Question of the Week # 396

396)  A 45 year old woman presents to your office for annual physical examination. She reports that she has had a fasting lipid panel done 6 months ago and her HDL – C was low at 25 mg%. She requests to be treated for this. She started healthy diet rich in fruits and vegetables. She used to smoke about 4 cigarettes/ day earlier but quit smoking after she came to know about her lipid results. She occasionally uses red wine in moderate amounts. She has also started aerobic exercises at least 3 days per week. Physical examination is unremarkable. A repeat lipid panel reveals Total cholesterol 128 mg%, LDL-C 80mg%, Triglycerides 100mg%, HDL-C 28mg%. Which of the following is the most appropriate next step?

A) Fenofibrate

B) Niacin

C) Ezetemibe

D) Atorvastatin

E) Omega-3-Fatty Acids

12 Responses

  1. b

  2. B) Niacin

    • Isolated low HDL with no risk factors does not require drug therapy

      E) Omega-3-Fatty Acids

      • Correct! Current guidelines from ATP III recommend treating Isolated Low HDL only in presence of CAD or CAD equivalent ( Framingham 10 year risk > 20%) after the goals of LDL and Non-HDL have been met.

        There is no evidence-based recommendation for pharmacotherapy for isolated low HDL in other group of patients with no history of CAD or CAD equivalent ( no risk factors for having > 20% 10 year CAD risk. Since this woman wants some kind of intervention, omega 3 fatty acids can be recommended which can increase HDL-C to some extent ( 5 to10%)

        Niacin is the most potent of any drug to increase HDL ( 30%). The HDL increasing effect of Niacin is more pronounced when there is concomitant hypertriglyceredemia.

        Fibrates can also modestly increase HDL-C by about 20% when low HDL-C is concomitant with hypertriglyceredemia. In the absence of high triglycerides, fibrates may increase HDL-C only by 5%.

        So, omega is the best option for her.

  3. B

  4. E.

    FROM THE INTERNET : The Role of HDL Cholesterol in Reducing Cardiovascular Risk

    Low levels of high-density lipoprotein cholesterol (HDL-C) can significantly increase one’s cardiovascular risk and be challenging to treat. Coronary artery disease risk remains elevated in patients with low HDL-C even after metabolic improvement for obesity, blood pressure, total cholesterol and LDL-C. The term “isolated low HDL cholesterol” refers to the situation in which total cholesterol or LDL-C are in the “ideal range” but the HDL-C is low. Although infrequently encountered clinically, several genetic diseases are associated with low HDL including Tangiers disease, familial hypoalphalipoproteinemia, fish-eye disease, and lecithin:cholesterol acyl transferase deficiency. Only Tangier’s disease and familial hypoalphalipoproteinemia are associated with premature coronary artery disease.

    A low HDL-C level is thought to accelerate the development of atherosclerosis because of impaired reverse cholesterol transport and possibly because of the absence of other protective effects of HDL-C, such as decreased oxidation of other lipoproteins.

    Cells within peripheral tissues produce all the cholesterol needed for cellular homeostasis. However, the liver is the only organ capable of degrading cholesterol. Therefore, cholesterol must be transported through blood to the liver for processing, degradation, and secretion into bile. Because cholesterol is an insoluble molecule, it must be packaged and transported by special particles in the plasma called lipoproteins. High-density lipoproteins are responsible for movement of most cholesterol from peripheral tissues back to the liver. Because the liver is the center of cholesterol homeostasis in the body, cholesterol that moves from peripheral tissues to the liver is considered to be moving in the reverse direction. HDL-C is believed to protect against atherosclerosis in part through the process of reverse cholesterol transport, whereby excess free cholesterol (FC) is removed from cells in peripheral tissues (such as macrophages within the arterial wall) and returned to the liver for excretion in the bile. FC is generated in part by the hydrolysis of intracellular cholesteryl ester (CE) stores.

    Several key molecules play a role in reverse cholesterol transport, including ATP-binding cassette protein A1 (ABCA1), lecithin:cholesterol acyltransferase (LCAT), and scavenger receptor class-B, type I (SR-BI). Pharmacological enhancement of this pathway could, in theory, help reduce atherosclerosis. Elevated levels of HDL-C have been associated with a reduced risk for CHD, which may occur by at least three mechanisms: (1) promotion of peripheral cholesterol transport, (2) enhanced antioxidant/anti-inflammatory effects, and (3) favorable antithrombotic effects.

    Diagnosing and Managing Low HDL Cholesterol

    Low HDL-C is defined as a level 60 % of total daily calories), certain medications (progestational drugs, anabolic steroids and beta blockers) can potentiate low HDL-C levels. Low HDL-C is the strongest predictor of subsequent cardiovascular events in patients with angiographically proven CAD and “desirable” levels of total cholesterol.

    Unfortunately, the ATP III report did NOT provide guidelines suggesting a specific level to which a low HDL-C should be raised. According to the study’s executive summary: “Although clinical trial results suggest that raising HDL-C will reduce risk, the evidence is insufficient to specify a goal of therapy. Furthermore, currently available drugs do not robustly raise HDL-C.”

    The panel stated that low HDL levels should be managed in the following manner:

    Reducing LDL cholesterol levels is the primary goal.
    Identify patients whose diet is very low in fat. A low HDL-C level in this setting is rarely associated with an increased risk for premature CHD.
    Identify and correct secondary factors.
    Instruct patients who smoke to stop smoking, tell persons who are overweight to manage their weight, and encourage individuals who are sedentary to engage in regular exercise.
    Whenever possible, eliminate medications associated with low HDL-C levels.
    Control diabetes optimally, and aggressively treat LDL-C, regardless of HDL-C levels.
    When a low HDL-C is associated with high triglycerides (200-499 mg/dL), secondary priority goes to achieving the non- HDL-C goal.
    For example, for patients with established CHD or a CHD risk equivalent (10-year risk for CHD >20%), the LDL-C goal is under 100 mg/dL, and the goal for non- HDL-C (Total cholesterol minus HDL cholesterol) is below 130 mg/dL.
    In persons with multiple (2+) risk factors and 10-year risk of equal to or less than 20%, the LDL-C goal is <130 mg/dL, while the non- HDL-C goal is <160 mg/dL.
    In persons with 0-1 risk factor, the LDL-C goal is <160 mg/dL, and that for the non- HDL-C is <190 mg/dL.
    Managing isolated low HDL-C is also important. According to the ATP III, if a patient's TG levels are below 200 mg/dL, the administration of drugs that increase HDL-C (fibrates or nicotinic acid) can be considered. Treatment for isolated low HDL cholesterol is provided mainly to patients with CHD and CHD risk equivalents.
    Niacin is the most effective agent currently available. However, many patients with isolated low HDL-C do not respond well to niacin. Most patients who receive niacin also have high LDL-C levels that are being managed pharmacologically, and niacin is added to raise their HDL-C level if it is low.
    Gemfibrozil and fenofibrate modestly raise the HDL-C level. They are most effective in the setting of concomitant hypertriglyceridemia.
    Statins only mildly raise HDL-C levels. They are not recommended for this purpose alone.
    Alcohol tends to raise some HDL-C subfractions. However, no clinical trial data are available to demonstrate any positive role for raising HDL-C levels with alcohol in order to reduce cardiovascular events in patients with CHD.
    Consider estrogen replacement therapy for postmenopausal women, because this can substantially raise HDL-C levels.
    It is unclear whether pharmacologic agents should be used to raise the HDL-C level in otherwise healthy persons, because no published clinical trials are available that demonstrate a benefit. Nonetheless, individuals at high risk require further assessment for CHD risk, with an evaluation that includes a family history, measurements of apo and lipoprotein Lp(a), and cardiac CT imaging.

  5. for the exam I would answer B. In real life, E

    • E for both lives – Exam and Real … because Exam is based on guidelines and NCEP/ ATP III does not recommend treating isolated low HDL in patients with 10 year CAD risk < 20%

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