"Uninformed consent" in clinical trials with cancer patients: A qualitative analysis of patients' and support persons' communication experiences and needs.

OBJECTIVE: Cancer patients are often overwhelmed when being informed about clinical trials. However, there is a lack of evidence-based strategies to improve physician-patient communication in this area. This study assessed the experiences and needs of cancer patients and their support persons (SPs) during the informed consent (IC) process prior to participation in clinical trials. METHODS: 17 semi-structured interviews with cancer patients and their SP were conducted and analysed using a framework analysis. RESULTS: Most respondents reported feeling well informed about the clinical trial. However, core aspects of the study were often not understood highlighting a dissonance between perceived and actual recall and understanding. Many participants trusted that the trial recommended was the best available care and only skimmed the consent form or did not read it at all. CONCLUSIONS: This is the first German study to analyse both cancer patients' and SPs' perspectives on IC processes. Although many feel well informed, our results suggest a significant gap in recall and understanding of core components of clinical trials which hinders IC. PRACTICE IMPLICATIONS: Further interventional research is required to improve the consent processes prior to clinical trials in order to provide optimal, patient-centred care.

Metabolic stress and disease-stage specific basigin expression of peripheral blood immune cell subsets in COVID-19 patients

Coronavirus disease 2019 (COVID-19) is driven by dysregulated immune responses yet the role of immunometabolism in COVID-19 pathogenesis remains unclear. By investigating 47 patients with confirmed SARS-CoV-2 infection and 16 uninfected controls, we found an immunometabolic dysregulation specific for patients with progressed disease that was reversible in the recovery phase. Specifically, T cells and monocytes exhibited increased mitochondrial mass, accumulated intracellular ROS and these changes were accompanied by disrupted mitochondrial architecture. Basigin (CD147), but not established markers of T cell activation, was up-regulated on T cells from progressed COVID-19 patients and correlated with ROS accumulation, reflected in the transcriptome. During recovery, basigin and ROS decreased to match the uninfected controls. In vitro analyses confirmed the correlation and showed a down-regulation of ROS by dexamethasone treatment. Our findings provide evidence of a basigin-related and reversible immunometabolic dysregulation in COVID-19.