No abstract available.
Hydroxymethylglutaryl-CoA Reductase Inhibitors*

No abstract available.
Hydroxymethylglutaryl-CoA Reductase Inhibitors*

No abstract available.
Hydroxymethylglutaryl-CoA Reductase Inhibitors*

Introduction: Postprandial lipemia represent an important risk factor for lifetime development of cardiovascular disease in patients with type 2 diabetes mellitus. Daily administration alone or combined statin and fi brate therapy has been shown to be an effective therapeutic approach but brings about serious logistics problem in our local setting. To address this concern, we report this observation where alternate day statin and fi brate treatment given alone or in combination in type 2 diabetes mellitus and similar effectiveness in lowering postprandial dyslipidemia has been obtained. Methodology: This is a retrospective case study in an endocrine clinic involving 53 patients seen from April 2014 to October 2015. The patients were on statin and fi brate combination (atorvastatin 20- 40mg and gemfi brozil 300-600 mg or fenofi brate 145-160mg), statin alone (atorvastatin 20-40mg) and fi brate alone (gemfi brozil 300-600mg/fenofi - brate 145-160mg) given on alternate days. Percent reductions of cholesterol, triglycerides, LDL for combined statin and fi brate; cholesterol and LDL for atorvastatin alone; and triglyceride for fi brate alone were determined. Results: In this preliminary report, 26 patients have available data. Follow-up period range was 4 to 48 weeks (mean 22.76+ 11.8 weeks). Alternate statin and fi brate (gemfi brozil) treatment yielded percent reductions from baseline as follows: cholesterol 7%, triglycerides 15%, and LDL 37% (P values= 0.02, 0.10 and 0.019, respectively). On the other hand, alternate statin and fi brate (fenofi brate) yielded percent reduction from baseline as follows: cholesterol 41% and LDL 20.4% (P=0.15 and 0.13, respectively). The population is small, the decrease did not yield signifi cant difference from baseline, however there is a tendency for triglyceride to decrease (P=0.09) with the combined statin and fenofi brate. With statin alone the percent reduction from baselinewere as follows: cholesterol 39% and LDL 62% (P= 0.29 and 0.11, respectively). No percent reduction of triglyceride is seen with fi brate given on alternate day with P= 0.19 The monthly cost reduction with combined alternate statin and fi brate treatment is at 34-48% while alternate day administration of the statin reduced cost by 60%. Conclusion This study showed lowering of postprandial total cholesterol, triglyceride and LDL with alternate statin and fi brate treatment, and total cholesterol and LDL with alternate day statin. The cost of treatment was also signifi cantly lowered with the alternate regimen. However, a follow through study with adequate sample size is recommended to support these observations.
Hydroxymethylglutaryl-CoA Reductase Inhibitors

No abstract available.
Acromegaly* ; Hydroxymethylglutaryl-CoA Reductase Inhibitors*

No abstract available.
Hydroxymethylglutaryl-CoA Reductase Inhibitors* ; Stroke*

No abstract available.
Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Inflammation

No abstract available.
Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Urticaria

No abstract available.
Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors*

Objective. Several studies showed that genetic factors affect responsiveness to statins among different populations. This study investigated the associations of candidate genetic variants with poor response to statins among Filipinos.

Methods. In this unmatched case-control study, dyslipidemic participants were grouped into statin responders and poor responders based on the degree of reduction in LDL-c from baseline. DNA from blood samples were genotyped and analyzed. The association of candidate variants with statin response was determined using chi-square and logistic regression analysis.

Results. We included 162 adults on statins (30 poor responders as cases, 132 good responders as controls). The following variants are nominally associated with poor response to statin among Filipinos at a per-comparison error rate of 0.05: rs173539 near CETP (OR=3.05, p=0.015), rs1800591 in MTTP (OR=3.07, p=0.021), and rs1558861 near the BUD13-ZPR1-APOA5 region (OR=5.08, p=0.004).

Conclusion. Genetic variants near CETP, MTTP and the BUD13-ZPR1-APOA5 region are associated with poor response to statins among Filipinos. Further study is recommended to test the external validity of the study in the general Filipino population.