Case 15 Andrea De Mesa

Patient history A 44 y/o male, single, undergoes cardiovascular screening on advice of his attending physician. He is a smoker of 1 pack/day, hypertensive (BP=140/100), with family history of NIDDM, but currently has no symptoms of polyuria, polydipsia nor polyphagia. He is 10lbs overweight and exercises only on Sundays. His father died of MI at 66 years old.

NORMAL VALUES Total Cholesterol < 200 mg/dl DESIRABLE mg/dl BORDERLINE to HIGH ≥240 mg/dl VERY HIGH FBS <100 mg/dl DESIRABLE mg/dl IMPARED FBS >126 mg/dl DIABETES

LDL <100 mg/dl OPTIMAL mg/dl NEAR OPTIMAL mg/dl BORDERLINE HIGH mg/dl HIGH >190 mg/dl VERY HIGH TRIGLYCERIDES <150 mg/dl NORMAL mg/dl BORDERLINE HIGH mg/dl HIGH >500 mg/dl VERY HIGH

Laboratory examinations FBS = 120mg%  prediabetic state TAG = 190mg%  borderline high Total cholesterol = 250mg%  very high LDL = 165mg%  high ECG = LVH, RSR Treadmill = hypertensive BP response, as high as 220/110mmHg, (-) for ischemia

Dx:Primary Hypercholesterolemia (elevated LDL) genetic disease that is related to the common disease hypercholesterolemia. patients suffering from FH have a much more serious condition. They have a much higher chance of suffering from heart attacks and stroke. Result of the overproduction and/or underutilization of Low-Density Lipoprotein (LDL). There is a mutation in the genetic encoding for the LDL receptors (LDLR gene) that are located on the surface of the liver cells.Low-Density Lipoprotein (LDL).LDL receptors

Causes: consumption of a high-cholesterol diet and/or the genetic disease familial hypercholesterolemia (FH). It is generally believed that the typical high fat, high cholesterol, high protein, low fiber U.S. diet is largely responsible for the unfortunate statistic of 600,000 deaths annually. Obesity and a sedentary life style add to the risk. Cholesterol causes deposits to form inside blood vessels.

Predisposing factors in developing CAD Male > 45 years of age Female > 55 years of age Cigarette smoking Hypertension >140/90 Low HDL Obesity Body mass index (BMI) > 25kg/m 2 Waist circumference: male >40 in; female >35 in

Treatment Px was advised to quit smoking Behavioral modification Lifestyle change was encouraged Advised to have dietary maneuvers for a period of at least 4 weeks

After advised regimen: 4wks later Fasting LDL-cholesterol determination revealed 165mg%. No significant change from the first lipid profile determination Another dietary intervention lasting for at least 4wks was instituted followed by another fasting LDL-cholesterol determination revealing LDL of 140mg%

Medications: HMG CoA REDUCTASE INHIBITORS Mechanism of Action Inhibitors of HMG CoA reductase block synthesis of cholesterol in the liver by competitively inhibiting HMG CoA reductase activity thus ↓LDL and TAG and ↑ HDL cholesterol.

Therapeutic Uses The initial choice of which statin to use depends on the degree of cholesterol lowering desired. Useful alone or in combination with bile acid binding resins or niacin. Lovastatin, Simvastatin, Pravastatin, Atorvastatin, Resuvastatin

For greater lowering of LDL, particularly in subjects with familial hypercholesterolemia, higher doses of lovastatin or simvastatin usually are required. A baseline determination of CPK activity and a panel of liver function tests should be obtained before beginning therapy, and analysis of liver transaminases should be repeated at 2 to 3 month intervals after that.

Adverse Effects The most important adverse effects are increases in hepatic transaminases in serum and myopathy. Increase creatinine kinase activity. Myopathy may be worsen if used with clofibrate, niacin, cyclosporine and erythromycin. May also cause lens opacity, lupus-like hypersensitivity and rhabdomyolysis

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