One-Year Outcomes after Ledipasvir/Sofosbuvir Treatment of Chronic Hepatitis C in Teenagers with and without Significant Liver Fibrosis—A Case Series Report

Abstract

One-year outcomes after therapy with ledipasvir/sofosbuvir (LDV/SOF) in children with chronic hepatitis C (CHC) presenting with and without significant liver fibrosis were analyzed. We included patients aged 12–17 years treated with LDV/SOF, presenting with significant fibrosis (F ≥ 2 on the METAVIR scale) in transient elastography (TE) at the baseline and we compared the outcomes with that of patients without fibrosis. Patients were followed every 4 weeks during the treatment, at the end of the therapy, at week 12 posttreatment, and one year after the end of treatment. Liver fibrosis was established using noninvasive methods: TE, aspartate transaminase-to-platelet ratio index (APRI), and Fibrosis-4 index (FIB-4). There were four patients with significant fibrosis at baseline: one with a fibrosis score of F2 on the METAVIR scale, and three with cirrhosis (F4) at baseline. One year after the end of treatment, the hepatitis C viral load was undetectable in three of them. One patient was lost to follow-up after week 4. In two out of the four patients, a significant improvement and regression of liver fibrosis was observed (from stage F4 and F2 to F0-F1 on the METAVIR scale). In one patient, the liver stiffness measurement median increased 12 weeks after the end of the treatment and then decreased, but still correlated with stage F4. An improvement in the APRI was observed in all patients. In four patients without fibrosis, the treatment was effective and no progression of fibrosis was observed. A one-year observation of teenagers with CHC and significant fibrosis treated with LDV/SOF revealed that regression of liver fibrosis is possible, but not certain. Further observations in larger groups of patients are necessary to find predictors of liver fibrosis regression.

Efficacy and Safety of the Treatment of Chronic Hepatitis C with Sofosbuvir/Ledipasvir in Children Aged 5 to 10 Years with Comorbidities—A Brief Report

“…Interestingly, there was a significant improvement in her LSM at 12 weeks posttreatment to 5.7 kPa, correlating to F0-1 on the Metavir scale. This is consistent with our previous observations in teenagers that suggested the possibility of regression of liver fibrosis after treatment with SOF/LDV [ 17 ]. However, antiviral treatment should not be delayed, and the problem lies in the lack of availability of therapies for children with CHC in national therapeutic programs.…”

Efficacy and safety of treatment with sofosbuvir/velpatasvir in patients aged 6–18 years with chronic hepatitis C—Results of the PANDAA‐PED study

“…In one patient, who presented at baseline with LSM referring to F3 on the Metavir scale, a significant improvement was revealed (to F3). Cases of significant regression of liver fibrosis (from stage F4 and F2 to F0‐F1 on the METAVIR scale) in children treated with DAAs (sofosbuvir/ledipasvir, SOF/LDV) were previously reported 21 . On the other hand, the mean CAP increased in the analysed period, and two cases of liver steatosis were reported (S1 and S3) in children with normal CAP at baseline.…”

“…Most of AEs were related to infections or injuries, and not related to the treatment. Thirty-three AEs were considered possibly or probably related to the administration of SOF/VEL, all of them were described as mild (21) or moderate (12).…”

Defer no more: advances in the treatment and prevention of chronic hepatitis C virus infection in children

“…In addition to curative response, DAA-based treatment may halt or reverse existing liver damage. Several studies in children have demonstrated overall improvements in noninvasive assessments of liver stiffness at 12 weeks and 1 year posttreatment, suggestive of possible reversal of liver damage [35–37,38 ▪ ]. However, persistently elevated liver stiffness measures have been documented in some children after HCV cure, such that post-SVR liver monitoring is recommended in children with pretreatment fibrosis [35–37,38 ▪ ,39].…”