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59 Year Old Female with Familial Hypercholesterolemia

59 Year Old Female with Familial Hypercholesterolemia. Case Categories Primary Prevention Secondary Prevention Pediatric Case Familial Hypertriglyceridemia Diabetes Metabolic Syndrome Low HDL Familial Combined Hyperlipidemia Familial Hypercholesterolemia Elevated Lipoprotein (a)

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59 Year Old Female with Familial Hypercholesterolemia

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  1. 59 Year Old Female with Familial Hypercholesterolemia Case Categories Primary Prevention Secondary Prevention Pediatric Case Familial Hypertriglyceridemia Diabetes Metabolic Syndrome Low HDL Familial Combined Hyperlipidemia Familial Hypercholesterolemia Elevated Lipoprotein (a) Statin Intolerance Case category: Primary Prevention, Familial Hypercholesterolemia History of present illness: 59 year old female with familial hypercholesterolemia. Initial NMR 5 years ago showed LDL-P >2050, LDL-C >130 and low HDL. Stable for several years on Crestor 10 and Niaspan 1000. Recent follow-up shows increase in glucose and HbA1c at 5.8. She also is reporting new muscle aches and GI reflux symptoms.

  2. Patient Information

  3. Patient History

  4. Current Medications

  5. Labs Worth Noting on Crestor 10 and Niaspan 1000

  6. Questions to Consider • Question 1: Address severity of reflux symptoms and determine if further GI work up needed. Assess dose of aspirin, can lower dose be used? (She is not taking aspirin currently. Reflux is currently being treated with OTC Prilosec. Niaspan may exacerbate reflux symptoms. No symptoms suggestive of active peptic ulcer disease.) • Question 2: Any symptoms of polyuria, polyphagia, carb craving? Postprandial symptoms? • Question 3: What type of CO Q 10 and dose used? (Currently 200 ubiquinone being used.)

  7. Labs on Crestor 10 and Niaspan 1000 (1 of 1) Discordance between normal HDL cholesterol and low HDL particle concentration. Niaspan has more of an effect on HDL cholesterol as it increases the size of the HDL particles. It does not typically increase the actual number of HDL particles. She appears to be at goal for her level of risk. LDL–P is very close to optimal <1000 with normal non-HDL and traditional lipid parameters.

  8. NMR LipoProfile • There is no evidence of insulin resistance on NMR despite the increase in HbA1C to 5.8. This may be due to Niaspan increase in glucose but does not appear to be related to underlying insulin resistant state. Niaspan does improve the lipoprotein parameters used to calculate insulin resistance score (i.e. increases size of HDL particles, decreases small dense LDL-P etc.). In our experience, if there is insulin resistance in the setting of Niaspan, we see abnormal IR score. It is not seen here. Crestor may increase glucose as well (as seen in JUPITER trial).

  9. NMR LipoProfile • Insert NMR Lipoprofile 051711 MR59 Insert

  10. Other Labs on Crestor 10 and Niaspan 1000

  11. Initial Treatment & Management • Stop Niaspan 1000. Niaspan may be contributing to higher glucose level. Increase Crestor from 10 mg to 20 mg/day to attempt to keep LDL-P at goal recognizing Crestor could be contributing to glucose elevation as well. • Increase CO Q 10 to 300-600 mg/day ubiquinol for muscle aching. • Reduce dose of vitamin D3 from 5000 to 2000 IU/day.

  12. Discussion (1 of 2)

  13. Discussion (2 of 2)

  14. Follow Up Off Niaspan 1000 and On Crestor 20 (1 of 2) • Familial Hypercholesterolemia – Deteriorated. • Discontinued Niaspan 1000 last visit and increased Crestor from 10 to 20 mg. She is experiencing more muscle aches on high dose of Crestor. Taking CO Q 10, but a low dose of 100. • LDL-P increased from 1056 to 1432. Triglycerides increased from 39 to 59, but still normal. HDL dropped from 52 to 47. • Small LDL-P increased from <90 to 815. Optimal is <600. • All inflammatory markers are normal. • E3E4 genotype may be a reason statin is less effective at higher dose. • Restart Niaspan 1000 mg/day and reduce Crestor to 10 mg/day. Reflux has improved which was the reason for stopping initially. • Reducing statin will help with muscle aching. • Borderline HbA1c – Unchanged. • Glucose and HbA1c did not change off Niaspan. • There is no change in insulin resistance markers overall on NMR. IR-score is actually worse off Niaspan. Niaspan does have favorable effects on several insulin resistance markers, increasing HDL particles and reducing small dense LDL. • Start a low carb diet and increase exercise. If needed, will start metformin. • Crestor may also have contributed to increase in HbA1c, but the clinical significance of this is unknown.

  15. Follow Up Off Niaspan 1000 and On Crestor 20 (2 of 2) • Vitamin D Deficiency – Improved. • Vitamin D levels were too high last visit. Reduced vitamin D3 from 5000 to 2000 IU/day. • Levels decreased from 104 to 84. Clinically, optimal benefit of reducing myalgias from statins is in the 50-90 range. • Continue vitamin D3 2000 IU/day.

  16. Follow Up Labs Off Niaspan 1000 and On Crestor 20 (1 of 4)

  17. Follow Up Labs Off Niaspan 1000 and On Crestor 20 (2 of 4)

  18. Follow Up Labs Off Niaspan 1000 and On Crestor 20 (3 of 4)

  19. Follow Up Labs Off Niaspan 1000 and On Crestor 20 (4 of 4)

  20. NMR LipoProfile • Insert NMR Lipoprofile 011012 MR59 Insert

  21. Case Summary

  22. Clinical Pearls: Combination therapy • In this case, glucose elevations were noted in a patient with otherwise stable lipoproteins and CV risk factors on long term therapy with Niaspan and Crestor. We elected to trial off Niaspan to see if this would improve glucose and mild reflux symptoms. With switch from combination therapy with statin/niacin to higher dose statin (Crestor 20), LDL–P and insulin resistance actually worsened significantly. The traditional lipids changed slightly but did not move outside the normal range. Without advanced testing, may not have realized the change for the worse with switch to statin monotherapy. Resuming Niaspan is appropriate. Combination therapy is typically the best approach for patients with E3E4 genotype as well. The long term effect of Niaspan on HbA1C and glucose not seen in previous clinical trials so no need to avoid this therapy in metabolic syndrome/prediabetes or even controlled diabetes.

  23. References (1 of 2) Familial Hypercholesterolemia • Cromwell WC, Otvos JD, Keyes MJ, et al. LDL particle number and risk of future cardiovascular disease in the Framingham offspring study – implications for LDL management. J ClinLipidol. 2007 Dec;1(6):583-92. • Brunzell JD, Davidson M, Furberg CD, et al. Lipoprotein management in patients with cardiometabolic risk: consensus statement from the American Diabetes Association and the American College of Cardiology Foundation. Diabetes Care. 2008 Apr;31(4):811-22. • Nicholls SJ, Ballantyne CM, Barter PJ, et al. Effect of two intensive statin regimens on progression of coronary disease. N Engl J Med. 2011 Dec 1;365(22):2078-87. • Ballantyne C, Herd JA, Stein E, et al. Apolipoprotein E genotypes and response of plasma lipids and progression-regression of coronary atherosclerosis to lipid-lowering drug therapy. J Am CollCardiol2000;36:1572-8. • Jafri H, Alsheikh-Ali AA, Mooney P, et al. Extended-release niacin reduces LDL particle number without changing total LDL cholesterol in patients with stable CAD. J ClinLipidol. 2009;3:45-50. • Ridker PM, Danielson E, Fonseca FA, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008 Nov 20;359(21):2195-207. • Elam MB, Hunninghake DB, Davis KB, et al. Effect of niacin on lipid and lipoprotein levels and glycemic control in patients with diabetes and peripheral arterial disease: the ADMIT study: A randomized trial. Arterial Disease Multiple Intervention Trial. JAMA. 2000 Sep 13;284(10):1263-70. • Grundy SM, Vega GL, McGovern ME, et al. Efficacy, safety, and tolerability of once-daily niacin for the treatment of dyslipidemia associated with type 2 diabetes: results of the assessment of diabetes control and evaluation of the efficacy of niaspan trial. Arch Intern Med. 2002 Jul 22;162(14):1568-76.

  24. References (2 of 2) Borderline HbA1c • AACE Diabetes Care Plan Guidelines, EndocrPract. 2011;17 (Suppl 2). Vitamin D Deficiency • Dobnig H, Pilz S, Scharnagl H, et al. Independent association of low serum 25-hydroxyvitamin d and 1,25-dihydroxyvitamin d levels with all-cause and cardiovascular mortality. Arch Intern Med. 2008;168(12):1340-1349. • Cannell J, Hollis B, Zasloff M, et al. Diagnosis and treatment of vitamin D deficiency. Pharmacotherapy. 2008;9(1):1-12. • Giovannucci E, Liu Y, Hollis B, Rimm E. 25-hydroxyvitamin d and risk of myocardial infarction in men. Arch Intern Med. 2008;168(11):1174-1180. • Holick M. Vitamin D Deficiency. N Engl J Med. 2007;357:266-81. • Michos E and Blumenthal R. Vitamin D Supplementation and Cardiovascular Disease Risk. Circulation. 2007;115(7):827-828. • Hathcock J, Shao A, Vieth R, et al. Risk assessment for vitamin D. Am J ClinNutr. 2007;85:6-18. • Jockers B. Vitamin D sufficiency: An approach to disease prevention. The American Journal for Nurse Practitioners. 2007;11(10):43-50. • Perez-Castrillon J, Vega G, Abad L, et al. Effects of atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Am J Cardiol. 2007;99(7):903-4.

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