This study evaluated whether the assessment of hepatitis C virus (HCV)-RNA at 12 weeks (FW+12) post-treatment follow-up was as applicable as FW+24 to evaluate sustained virological response (SVR) using the highly sensitive real-time polymerase chain reaction (PCR) HCV assay.
Two hundred and twenty-two patients with chronic hepatitis C were included in this study. Pegylated interferon (Peg-IFN) and ribavirin were administered for 24-72 weeks based on the genotype and viral load. Serum HCV-RNA was measured using real-time PCR at pretreatment, the end of treatment, FW+4, FW+8, FW+12, FW+16, FW+20 and FW+24. Two hundred patients had a virological response at the end of treatment. One hundred and forty-eight of 200 (74.0%) patients with a virological response at the end of treatment had an SVR at the FW+24. The positive predictive value (PPV) to identify patients with SVR at FW+4, FW+8, FW+12 was 87.1, 96.1, 98.0%, respectively. The viral load showed a reversion to the basal level as early as 8 weeks in relapse patients. There were only three patients who relapsed after FW+12 and all three of these patients were females with genotype Ib and a high viral load.
The assessment of serum HCV-RNA FW+12, using the highly sensitive real-time PCR assay, is almost as effective as FW+24 to predict SVR. However, there are false negatives in female patients with a high viral load of genotype Ib when the SVR is predicted by FW+12. The current standard with FW+24 is reasonable, but the assessment of serum HCV-RNA FW+12 may be effective in most patients.
[Show abstract][Hide abstract] ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is one of the five most lethal malignancies worldwide and survival has not improved substantially in the past 30 years. Desmoplasia (abundant fibrotic stroma) is a typical feature of PDAC in humans, and stromal activation commonly starts around precancerous lesions. It is becoming clear that this stromal tissue is not a bystander in disease progression. Cancer-stroma interactions effect tumorigenesis, angiogenesis, therapy resistance and possibly the metastatic spread of tumour cells. Therefore, targeting the tumour stroma, in combination with chemotherapy, is a promising new option for the treatment of PDAC. In this Review, we focus on four issues. First, how can stromal activity be used to detect early steps of pancreatic carcinogenesis? Second, what is the effect of perpetual pancreatic stellate cell activity on angiogenesis and tissue perfusion? Third, what are the (experimental) antifibrotic therapy options in PDAC? Fourth, what lessons can be learned from Langton's Ant (a simple mathematical model) regarding the unpredictability of genetically engineered mouse models?
[Show abstract][Hide abstract] ABSTRACT: Although the anti-hepatitis C virus (HCV) effect of statins in vitro and clinical efficacy of fluvastatin combined with Pegylated interferon (PEG-IFN)/ribavirin therapy for chronic hepatitis C (CHC) have been reported, the details of clinical presentation are largely unknown. We focused on viral relapse that influences treatment outcome, and performed a post-hoc analysis by using data from a randomized controlled trial.
Thirty-four patients in the fluvastatin group and 33 patients in the non-fluvastatin group who achieved virological response (complete early virological response [cEVR] or late virological response [LVR]) with PEG-IFN/ribavirin therapy were subjected to this analysis. Factors contributing to viral relapse were identified by using multiple logistic regression analysis.
Relapse rate in patients with cEVR was significantly lower in the fluvastatin group (2 of 23, 8.7%) than in the non-fluvastatin group (9 of 26, 34.6%; P = 0.042). The use of fluvastatin decreased relapse rate in patients with LVR (27.3% vs 57.1%), though not significantly. Overall, relapse rate was significantly lower in the fluvastatin group (14.7%; 5 of 34) than in the non-fluvastatin group (39.4%; 13 of 33; P = 0.027). Multivariate analysis identified absence of fluvastatin (P = 0.027, odds ratio [OR] = 3.98, 95% confidence interval [CI] = 1.05–15.11) and low total ribavirin dose (P = 0.002, OR = 2.41, 95% CI = 1.38–4.19) as independent factors contributing to relapse.
The concomitant addition of fluvastatin significantly suppressed viral relapse, resulting in the improvement of sustained virological response rate, in PEG-IFN/ribavirin therapy for CHC patients with HCV genotype 1b and high viral load.
Journal of Gastroenterology and Hepatology 09/2012; 28(1). DOI:10.1111/j.1440-1746.2012.07267.x · 3.50 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Studies of cell lines and of animal models of pancreatic cancer have raised a number of provocative questions about the nature and origins of human pancreatic cancer and have provided several leads into exciting new approaches for the treatment of this deadly cancer. In addition, clinicians with little or no contact with human pathology have challenged the way that pancreatic pathology is practiced, suggesting that "genetic signals" may be more accurate than today's multimodal approach to diagnoses. In this review, we consider 8 provocative issues in pancreas pathology, with an emphasis on "the evidence derived from man."
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