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   <subfield code="a">10.1007/s10620-010-1417-9</subfield>
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   <subfield code="a">Prevalence and Impact of Hepatic Steatosis on the Response to Antiviral Therapy in Saudi Patients with Genotypes 1 and 4 Chronic Hepatitis C</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Abdallah AlQaraawi, Faisal Sanai, Hussa Al-Husseini, Ali Albenmousa, Abdulmalik AlSheikh, Lubna Ahmed, Ahmad Hersi, Molfi Al-Otaibi, Mohammed Syed, Safiyya Ali, Waleed Al-hamoudi, Khalid Alswat, Ayman Abdo]</subfield>
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   <subfield code="a">Background: Hepatic steatosis in hepatitis C virus (HCV)-infected patients has been shown to enhance the progression of liver fibrosis and decrease the response to antiviral therapy. Aims: We aimed to determine the role of HCV genotype 4 (HCV-G4) in the prevalence of hepatic steatosis, its impact on antiviral therapy, and its associations and predictive factors in comparison to HCV-G1-infected patients. Methods: Treatment-naïve HCV patients who were started on pegylated interferon a-2b plus ribavirin therapy in two centers in Saudi Arabia were included. The severity of steatosis was assessed using the METAVIR and NAS (non-alcoholic fatty liver disease [NAFLD] activity score) scoring systems. Sustained virological response (SVR) was studied in relation to the degree of steatosis. Associations between steatosis and multiple demographic, laboratory, and virological factors were examined. HCV-G1 and HCV-G4 patients were compared. Results: A total of 116 patients (HCV-G4 85 [73.3%]; HCV-G1 31 [26.7%]) were included. The mean age was 50.4±10.7years and 56.9% were males. In terms of steatosis grading using the NAS scoring system, 50% had steatosis grade 0, 26.7% grade 1, 14.7% grade 2, and 8.6% grade 3, while the overall staging of steatosis revealed that 43.1% had mild steatosis, 42.2% moderate, and 14.7% severe. Gamma-glutamyl transpeptidase (GGT), platelet count, body mass index (BMI), cholesterol level, presence of hyperlipidemia, liver histology stage, and grade were significantly correlated with hepatic steatosis in one or more of the statistical analyses. Twenty-two out of 55 patients (40.0%) had an SVR in the mild steatosis group, compared to 52.7% in the moderate group and 7.3% in the severe group (P=0.03). The HCV genotype did not correlate with steatosis or SVR. Conclusion: Our study confirms the high prevalence of steatosis in HCV-G4 and HCV-G1 patients, but with no difference in the grade or score of steatosis between the two genotypes. The grade of steatosis correlates with GGT, platelet count, and BMI, while the NAS score of steatosis correlates with response to antiviral therapy.</subfield>
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   <subfield code="a">Springer Science+Business Media, LLC, 2010</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Hepatitis C</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Steatosis</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Histology</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Genotype 4</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">NAS score</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Inflammation</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Fibrosis</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Interferon</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">AlQaraawi</subfield>
   <subfield code="D">Abdallah</subfield>
   <subfield code="u">Department of Medicine, College of Medicine, King Saud University, P.O. Box 2925 (59), 11461, Riyadh, Saudi Arabia</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Sanai</subfield>
   <subfield code="D">Faisal</subfield>
   <subfield code="u">Department of Hepatobiliary Sciences, King Abdulaziz Medical City, Riyadh, Saudi Arabia</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Al-Husseini</subfield>
   <subfield code="D">Hussa</subfield>
   <subfield code="u">Department of Pathology, Riyadh Military Hospital, Riyadh, Saudi Arabia</subfield>
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   <subfield code="a">Albenmousa</subfield>
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   <subfield code="u">Hepatology Unit, Department of Medicine, Riyadh Military Hospital, Riyadh, Saudi Arabia</subfield>
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   <subfield code="a">AlSheikh</subfield>
   <subfield code="D">Abdulmalik</subfield>
   <subfield code="u">Department of Pathology, College of Medicine, King Saud University, Riyadh, Saudi Arabia</subfield>
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   <subfield code="a">Ahmed</subfield>
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   <subfield code="u">Department of Pathology, College of Medicine, King Saud University, Riyadh, Saudi Arabia</subfield>
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   <subfield code="a">Hersi</subfield>
   <subfield code="D">Ahmad</subfield>
   <subfield code="u">Department of Medicine, College of Medicine, King Saud University, P.O. Box 2925 (59), 11461, Riyadh, Saudi Arabia</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Al-Otaibi</subfield>
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   <subfield code="u">Hepatology Unit, Department of Medicine, Riyadh Military Hospital, Riyadh, Saudi Arabia</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Syed</subfield>
   <subfield code="D">Mohammed</subfield>
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   <subfield code="a">Ali</subfield>
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   <subfield code="u">Liver Disease Research Center, King Saud University, Riyadh, Saudi Arabia</subfield>
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   <subfield code="a">Al-hamoudi</subfield>
   <subfield code="D">Waleed</subfield>
   <subfield code="u">Department of Medicine, College of Medicine, King Saud University, P.O. Box 2925 (59), 11461, Riyadh, Saudi Arabia</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Alswat</subfield>
   <subfield code="D">Khalid</subfield>
   <subfield code="u">Department of Medicine, College of Medicine, King Saud University, P.O. Box 2925 (59), 11461, Riyadh, Saudi Arabia</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Abdo</subfield>
   <subfield code="D">Ayman</subfield>
   <subfield code="u">Department of Medicine, College of Medicine, King Saud University, P.O. Box 2925 (59), 11461, Riyadh, Saudi Arabia</subfield>
   <subfield code="4">aut</subfield>
  </datafield>
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   <subfield code="t">Digestive Diseases and Sciences</subfield>
   <subfield code="d">Springer US; http://www.springer-ny.com</subfield>
   <subfield code="g">56/4(2011-04-01), 1222-1228</subfield>
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   <subfield code="u">Department of Medicine, College of Medicine, King Saud University, P.O. Box 2925 (59), 11461, Riyadh, Saudi Arabia</subfield>
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