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.

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.

The diffusion of SARS-CoV-2, starting from China in December 2019, has led to a pandemic, reaching Italy in February 2020. Previous studies in Asia have shown that the median duration of SARS-CoV-2 viral shedding was approximately 12–20 days. We considered a cohort of patients recovered from COVID-19 showing that the median disease duration between onset and end of COVID-19 symptoms was 27.5 days (interquartile range (IQR): 17.0–33.2) and that the median duration between onset of symptoms and microbiological healing, defined by two consecutive negative nasopharyngeal swabs, was 38 days (IQR: 31.7–50.2). A longer duration of COVID-19 with delayed clinical healing (symptom-free) occurred in patients presenting at admission a lower PaO₂/FiO₂ ratio (p < 0.001), a more severe clinical presentation (p = 0.001) and a lower lymphocyte count (p = 0.035). Moreover, patients presenting at admission a lower PaO₂/FiO₂ ratio and more severe disease showed longer viral shedding (p = 0.031 and p = 0.032, respectively). In addition, patients treated with corticosteroids had delayed clinical healing (p = 0.013).

COVID-19 patients may manifest thrombocytopenia and some of these patients succumb to infection due to coagulopathy. The aim of our study was to examine platelet count values in patients infected with SARS-CoV-2, comparing them to a control group consisting of non-COVID-19 patients. Moreover, we evaluated the correlation between the platelet value and the respiratory alteration parameters and the outcome (hospitalization and mortality) in COVID-19 patients. The mean platelet values (×10⁹/L) differed between patients with positive or negative SARS-CoV-2 swabs (242.1 ± 92.1 in SARS-CoV-2 negative vs. 215.2 ± 82.8 in COVID-19 patients, p < 0.001). In COVID-19 patients, the platelet count correlated with the A-aO₂ gradient (p = 0.001, rho = −0.149), with its increase over the expected (p = 0.013; rho = −0.115), with the PaO₂ values (p = 0.036; rho = 0.093), with the PCO₂ values (p = 0.003; rho = 0.134) and with the pH values (p = 0.016; rho = −0.108). In COVID-19 negative patients, the platelet values correlated only with the A-aO₂ gradient: (p = 0.028; rho = −0.101). Patients discharged from emergency department had a mean platelet value of 234.3 ± 68.7, those hospitalized in ordinary wards had a mean value of 204.3 ± 82.5 and in patients admitted to sub-intensive/intensive care, the mean value was 201.7 ± 75.1. In COVID-19 patients, the survivors had an average platelet value at entry to the emergency department of 220.1 ± 81.4, while that of those who died was 206.4 ± 87.7. Our data confirm that SARS-CoV-2 infection may induce thrombocytopenia, and that the reduction in platelet counts could be correlated with the main blood gas parameters and with clinical outcome; as a consequence, platelet count could be an important prognostic factor to evaluate and stratify COVID-19 patients.

It seems that during SARS-CoV-2 infection, total cholesterol, LDL-C, and HDL-C values decrease and lipids could play a fundamental role in viral replication. Moreover, it has been shown that SARS-CoV-2 infection could influence thyroid function. We performed a retrospective analysis of 118 hospitalized patients with COVID-19, comparing pre-infection lipid profile (53 patients) and thyroid-stimulating hormone (TSH) values (45 patients) to those measured on admission. Our aim was to evaluate whether SARS-CoV-2 infection could be involved in thyroid and lipid profile alterations and study possible correlations with disease severity and clinical outcome. Median baseline values at the admission time were: total cholesterol at 136.89 ± 42.73 mg/dL, LDL-C 81.53 ± 30.35 mg/dL, and HDL-C 32.36 ± 15.13 mg/dL; and triglycerides at 115.00 ± 40.45 mg/dL, non-HDL-C 104.53 ± 32.63 md/dL, and TSH 1.15 ± 1.08 μUI/mL. Median values of pre-infection total cholesterol, HDL-C, and TSH were significantly higher than those measured at the admission time (p value < 0.05). The C-reactive protein (CRP) negatively correlated with LDL-C (p = 0.013) and HDL-C (p = 0.05). Our data underline a possible impact of SARS-CoV-2 infection on thyroid function. Moreover it suggests a possible relation between COVID-19 and the lipid profile with a negative correlation between CRP, LDL-C, and HDL-C values, proposing the hypothesis that lipid lowering could follow the rising of the COVID-19 inflammatory state.