Background: Few studies have focused on the treatment of tuberculosis (TB) during pregnancy. This study aimed to evaluate the risk of adverse events, particularly liver toxicity, in pregnant women during treatment for active TB. Methods: We conducted a retrospective study on pregnant and age-matched non-pregnant women receiving treatment for active TB at four hospitals in Western Sweden between 1992 and 2017. Results: A total of 135 women were included, 40 pregnant and 95 non-pregnant. The frequency of severe hepatotoxicity was 40% in pregnant women and 6% among non-pregnant women (p < 0.001) (odds ratio 9.9; 95% confidence interval 3.5-28.0). Temporary drug withdrawal due to elevated transaminase levels was more frequent for pregnant than non-pregnant women (40% vs 9.5%; p < 0.001) (odds ratio 6.4; 95% confidence interval 2.5-16.2). There was one fatal case of hepatotoxicity in a pregnant woman. Conclusion: Severe hepatotoxicity was significantly more frequent in pregnant women compared to nonpregnant women. Careful monitoring of liver transaminases while receiving TB treatment during pregnancy is mandatory, as well as ensuring adequate measures with adjustment of drug regimen and temporary drug withdrawals when a rise in liver enzymes is noted.

Background:The prevalence and importance of cardiac dysfunction in critically ill patients with COVID-19 in Sweden is not yet established. The aim of the study was to assess the prevalence of cardiac dysfunction and elevated pulmonary artery pressure (PAP), and its influence on mortality in patients with COVID-19 in intensive care in Sweden. Methods:This was a multicentre observational study performed in five intensive care units (ICUs) in Sweden. Patients admitted to participating ICU with COVID-19 were examined with echocardiography within 72 h from admission and again after 4 to 7 days. Cardiac dysfunction was defined as left ventricular (LV) dysfunction (ejection fraction <50% and/or regional hypokinesia) or right ventricular (RV) dysfunction (defined as TAPSE <17 mm or visually assessed moderate/severe RV dysfunction). Results:We included 132 patients, of whom 127 (96%) were intubated. Cardiac dysfunction was found in 42 (32%) patients. Most patients had cardiac dysfunction at the first assessment (n = 35) while a few developed cardiac dysfunction later (n = 7) and some changed type of dysfunction (n = 3). LV dysfunction was found in 21 and | 607 HOLMQVIST eT aL.

Introduction: The importance of cardiac dysfunction in critically ill patients with COVID-19 is not well studied. The aim of the study was to assess the incidence, clinical risk factors, and prognosis of cardiac dysfunction in critical illness caused by COVID-19, and to evaluate if cardiac biomarkers can detect this condition.Methods: This was a multicentre observational study performed in five intensive care units (ICUs) in Sweden. Patients admitted to participating ICU with COVID-19 were examined with echocardiography within 72 hours from admission to the ICU and again after four to seven days. Cardiac biomarkers and clinical data were collected at the time of echocardiography. Cardiac dysfunction was defined as either left ventricular (LV) dysfunction (having an ejection fraction < 50% and/or regional hypokinesia) or right ventricular (RV) dysfunction (having a tricuspid annular plane systolic excursion (TAPSE) < 17mm or a moderate/severe RV dysfunction assessed visually).Results: We included 132 patients of whom 94 (71%) were included prospectively. The vast majority were intubated (n=127). At the time of admission to ICU, 35 (27%) patients had cardiac dysfunction and 7 patients (5%) had cardiac dysfunction detected later in the ICU-period. LV dysfunction was found in 18 patients and RV dysfunction in 17 patients, 7 patients had both RV and LV dysfunction. Noradrenaline > 0.20µg/kg/min was the only clinical variable associated with a higher risk of cardiac dysfunction. RV dysfunction was associated with an increased risk of death in a risk-adjusted model (OR 3.98, p = 0.013). Troponin and N-terminal pro b-type natriuretic peptide (NTproBNP) had moderate values in detecting cardiac dysfunction (AUC 0.729 and AUC 0.744, respectively). A combination of troponin < 1.44 times the upper reference limit and NTproBNP < 857ng/L had 85% probability of excluding cardiac dysfunction.Conclusions: Cardiac dysfunction is common in critically ill patients with COVID-19. Although not easily detected with clinical variables, cardiac biomarkers might be helpful. RV dysfunction is associated with an increased risk of death, these patients might benefit from further investigation or treatments. Trial registration: Registered on 24 Aug 2020 at Clinicaltrials.gov; registration number NCT04524234.

Background Chloroquine was promoted as a COVID-19 therapeutic early in the pandemic. Most countries have since discontinued the use of chloroquine due to lack of evidence of any benefit and the risk of severe adverse events. The primary aim of this study was to examine if administering chloroquine during COVID-19 imposed an increased risk of ischemic heart injury or heart failure. Methods Medical records, laboratory findings, and electrocardiograms of patients with COVID-19 who were treated with 500 mg chloroquine phosphate daily and controls not treated with chloroquine were reviewed retrospectively. Controls were matched in age and severity of disease. Results We included 20 patients receiving chloroquine (500 mg twice daily) for an average of five days, and 40 controls. The groups were comparable regarding demographics and biochemical analyses including C-reactive protein, thrombocytes, and creatinine. There were no statistically significant differences in cardiac biomarkers or in electrocardiograms. Median troponin T was 10,8 ng/L in the study group and 17.9 ng/L in the control group, whereas median NT-proBNP was 399 ng/L in patients receiving chloroquine and 349 ng/L in the controls. Conclusions We found no increased risk of ischemic heart injury or heart failure as a result of administering chloroquine. However, the use of chloroquine to treat COVID-19 outside of clinical trials is not recommended, considering the lack of evidence of its effectiveness, as well as the elevated risk of fatal arrythmias.