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العنوان
Role of liver fibrosis using indirect serological markers in prediction of non-responders and relapsers to sofosbuvir-based treatment in patients with HCV infection/
المؤلف
Helmy,Ahmed Mohamed .
هيئة الاعداد
باحث / أحمد محمد حلمي متولي زكي
مشرف / راويةعبد السلام الفقي
مشرف / عصام محمد بيومي
مشرف / عزة إمام محمد
تاريخ النشر
2017.
عدد الصفحات
207.p;
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب الباطني
تاريخ الإجازة
1/10/2017
مكان الإجازة
جامعة عين شمس - كلية الطب - internal medicine
الفهرس
Only 14 pages are availabe for public view

from 206

from 206

Abstract

Background.
Sustained virological response rates (SVRs) to directly acting antiviral (DAA) therapy for hepatitis C virus (HCV) are lower in decompensated cirrhosis. Markers of innate immunity predict nonresponse to interferon-based HCV treatment; however, whether they are associated with the response to DAAs in patients with decompensation is not known.
Methods.
Information on demographics, adherence, viral kinetics, and resistance were gathered prospectively from a cohort with decompensated cirrhosis treated with 12 weeks of DAAs. C-X-C motif chemokine-10 (CXCL-10) level and T-cell and natural killer (NK) cell phenotype were analyzed pretreatment and at 4 and 12 weeks of treatment.
Results.
Of 32 patients, 24 of 32 (75%) achieved SVR (responders). Eight of 32 (25%) experienced relapse after the end of treatment (nonresponders). There were no differences in demographics or adherence between groups. Nonresponders had higher CXCL-10; 320 pg/mL (179461) vs 109 pg/mL (88170) in responders (P < .001) and differential CXCL-10 dynamics. Nonresponders had lower NK cell frequency, higher expression of activation receptor NKp30, and lower frequency of the NK subset CD56−CD16+.
Conclusions.
Nonresponders to DAAs displayed a different NK phenotype and CXCL-10 profile to responders. Nonresponders did not have poorer adherence or baseline virological resistance, and this shows that immunological parameters are associated with treatment response to interferon-free treatment for HCV in individuals with decompensated cirrhosis.