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Background: Drug concentration in blood or urine is an acknowledged method to detect nonadherence. Observational studies suggest that informing patients about low or absent serum drug levels improves blood pressure (BP). We performed a multicenter randomized clinical trial to test the hypothesis that therapeutic drug monitoring (TDM) could improve drug adherence and BP in patients with uncontrolled hypertension (HT)., Methods: Patients were ≥18 years on stable treatment with at least 2 antihypertensive agents. We planned to randomize 80 nonadherent patients with a systolic daytime ambulatory BP ≥135 mm Hg to TDM intervention or not. The control group and the study personnel who measured BP remained uninformed about serum drug measurements throughout. All patients and physicians were blinded for BPs. Lifestyle advice and detailed information on the disease process and the importance of BP treatment were given to both groups., Results: From 2017 to 2022, we randomized 46 diagnosed nonadherent from a total of 606 patients with uncontrolled HT. The TDM group had a 6.7 (±14.5) mm Hg reduction from 147.9 (±10.3) to 141.1 (±14.1) mm Hg, and the control group experienced a 7.3 (±13.2) mm Hg reduction from 147.1 (±9.2) to 139.1 (±17.4) mm Hg, P = 0.9 between groups. Adherence improved in both groups, 73% in the TDM group and 59% in the control group became adherent at 3 months, P = 0.51., Conclusions: In our prospective multicenter clinical trial of uncontrolled and nonadherent hypertensive patients, we found no additional effect of TDM on BP and drug adherence compared with standard care., Clinical Trials Registration: Trial Number NCT03209154, www.clinicaltrials.gov., (© The Author(s) 2024. Published by Oxford University Press on behalf of American Journal of Hypertension, Ltd.)

Objectives Background: Under normal conditions, pulmonary megakaryocytes are an important source of circulating thrombocytes, causing thrombocyte counts to be higher in arterial than venous blood. In critical COVID-19, thrombocytes may be removed from the circulation by the lungs because of immunothrombosis, possibly causing venous thrombocyte counts to be higher than arterial thrombocyte counts. In the present study, we investigated time-dependent changes in pulmonary turnover of thrombocytes during critical COVID-19 by measuring arteriovenous thrombocyte differences. We hypothesized that the early stages of the disease would be characterized by a net pulmonary removal of circulating thrombocytes because of immunothrombosis and that later stages would be characterized by a net pulmonary release of thrombocytes as normal pulmonary function is restored., Design: Cohort study with repeated measurements of arterial and central venous thrombocyte counts., Setting: ICU in a large university hospital., Patients: Thirty-one patients with critical COVID-19 that were admitted to the ICU and received invasive or noninvasive mechanical ventilation., Interventions: None., Measurements and Main Results: We found a significant positive association between the arteriovenous thrombocyte difference and time since symptom debut. This finding indicates a negative arteriovenous thrombocyte difference and hence pulmonary removal of thrombocytes in the early stages of the disease and a positive arteriovenous thrombocyte difference and hence pulmonary release of thrombocytes in later stages. Most individual arteriovenous thrombocyte differences were smaller than the variance coefficient of the analysis., Conclusions: The results of this study support our hypothesis that early stages of critical COVID-19 are characterized by pulmonary removal of circulating thrombocytes because of immunothrombosis and that later stages are characterized by the return of normal pulmonary release of thrombocytes. However, in most cases, the arteriovenous thrombocyte difference was too small to say anything about pulmonary thrombocyte removal and release on an individual level., (Copyright © 2024 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of the Society of Critical Care Medicine.)

To examine whether interleukin-6 in critical coronavirus disease 2019 is higher in arterial than in central venous blood, as a sign of predominantly local pulmonal rather than systemic interleukin-6 production., Design: Prospective cohort pilot study with repeated weekly measurements of interleukin-6 in arterial and central venous blood. Respiratory function, assessed with Pao 2 /Fio 2 ratio, was measured at the time of blood sampling., Setting: ICU at a university hospital., Subjects: Nine adult patients with critical coronavirus disease 2019, actively treated and receiving mechanical ventilation., Measurements and Main Results: No difference between arterial and central venous interleukin-6 was found. There was a significant negative relationship between interleukin-6 concentration and P/F ratio in both arterial ( p = 0.04) and central venous ( p = 0.03) blood., Conclusions: The absence of an arteriovenous interleukin-6 difference implies that interleukin-6 in critical coronavirus disease 2019 is mainly produced outside the lungs as part of a systemic inflammatory response syndrome and act as a driver of local inflammation and damage in the lungs., Competing Interests: The authors have disclosed that they do not have any potential conflicts of interest., (Copyright © 2021 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of the Society of Critical Care Medicine.)