Background and aims Coronavirus disease 2019 (COVID-19) pandemic is ongoing. Except for lung injury, it is possible that COVID-19 patients develop liver injury. Thus, we conducted a systematic review and meta-analysis to explore the incidence, risk factors, and prognosis of abnormal liver biochemical tests in COVID-19 patients. Methods PubMed, Embase, Cochrane Library, China National Knowledge Infrastructure (CNKI), VIP, and Wanfang databases were searched. The incidence of abnormal liver biochemical tests, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (GGT), total bilirubin (TBIL), and albumin (ALB), was pooled. Risk ratio (RR) was calculated to explore the association of abnormal liver biochemical tests with severity and prognosis of COVID-19 patients. Results Forty-five studies were included. The pooled incidence of any abnormal liver biochemical indicator at admission and during hospitalization was 27.2% and 36%, respectively. Among the abnormal liver biochemical indicators observed at admission, abnormal ALB was the most common, followed by GGT, AST, ALT, TBIL, and ALP (39.8%, 35.8%, 21.8%, 20.4%, 8.8%, and 4.7%). Among the abnormal liver biochemical indicators observed during hospitalization, abnormal ALT was more common than AST and TBIL (38.4%, 28.1%, and 23.2%). Severe and/or critical patients had a significantly higher pooled incidence of abnormal liver biochemical indicators at admission than mild and/or moderate patients. Non-survivors had a significantly higher incidence of abnormal liver biochemical indicators than survivors (RR = 1.34, p = 0.04). Conclusions Abnormal liver biochemical tests are common in COVID-19 patients. Liver biochemical indicators are closely related to the severity and prognosis of COVID-19 patients.

Cachexia is a prevalent pathological condition associated with chronic heart failure. Its occurrence predicts increased morbidity and mortality independent of important clinical variables such as age, ventricular function, or heart failure functional class. The clinical consequences of cachexia are dependent on both weight loss and systemic inflammation, which accompany cachexia development. Skeletal muscle wasting is an important component of cachexia; it often precedes cachexia development and predicts poor outcome in heart failure. Cachexia clinically affects several organs and systems. It is a multifactorial condition where underlying pathophysiological mechanisms are not completely understood making it difficult to develop specific prevention and treatment therapies. Preventive strategies have largely focused on muscle mass preservation. Different treatment options have been described, mostly in small clinical studies or experimental settings. These include nutritional support, neurohormonal blockade, reducing intestinal bacterial translocation, anemia and iron deficiency treatment, appetite stimulants, immunomodulatory agents, anabolic hormones, and physical exercise regimens. Currently, nonpharmacological therapy such as nutritional support and physical exercise are considered central to cachexia prevention and treatment.

Management of cirrhosis complications has greatly improved, increasing survival and quality of life of the patients. Despite that, some of these complications are still overlooked and scarcely treated, particularly those that are not related to the liver. This is the case of osteoporosis, the only cirrhosis complication that is not solved after liver transplantation, because bone loss often increases after immunosuppressant therapy. In this review, the definitions of bone conditions in cirrhotic patients are analyzed, focusing on the more common ones and on those that have the largest impact on this population. Risk factors, physiopathology, diagnosis, screening strategies, and treatment of osteoporosis in cirrhotic patients are discussed, presenting the more striking data on this issue. Therapies used for particular conditions, such as primary biliary cirrhosis and liver transplantation, are also presented.

Hepatic encephalopathy (HE) is one of the worst complications of liver disease and can be greatly influenced by nutritional status. Ammonia metabolism, inflammation and muscle wasting are relevant processes in HE pathophysiology. Malnutrition worsens the prognosis in HE, requiring early assessment of nutritional status of these patients. Body composition changes induced by liver disease and limitations superimposed by HE hamper the proper accomplishment of exams in this population, but evidence is growing that assessment of muscle mass and muscle function is mandatory due to the role of skeletal muscles in ammonia metabolism. In this review, we present the pathophysiological aspects involved in HE to support further discussion about advantages and drawbacks of some methods for evaluating the nutritional status of cirrhotic patients with HE, focusing on body composition.

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Heart failure patients often develop cachexia, which is an independent factor for survival reduction. Cachexia can be diagnosed when there is loss of more than 6% of the body weight, in the absence of other diseases. Even though its pathophysiology has not yet been completely clarified, various factors seem to be involved, such as reduction in food consumption, gastrointestinal tract abnormalities, immunologic and neuro-hormonal activation and changes in the relationship between anabolic and catabolic processes. Since there is not specific therapy for heart failure-induced cachexia, management is based on nutritional support, neuro-hormonal blockade, control of edema and anemia and exercise. Drugs with anabolic and immunomodulating properties are being evaluated and clinical and non-clinical trials.

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Oral administration of solid dosage forms is usually preferred in drug therapy. Conventional imaging methods are essential tools to investigate the in vivo performance of these formulations. The non-invasive technique of ac biosusceptometry has been introduced as an alternative in studies focusing on gastrointestinal motility and, more recently, to evaluate the behaviour of magnetic tablets in vivo. The aim of this work was to employ a multisensor ac biosusceptometer system to obtain magnetic images of disintegration of tablets in vitro and in the human stomach. The results showed that the transition between the magnetic marker and the magnetic tracer characterized the onset of disintegration (t(50)) and occurred in a short time interval (1.1 +/- 0.4 min). The multisensor ac biosusceptometer was reliable to monitor and analyse the in vivo performance of magnetic tablets showing accuracy to quantify disintegration through the magnetic images and to characterize the profile of this process.