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Tranexamic acid as an adjunct to resuscitative endovascular balloon occlusion of the aorta does not worsen outcomes in a porcine model of hemorrhage.

Trauma Surg Acute Care Open

January 2025

Expeditionary and Trauma Medicine, Naval Medical Research Unit San Antonio, JBSA-Fort Sam Houston, Texas, USA.

Background: Non-compressible torso hemorrhage (NCTH) represents a leading cause of preventable mortality in trauma. Resuscitative endovascular balloon occlusion of the aorta (REBOA) stabilizes NCTH but may predispose patients to thrombus generation. REBOA must therefore be prospectively evaluated for coagulation risks with concomitant usage of anti-fibrinolytic tranexamic acid (TXA).

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Tanimilast is an inhaled phosphodiesterase-4 inhibitor currently in phase III clinical development for treating chronic obstructive pulmonary disease and asthma. This trial aimed to characterize the pharmacokinetics, mass balance, and metabolite profiling of tanimilast. Eight healthy male volunteers received a single dose of nonradiolabeled tanimilast via powder inhaler (Chiesi NEXThaler [3200 μg]), followed by a concomitant intravenous infusion of a microtracer ([C]-tanimilast: 18.

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Characterization of human alcohol dehydrogenase 4 and aldehyde dehydrogenase 2 as enzymes involved in the formation of 5-carboxylpirfenidone, a major metabolite of pirfenidone.

Drug Metab Dispos

January 2025

Drug Metabolism and Toxicology, Faculty of Pharmaceutical Sciences, Kanazawa University, Kakuma-machi, Kanazawa, Japan; WPI Nano Life Science Institute (WPI-NanoLSI), Kanazawa University, Kakuma-machi, Kanazawa, Japan.

Pirfenidone (PIR) is used in the treatment of idiopathic pulmonary fibrosis. After oral administration, it is metabolized by cytochrome P450 1A2 to 5-hydroxylpirfenidone (5-OH PIR) and further oxidized to 5-carboxylpirfenidone (5-COOH PIR), a major metabolite excreted in the urine (90% of the dose). This study aimed to identify enzymes that catalyze the formation of 5-COOH PIR from 5-OH PIR in the human liver.

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Introduction: Sotalol is a beta-adrenoceptor blocking drug with unique physical and pharmacologic properties. Unlike most beta-adrenoceptor blocking drugs, sotalol is amenable to extracorporeal removal and causes QT interval prolongation and ventricular dysrhythmias. These properties have implications for treating sotalol poisoning.

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Background: Adalimumab biosimilar MSB11022 (Idacio®) has been approved for the same indications as its originator (Humira®), based on findings from clinical trials in plaque psoriasis. Data on its efficacy and safety in inflammatory bowel disease, however, are scarce.

Methods: Retrospective, observational study of 44 patients with inflammatory bowel disease: 30 were treated with originator adalimumab, five were directly started on MSB11022, and nine switched from originator to biosimilar adalimumab.

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