There is growing evidence of activated microglia and inflammatory processes in the cerebral cortex in amyotrophic lateral sclerosis (ALS). Activated microglia is characterized by increased expression of the 18 kDa translocator protein (TSPO) in the brain and may be a useful biomarker of inflammation. In this study, we evaluated neuroinflammation in ALS patients using a radioligand of TSPO, 18F-DPA-714. Ten patients with probable or definite ALS (all right-handed, without dementia, and untreated by riluzole or other medication that might bias the binding on the TSPO), were enrolled prospectively and eight healthy controls matched for age underwent a PET study. Comparison of the distribution volume ratios between both groups were performed using a Mann-Whitney’s test. Significant increase of distribution of volume ratios values corresponding to microglial activation was found in the ALS sample in primary motor, supplementary motor and temporal cortex (p = 0.009, p = 0.001 and p = 0.004, respectively). These results suggested that the cortical uptake of 18F-DPA-714 was increased in ALS patients during the “time of diagnosis” phase of the disease. This finding might improve our understanding of the pathophysiology of ALS and might be a surrogate marker of efficacy of treatment on microglial activation.

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F-FDG uptake is predictive for microvascular invasion and tumor differentiation. This examination has a prognostic value regarding tumor recurrence after liver transplantation for HCC.

Aims Rituximab is an anti‐CD20 monoclonal antibody approved in non‐Hodgkin lymphoma (NHL). This study aimed to assess the relationship between antigen mass and nonlinear pharmacokinetics of rituximab in NHL patients. Methods In a retrospective cohort of 25 NHL patients treated with rituximab, antigen mass was assessed at baseline by measuring metabolic tumour volume (MTV) by positron emission tomography. Rituximab pharmacokinetics was described using a semimechanistic 2‐compartment model including a latent target antigen. Rituximab target‐mediated elimination was described as irreversible binding between rituximab and it target. Histology (follicular or diffuse large B‐cell lymphomas), initial MTV and body weight were tested as covariates on pharmacokinetic parameters. Results The model allowed a satisfactory description of rituximab serum concentrations. Target‐mediated elimination was maximum at the beginning of treatment and became negligible towards the end of follow‐up. The second‐order elimination of rituximab due to target binding and complex elimination increased with baseline MTV. Central volume of distribution increased with body weight (P = .022) and baseline MTV (P = .005). Conclusions This study quantified for the first time the target‐mediated elimination of rituximab in NHL patients and confirmed rituximab retention by antigen mass.

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