Visceral adiposity index is associated with histological findings and high viral load in patients with chronic hepatitis C due to genotype 1.
Metabolic factors have been associated with liver damage in patients with genotype 1 chronic hepatitis C (G1 CHC). We tested visceral adiposity index (VAI), a new marker of adipose dysfunction in G1 CHC, patients to assess its association with host and viral factors and its link to both histological findings and sustained virological response (SVR). Two hundred thirty-six consecutive G1 CHC patients were evaluated by way of liver biopsy and anthropometric and metabolic measurements, including insulin resistance (IR), homeostasis model assessment (HOMA), and VAI using waist circumference, body mass index, triglycerides, and high-density lipoprotein cholesterol. All biopsies were scored by one pathologist for staging and grading and graded for steatosis, which was considered moderate to severe if ≥ 30%. Multiple linear regression analysis revealed that VAI score was independently associated with higher HOMA score (P = 0.009), log10 hepatitis C virus RNA levels (P = 0.01), necroinflammatory activity (P = 0.04), and steatosis (P = 0.04). Multiple logistic regression analysis revealed that IR (OR 3.879, 95% CI 1.727-8.713, P = 0.001), higher VAI score (OR 1.472, 95% CI 1.051-2.062, P = 0.02), and fibrosis (OR 2.255, 95% CI 1.349-3.768, P = 0.002) were linked to steatosis ≥ 30%. Logistic regression analysis revealed that older age (OR 1.030, 95% CI 1.002-1.059, P = 0.03), higher VAI score (OR 1.618, 95% CI 1.001-2.617, P = 0.04), and fibrosis (OR 2.608, 95% CI 1.565-4.345, P < 0.001) were independently associated with moderate to severe necroinflammatory activity. No independent associations were found between VAI score and both fibrosis and SVR.


CONCLUSIONS
In G1 CHC patients, higher VAI score is independently associated with both steatosis and necroinflammatory activity and has a direct correlation with viral load.
Petta
Salvatore
S
Dipartimento Biomedico Di Medicina Interna e Specialistica, Cattedra di Gastroenterologia, DiBiMIS, Palermo, Italy. petsa@inwind.it
Amato
Marco
M
Cabibi
Daniela
D
Cammà
Calogero
C
Di Marco
Vito
V
Giordano
Carla
C
Galluzzo
Aldo
A
Craxì
Antonio
A
D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000428:Alcohol Drinking / Q000235:genetics / Q000473:pathology; D000998:Antiviral Agents / Q000627:therapeutic use; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D008076:Cholesterol, HDL / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000150:complications; D005234:Fatty Liver / Q000235:genetics / Q000473:pathology / Q000821:virology; D005260:Female; D005838:Genotype; D019698:Hepatitis C, Chronic / Q000150:complications / Q000235:genetics* / Q000473:pathology / Q000821:virology*; D006801:Humans; D006973:Hypertension / Q000150:complications; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use; D050152:Intra-Abdominal Fat / Q000033:anatomy & histology* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols / Q000627:therapeutic use; D012367:RNA, Viral / Q000235:genetics; D011994:Recombinant Proteins; D019562:Viral Load; D055105:Waist Circumference
D000998:Antiviral Agents; D001786:Blood Glucose; D008076:Cholesterol, HDL; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D000410:Alanine Transaminase; C100416:peginterferon alfa-2a