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Metabolic Syndrome Medication

  • Author: Stanley S Wang, MD, JD, MPH; Chief Editor: Yasmine Subhi Ali, MD, FACC, FACP, MSCI  more...
 
Updated: Dec 27, 2015
 

Medication Summary

An insulin-sensitizing agent, such as metformin, is typically used at the start of hyperglycemia treatment in patients with metabolic syndrome. Some literature suggests that metformin may help to reverse the pathophysiologic changes of metabolic syndrome. This includes when it is used in combination with lifestyle changes[96] or with peroxisome proliferator-activated receptor agonists, such as fibrates[97] and thiazolidinediones,[98] each of which may produce favorable metabolic alterations as single agents in patients with metabolic syndrome.[99]

When statin therapy and therapeutic lifestyle modifications are not successful, niacin may aid in the management of reduced HDL-C and in the treatment of elevated triglycerides.

Aspirin may contribute to the primary prevention of cardiovascular complications in metabolic syndrome, particularly in patients with at least an intermediate risk of suffering a cardiovascular event (ie, >6% 10-y risk).[101, 102]

Additional therapies have found early support from more recent data. For example, a small trial of high-dose resveratrol therapy (1000 mg daily) was found to lead to greater new bone formation and mineralization in men with MetS.{ref1-INVALID REFERENCE}[122]

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Antidiabetics, Biguanides

Class Summary

These agents reduce blood glucose levels.

Metformin (Glucophage, Fortamet, Glumetza, Riomet)

 

Metformin reduces hepatic glucose output, decreases intestinal absorption of glucose, and increases glucose uptake in the peripheral tissues (muscle and adipocytes). It is a major drug for use in patients who are obese and have type 2 diabetes. Metformin enhances weight reduction and improves lipid profile and vascular integrity. Individualize treatment with monotherapy or in combination with insulin or sulfonylureas.

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Antidiabetics, Thiazolidinediones

Class Summary

Thiazolidinediones may produce favorable metabolic alterations as single agents in patients with metabolic syndrome. These agents are highly selective agonists for the peroxisome proliferator-activated receptor-gamma (PPAR-gamma). Activation of PPAR-gamma receptors regulate insulin-responsive gene transcription involved in glucose production, transport, and use, thereby reducing blood glucose concentrations and reducing hyperinsulinemia.

Rosiglitazone (Avandia)

 

Rosiglitazone is available only via a restricted access program. It is an insulin sensitizer with a major effect in the stimulation of glucose uptake in skeletal muscle and adipose tissue. It lowers plasma insulin levels and is used to treat type 2 diabetes associated with insulin resistance.

Pioglitazone (Actos)

 

Pioglitazone improves target cell response to insulin without increasing insulin secretion from the pancreas. It decreases hepatic glucose output and increases insulin-dependent glucose use in skeletal muscle and, possibly, in liver and adipose tissue.

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Lipid-Lowering Agents, Statins

Class Summary

Management of elevated LDL-C includes consideration of all statins (3-hydroxy-3-methylglutaryl coenzyme A [HMG-CoA] reductase inhibitors) at all indicated ranges, as there are several formulations available with different doses and potencies. Statins affect the lipid profile favorably and provide possible pleiotropic benefits. The choice of drug and dose should be based on guidelines but individualized to the patient.

Atorvastatin (Lipitor)

 

Atorvastatin is an HMG-CoA reductase inhibitor that inhibits the rate-limiting step in cholesterol biosynthesis by competitively inhibiting HMG-CoA reductase.

Rosuvastatin (Crestor)

 

Rosuvastatin is an HMG-CoA reductase inhibitor that inhibits the rate-limiting step in cholesterol biosynthesis by competitively inhibiting HMG-CoA reductase.

Fluvastatin (Lescol, Lescol XL)

 

Fluvastatin is an HMG-CoA reductase inhibitor that inhibits the rate-limiting step in cholesterol biosynthesis by competitively inhibiting HMG-CoA reductase.

Lovastatin (Altoprev, Mevacor)

 

Lovastatin is an HMG-CoA reductase inhibitor that inhibits the rate-limiting step in cholesterol biosynthesis by competitively inhibiting HMG-CoA reductase.

Simvastatin (Zocor)

 

Pravastatin (Pravachol)

 

Pitavastatin (Livalo)

 
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ACE Inhibitors

Class Summary

ACE inhibitors prevent the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, and lower aldosterone secretion. They are effective and well-tolerated drugs with no adverse effects on plasma lipid levels or glucose tolerance. They prevent the progression of diabetic nephropathy and other forms of glomerulopathies but appear to be less effective in black patients than in white patients.

Patients with high plasma renin activity may have an excessive hypotensive response to ACE inhibitors. Patients with bilateral renal vascular disease or with single kidneys, whose renal perfusion is maintained by high levels of angiotensin II, may develop irreversible acute renal failure when treated with ACE inhibitors.

ACE inhibitors are contraindicated in pregnancy. Cough and angioedema are less common with newer members of this class than with captopril. Serum potassium and serum creatinine concentrations should be monitored for the development of hyperkalemia and azotemia. Examples of agents from this class include captopril, lisinopril, and enalapril.

Captopril

 

Captopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. It is rapidly absorbed, but bioavailability is significantly reduced with food intake. Captopril achieves a peak concentration in 1 hour and has a short half-life. It is cleared by the kidney; impaired renal function requires reduction of the dosage. The drug is absorbed well orally.

Give captopril at least 1 hour before meals. If it is added to water, use it within 15 minutes. The dose can be low initially, then titrated upward as needed and as tolerated by the patient.

Enalapril (Vasotec)

 

Enalapril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. It helps control blood pressure and proteinuria. It decreases the pulmonary-to-systemic flow ratio in the catheterization laboratory and increases systemic blood flow in patients with relatively low pulmonary vascular resistance.

Enalapril has a favorable clinical effect when administered over a long period. It helps prevent potassium loss in distal tubules. The body conserves potassium; thus, less oral potassium supplementation is needed.

Lisinopril (Prinivil, Zestril)

 

Lisinopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Benazepril (Lotensin)

 

Benazepril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

When pediatric patients are unable to swallow tablets or the calculated dose does not correspond with tablet strength, an extemporaneous suspension can be compounded. Combine 300 mg (15 tablets of 20-mg strength) in 75 mL of Ora-Plus suspending vehicle and shake well for at least 2 minutes. Let the tabs sit and dissolve for at least 1 hour, and then shake again for 1 minute. Add 75 mL of Ora-Sweet. The final concentration is 2 mg/mL, with a total volume of 150 mL. The expiration time is 30 days with refrigeration.

Fosinopril

 

Fosinopril is a competitive ACE inhibitor. It prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. It decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction.

Quinapril (Accupril)

 

Quinapril is a competitive ACE inhibitor. It reduces angiotensin II levels, decreasing aldosterone secretion.

Ramipril

 
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Angiotensin II Receptor Blockers (ARBs)

Class Summary

ARBs lower blood pressure by blocking the final receptor (ie, angiotensin II) in the renin-angiotensin axis. Like ACE inhibitors, they are contraindicated in pregnancy. Serum electrolyte and creatinine levels should be monitored.

Irbesartan (Avapro)

 

Irbesartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II at the tissue receptor site. It may induce a more complete inhibition of renin-angiotensin system than do ACE inhibitors, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema.

Losartan (Cozaar)

 

Losartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. It may induce a more complete inhibition of renin-angiotensin system than do ACE inhibitors, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema. It is suitable for patients unable to tolerate ACE inhibitors.

Olmesartan (Benicar)

 

Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking the binding of angiotensin II to angiotensin I receptors in vascular smooth muscle. Its action is independent of the pathways for angiotensin II synthesis.

Valsartan (Diovan)

 

Valsartan is a prodrug that produces direct antagonism of angiotensin II receptors. It displaces angiotensin II from angiotensin I receptors and may lower blood pressure by antagonizing angiotensin I–induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses.

Valsartan may induce a more complete inhibition of renin-angiotensin system than do ACE inhibitors, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema. It is suitable for patients unable to tolerate ACE inhibitors.

Telmisartan

 
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Lipid-lowering Agents, Non-Statin

Class Summary

These agents are used to improve lipid profile in patients.

Niacin (Niacor, Niaspan, Slo-Niacin)

 

Niacin is used in tissue respiration, lipid metabolism, and glycogenolysis. Nicotinic acid has lipid-lowering properties, but nicotinamide and niacinamide do not. Inositol hexanicotinate is a "no flush" form that may not release enough niacin to be effective.

Niacin is available as a prescription, Niaspan, or over the counter as Slo-Niacin. Allergies are common, but another form may be tolerated. In addition to improving low HDL-C levels, niacin may lower triglycerides and LDL-C levels.

Fenofibrate (TriCor, Triglide, Lipofen, Lofibra)

 

Fenofibrate increases VLDL catabolism by enhancing synthesis of lipoprotein lipase, fatty acid oxidation, and elimination of triglyceride-rich particles. This results in decreased triglyceride levels by 30-60%; HDL may increase.

Fenofibric acid (Trilipix, Fibricor)

 

Fenofibric acid increases VLDL catabolism by enhancing synthesis of lipoprotein lipase, fatty acid oxidation, and elimination of triglyceride-rich particles. This results in decreased triglyceride levels by 30-60%; HDL may increase.

Gemfibrozil (Lopid)

 

Gemfibrozil may decrease serum VLDL levels by inhibiting lipolysis, decreasing subsequent hepatic fatty acid uptake, and by inhibiting hepatic secretion of VLDL.

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Lipid-Lowering Agents, Non-Statin

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Antiplatelet Agents, Cardiovascular

Class Summary

These agents inhibit platelet aggregation.

Aspirin (Ecotrin, Ascriptin, Bayer Aspirin, Buffinol)

 

Aspirin is an odorless, white, powdery substance available in 81mg, 325mg, and 500mg form for oral use. When exposed to moisture, aspirin hydrolyzes into salicylic acid and acetic acids.

Aspirin is a stronger inhibitor of prostaglandin synthesis and platelet aggregation than are other salicylic acid derivatives. The acetyl group is responsible for inactivation of cyclooxygenase via acetylation. Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero order pharmacokinetics.

Aspirin irreversibly inhibits platelet aggregation by inhibiting platelet cyclooxygenase. This, in turn, inhibits conversion of arachidonic acid to prostaglandin I2 (potent vasodilator and inhibitor of platelet activation) and thromboxane A2 (potent vasoconstrictor and platelet aggregating agent). Platelet inhibition lasts for the life of the cell (approximately 10 days).

Aspirin may be used in low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis. It reduces the likelihood of myocardial infarction and is also very effective in reducing the risk of stroke. Early administration of aspirin in patients with acute myocardial infarction may reduce cardiac mortality in the first month.

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Contributor Information and Disclosures
Author

Stanley S Wang, MD, JD, MPH Clinical Cardiologist, Austin Heart South; Director of Legislative Affairs, Austin Heart; Director, Sleep Disorders Center at Heart Hospital of Austin; Assistant Professor of Medicine (Adjunct), University of North Carolina School of Medicine

Stanley S Wang, MD, JD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, American Society of Echocardiography, Texas Medical Association, American Academy of Sleep Medicine, American Stroke Association, American Society of Nuclear Cardiology

Disclosure: Nothing to disclose.

Chief Editor

Yasmine Subhi Ali, MD, FACC, FACP, MSCI President, Nashville Preventive Cardiology, PLLC; Assistant Clinical Professor of Medicine, Vanderbilt University School of Medicine

Yasmine Subhi Ali, MD, FACC, FACP, MSCI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, Tennessee Medical Association, National Lipid Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: MCG Health, LLC; MedStudy<br/>Serve(d) as a speaker or a member of a speakers bureau for: MedStudy<br/>Received honoraria from MedStudy for independent contractor; Received salary from MCG Health, LLC for employment; Received fees from About.com for independent contractor.

Acknowledgements

Justin D Pearlman, MD, ME, PhD, FACC, MA Chief, Division of Cardiology, Director of Cardiology Consultative Service, Director of Cardiology Clinic Service, Director of Cardiology Non-Invasive Laboratory, Director of Cardiology Quality Program KMC, Dartmouth-Hitchcock Medical Center, Dartmouth Medical School

Justin D Pearlman, MD, ME, PhD, FACC, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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