Testicular DLCL is characterized by a particularly high risk of extranodal relapse even in cases with localized disease at diagnosis. Anthracycline-based chemotherapy, CNS prophylaxis, and contralateral testicular irradiation seem to improve the outcome. Their efficacy is under evaluation in a prospective clinical trial.

Background: There is uncertainty as to the contribution of cancer patients' features on severity and mortality from Covid-19 and little guidance as to the role of anticancer and anti-Covid-19 therapy in this population.Methods: OnCovid is a retrospective observational study conducted across 19 European centers that recruited cancer patients aged >18 and diagnosed with Covid-19 between 26/02 and 01/04/2020. Uni-and multivariable regression models were used to evaluate predictors of Covid-19 severity and mortality.Results: We identified 890 patients from UK (n¼218, 24%), Italy (n¼343, 37%), Spain (n¼323, 36%) and Germany (n¼6, 1%). Most patients were male (n¼503, 56%) had a diagnosis of solid malignancy (n¼753, 84%) and 556 (62%) had active disease. Mean (AESD) patient age was 68AE13 years, and 670 (75%) had >1 co-morbidity, most commonly hypertension (n¼386, 43%). Commonest presenting symptoms were fever (n¼569, 63%) and cough (n¼448, 50%), beginning 6.3 (AE9.5 SD) days before diagnosis. Most patients (n¼565, 63%) had >1 complication from Covid-19, including respiratory failure (n¼527, 59%) and acute respiratory distress syndrome (n¼127, 22%). In total, 110 patients (14%) were escalated to high-dependency or intensive care. At time of analysis, 299 patients had died (33%). Multi-variate logistic regression identified male gender, age>65 (p<0.0001) presence of >2 comorbidities (p¼0.001) active malignancy (p¼0.07) as predictors of complicated Covid-19. Mortality was associated with active malignancy (p<0.0001), age>65 and co-morbid burden (p¼0.002). Provision of chemotherapy, targeted therapy or immunotherapy was not associated with higher mortality. Exposure to anti-malarials alone (chloroquine/ hydroxychloroquine, n¼182, p<0.001) or in combination with anti-virals (n¼195, p<0.001) or tocilizumab (n¼51, p¼0.004) was associated with improved mortality compared to patients who did not receive any of these therapies (n¼446) independent of patients' gender, age, tumour stage and severity of Covid-19.Conclusions: This study highlights the clinical utility of demographic factors for individualized risk-stratification of patients and supports further research into emerging anti Covid-19 therapeutics in SARS-Cov-2 infected cancer patients. Clinical trial identification: NCT04393974.Legal entity responsible for the study: Imperial College London.

A few cases of parkinsonism linked to COVID-19 infection have been reported so far, raising the possibility of a post-viral parkinsonian syndrome. The objective of this review is to summarize the clinical, biological, and neuroimaging features of published cases describing COVID-19-related parkinsonism and to discuss the possible pathophysiological mechanisms. A comprehensive literature search was performed using NCBI’s PubMed database and standardized search terms. Thirteen cases of COVID-19-related parkinsonism were included (7 males; mean age: 51 years ± 14.51, range 31–73). Patients were classified based on the possible mechanisms of post-COVID-19 parkinsonism: extensive inflammation or hypoxic brain injury within the context of encephalopathy (n = 5); unmasking of underlying still non-symptomatic Parkinson’s Disease (PD) (n = 5), and structural and functional basal ganglia damage (n = 3). The various clinical scenarios show different outcomes and responses to dopaminergic treatment. Different mechanisms may play a role, including vascular damage, neuroinflammation, SARS-CoV-2 neuroinvasive potential, and the impact of SARS-CoV-2 on α-synuclein. Our results confirm that the appearance of parkinsonism during or immediately after COVID-19 infection represents a very rare event. Future long-term observational studies are needed to evaluate the possible role of SARS-CoV-2 infection as a trigger for the development of PD in the long term.

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