Hypercoagulability progresses to hypocoagulability during evolution of acetaminophen-induced acute liver injury in pigs

Increases in prothrombin time (PT) and international normalised ratio (INR) characterise acute liver injury (ALI) and failure (ALF), yet a wide heterogeneity in clotting abnormalities exists. This study defines evolution of coagulopathy in 10 pigs with acetaminophen (APAP)-induced ALI compared to 3 Controls. APAP administration began at 0 h and continued to ‘ALF’, defined as INR >3. In APAP pigs, INR was 1.05 ± 0.02 at 0 h, 2.15 ± 0.43 at 16 h and > 3 at 18 ± 1 h. At 12 h thromboelastography (TEG) demonstrated increased clot formation rate, associated with portal vein platelet aggregates and reductions in protein C, protein S, antithrombin and A Disintegrin and Metalloprotease with Thrombospondin type 1 repeats–13 (ADAMTS-13) to 60%, 24%, 47% and 32% normal respectively. At 18 ± 1 h, INR > 3 was associated with: hypocoagulable TEG profile with heparin-like effect; falls in thrombin generation, Factor V and Factor VIII to 52%, 19% and 17% normal respectively; further decline in anticoagulants; thrombocytopenia; neutrophilia and endotoxemia. Multivariate analysis, found that ADAMTS-13 was an independent predictor of a hypercoagulable TEG profile and platelet count, endotoxin, Protein C and fibrinogen were independent predictors of a hypocoagulable TEG profile. INR remained normal in Controls. Dynamic changes in coagulation occur with progression of ALI: a pro-thrombotic state progresses to hypocoagulability

Stunting is preceded by intestinal mucosal damage and microbiome changes and Is associated with systemic inflammation in a cohort of Peruvian infants

Stunting, defined as height-for-ag

Assessment of endogenous fibrinolysis in clinical using novel tests - Ready for clinical roll-out?

© The Author(s) 2021. This article is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.The occurrence of thrombotic complications, which can result in excess mortality and morbidity, represent an imbalance between the pro-thrombotic and fibrinolytic equilibrium.The mainstay treatment of these complications involves the use of antithrombotic agents but despite advances in pharmacotherapy, there remains a significant proportion of patients who continue to remain at risk.Endogenous fibrinolysis is a physiological counter-measure against lasting thrombosis and may be measured using several techniques to identify higher risk patients who may benefit from more aggressive pharmacotherapy. However, the assessment of the fibrinolytic systemis not yet accepted into routine clinical practice.In this review, we will revisit the different methods of assessing endogenous fibrinolysis (factorial assays, turbidimetric lysis assays, viscoelastic and the global thrombosis tests), including the strengths, limitations, correlation to clinical outcomes of each method and howwe might integrate the assessment of endogenous fibrinolysis into clinical practice in the future.Peer reviewedFinal Published versio

[Changes in the heart rhythm and slow-release beta-2 agonist therapy (peroral) in asthmatic patients. A Holter study]. Alterazioni del ritmo cardiaco e terapia beta-2-agonista a lento rilascio (per via orale) in pazienti asmatici. Studio Holter.

Slow-release formulations of salbutamol, used in asthmatic patients, may have few effects on cardiac rhythm. This study was designed to compare incidence and type of cardiac arrhythmias in a group of ten patients with stable bronchial asthma before and after 6 weeks treatment with a slow-release formulation of salbutamol. After a baseline spirometric and electrocardiographic evaluation, patients received placebo for a two-weeks period. At the end of this period patients repeated spirometry and carried out a 24-hour-ambulatory-E-Holter-monitoring. Subsequently, patients received for 6 weeks a treatment with a slow-release formulation of oral salbutamol. At the end of this period patients repeated spirometry, a 24-hour-ambulatory-EG-Holter-monitoring and potassium serum levels were controlled. We concluded from our study that, in patients with moderate bronchial asthma the treatment with an oral formulation of slow-release salbutamol may carry out a significant and durable bronchodilator effect, without causing important cardiac arrhythmias.Slow-release formulations of salbutamol, used in asthmatic patients, may have few effects on cardiac rhythm. This study was designed to compare incidence and type of cardiac arrhythmias in a group of ten patients with stable bronchial asthma before and after 6 weeks treatment with a slow-release formulation of salbutamol. After a baseline spirometric and electrocardiographic evaluation, patients received placebo for a two-weeks period. At the end of this period patients repeated spirometry and carried out a 24-hour-ambulatory-E-Holter-monitoring. Subsequently, patients received for 6 weeks a treatment with a slow-release formulation of oral salbutamol. At the end of this period patients repeated spirometry, a 24-hour-ambulatory-EG-Holter-monitoring and potassium serum levels were controlled. We concluded from our study that, in patients with moderate bronchial asthma the treatment with an oral formulation of slow-release salbutamol may carry out a significant and durable bronchodilator effect, without causing important cardiac arrhythmias