recovery (FLAIR) suggestive of a vascular origin. Her symptoms progressed by aphasia and weakness of the right leg corresponding to increased size and number of cerebral lesions. A lumbar puncture showed no malignant cells and no evidence of inflammation. A PCR analysis was negative for Toxoplasma gondii, HSV, VCV, CMV, EBV, and enterovirus but positive for JC-DNA (215.000 copies/ml). A rapid progression leads to death two months after onset of symptoms. Conclusions: Antibody deficiency syndrome corresponding to CLL under treatment with chemotherapy and rituximab lead to a severe immunosuppression enabling unusual viral infections such as PML. No significant financial relationships to disclose.