Non-alcoholic fatty liver disease (NAFLD) is defined as a chronic liver disease characterized by excessive fat accumulation in the liver without another obvious cause (no excessive alcohol consumption, hepatotoxic medications, toxins, viral infections, genetic hepatic diseases), therefore it is an exclusion diagnosis. The term NAFLD literally refers to non-alcohol related hepatopathy and does not adequately correlate with metabolic dysfunction and related cardiovascular risks. Therefore, researchers and scientific societies have moved towards changing the terminology. The novel nomenclature for a metabolic-associated fatty liver disease (MAFLD) has been proposed in 2020 by a group of experts to overcome the issues related to the old terminology. The diagnosis of MAFLD is based on the presence of hepatic steatosis and at least one between these three conditions: type 2 diabetes mellitus (T2DM), obesity or metabolic dysregulation. MAFLD has been shown to be an independent risk factor for cardiovascular diseases and atherosclerosis. It is better related to the main risk factors for atherosclerosis and cardiovascular diseases than NAFLD, such as dyslipidemia, T2DM and hypertension. The aim of this review is to highlight the reasons why the term NAFLD is moving to the term MAFLD, what are the conceptual basis of this choice and its clinical implications, particularly in the cardiovascular field.

Thoracic ultrasound seems to adapt to the screening for lung involvement of patients with suspected or ascertained SARS-COVID-19 infection due to its characteristics of easy applicability. It can be also a relevant method in monitoring patients. B lines are early finding of COVID-19, even in mild-symptomatic subjects; in the most serious cases such as pre-ARDS or ARDS, the B lines end up filling the ultrasound image almost completely, until it merges, so as to create a single hyperechoic image named as “white lung”, with distortion and irregularity of the pleural line. In advanced stage, lung consolidations are present, representing pulmonary pathological areas that are no longer normally ventilated.

The renin-angiotensin system (RAS) plays a main role in regulating blood pressure and electrolyte and liquid balance. Previous evidence suggests that RAS may represent an important target for the treatment of lung pathologies, especially for acute respiratory distress syndrome and chronic fibrotic disease. The scientific community has recently focused its attention on angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor 1 (AT1R) inhibitors and their possible benefit/harms for patients infected by Coronavirus disease (COVID-19) who experience pneumonia, but there are still some doubts about the effects of these drugs in this setting.

Impaired coagulation, liver dysfunction and COVID-19: Discovering an intriguing relationship

Background: The metabolic syndrome (MetS) is a cluster of risk factors for the development of cardiovascular diseases (CVD) and type 2 diabetes (T2DM). According to several meta-analyses, it has been shown that the cardiovascular (CV) risk conferred by the MetS is higher in women in comparison with men. There are many possible reasons to explain a higher CV risk in women with MetS: the most important differences can be attributed to distribution of central adiposity, lipid profile and hormones, but also differences in platelet biology and biochemistry play an important role. Methods: In this article we performed a research using PubMed database reviewing the evidence in literature (in particular clinical trials and meta-analyses) or lack of evidence/ biased information regarding the distribution by gender of MetS components and associated CV risk and we intended to provide a consequent gender perspective to the treatment of MetS and CV risk. Results: Twenty-three papers were evaluated searching for sex differences in the prevalence of MetS and CV risk. We also identified fifty-six papers dealing with sex differences in adiposity, insulin resistance and hormonal regulation. In terms of gender-specific expression of MetS in chronic disease we analyzed thirty-one papers focusing the attention on non-alcoholic fatty liver disease, polycystic ovarian syndrome, gestational diabetes mellitus, rheumatoid arthritis and HIV infection. We also evaluated twenty papers focusing on gender differences in platelet biology/reactivity and thirty-three papers on the gender approach in the treatment of MetS. The CV risk conferred by MetS segregates differently according to gender; differences between sexes may depend on the different representation of MetS components, gender-specific genetic, acquired metabolic and hormonal milieu and finally on a differential interaction between known risk factors and genderspecific properties, resulting in different degrees of pathophysiological events eventually leading to atherothrombosis. Regarding a potential sex-related therapeutic approach, even if gender-related differences exist in the pharmacokinetics of drugs for differences in body composition, plasma protein binding, metabolizing enzymes and difference in excretion characteristics, we have to acknowledge that women are under-represented in clinical trials, thus preventing from adequately challenging the efficacy and safety of drugs in this gender. Conclusion: While ncreasing knowledge exists regarding pathophysiological differences between genders in the prevalence of MetS components as well as in the associated cardiometabolic risk, underrepresentation of women in clinical trials and underutilization of guideline therapy, for instance in women with ischemic heart disease, largely flaw the interpretation of epidemiological and clinical evidence. Efforts should be undertaken to fight the so-called “Yentl syndrome” and to promote gender-specific drug trials, or at least studies where subgroup analyses by gender are pre-specified.