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Keech A, Simes RJ, Barter P, et al. FIELD study investigators. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus the FIELD study ; : randomised controlled trial. Lancet. 2005 Nov 26; 366 9500 ; : 1849-61. INTERPRETATION: Fenofibrate did not significantly reduce the risk of the primary outcome of coronary events. It did reduce total cardiovascular events, mainly due to fewer non-fatal myocardial infarctions and revascularisations. The higher rate of starting statin therapy in patients allocated placebo might have masked a moderately larger treatment benefit. But some non-significant concerns with fenofibrate vs placebo such as: an in cardiac mortality 2.2 vs 1.9%, an in total CVD events for those with previous CVD 25.5 vs 25.1%, an excess in non-cardiovascular disease deaths 4.4 vs 4% & an in total mortality 7.3 vs 6.6% ; . But may benefit albuminuria & retinopthy. InfoPOEMs: In this study, patients with type 2 diabetes treated with fenofibrate Antara, Lofibra, Trifor ; had no significant reduction in coronary events compared with patients treated with placebo. There was a small reduction, however, in nonfatal myocardial infarctions, total cardiovascular disease, and revascularization. LOE 1b 32. Houslay E, et al. Progressive coronary calcification despite intensive lipid-lowering therapy: a randomised controlled trial. Heart. 2006 Jan 31; [Epub ahead of print] 33. Nissen SE, et al. Effect of Very High-Intensity Statin rosuvastatin 40mg d, 2yr, n 507 ; Therapy on Regression of Coronary Atherosclerosis: The ASTEROID Trial.JAMA. 2006 Mar 13; [Epub ahead of print] 34. Hooper L, et al. Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: systematic review. BMJ. 2006 Mar 24; [Epub ahead of print] 35. Costa J, Borges M, David C, Carneiro AV. Efficacy of lipid lowering drug treatment for diabetic and non-diabetic patients: meta-analysis of randomised controlled trials. BMJ. 2006 Apr 3; [Epub ahead of print] 36. Manuel DG, et al. Effectiveness and efficiency of different guidelines on statin treatment for preventing deaths from coronary heart disease: modelling study. BMJ. 2006 Jun 17; 332 7555 ; : 1419. Epub 2006 May 31. 37. Knopp RH, et al. Efficacy and Safety of Atorvastatin in the Prevention of Cardiovascular End Points in Subjects With Type 2 Diabetes: The Atorvastatin Study for Prevention of Coronary Heart Disease Endpoints in NonInsulin-Dependent Diabetes Mellitus ASPEN ; . Diabetes Care. 2006 Jul; 29 7 ; : 1478-85. 38. Amarenco P, et al.; Stroke Prevention by Aggressive Reduction in Cholesterol Levels SPARCL ; Investigators. High-dose atorvastatin after stroke or transient ischemic attack. N Engl J Med. 2006 Aug 10; 355 6 ; : 549-59. Kent DM. Stroke--an equal opportunity for the initiation of statin therapy. N Engl J Med. 2006 Aug 10; 355 6 ; : 613-5. ; 39. Hayward RA, Hofer TP, Vijan S. Narrative review: lack of evidence for recommended low-density lipoprotein treatment targets: a solvable problem. Ann Intern Med. 2006 Oct 3; 145 7 ; : 520-30. 40. Cannon CP, Braunwald E, McCabe CH, et al. Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 Investigators. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med. 2004 Apr 8; 350 15 ; : 1495-504. Epub 2004 Mar 8. Erratum in: N Engl J Med. 2006 Feb 16; 354 7 ; : 778. Ahmed S, Cannon CP, Murphy SA, et al.Acute coronary syndromes and diabetes: Is intensive lipid lowering beneficial? Results of the PROVE IT-TIMI 22 trial. Eur Heart J. 2006 Oct; 27 19 ; : 2323-9. Epub 2006 Sep 5. ; 41. Nakamura H, et al. Primary prevention of cardiovascular disease with pravastatin in Japan MEGA Study ; : a prospective randomised controlled trial. Lancet. 2006 Sep 30; 368 9542 ; : 1155-63. 42. Taylor AJ, et al. Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol ARBITER ; 2: a double-blind, placebo-controlled study of extended-release niacin on atherosclerosis progression in secondary prevention patients treated with statins. Circulation. 2004 Dec 7; 110 23 ; : 3512-7. Epub 2004 Nov 10. Erratum in: Circulation. 2004 Dec 7; 110 23 ; : 3615. Circulation. 2005 Jun 21; 111 24 ; : e446. 43. Thavendiranathan P, Bagai A, Brookhart MA, Choudhry NK. Primary Prevention of Cardiovascular Diseases With Statin Therapy: A Meta-analysis of Randomized Controlled Trials. Arch Intern Med. 2006 Nov 27; 166 21 ; : 2307-13. Subjects taking statins for a mean of 4.3 years n 42 848 ; had a lower incidence of heart attack, stroke, revascularization, and other events than controls. The authors estimate the following numbers needed to treat for 4.3 years: 60, to prevent one major coronary event; 268 for stroke; 61 for nonfatal myocardial infarction and 93 for revascularization. In patients without CV disease, statin therapy decreases the incidence of major coronary and cerebrovascular events and revascularizations but not coronary heart disease or overall mortality 44. Wanner C, Krane V, Marz W, et al.; German Diabetes and Dialysis Study Investigators 4D ; . Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005 Jul 21; 353 3 ; : 238-48. It lowered 100 points by changing from tricor to over 900 my levels are much better now that im on the tricor i couldnt tolerate the nispan at all and i cannot.

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TRANSACTIVATION RESPONSE OF VDRB1 IS PROMOTER- CELL- AND LIGAND-SPECIFIC C Fong, LM Esteban, SJ Allison, JL Flanagan, D Amr * , C Liddle * , JA Eisman & EM Gardiner Bone and Mineral Research Program, Garvan Institute of Medical Research, Sydney, NSW * Department of Clinical Pharmacology and Toxicology, Westmead Hospital, Westmead, NSW The vitamin D receptor VDR ; mediates the effects of 1, 25 OH ; 2D3, the active form of vitamin D. The human VDRB1 isoform differs from the originally described VDRA by an N-terminal extension of 50 amino acids. We investigated cell-, promoterand ligand-specific transactivation by VDRB1. Relative activities of the VDR isoforms on two cytochrome P450 gene promoters, CYP24 and CYP3A4, were studied in COS1 and HEK293 cell lines. Transactivation was induced by 1, 25 OH ; 2D3 or the secondary bile acid, lithocholic acid LCA ; , a recently reported VDR activator.

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Baseline characteristics. There were no significant differences between the two groups in baseline clinical characteristics except a higher prevalence of hypertension in group I versus group II Table 1 ; . Angiographic and procedural characteristics. The patients in group II had more unfavorable anatomical and procedural characteristics than those in group I Table 2 ; . A long stent 30 mm was more frequently deployed in group II, and the number of implanted stents per patient was also higher in group II than in group I. Primary end point at one month. A complete 30-day follow-up was available for all eligible patients. The primary end point of stent thrombosis or MACE was 0.8% in group I and 0.3% in group II p 0.085 ; . The incidence of stent thrombosis was significantly lower in group II than in group I 0.5% in group I vs. 0.1% in group II, p 0.024 ; Table 3 ; . Acute stent thrombosis occurred in three patients, whereas subacute stent thrombosis occurred in seven patients, with a mean time of occurrence of 5.9 9.1 days after the procedure. Of all ten patients with stent thrombosis, three all from group I ; had undergone primary stenting for AMI, whereas the other seven six in group I and one in group II ; had undergone elective stenting Table 3 ; . Eight patients died during the 30-day follow-up period: five four cardiac deaths and one noncardiac death ; in group I and three cardiac deaths in group II. Secondary end point at one month. Twenty-one patients 11 in group I and 10 in group II ; experienced major bleeding requiring transfusion Table 4 ; . The secondary end point of the occurrence of adverse events was similar in both groups 28 patients [1.8%] in group I vs. 37 patients [2.6%] in group I; p 0.140 ; . The incidence of adverse side effects, for example, tricor medicine side effects.

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