Long-term reversal of hypocholesterolaemia in patients with chronic hepatitis C is related to sustained viral response and viral genotype

被引:31
作者
Fernandez-Rodriguez, C. M.
Lopez-Serrano, P.
Alonso, S.
gutierrez, M. L.
Lledo, J. L.
Perez-Calle, J. L.
Temino, R.
Cacho, G.
Nevado, M.
Casas, M. L.
Gasalla, J. M.
Bonets, B.
机构
[1] Fdn Hosp Alcorcon, Unit Gastroenterol & Liver Dis, Madrid 28922, Spain
[2] Fdn Hosp Alcorcon, Unit Pathol, Madrid 28922, Spain
[3] Fdn Hosp Alcorcon, Lab Unit, Madrid 28922, Spain
[4] Fdn Hosp Alcorcon, Paediat Endocrinol Unit, Area Paediat, Madrid 28922, Spain
关键词
D O I
10.1111/j.1365-2036.2006.03000.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Genotype-3 of hepatitis C virus (HCV) has been associated with serum lipid changes (reversible with sustained viral response) and liver steatosis. To characterize the relationships among hepatic steatosis, cholesterol and sustained viral response in these patients. Patients (n = 215) with chronic hepatitis C (157 with genotype-1 of HCV) had age, body mass index, gender, alcohol intake, glycaemia, serum lipids, transaminases, grade and stage (METAVIR and Scheuer), degree of liver steatosis, sustained viral response, insulinaemia, leptinaemia, beta-hydroxybutyrate and glycerol measured, and were compared with 32 hepatitis B virus (HBV)-infected subjects. Genotype-3 of HCV patients had age-adjusted hypocholesterolaemia and more frequent hepatic steatosis (P < 0.001). Steatosis was inversely correlated with serum cholesterol (P < 0.01) and directly with viral load (P < 0.03). In patients with genotype-3 of HCV and sustained viral response, serum cholesterol increased from 138 (95% CI: 120-151) to 180 mg/dL (95% CI: 171-199) 12 months after treatment conclusion (P < 0.0001). By contrast, cholesterol values were unchanged in genotype-3 of HCV non-responders and in patients with genotype-1 of HCV regardless of response. Rising cholesterol in sustained viral response did not parallel the changes in beta-hydroxybutyrate. Besides causing hepatic steatosis, genotype-3 specifically decreases serum cholesterol. This interference with the metabolic lipid pathway is related to viral load, is reversed with sustained viral response, and seems unrelated to mitochondrial dysfunction.
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页码:507 / 512
页数:6
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共 31 条
  • [1] An in vitro model of hepatitis C virus genotype 3a-associated triglycerides accumulation
    Abid, K
    Pazienza, V
    de Gottardi, A
    Rubbia-Brandt, L
    Conne, B
    Pugnale, P
    Rossi, C
    Mangia, A
    Negro, F
    [J]. JOURNAL OF HEPATOLOGY, 2005, 42 (05) : 744 - 751
  • [2] Steatosis accelerates the progression of liver damage of chronic hepatitis C patients and correlates with specific HCV genotype and visceral obesity
    Adinolfi, LE
    Gambardella, M
    Andreana, A
    Tripodi, MF
    Utili, R
    Ruggiero, G
    [J]. HEPATOLOGY, 2001, 33 (06) : 1358 - 1364
  • [3] Hepatitis C virus and other Flaviviridae viruses enter cells via low density lipoprotein receptor
    Agnello, V
    Abel, G
    Elfahal, M
    Knight, GB
    Zhang, QX
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (22) : 12766 - 12771
  • [4] Liver fibrosis is not associated with steatosis but with necroinflammation in French patients with chronic hepatitis C
    Asselah, T
    Boyer, N
    Guimont, MC
    Cazals-Hatem, D
    Tubach, F
    Nahon, K
    Daïkha, H
    Vidaud, D
    Martinot, M
    Vidaud, M
    Degott, C
    Valla, D
    Marcellin, P
    [J]. GUT, 2003, 52 (11) : 1638 - 1643
  • [5] Hepatitis C virus core protein shows a cytoplasmic localization and associates to cellular lipid storage droplets
    Barba, G
    Harper, F
    Harada, T
    Kohara, M
    Goulinet, S
    Matsuura, Y
    Eder, G
    Schaff, Z
    Chapman, MJ
    Miyamura, T
    Brechot, C
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (04) : 1200 - 1205
  • [6] Barbaro G, 1999, AM J GASTROENTEROL, V94, P2198, DOI 10.1111/j.1572-0241.1999.01294.x
  • [7] High body mass index is an independent risk factor for nonresponse to antiviral treatment in chronic hepatitis C
    Bressler, BL
    Guindi, M
    Tomlinson, G
    Heathcote, J
    [J]. HEPATOLOGY, 2003, 38 (03) : 639 - 644
  • [8] Worsening of steatosis is an independent factor of fibrosis progression in untreated patients with chronic hepatitis C and paired liver biopsies
    Castéra, L
    Hézode, C
    Roudot-Thoraval, F
    Bastie, A
    Zafrani, ES
    Pawlotsky, JM
    Dhumeaux, D
    [J]. GUT, 2003, 52 (02) : 288 - 292
  • [9] Hepatitis C virus-induced hepatocellular steatosis
    Castera, L
    Chouteau, P
    Hezode, C
    Zafrani, ES
    Dhumeaux, D
    Pawlotsky, JM
    [J]. AMERICAN JOURNAL OF GASTROENTEROLOGY, 2005, 100 (03) : 711 - 715
  • [10] Effect of antiviral treatment on evolution of liver steatosis in patients with chronic hepatitis C:: indirect evidence of a role of hepatitis C virus genotype 3 in steatosis
    Castéra, L
    Hézode, C
    Roudot-Thoraval, F
    Lonjon, I
    Zafrani, ES
    Pawlotsky, JM
    Dhumeaux, D
    [J]. GUT, 2004, 53 (03) : 420 - 424