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Sökning: WFRF:(Nakata A)

  • Resultat 1-10 av 19
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  • 2017
  • swepub:Mat__t
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  • Pellegrino, T, et al. (författare)
  • Moderated Poster Session 3 : Monday 4 May 2015, 10
  • 2015
  • Ingår i: European Heart Journal Cardiovascular Imaging. - : Oxford University Press (OUP). - 2047-2404 .- 2047-2412. ; 16 Suppl 1
  • Tidskriftsartikel (refereegranskat)
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6.
  • Nyberg, F, et al. (författare)
  • Interstitial lung disease in gefitinib-treated Japanese patients with non-small-cell lung cancer: genome-wide analysis of genetic data
  • 2011
  • Ingår i: Pharmacogenomics. - : Future Medicine Ltd. - 1744-8042 .- 1462-2416. ; 12:7, s. 965-975
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim: To investigate potential relationships between SNPs and acute interstitial lung disease (ILD) events in Japanese non-small-cell lung cancer patients receiving gefitinib. Materials & methods: Japanese non-small-cell lung cancer patients treated with gefitinib from a prospective pharmacoepidemiological cohort with a nested case–control study component (‘CCS’; 52 ILD cases, 139 controls) and a retrospective study (28 ILD cases, 55 controls) were genotyped for nearly 500,000 SNPs. Associations between genotype and ILD were evaluated using Fisher’s exact test and logistic regression modeling, and false discovery rate analysis was used to adjust for the large number of statistical tests. Results: The CCS data provided some false discovery rate evidence that the significance of top-ranking SNPs exceeded levels expected by chance, suggesting some genuine associations. However, replication analyses using retrospective study data were not supportive and there was little evidence of strong genetic associations from a combined analysis. Adjustment of CCS analyses for clinical variables provided little additional convincing evidence. Significant gene–gene interactions between SNP pairs using CCS data were not confirmed in retrospective study replication analyses. Conclusion: Although it is not possible to exclude genetic influences in ILD etiology, common sequence variation is unlikely to explain a major component of ILD risk. Our top results may provide a useful hypothesis-generating starting point for further research. Presented, in part, at the 26th ICPE: International Conference on Pharmacoepidemiology & Therapeutic Risk Management, Brighton, UK, 19–22 August 2010. Original submitted 1 December 2010; Revision submitted 22 February 2011
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  • Rhee, CM, et al. (författare)
  • Serum Thyrotropin Elevation and Coronary Artery Calcification in Hemodialysis Patients
  • 2022
  • Ingår i: Cardiorenal medicine. - : S. Karger AG. - 1664-5502 .- 1664-3828. ; 12:3, s. 106-116
  • Tidskriftsartikel (refereegranskat)abstract
    • <b><i>Introduction:</i></b> Hypothyroidism is highly prevalent in end-stage kidney disease patients, and emerging data show that lower circulating thyroid hormone levels lead to downregulation of vascular calcification inhibitors and coronary artery calcification (CAC) in this population. To date, no studies have examined the association of serum thyrotropin (TSH), the most sensitive and specific single biochemical metric of thyroid function, with CAC risk in hemodialysis patients. <b><i>Methods:</i></b> In secondary analyses of patients from the <i>Anti-Inflammatory and Anti-Oxidative Nutrition in Hypoalbuminemic Dialysis Patients</i> trial, we examined serum TSH levels and CAC risk assessed by cardiac computed tomography scans collected within a 90-day period. We evaluated the relationship between serum TSH with CAC Volume (VS) and Agatston score (AS) (defined as &#x3e;100 mm<sup>3</sup> and &#x3e;100 Houndsfield Units, respectively) using multivariable logistic regression. <b><i>Results:</i></b> Among 104 patients who met eligibility criteria, higher TSH levels in the highest tertile were associated with moderately elevated CAC VS and AS in case-mix-adjusted analyses (ref: lowest tertile): adjusted ORs (95% CIs) 4.26 (1.18, 15.40) and 5.53 (1.44, 21.30), respectively. TSH levels &#x3e;3.0 mIU/L (ref: ≤3.0 mIU/L) were also associated with moderately elevated CAC VS and AS. In secondary analyses, point estimates of incrementally lower direct free thyroxine levels trended toward elevated CAC VS and AS, although associations did not achieve statistical significance. <b><i>Conclusions:</i></b> In hemodialysis patients, higher serum TSH was associated with elevated CAC VS and AS. Further studies are needed to determine if thyroid hormone supplementation can attenuate CAC burden in this population.
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9.
  • Rhee, CM, et al. (författare)
  • Serum Thyrotropin Elevation and Coronary Artery Calcification in Hemodialysis Patients
  • 2022
  • Ingår i: Cardiorenal medicine. - : S. Karger AG. - 1664-5502 .- 1664-3828. ; 12:3, s. 106-116
  • Tidskriftsartikel (refereegranskat)abstract
    • <b><i>Introduction:</i></b> Hypothyroidism is highly prevalent in end-stage kidney disease patients, and emerging data show that lower circulating thyroid hormone levels lead to downregulation of vascular calcification inhibitors and coronary artery calcification (CAC) in this population. To date, no studies have examined the association of serum thyrotropin (TSH), the most sensitive and specific single biochemical metric of thyroid function, with CAC risk in hemodialysis patients. <b><i>Methods:</i></b> In secondary analyses of patients from the <i>Anti-Inflammatory and Anti-Oxidative Nutrition in Hypoalbuminemic Dialysis Patients</i> trial, we examined serum TSH levels and CAC risk assessed by cardiac computed tomography scans collected within a 90-day period. We evaluated the relationship between serum TSH with CAC Volume (VS) and Agatston score (AS) (defined as &#x3e;100 mm<sup>3</sup> and &#x3e;100 Houndsfield Units, respectively) using multivariable logistic regression. <b><i>Results:</i></b> Among 104 patients who met eligibility criteria, higher TSH levels in the highest tertile were associated with moderately elevated CAC VS and AS in case-mix-adjusted analyses (ref: lowest tertile): adjusted ORs (95% CIs) 4.26 (1.18, 15.40) and 5.53 (1.44, 21.30), respectively. TSH levels &#x3e;3.0 mIU/L (ref: ≤3.0 mIU/L) were also associated with moderately elevated CAC VS and AS. In secondary analyses, point estimates of incrementally lower direct free thyroxine levels trended toward elevated CAC VS and AS, although associations did not achieve statistical significance. <b><i>Conclusions:</i></b> In hemodialysis patients, higher serum TSH was associated with elevated CAC VS and AS. Further studies are needed to determine if thyroid hormone supplementation can attenuate CAC burden in this population.
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