DAA treatment is not associated with a higher risk of HCC in persons with cirrhosis with chronic HCV infection in the short term. Previously reported higher rates of HCC associated with DAA treatment may be explained by both the presence of relatively fewer baseline HCC risk factors in persons treated with IFN as well as selection bias, given that DAA regimens were used to treat persons at higher risk for developing HCC. (Hepatology 2018;67:2244-2253).
Purpose. To determine the immune response after dendritic cell (DC) vaccine and cytokine-induced killer cells (CIK) therapy and assess its associated toxicity, survival benefit, and changes in the quality of life (QOL) of advanced colorectal cancer (CRC) patients. Methods. We recruited 100 patients with unresectable CRC orrelapsed CRC after surgery who received DC vaccine and CIK cells (group immunotherapy, group I), and, as a control, 251 patients who had similar characteristics and underwent similar treatments, except for this immunotherapy (group nonimmunotherapy, group NI). After a follow-up period of 489.2 ± 160.4 days, overall survival (OS) of the two groups was compared using the Kaplan-Meier method. Results. In group I, 62% of patients developed a positive delayed type hypersensitivity response, and most patients showed an improvement in physical strength (75.2%), appetite (74.2%), sleeping (72.1%), and body weight (70.1%). Adverse events were fever (29.5%), insomnia (19.2%), anorexia (9.1%), sore joints (5.4%), and skin rash (1.0%). No toxicity was observed in patients treated with DC vaccine and CIK therapy. OS was significantly longer in group I than in group NI (P = 0.043). Conclusion. DC vaccine and CIK therapy were safe and could induce an immune response against CRC, thereby improving QOL and prolonging OS.
Summary
Background
Directly acting antiviral agents (DAA) have been associated with hepatic decompensation, especially in patients with pre‐treatment cirrhosis, but this risk is not well defined.
Aim
To determine the incidence of hepatic decompensation, liver transplantation, death and worsening renal function in patients treated with a Paritaprevir/ritonavir, Ombitasvir, Dasabuvir (PrOD), sofosbuvir/simeprevir or sofosbuvir/ledipasvir regimen.
Methods
We followed ERCHIVES participants treated with the above regimens for up to 12 weeks post‐treatment. We excluded those with HIV, HBsAg+ and pre‐existing diagnosis of hepatic decompensation and hepatocellular carcinoma.
Results
Of 3728 persons on PrOD, 1578 on sofosbuvir/simeprevir and 10 440 on sofosbuvir/ledipasvir, incidence rates (95% CI) of hepatic decompensation/1000 patient‐years were 10.6 (5.89–17.36) for the PrOD, 32.4 (20.74–48.16) for the sofosbuvir/simeprevir and 13.0 (9.74–17.10) for the sofosbuvir/ledipasvir. Among those with baseline cirrhosis, these rates were 36.9 (19.1–64.5), 61.8 (38.2–94.5) and 41.1 (29.9–55.2) respectively, while among those without cirrhosis at baseline, these rates were 2.7 (0.6–8.0), 7.5 (1.5–21.8) and 2.7 (1.2–5.4). Advanced fibrosis was associated with increased risk of hepatic decompensation in all groups [HR (95% CI) per 0.5 unit increase in FIB‐4 score: PrOD 1.11 (1.07–1.16); sofosbuvir/simeprevir 1.03 (1.01–1.05); sofosbuvir/ledipasvir 1.02 (1.01–1.03)]. There were no deaths. Proportion of persons with eGFR decrease >30 ml/min/1.73 m2 was higher among the PrOD group, but presence of cirrhosis did not appear to affect this.
Conclusions
The incidence of hepatic decompensation in persons treated with PrOD, up to 12 weeks after completion of treatment, was comparable to those treated with sofosbuvir/ledipasvir regimen, and was lower than among those treated with a sofosbuvir/simeprevir regimen. Such risk was predominantly observed in those with pre‐treatment cirrhosis.
BackgroundAs an acute-phase protein, serum amyloid A (SAA) is expressed primarily in the liver. However, its expression in extrahepatic tissues, especially in tumor tissues, was also demonstrated recently. In our study, we investigated the expression of SAA in uterine cervical carcinomas, and our results suggested its potential as a serum biomarker.MethodsQuantitative real-time polymerase chain reaction (RT-PCR), immunohistochemistry (IHC) and enzyme-linked immunosorbent assay (ELISA) were used to evaluate the SAA gene and protein expression levels in the tissues and sera of patients with non-neoplastic lesions (NNLs), cervical intraepithelial neoplasia (CIN) and cervical carcinoma (CC).ResultsCompared with NNLs, the SAA gene (SAA1 and SAA4) expression levels were significantly higher in uterine CC (mean copy numbers: 138.7 vs. 5.01, P < 0.000; and 1.8 vs. 0.079, P = 0.001, respectively) by real-time PCR. IHC revealed cytoplasmic SAA protein staining in tissues from adenocarcinoma and squamous cell carcinoma of the cervix. The median serum concentrations (μg/ml) of SAA were 6.02 in patients with NNLs and 10.98 in patients with CIN (P = 0.31). In contrast, the median serum SAA concentration was 23.7 μg/ml in uterine CC patients, which was significantly higher than the SAA concentrations of the NNL group (P = 0.002) and the CIN group (P = 0.024).ConclusionsOur data suggested that SAA might be a uterine CC cell product. High SAA concentrations in the serum of CC patients may have a role in monitoring disease occurrence and could have therapeutic applications.Virtual slidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1433263219102962.
FIB-4 score is a better predictor of HD and HCC in HCV-positive persons. A score of <3 is associated with a low risk of HD and HCC 1 and 3 years after HCV diagnosis.
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