ABSTRACT
AIM: To assess the respective performances of a HCV screening program in a hospital setting and a HCV screening model applied concomitantly in a primary care centre. METHODS: Adult patients consecutively admitted to hospital for ambulatory surgery were screened for anti-HCV antibodies (hospital screening cohort, HPSC), as were patients receiving blood tests for medical reasons in a primary care centre (primary care screening cohort, PCSC). Serum anti-HCV and HCV RNA levels were tested by ELISA and real-time PCR, respectively. RESULTS: Seroprevalence of HCV infection was 2.2 % in the HPSC and 1.4 % in the PCSC (p = 0.044). All viraemic patients (0.2 % in HPSC and 0.1 % in PCSC) were treated with direct-acting antivirals and 85.7 % experienced a sustained virological response. CONCLUSIONS: Hospital-based HCV screening outperformed primary care-centered screening, significantly increasing HCV case findings.
Subject(s)
Hepatitis C, Chronic , Hepatitis C , Adult , Humans , Hepacivirus/genetics , Antiviral Agents/therapeutic use , Seroepidemiologic Studies , Hepatitis C, Chronic/diagnosis , Hepatitis C, Chronic/drug therapy , Hepatitis C/diagnosis , Hepatitis C/drug therapy , Hepatitis C/epidemiology , Hospitals , Hepatitis C Antibodies/therapeutic use , Primary Health CareABSTRACT
Non-alcoholic fatty liver disease (NAFLD) is currently the most common chronic liver disease worldwide and comprises varied grades of intrahepatic lipid accumulation, inflammation, ballooning, and fibrosis; the most severe cases result in cirrhosis and liver failure. There is extensive clinical and experimental evidence indicating that chronic intermittent hypoxia, featuring a respiratory disorder of growing prevalence worldwide termed obstructive sleep apnea, could contribute to the progression of NAFLD from simple steatosis, also termed non-alcoholic fatty liver or hepatosteatosis, to non-alcoholic steatohepatitis; however, the molecular mechanisms by which hypoxia might contribute to hepatosteatosis setup and progression still remain to be fully elucidated. In this review, we have prepared an overview about the link between hypoxia and lipid accumulation within the liver, focusing on the impact of hypoxia on the molecular mechanisms underlying hepatosteatosis onset.
