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Steatosis accelerates the progression of liver damage of chronic hepatitis C patients and correlates with specific HCV genotype and visceral obesity.
Hepatology 2001; 33(6):1358-64Hep

Abstract

The role of steatosis in the progression of liver damage in chronic hepatitis C (CHC) was studied. Enrolled were 180 consecutive liver biopsy-proven CHC patients and 41 additional subjects with a known duration of infection. We evaluated the histological activity index (HAI), grade of fibrosis and steatosis, body mass index (BMI; kg/m(2)), distribution of body fat, HCV genotype, and levels of HCV RNA. Eighty six (48%) patients showed steatosis, and a higher prevalence was observed in genotype 3a infection (P <.01). A correlation between the grade of steatosis and fibrosis was observed (P <.001). Fibrosis was also associated with age (P <.001). After adjusting for age, the association between steatosis and fibrosis remained significant. The grade of steatosis also correlated with the HAI (P <.007) with a significant increase in periportal necrosis. No relation was found between steatosis and age, gender, iron storage, or levels of HCV RNA. Patients with a high grade of steatosis (>30%) showed higher serum levels of gamma-GT and ALT (P <.001). Overall, steatosis was not significantly associated to BMI. Analysis by single genotype showed a significant association between the grade of steatosis and BMI in type 1 infection r =.689; P <.001) and with levels of HCV RNA in type 3a infection r =.786; P <.001). Visceral fat distribution rather than BMI proved to be associated with steatosis (P <.001). Data obtained from patients with a known date of infection confirmed that steatosis grades 3-4 were associated with a higher annual rate of fibrosis progression, and showed that alcohol and steatosis act together in increasing fibrosis (P <.05). Our data indicate that steatosis is an important cofactor in increasing liver necroinflammatory activity and in accelerating fibrosis in CHC. Visceral obesity and genotype 3a play a role in the development of steatosis.

Authors+Show Affiliations

Internal Medicine & Hepatology, Second University of Naples, Naples, Italy. luigielo.adinolfi@unina2.itNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11391523

Citation

Adinolfi, L E., et al. "Steatosis Accelerates the Progression of Liver Damage of Chronic Hepatitis C Patients and Correlates With Specific HCV Genotype and Visceral Obesity." Hepatology (Baltimore, Md.), vol. 33, no. 6, 2001, pp. 1358-64.
Adinolfi LE, Gambardella M, Andreana A, et al. Steatosis accelerates the progression of liver damage of chronic hepatitis C patients and correlates with specific HCV genotype and visceral obesity. Hepatology. 2001;33(6):1358-64.
Adinolfi, L. E., Gambardella, M., Andreana, A., Tripodi, M. F., Utili, R., & Ruggiero, G. (2001). Steatosis accelerates the progression of liver damage of chronic hepatitis C patients and correlates with specific HCV genotype and visceral obesity. Hepatology (Baltimore, Md.), 33(6), pp. 1358-64.
Adinolfi LE, et al. Steatosis Accelerates the Progression of Liver Damage of Chronic Hepatitis C Patients and Correlates With Specific HCV Genotype and Visceral Obesity. Hepatology. 2001;33(6):1358-64. PubMed PMID: 11391523.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Steatosis accelerates the progression of liver damage of chronic hepatitis C patients and correlates with specific HCV genotype and visceral obesity. AU - Adinolfi,L E, AU - Gambardella,M, AU - Andreana,A, AU - Tripodi,M F, AU - Utili,R, AU - Ruggiero,G, PY - 2001/6/8/pubmed PY - 2001/6/29/medline PY - 2001/6/8/entrez SP - 1358 EP - 64 JF - Hepatology (Baltimore, Md.) JO - Hepatology VL - 33 IS - 6 N2 - The role of steatosis in the progression of liver damage in chronic hepatitis C (CHC) was studied. Enrolled were 180 consecutive liver biopsy-proven CHC patients and 41 additional subjects with a known duration of infection. We evaluated the histological activity index (HAI), grade of fibrosis and steatosis, body mass index (BMI; kg/m(2)), distribution of body fat, HCV genotype, and levels of HCV RNA. Eighty six (48%) patients showed steatosis, and a higher prevalence was observed in genotype 3a infection (P <.01). A correlation between the grade of steatosis and fibrosis was observed (P <.001). Fibrosis was also associated with age (P <.001). After adjusting for age, the association between steatosis and fibrosis remained significant. The grade of steatosis also correlated with the HAI (P <.007) with a significant increase in periportal necrosis. No relation was found between steatosis and age, gender, iron storage, or levels of HCV RNA. Patients with a high grade of steatosis (>30%) showed higher serum levels of gamma-GT and ALT (P <.001). Overall, steatosis was not significantly associated to BMI. Analysis by single genotype showed a significant association between the grade of steatosis and BMI in type 1 infection r =.689; P <.001) and with levels of HCV RNA in type 3a infection r =.786; P <.001). Visceral fat distribution rather than BMI proved to be associated with steatosis (P <.001). Data obtained from patients with a known date of infection confirmed that steatosis grades 3-4 were associated with a higher annual rate of fibrosis progression, and showed that alcohol and steatosis act together in increasing fibrosis (P <.05). Our data indicate that steatosis is an important cofactor in increasing liver necroinflammatory activity and in accelerating fibrosis in CHC. Visceral obesity and genotype 3a play a role in the development of steatosis. SN - 0270-9139 UR - https://www.unboundmedicine.com/medline/citation/11391523/Steatosis_accelerates_the_progression_of_liver_damage_of_chronic_hepatitis_C_patients_and_correlates_with_specific_HCV_genotype_and_visceral_obesity_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0270913901658336 DB - PRIME DP - Unbound Medicine ER -