COVID-19-induced liver injury in adult patients: A brief overview

Coronavirus disease has spread worldwide since 2019, causing important pandemic issues and various social health problems to date. Little is known about the origin of this virus and the effects it has on extra-pulmonary organs. The different mechanisms of the virus and the influence it has on humans are still being studied, with hopes of finding a cure for the disease and the pathologies associated with the infection. Liver damage caused by coronavirus disease 2019 (COVID-19) is sometimes underestimated and has been of important clinical interest in the past few years. Hepatic dysfunctions can manifest in different forms which can sometimes be mild and without specific signs and symptoms or be severe with important clinical implications. There are several studies that have tried to explain the mechanism of entry (hepatotropism) of the virus into hepatocytes and the effects the virus has on this important organ. What clearly emerges from the current literature is that hepatic injury represents an important clinical aspect in the management of patients infected with COVID-19, especially in frail patients and those with comorbidities. The aim of our brief overview is to summarize the current literature regarding the forms of hepatic damage, complications, mechanisms of pathology, clinical features of liver injury, influence of comorbidities and clinical management in patients with COVID-19 infection.     

Validity,potential clinical utility and comparison of a consumer activity tracker and a research‐grade activity tracker in insomnia disorder II: Outside the laboratory

Accurate assessment of sleep can be fundamental for monitoring, managing and evaluating treatment outcomes within diseases. A proliferation of consumer activity trackers gives easy access to objective sleep. We evaluated the performance of a commercial device (Fitbit Alta HR) relative to a research‐grade actigraph (Actiwatch Spectrum Pro) in measuring sleep before and after a cognitive behavioural intervention in insomnia disorder. Twenty‐five individuals with DSM‐5 insomnia disorder (M = 50.6 ± 15.9 years) wore Fitbit and Actiwatch and completed a sleep diary during an in‐laboratory polysomnogram, and for 1 week preceding and following seven weekly sessions of cognitive‐behavioural intervention for insomnia. Device performance was compared for sleep outcomes (total sleep time, sleep latency, sleep efficiency and wake after sleep onset). The analyses assessed (a) agreement between devices across days and pre‐ to post‐treatment, and (b) whether pre‐ to post‐treatment changes in sleep assessed by devices correlated with clinical measures of change. Devices generally did not significantly differ from each other on sleep variable estimates, either night to night, in response to sleep manipulation (pre‐ to post‐treatment) or in response to changes in environment (in the laboratory versus at home). Change in sleep measures across time from each device showed some correlation with common clinical measures of change in insomnia, but not insomnia diagnosis as a categorical variable. Overall, the Fitbit provides similar estimates of sleep outside the laboratory to a research grade actigraph. Despite the similarity between Fitbit and Actiwatch performance, the use of consumer technology is still in its infancy and caution should be taken in its interpretation.     

Elevated serum uric acid is associated with a greater inflammatory response and with short- and long-term mortality in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention

Background and aimsDespite elevated serum uric acid (eSUA) has been identified as independent risk factor for cardiovascular diseases, its prognostic value in the setting of ST-segment elevation myocardial infarction (STEMI) is still controversial. Although the mechanisms of this possible relationship are unsettled it has been suggested that eSUA could trigger the inflammatory response. This study sought to investigate the association between eSUA with short- and long-term mortality and with inflammatory response in patients with STEMI treated with primary percutaneous coronary intervention (pPCI).Methods and resultsBlood samples were collected on admission and at 24 and 48 h after pPCI: the inflammatory biomarkers C-reactive protein (CRP), neutrophil count and neutrophil to lymphocytes ratio (NLR) were considered. Baseline eSUA was defined as ≥6.8 mg/dl. Cumulative 30-days and 1-year mortalities were estimated using the Kaplan-Meyer analysis. Multivariable analyses were performed by Cox proportional hazard models.In the 2369 patients with STEMI considered, 30-day mortality was 5.8% among patients with eSUA and 2% among patient with normal SUA level (p < 0.001); 1-year mortality was 8.5% vs 4%, respectively (p < 0.001). At multivariable analyses eSUA was an independent predictor of 30-day mortality (HR 1.196, 95%CI 1.006–1.321, p = 0.042) and 1-year mortality (HR 1.178, 95%CI 1.052–1.320, p = 0.005). eSUA patients presented higher values in on admission CRP (p < 0.001) and in neutrophil count and NLR at 24 h (respectively, p = 0.020 and p < 0.001) and at 48 h (p = 0.018 and p < 0.001) compared to patients with normal SUA levels.ConclusionsElevated serum uric acid is associated with higher short- and long-term mortality and with a greater inflammatory response after reperfusion in patients with STEMI treated with primary PCI.