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  • 1
    Electronic Resource
    Electronic Resource
    Psoriasis patients who are homozygous for the HLA-Cw*0602 allele have a 2·5-fold increased risk of developing psoriasis compared with Cw6 heterozygotes (2003)
    Oxford, UK : Blackwell Science Ltd
    British journal of dermatology 148 (2003), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary Background Psoriasis is strongly associated with certain human leucocyte-associated antigens, especially HLA-Cw*0602. Patients who are HLA-Cw*0602 positive have been reported to have more active disease and a younger age at disease onset than HLA-Cw6-negative patients. Objectives To ascertain whether there are differences in the clinical features and relative risk between HLA-Cw*0602 homozygous and heterozygous psoriasis patients. Methods One thousand and six patients with chronic plaque psoriasis were evaluated clinically and HLA-C typed. In addition, 512 unrelated controls were typed for HLA-C. Results Of the patients 646 (64·2%) were HLA-Cw*0602 positive, and 68 (6·8%) were homozygous for this allele. Heterozygosity was associated with a relative risk of developing psoriasis of 8·9 compared with 23·1 for the Cw6 homozygous patients. The homozygous patients also had an earlier disease onset (mean 15·0 vs. 17·8 years, P = 0·04). However, the Cw6 homozygotes did not differ from the heterozygotes with respect to disease severity, guttate onset, distribution of plaques, nail changes or any other clinical parameter recorded. Conclusions Homozygosity for the gene in the major histocompatibility complex region has a major additive impact on the risk of developing psoriasis and predisposes to an earlier disease onset, but does not have any marked influence on the phenotype or the severity of the disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2133.2003.05115.x
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  • 2
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    The effect of cholesteryl ester transfer protein inhibition on lipids, lipoproteins, and markers of HDL function after an acute coronary syndrome: the dal-ACUTE randomized trial (2014)
    Oxford University Press
    Details
    Publication Date: 2014-07-16
    Description: Aims The effects of cholesteryl ester transfer protein (CETP) inhibition on lipids, inflammation, and markers of high-density lipoprotein (HDL) function, following an acute coronary syndrome (ACS), are unknown. Methods and results The dal-ACUTE study randomized 300 patients (1 : 1) to dalcetrapib 600 mg/day or placebo within 1 week of an ACS. The primary endpoint was per cent change in HDL-cholesterol (HDL-C) after 4 weeks. Secondary endpoints included apolipoprotein levels, markers of HDL function, and inflammation. Dalcetrapib treatment increased HDL-C and apolipoprotein A1 by 33.7 and 11.8%, respectively (both P 〈 0.001) and total cholesterol efflux by 9.5% ( P = 0.003) after 4 weeks, principally via an increase in non-ATP-binding cassette transporter (ABC) A1-mediated efflux, without statistically significant changes in pre-β1-HDL levels. The increase in total efflux with dalcetrapib correlated most strongly with increases in apolipoprotein A1 and HDL-C ( r = 0.46 and 0.43, respectively) rather than the increase in pre-β1-HDL ( r = 0.32). Baseline and on-treatment ABCA1-mediated efflux correlated most strongly with pre-β1-HDL levels; in contrast, non-ABCA1-mediated efflux correlated better with apolipoprotein A1 and HDL-C levels. Conclusions High-density lipoprotein raised through CETP inhibition with dalcetrapib improves cholesterol efflux, principally via a non-ABCA1-mediated pathway. While HDL-C was increased by one-third, apolipoprotein A1 and total efflux were increased only by one-tenth, supporting the concept of dissociation between improvements in HDL function and HDL-C levels, which may be of relevance to ongoing trials and the development of therapeutic interventions targeting HDL.
    Print ISSN: 0195-668X
    Electronic ISSN: 1522-9645
    Topics: Medicine
    Published by Oxford University Press
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  • 3
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    Pharmacogenomic Determinants of the Cardiovascular Effects of Dalcetrapib [Original Articles] (2015)
    American Heart Association (AHA)
    Details
    Publication Date: 2015-04-22
    Description: Background— Dalcetrapib did not improve clinical outcomes, despite increasing high-density lipoprotein cholesterol by 30%. These results differ from other evidence supporting high-density lipoprotein as a therapeutic target. Responses to dalcetrapib may vary according to patients’ genetic profile. Methods and Results— We conducted a pharmacogenomic evaluation using a genome-wide approach in the dal-OUTCOMES study (discovery cohort, n=5749) and a targeted genotyping panel in the dal-PLAQUE-2 imaging trial (support cohort, n=386). The primary endpoint for the discovery cohort was a composite of cardiovascular events. The change from baseline in carotid intima-media thickness on ultrasonography at 6 and 12 months was evaluated as supporting evidence. A single-nucleotide polymorphism was found to be associated with cardiovascular events in the dalcetrapib arm, identifying the ADCY9 gene on chromosome 16 (rs1967309; P =2.41 x 10 –8 ), with 8 polymorphisms providing P 〈10 –6 in this gene. Considering patients with genotype AA at rs1967309, there was a 39% reduction in the composite cardiovascular endpoint with dalcetrapib compared with placebo (hazard ratio, 0.61; 95% confidence interval, 0.41–0.92). In patients with genotype GG, there was a 27% increase in events with dalcetrapib versus placebo. Ten single-nucleotide polymorphism in the ADCY9 gene, the majority in linkage disequilibrium with rs1967309, were associated with the effect of dalcetrapib on intima-media thickness ( P 〈0.05). Marker rs2238448 in ADCY9 , in linkage disequilibrium with rs1967309 ( r 2 =0.8), was associated with both the effects of dalcetrapib on intima-media thickness in dal-PLAQUE-2 ( P =0.009) and events in dal-OUTCOMES ( P =8.88 x 10 –8 ; hazard ratio, 0.67; 95% confidence interval, 0.58–0.78). Conclusions— The effects of dalcetrapib on atherosclerotic outcomes are determined by correlated polymorphisms in the ADCY9 gene. Clinical Trial Information— URL: http://www.clinicaltrials.gov . Unique identifiers: NCT00658515 and NCT01059682
    Keywords: Cardiovascular Pharmacology, Secondary prevention
    Print ISSN: 1942-325X
    Electronic ISSN: 1942-3268
    Topics: Medicine
    Published by American Heart Association (AHA)
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