Chronic hepatitis C virus (HCV) infection is a leading cause of progressive liver disease, cirrhosis, and hepatocellular carcinoma (HCC), posing a significant global health burden. The introduction of direct-acting antiviral (DAA) therapy has revolutionized treatment, achieving high rates of sustained virologic response (SVR) and dramatically reducing liver-related morbidity and mortality. However, the long-term metabolic consequences of viral eradication remain an area of concern. This study aimed to evaluate the impact of direct-acting antiviral (DAA) treatment on the progression of liver disease and the incidence of metabolic syndrome pre and post DAA treatment in patients with chronic hepatitis C. A total of 313 patients with chronic HCV, including with advanced fibrosis (F3 26.5%, F4 64.2%) or cirrhosis (62%), were observed for at least two years to a maximum of ten, after achieving a sustained virologic response (SVR). The data were gathered from physical examination findings, biochemical tests, fibroscan values, and other relevant metabolic indicators such as BMI, fasting glucose, lipid profile, and blood pressure at different time points: before treatment, at one year follow up and at the latest follow up. The analyses showed that there was a significant regression of fibrosis, the fibroscan scores were almost halved from the baseline, the Child-Pugh classifications also improved (Class C prevalence went from 7.4% to ~0% ) post-SVR. Additionally, the incidence of decompensated cirrhosis dropped by 68%, with significant decrease in portal hypertension, variceal bleeding (from 10% to 0%) and ascites (8% to 0.9%). These findings support the well-established role of DAAs in halting fibrogenesis and reversing important features of advanced liver disease, thus preventing decompensation and possibly reducing the need for long term hepatic transplantation. However, concurrent metabolic health assessment paradoxically showed undesirable worsening of metabolic parameters, with an increase of BMI, obesity rate (from 9.3% to 14.8%%), T2DM (more then doubled), dyslipidemia (8.9% to 43.4%) , hypertension (31% to 42.9%) and hepatic steatosis. To conclude, the results revealed that viral eradication through DAA treatment is a “double edged sword”, if on one side relieves hepatic damage on the other simultaneously reveals or exacerbates the patient’s metabolic vulnerabilities. This unforeseen dual nature of DAAs stresses the necessity to adopt a new standard of care based on an integrated multidisciplinary model able to provide an effective monitoring for both HCC and metabolic complications a to fully optimize patients outcomes.
Chronic hepatitis C virus (HCV) infection is a leading cause of progressive liver disease, cirrhosis, and hepatocellular carcinoma (HCC), posing a significant global health burden. The introduction of direct-acting antiviral (DAA) therapy has revolutionized treatment, achieving high rates of sustained virologic response (SVR) and dramatically reducing liver-related morbidity and mortality. However, the long-term metabolic consequences of viral eradication remain an area of concern. This study aimed to evaluate the impact of direct-acting antiviral (DAA) treatment on the progression of liver disease and the incidence of metabolic syndrome pre and post DAA treatment in patients with chronic hepatitis C. A total of 313 patients with chronic HCV, including with advanced fibrosis (F3 26.5%, F4 64.2%) or cirrhosis (62%), were observed for at least two years to a maximum of ten, after achieving a sustained virologic response (SVR). The data were gathered from physical examination findings, biochemical tests, fibroscan values, and other relevant metabolic indicators such as BMI, fasting glucose, lipid profile, and blood pressure at different time points: before treatment, at one year follow up and at the latest follow up. The analyses showed that there was a significant regression of fibrosis, the fibroscan scores were almost halved from the baseline, the Child-Pugh classifications also improved (Class C prevalence went from 7.4% to ~0% ) post-SVR. Additionally, the incidence of decompensated cirrhosis dropped by 68%, with significant decrease in portal hypertension, variceal bleeding (from 10% to 0%) and ascites (8% to 0.9%). These findings support the well-established role of DAAs in halting fibrogenesis and reversing important features of advanced liver disease, thus preventing decompensation and possibly reducing the need for long term hepatic transplantation. However, concurrent metabolic health assessment paradoxically showed undesirable worsening of metabolic parameters, with an increase of BMI, obesity rate (from 9.3% to 14.8%%), T2DM (more then doubled), dyslipidemia (8.9% to 43.4%) , hypertension (31% to 42.9%) and hepatic steatosis. To conclude, the results revealed that viral eradication through DAA treatment is a “double edged sword”, if on one side relieves hepatic damage on the other simultaneously reveals or exacerbates the patient’s metabolic vulnerabilities. This unforeseen dual nature of DAAs stresses the necessity to adopt a new standard of care based on an integrated multidisciplinary model able to provide an effective monitoring for both HCC and metabolic complications a to fully optimize patients outcomes.
Metabolic syndrome pre and post DAA treatment in patients with chronic hepatitis C
BOCCHIOTTI, ERIKA
2023/2024
Abstract
Chronic hepatitis C virus (HCV) infection is a leading cause of progressive liver disease, cirrhosis, and hepatocellular carcinoma (HCC), posing a significant global health burden. The introduction of direct-acting antiviral (DAA) therapy has revolutionized treatment, achieving high rates of sustained virologic response (SVR) and dramatically reducing liver-related morbidity and mortality. However, the long-term metabolic consequences of viral eradication remain an area of concern. This study aimed to evaluate the impact of direct-acting antiviral (DAA) treatment on the progression of liver disease and the incidence of metabolic syndrome pre and post DAA treatment in patients with chronic hepatitis C. A total of 313 patients with chronic HCV, including with advanced fibrosis (F3 26.5%, F4 64.2%) or cirrhosis (62%), were observed for at least two years to a maximum of ten, after achieving a sustained virologic response (SVR). The data were gathered from physical examination findings, biochemical tests, fibroscan values, and other relevant metabolic indicators such as BMI, fasting glucose, lipid profile, and blood pressure at different time points: before treatment, at one year follow up and at the latest follow up. The analyses showed that there was a significant regression of fibrosis, the fibroscan scores were almost halved from the baseline, the Child-Pugh classifications also improved (Class C prevalence went from 7.4% to ~0% ) post-SVR. Additionally, the incidence of decompensated cirrhosis dropped by 68%, with significant decrease in portal hypertension, variceal bleeding (from 10% to 0%) and ascites (8% to 0.9%). These findings support the well-established role of DAAs in halting fibrogenesis and reversing important features of advanced liver disease, thus preventing decompensation and possibly reducing the need for long term hepatic transplantation. However, concurrent metabolic health assessment paradoxically showed undesirable worsening of metabolic parameters, with an increase of BMI, obesity rate (from 9.3% to 14.8%%), T2DM (more then doubled), dyslipidemia (8.9% to 43.4%) , hypertension (31% to 42.9%) and hepatic steatosis. To conclude, the results revealed that viral eradication through DAA treatment is a “double edged sword”, if on one side relieves hepatic damage on the other simultaneously reveals or exacerbates the patient’s metabolic vulnerabilities. This unforeseen dual nature of DAAs stresses the necessity to adopt a new standard of care based on an integrated multidisciplinary model able to provide an effective monitoring for both HCC and metabolic complications a to fully optimize patients outcomes.File | Dimensione | Formato | |
---|---|---|---|
Bocchiotti Erika 895318.pdf
non disponibili
Dimensione
3.67 MB
Formato
Adobe PDF
|
3.67 MB | Adobe PDF |
I documenti in UNITESI sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
https://hdl.handle.net/20.500.14240/164870