PMC

(A) Partial thrombin time at baseline and the trough steady state after rivaroxaban treatment. Box plots are shown; the bottom and top of the box are the first and third quartiles, and the band inside the box is the second quartile (the median). PT, prothrombin time; trough = trough steady state at 4 weeks of rivaroxaban treatment. (B) Prothrombin fragment 1 + 2 at baseline and the trough steady state after rivaroxaban treatment. F1 + 2, prothrombin fragment 1 + 2; trough = trough steady state at 4 weeks of rivaroxaban treatment. (C) Thrombin–antithrombin complex at baseline and the trough steady state after rivaroxaban treatment. TAT, thrombin–antithrombin complex; trough = trough steady state at 4 weeks of rivaroxaban treatment. (D) D‐dimer at baseline and the trough steady state on rivaroxaban treatment. Trough = trough steady state at 4 weeks of rivaroxaban treatment

TNF bioactivity, DAS28, and IFX trough concentration at W22 in function of presence of IFX with or without ATI at W22 and IFX trough concentration and ATI at W22 and clinical response at W22. High TNF bioactivity was observed in the group “Low IFX trough concentration with ATI,” but not in the groups “Low IFX trough concentration without ATI” and “High IFX trough concentration without ATI” ((a) Kruskal-Wallis rank sum test; p < 0.0001). DAS28 was higher in the “Low IFX trough concentration with ATI” group compared to the two others ((b) Kruskal-Wallis rank sum test; p = 0.0266). IFX trough concentration at W22 was heterogeneous in the three groups ((c) Kruskal-Wallis rank sum test; p < 0.0001) with highest IFX trough concentration in the group “High IFX trough concentration without ATI.” Furthermore, IFX trough concentration was higher in the group “Low IFX trough concentration without ATI” than in the group “Low IFX trough concentration with ATI” ((c) p < 0.0001). IFX trough concentration was higher in the group “High IFX trough concentration without ATI” than in the group “Low IFX trough concentration without ATI” ((c) p = 0.0002). A trend for high IFX trough concentration and good EULAR response was observed at W22 ((d) Kruskal-Wallis rank sum test p = 0.1526). Oppositely, ATI concentration was not detectable in good response and high in Null response at W22 ((e) Kruskal-Wallis rank sum test p = 0.0047). At W22, a trend between TNF bioactivity and EULAR response (f). TNF bioactivity was not detectable in good response and high in Null response at W22 (Kruskal-Wallis rank sum test; NS). The box plots show the median values and the first and third quartiles at each time. The T bars represent the rest of the data with a maximum of 1.5 times the interquartile range. Circles represent values lower or higher than 1.5 times the interquartile range. TNF: tumor necrosis factor; ATI: antibodies towards IFX; W: week; Low ITL: ITL lower than 2 μg/mL; High IFX trough concentration: infliximab trough concentration higher than 2 μg/mL; presence or absence of ATI was determined with a cut-off at 20 ng/mL.

Tacrolimus trough concentrations before and after clotrimazole discontinuation. Median tacrolimus trough concentrations before and after clotrimazole discontinuation were 10.5 ng/ml (IQR 8.4–12.2) and 6.6 ng/ml (IQR 5–8.7), respectively. The goal tacrolimus trough concentration of 8–12 ng/ml is highlighted in gray

(A): range of observed Colistimethate sodium (CMS) and Colistin levels of samples taken 30 min after injection (CMS and Colistin peak levels) or immediately prior to injections of CMS (CMS and Colistin trough levels). A total of 779 samples were analyzed (CMS peak n = 385, CMS trough n = 388, Colistin peak n = 388, Colistin trough n = 394). Box indicates 25–75th percentile including median. Whiskers indicate 2.5–97.5 percentile. Outliers are plotted individually. * p > 0.001 for t-test comparing CMS trough vs CMS peak levels. (B–D): Linear correlation (Pearson) of Colistin peak and trough levels (B) CMS trough and Colistin trough levels (C) and CMS peak versus Colistin trough levels (D).