Effects of amlodipine-atorvastatin combination on inflammation markers and insulin sensitivity in normocholesterolemic obese hypertensive patientsFogari, Roberto; Preti, Paola; Zoppi, Annalisa; Lazzari, Pierangelo; Corradi, Luca; Fogari, Elena; Ciccarelli, Leonardina; Derosa, Giuseppe
doi: 10.1007/s00228-006-0176-1pmid: 16896785
Amlodipine monotherapy decreased both SBP (−17.1 mm Hg, p=0.008 vs. placebo) and DBP (−14.3 mm Hg, p=0.008) as well as TNF-α (from 3.66±1.6 to 3.09±1.1 pg/ml, p=0.045) and HOMA-IR (from 4.58±0.7 to 3.88±0.6, p=0.007). The amlodipine-atorvastatin combination produced a decrease in SBP (−22.5 mm Hg, p=0.0007 vs. placebo, p=0.039 vs. amlodipine), DBP (−17.7 mm Hg, p=0.0007 vs. placebo; p=0.04 vs. amlodipine), TNF-α (2.59±0.9 pg/mL, p=0.007 vs. placebo and p=0.038 vs. amlodipine) and HOMA-IR (2.86±0.4, p=0.0008 vs. placebo and p=0.007 vs. amlodipine). The combination reduced IL-6 (from 7.93±1.9 to 5.59±1.2 pg/mL, p=0.008 vs. placebo and p=0.007 vs. amlodipine) and TC (from 4.3±0.5 to 3.6±0.4 mmol/L, p=0.008 vs. placebo and vs. amlodipine). HOMA-IR changes significantly correlated with TNF-α changes (r=0.38, p<0.05) during combination but not during amlodipine monotherapy. In normocholesterolemic, obese hypertensive patients, the amlodipine-atorvastatin combination decreased inflammatory markers and IR more than amlodipine monotherapy and produced a greater SBP and DBP reduction.
UGT1A polymorphisms in a Swedish cohort and a human diversity panel, and the relation to bilirubin plasma levels in males and femalesMercke Odeberg, J.; Andrade, J.; Holmberg, K.; Hoglund, P.; Malmqvist, U.; Odeberg, J.
doi: 10.1007/s00228-006-0166-3pmid: 16909274
In a Swedish cohort, several genetic variants in the UGT1A gene are common, but prevalence in a population may differ because of ethnicity. A phenotype based on bilirubin levels has limitations in serving as an indicator of pharmacogenetic differences in glucuronidation due to the influence of gender. Because of possible substrate overlap regarding different UGT1A isoforms, determination of haplotypes of potential cis-acting polymorphisms in the UGT1A gene should be considered in pharmacogenetic association studies regarding drugs that undergo glucuronidation.