About 63% from the study participants were male, and 37% were female — with an average chronilogical age of 58. Almost 56% had not been in HCV treatment before.
About 27.7% from the study had stage F3 (severe) fibrosis. Just a little over 72% had cirrhosis (65.3% with Child-Pugh class A and sevenPercent with Child-Pugh class B). Comorbidities were somewhat common, with 11.2% getting diabetes, 14.8% getting coronary disease and 5.3% obesity.
When it comes to genotypes:
- Genotype 1a was discovered in 19.1% of participants.
The DAA regimens were also varied:
- Sofosbuvir (Sovaldi) + ribavirin for 12-24 days in 18.3% of participants.
Rates of cure, also known as SVR12 (sustained virologic response 12 days after ending therapy), varied according to liver disease stage. About 97.2% of individuals with F3 fibrosis achieved SVR12, while 92.7% of individuals with cirrhosis (Child A) and 80% of individuals with cirrhosis (Child B) achieved SVR12.
They discovered that throughout the study period 41 participants acquired HCC to have an HCC incidence rate of just one.64%. This incidence rate differed by liver disease stage. For individuals with F3 fibrosis, the incidence was .23%. For individuals with cirrhosis (Child A), the incidence rate was 1.64%. And, for individuals with cirrhosis (Child B), the incidence rate was 2.92%. The main difference between the 3 groups was statistically significant (P = .05), as the difference backward and forward cirrhosis groups wasn’t (P = .259).
The general HCC incidence rate present in this group was less than historic incidence rates present in untreated individuals coping with HCV within the same region, they noted, with Romano highlighting that 2.8% and three.9% were past incidence rates.
Further analyzing the information, they discovered that HCC risk was connected with elevated liver enzymes and occasional platelet count, although not along with other factors, including gender, age, HCV genotype and DAA regimen. Particularly, the very best predictor of HCC risk was APRI score, which measures liver scarring. Individuals by having an APRI score below 2.5 had an HCC incidence rate of just one.52, while individuals by having an APRI score more than or comparable to 2.5 had an incidence rate of three.27 (P = .02).
"The outcomes of the study, while confirming that DAAs treatment does not boost the overall chance of HCC, indicate that there’s no medicinal protection against HCC despite effective antiviral therapy, a minimum of throughout the first six to 12 several weeks after initiation of treatment[,]" stated lead study author Alfredo Alberti, M.D., based on the study pr release. "Therefore, it’s mandatory that patients given DAAs with advanced liver disease should continue being monitored for HCC," Alberti concluded.
Warren Tong may be the senior science editor for TheBody.com and TheBodyPRO.com.
Follow Warren on Twitter: @WarrenAtTheBody.