The obtained efficacy estimates were synthesized with a mixed treatment comparison meta-analysis. Treatment benefit and degree of disease activity, as reflected with Bath Ankylosing Spondylitis Functional
Index (BASFI) and Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) scores, were related to QALYs and AS-specific costs (related to BASDAI). Other cost outcomes related to drug acquisition, and gastrointestinal and cardiovascular safety. Uncertainty in the source data was translated into uncertainty in cost-effectiveness estimates and therefore decision uncertainty. Costs and outcomes were discounted at 3.5% per annum.
Results: There was a >98% probability that treatment with etoricoxib results in greater QALYs than the other interventions. Over a 30-year time horizon, starting AS treatment with etoricoxib was associated with about 0.4 more QALYs than SBE-β-CD clinical trial the other interventions. At 2 years there was a 77% probability that etoricoxib had the lowest cost. This increased to >99%
at 30 years. Etoricoxib is expected to save pound 13 620 (year 2007 values) relative to celecoxib (200/400 mg), 9957 pound relative to diclofenac and 9863 relative to naproxen. For a willingness-to-pay ceiling ratio of 20 000 per QALY, there was a >97% probability that etoricoxib was the most cost-effective treatment. Additional analysis with different assumptions, including celecoxib 200 mg, and ignoring cost-offsets associated with improvements SNX-5422 solubility dmso in disease activity, supported these findings.
Conclusions: This economic evaluation suggests that, from the UK NHS perspective, etoricoxib
is the most cost-effective initial NSAID treatment for AS patients.”
“Fibroblast growth factors (FGFs) and their receptors (FGFRs) have been implicated in prostate growth and are overexpressed in benign prostatic hyperplasia (BPH). In this study, we investigated whether single nucleotide polymorphisms (SNPs) of the FGFR genes (FGFR1 and FGFR2) were associated with BPH and its clinical phenotypes in a population of Korean men. We genotyped four SNPs in the exons of FGFR1 and FGFR2 (rs13317 in FGFR1; rs755793, rs1047100, and rs3135831 in FGFR2) using direct sequencing in www.selleckchem.com/products/3-deazaneplanocin-a-dznep.html 218 BPH patients and 213 control subjects. No SNPs of FGFR1 or FGFR2 genes were associated with BPH. However, analysis according to clinical phenotypes showed that rs1047100 of FGFR2 was associated with prostate volume in BPH in the dominant model (GA/AA versus GG, P = 0.010). In addition, a significant association was observed between rs13317 of FGFR1 and international prostate symptom score (IPSS) in the additive (TC versus CC versus TT, P = 0.0022) and dominant models (TC/CC versus TT, P = 0.005). Allele frequency analysis also showed significant association between rs13317 and IPSS (P = 0.005). These results suggested that FGFR genes could be related to progression of BPH.