P757 REDUCING POLYMORPHISMS CONSISTING OF (TA)N DINUCLEOTIDE REPEAT NEAR IL28B GENE ASSOCIATE WITH THE DEVIATION OF IL28B SNPS AND AFFECT VIRAL RESPONSE OF PEGIFN/RBV

2014 ◽  
Vol 60 (1) ◽  
pp. S323
Author(s):  
M. Korenaga ◽  
M. Sugiyama ◽  
T. Takeda ◽  
Y. Aoki ◽  
S. Yoshio ◽  
...  
1999 ◽  
Vol 30 (4) ◽  
pp. 320-321 ◽  
Author(s):  
L. S. Ruth ◽  
T. J. Hopman ◽  
. Schug ◽  
C. F. Aquadro ◽  
A. T. Bowling ◽  
...  
Keyword(s):  

1999 ◽  
Vol 30 (6) ◽  
pp. 462-478
Author(s):  
P J Venta ◽  
Y Cao ◽  
L Alexander ◽  
V Yuzbasiyan-Gurkan

2000 ◽  
Vol 31 (2) ◽  
pp. 141-141 ◽  
Author(s):  
M C Roberts ◽  
J Murtaugh ◽  
S J Valberg ◽  
J R Mickelson ◽  
L J Alexander
Keyword(s):  

1994 ◽  
Vol 71 (06) ◽  
pp. 731-736 ◽  
Author(s):  
M W Mansfield ◽  
M H Stickland ◽  
A M Carter ◽  
P J Grant

SummaryTo identify whether genotype contributes to the difference in PAI-1 levels in type 1 and type 2 diabetic subjects and whether genotype relates to the development of retinopathy, a Hind III restriction fragment length polymorphism and two dinucleotide repeat polymorphisms were studied. In 519 Caucasian diabetic subjects (192 type 1, 327 type 2) and 123 Caucasian control subjects there were no differences in the frequency of the Hind III restriction alleles (type 1 vs type 2 vs control: allele 1 0.397 vs 0.420 vs 0.448; allele 2 0.603 vs 0.580 vs 0.552) nor in the allelic frequency at either dinucleotide repeat sequence. In 86 subjects with no retinopathy at 15 years or more from diagnosis of diabetes and 190 subjects with diabetic retinopathy there was no difference in the frequency of Hind III restriction alleles (retinopathy present vs retinopathy absent: allele 1 0.400 vs 0.467; allele 2 0.600 vs 0.533) nor in the allelic frequencies at either dinucleotide repeat sequence. The results indicate that there is no or minimal influence of the PAI-1 gene on either PAI-1 levels or the development of diabetic retinopathy in patients with diabetes mellitus.


2016 ◽  
Vol 25 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Tim Zimmermann ◽  
Dietrich Hueppe ◽  
Stefan Mauss ◽  
Peter Buggisch ◽  
Heike Pfeiffer-Vornkahl ◽  
...  

Background & Aims: Smoking has multiple effects on factors influencing hepatitis C and antiviral therapy, including lipid metabolism, fibrosis, platelet count and adherence aspects. The aim of this analysis was to determine the impact of smoking on hepatitis C virus antiviral therapy. Methods: Data of two cohorts of an observational multicenter study including therapy-naïve patients infected with genotype 1 hepatitis C virus (HCV) treated with dual antiviral therapy (n=7,796) with pegylated interferon alpha 2a in combination with ribavirin, or triple antiviral therapy (n=1,122) containing telaprevir or boceprevir, were analysed. Results: In the univariate matched pair analysis of dual antiviral therapy patients (n=584), smoking was significantly associated with lower sustained viral response rates (p=0.026, OR 0.69 CI: 0.50 – 0.96). The effect of smoking on sustained viral response remained significant (p=0.028, OR 0.67 CI: 0.47 – 0.96) in the multivariate analysis when adjusting for all other baseline parameters with a significant association in the univariate analysis, i.e. diabetes, fibrosis, body mass index, transaminases and baseline viral load. Under protease inhibitors the influence of smoking on virological response did not arise. Conclusions: Smoking has a negative impact on antiviral therapy in naïve patients infected with HCV genotype 1 independently of age, gender, history of drug use or alcoholic liver disease. The effects of smoking might be overcome by the new antiviral agents.Abbreviations: APRI: AST to platelet ratio index; DAA: direct antiviral agent; DT: dual antiviral therapy; EoTR: end of treatment response; RVR: rapid virological response; EVR: early virological response; HCV: hepatitis C virus; IFN: interferon alpha; MPA: Matched Pair Analysis; NS: non-smokers; PEG-IFN: pegylated interferon alpha 2a; PI: protease inhibitor; RBV: ribavirin; SAE: serious adverse event; SOC: standard of care; S: smokers; SVR: sustained viral response.    


2020 ◽  
Vol 7 (Supplement_1) ◽  
pp. S561-S562
Author(s):  
Jehan F Chowdhury ◽  
Anna Winston ◽  
Tanya Zeina ◽  
Hong Gi Shim ◽  
Tine Vindenes

Abstract Background Hepatitis C virus (HCV) is a leading cause of advanced liver disease and death. In the United States about 3.5 million people are living with HCV, but only 50% are aware of the infection, 16% are prescribed treatment, and only 9% achieve sustained viral response. The World Health Organization published an HCV elimination goal for 2030 that strives to achieve a 65% reduction in HCV-related deaths and 90% reduction in transmission. An important step toward this goal is micro-elimination at local hospitals by addressing care gaps in the HCV care cascade. Figure 1 Methods We created a retrospective cohort of patients who tested positive for HCV antibody (HCV Ab+) between 2016 and 2018 at Tufts Medical Center in Boston, Massachusetts. We assessed achievement of care cascade steps including HCV viral load (VL) testing, linkage to care, treatment initiation, and sustained viral response (SVR). We also assessed patient demographics, clinical factors and HCV risk factors. We used STATA/IC 14.1 to conduct bivariate analysis to identify factors associated with loss to follow-up across each care cascade step. Results A total of 24,308 HCV antibody tests were done during this timeframe, of which 5% (n=1,222) were HCV Ab+. After excluding duplicate tests, 1,041 unique patients with HCV Ab+ were included. This cohort had a mean age of 47 years and were 61% male, 66% white, 72% on public insurance, 12% HIV-positive, 13% HCV treatment-experienced. The most frequent HCV risk factor was injection drug use, occurring in 64% of patients. Of patients with HCV Ab+, 76% (n=791) were tested for an HCV VL, of which 50% (n=393) had detectable VL and 50% (n=398) had undetectable VL. Of the patients with a detectable VL, 58% (n=226) were linked with care. Following care linkage, 69% (n=155) initiated treatment, of which 90% (n=139) completed treatment, of which 97% (n=135) achieved SVR (Figure 1). Factors that were significantly associated with getting a VL test and linking to care included private insurance, HIV co-infection, absence of intravenous drug use and cirrhosis; however, these factors were not significantly associated with achieving subsequent steps. Conclusion Assessment of the HCV care cascade at our hospital allowed us to identify clear care gaps and areas needing improvement towards a local micro-elimination. Disclosures All Authors: No reported disclosures


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