No abstract

The actual Coronavirus Disease (COVID 19) pandemic is due to Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a member of the coronavirus family. Besides the respiratory involvement, COVID 19 patients frequently develop a pro-coagulative state caused by virus-induced endothelial dysfunction, cytokine storm and complement cascade hyperactivation. It is common to observe diffuse microvascular thrombi in multiple organs, mostly in pulmonary microvessels. Thrombotic risk seems to be directly related to disease severity and worsens patients' prognosis. Therefore, the correct understanding of the mechanisms underlying COVID-19 induced prothrombotic state can lead to a thorough assessment of the possible management strategies. Hence, we review the pathogenesis and therapy of COVID 19-related thrombosis disease, focusing on the available evidence on the possible treatment strategies and proposing an algorithm for the anticoagulation strategy based on disease severity. Keywords COVID-19 • SARS-CoV-2 • Thrombosis • Anticoagulation Highlights • SARS-CoV-2 induced complement hyperactivation, endothelial dysfunction and cytokine storm have a prothrombotic effect. • COVID 19 patients develop a pro-coagulative state directly related to disease severity. • In COVID 19 critical patients, thrombotic lesions in pulmunary microvessels have a prevalence twice higher than critical non-COVID 19 patients. • Anticoagulant treatment is associated with lower mortality. Hence, we propose an algorithm for the anticoagulation strategy based on disease severity.

The spread of hepatitis B virus (HBV) infection has gradually decreased in Italy in the last 5 decades as shown by the steady reduction in the incidence rates of acute hepatitis B, from 10/100000 inhabitants in 1984 to 0.85/100000 in 2012, and by the reduced prevalence of hepatitis B surface antigen (HBsAg)-positive cases among chronic hepatitis patients with different etiologies, from 60% in 1975 to about 10% in 2001. The prevalence of HBsAg chronic carriers in the general population also decreased from nearly 3% in the 1980s to 1% in 2010. Linked to HBV by its characteristics of defective virus, the hepatitis delta virus (HDV) has shown a similar epidemiological impact on the Italian population over time. The incidence of acute HDV infection decreased from 3.2/100000 inhabitants in 1987 to 0.8/100000 in 2010 and the prevalence of HDV infection in HBsAg chronic carriers decreased from 24% in 1990 to 8.5% in 2006. Before the beneficial effects of HBV mass vaccination introduced in 1991, the decreased endemicity of HBV and HDV infection in Italy paralleled the improvement in screening blood donations, the higher standard of living and impressive reduction in the birth rate associated with a marked reduction in the family size. A further contribution to the decline in HBV and HDV infections most probably came from the media campaigns to prevent the spread of human immunodeficiency virus infection by focusing the attention of the general population on the same routes of transmission of viral infections such as unsafe sexual intercourse and parenteral exposures of different kinds.

COVID-19 infection has a broad spectrum of severity ranging from an asymptomatic form to a severe acute respiratory syndrome that requires mechanical ventilation. Starting with the description of our case series, we evaluated the clinical presentation and evolution of COVID-19. This article is addressed particularly to physicians caring for patients with COVID-19 in their clinical practice. The intent is to identify the subjects in whom the infection is most likely to evolve and the best methods of management in the early phase of infection to determine which patients should be hospitalized and which could be monitored at home. Asymptomatic patients should be followed to evaluate the appearance of symptoms. Patients with mild symptoms lasting more than a week, and without evidence of pneumonia, can be managed at home. Patients with evidence of pulmonary involvement, especially in patients over 60 years of age, and/or with a comorbidity, and/or with the presence of severe extrapulmonary manifestations, should be admitted to a hospital for careful clinical-laboratory monitoring.

This is the first demonstration that TM6SF2 E167K variant is an independent predictor of liver steatosis in chronic hepatitis C.