eMedicine Specialties > Ophthalmology > Metabolic Disorders
Hyperlipoproteinemia: Treatment & Medication
Updated: Aug 14, 2007
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
- Systemic
- Drugs are used to lower cholesterol and triglyceride levels.
- Because of the possibility of adverse effects and the question of whether the triglyceride level is an independent risk factor for atherosclerosis, many physicians use drugs to reduce the triglyceride level only when the level exceeds 500 mg/100 mL.
- Examples of these drugs include lovastatin, pravastatin, and simvastatin.
- Supportive
- Weight reduction and a diet low in saturated fat and cholesterol are advocated.
- Patients should avoid alcohol and estrogen in certain types of hyperlipoproteinemias.
Surgical Care
Ileal bypass surgery and plasmapheresis to lower elevated serum lipids are used in selected cases of familial hypercholesterolemia. Only experienced physicians should use these therapies.
Consultations
Internist or family practitioner
Diet
A low-fat diet is recommended, including fruit, vegetables, chicken, and fish.
Medication
Drugs are used to lower cholesterol and triglyceride levels. Because of the possibility of adverse effects and the question of whether the triglyceride level is an independent risk factor for atherosclerosis, many physicians use drugs to reduce the triglyceride level only when the level exceeds 500 mg/100 mL.
HMG-CoA reductase inhibitors
These agents are competitive inhibitors of 3-hydroxy-3-methyl Co-A reductase, an enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis, resulting in up-regulation of LDL receptors in response to the decrease in intracellular cholesterol. The HMG-CoA reductase inhibitors are indicated for the secondary prevention of cardiovascular events and for the treatment of hypercholesterolemia and mixed dyslipidemia.
A number of HMG-CoA reductase inhibitors are indicated for patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments. However, these agents may be less effective in patients with rare homozygous familial hypercholesterolemia, possibly because these patients are lacking functional LDL receptors, making it more likely to raise serum transaminases.
Pravastatin (Pravachol)
Lipid-lowering compound; HMG-CoA reductase inhibitor; reduces cholesterol biosynthesis; orally administered in active form; rapidly absorbed (peak plasma 1-1.5 h). Therapeutic response is usually 1 wk. Highly effective in reducing total-C, LDL-C, and triglycerides in patients with heterozygous familial, presumed familiar forms of primary hypercholesterolemia, and mixed dyslipidemia.
Adult
10, 20, and 40 mg tab: Initially 10-20 mg PO hs; prior to dosing, establish lipid and liver functions and recheck at intervals of no less than 4 wk
Pediatric
<18 years: Not recommended
Effects increase with cholestyramine; increases toxicity of gemfibrozil, clofibrate, niacin, cyclosporine, and oral anticoagulants; itraconazole and ketoconazole increase toxicity of lovastatin; concurrent use with erythromycin may increase risk of rhabdomyolysis
Documented hypersensitivity; active liver disease
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Tell the patient to report promptly any unexplained muscle pain, tenderness, or weakness, especially if accompanied with malaise or fever
Lovastatin (Mevacor, Altocor)
This is a cholesterol-lowering agent, isolated from a strain of Aspergillus terreus. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, which is an early and rate-limiting step in the biosynthesis of cholesterol. Available in immediate-release (Mevacor) and sustained-release (Altocor) dosage forms.
Adult
Immediate-release: 20 mg PO qd with evening meal initially; may increase gradually to 20-80 mg/d in single or divided doses
Sustained-release: 10-20 mg PO hs initially; may increase dose q4wk, not to exceed 60 mg/d
Pediatric
Not established
Cyclosporine or other immunosuppressants; possible risk of polymyositis and rhabdomyolysis with erythromycin, gemfibrozil, and niacin; high risk of hepatotoxicity, avoid concomitant use with ethanol; oral anticoagulants may enhance clinical effects
Patients with active liver disease or unexplained elevations of serum transaminases; patients receiving immunosuppressive drugs; patients taking itraconazole, ketoconazole, gemfibrozil, niacin, erythromycin, clarithromycin, or nefazodone
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Liver function profiles of 6-12 wk of therapy; use cautiously in patients who consume large amounts of alcohol; renal failure; may contribute to progression of cataracts; monitor patients closely
Simvastatin (Zocor)
Inhibits 3-hydroxy-3-methylglutaryl-coenzyme A reductase, an enzyme in an early and rate-limiting step in the synthetic pathway of cholesterol. Peak plasma 1.3-2.4 h; peak antilipemic effects 3-4 mo.
Adult
Initially 5-10 mg PO qd pm; adjust dose every 4 wk per patient tolerance response; not to exceed 40 mg
Pediatric
Not established
Drugs that decrease levels or activity of endogenous steroids may increase risk of developing endocrine dysfunction; erythromycin, fibric acid derivatives, immunosuppressants, and high doses of niacin may increase risk of rhabdomyolysis, monitor closely if patient is taking cyclosporine and limit daily dose to 10 mg/d; ethanol increases risk of hepatotoxicity; warfarin may enhance effect; monitor patient at start of therapy and during dosage adjustments
Documented hypersensitivity; patients with active liver disease or conditions that cause unexplained persistent elevations of serum transaminase
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Use cautiously in patients who consume alcohol or who have liver or kidney disease; use only when patient diet and nonpharmacologic therapies have failed; test liver function as therapy starts and periodically thereafter; instruct patients to notify the doctor of adverse reactions and muscle aches and pains
Rosuvastatin (Crestor)
HMG-CoA reductase inhibitor, which, in turn, decreases cholesterol synthesis and increases cholesterol metabolism. Reduces total-C, LDL-C, and TG levels and increases HDL-C level. Used adjunctively with diet and exercise to treat hypercholesterolemia.
Adult
5-10 mg PO qd initially; may increase dose if needed, not to exceed 40 mg/d; for marked hypercholesterolemia (ie, LDL-C >190 mg/dL), initiate with 20 mg/d PO
Familial hypercholesterolemia: 20 mg PO qd initially; may increase dose if needed, not to exceed 40 mg/d
Pediatric
Not established
Cyclosporine or gemfibrozil significantly increase Cmax and AUC, thereby increasing myopathy and rhabdomyolysis risk; limit dose to 5 mg/d when coadministered with cyclosporine and 10 mg/d when coadministered with gemfibrozil; coadministration with aluminum and magnesium hydroxide antacids decreases plasma concentrations (administer antacids 2 h after rosuvastatin); may increase oral contraceptive plasma concentrations; alcohol may increase hepatotoxic risk
Documented hypersensitivity; active liver disease; unexplained serum transaminase elevation
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Common adverse effects include muscle aches, stomach pain, constipation, nausea, and weakness; may cause myopathy, rhabdomyolysis, and kidney failure; monitor LFTs (ie, baseline, 12 wk after drug initiation and any dose elevation, and semiannually), discontinue if elevation persists; decrease dose with CrCl <30 mL/min; doses 40 mg or greater associated with hematuria and proteinuria
Nicotinic acid derivatives
Niacin (vitamin B-3) inhibits the hepatic secretion of VLDL cholesterol. Niacin is effective in most categories of hyperlipidemia. Niacin has been demonstrated to lower LDL cholesterol by 32%, lower triglycerides by 20-50%, and raise HDL cholesterol by 43%. Niacin lowers lipoprotein (a) levels, which may be of some clinical importance because lipoprotein (a) levels have been associated with coronary heart disease in numerous epidemiological studies. The clinical benefit of lowering lipoprotein (a) levels has not been determined.
Niacin (Nicobid, Niaspan, Nicotinex)
Niacin functions in the body after conversion to nicotinamide adenine dinucleotide (NAD) in the NAD coenzyme system. Niacin in gram doses reduces total cholesterol, LDL-C, and triglycerides and increases high-density lipoprotein cholesterol. The magnitude of individual lipid and lipoprotein responses may be influenced by the severity and type of underlying lipid abnormality. Niacin should be taken at bedtime after a low-fat snack and individualized according to patient response.
Adult
Initially, dosage is gradually increased, starting with 375 mg and increasing until the patient responds
Recommended maintenance dose is 1000-2000 mg qd
Pediatric
Not established
May produce false elevations in some fluorometric determinations of plasma or urinary catecholamines; may potentiate the effects of ganglionic blocking agents and vasoactive drugs causing hypotension; concomitant aspirin may decrease the metabolic clearance of nicotinic acid
Documented hypersensitivity; unexplained hepatic dysfunction; active gastric ulcer disease; arterial bleeding
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Precautions
Closely observe patients with history of jaundice, hepatobiliary disease, or peptic ulcer; patients with diabetes may experience a dose-related rise in glucose intolerance; use cautiously in patients with angina; may cause an increase in prothrombin time; avoid with anticoagulants
More on Hyperlipoproteinemia |
| Overview: Hyperlipoproteinemia |
| Differential Diagnoses & Workup: Hyperlipoproteinemia |
 Treatment & Medication: Hyperlipoproteinemia |
| Follow-up: Hyperlipoproteinemia |
| References |
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References
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Crispin SM. Lipid deposition at the limbus. Eye. 1989;3 (Pt 2):240-50. [Medline].
Feldman EB. Nutrition and diet in relation to hyperlipidemia and atherosclerosis. In: Shields M, Olson JA, Shike M. Modern Nutrition in Health and Disease. 8th ed. 1992.
Gronemeyer A, Arsene S, Le Lez ML, Rateau J. [Central retinal artery occlusion or branch retinal artery occlusion in the young associated with high lipoprotein (a) levels]. J Fr Ophtalmol. Sep 2002;25(7):727-30. [Medline].
Jünemann A, Küchle M, Naumann GO. Epithelial iron line in juvenile corneal arcus lipoides. Cornea. Sep 1995;14(5):540-2. [Medline].
Wu CW, Lin PY, Liu YF, Liu TC, Lin MW, Chen WM, et al. Central corneal mosaic opacities in Schnyder's crystalline dystrophy. Ophthalmology. Apr 2005;112(4):650-3. [Medline].
Further Reading
Keywords
hyperlipidemia, chylomicronemia, hypercholesterolemia, dysbetalipoproteinemia, hypertriglyceridemia, mixed hyperlipoproteinemia, combined hyperlipoproteinemia, high cholesterol
