Bile acids are synthesized in the liver from cholesterol and excreted into the duodenum. Cholestyramine (Questran—Bristol-Myers
Squibb) is an ion exchange resin that interferes with the enteric absorption of bile acids and is approved for use in people
to lower cholesterol.18 Cholestyramine (1 to 2 g orally b.i.d.) results in increased cholesterol use for bile acid synthesis.3,18 As hepatic cholesterol concentration decreases, hepatic LDL receptors are upregulated to increase the removal of LDLs and
HDLs from the blood.18 Potential side effects of this medication include constipation, interference of oral medication absorption, and increased
VLDLs from uptake of LDLs.18 Because of the risk of increased VLDLs, use cholestyramine with caution in patients with concurrent hypertriglyceridemia.
The statins, which are methylglutaconyl-coenzyme A (HMG-CoA) reductase inhibitors, are the most potent cholesterol-lowering
drugs in people.18 HMG-CoA reductase is the rate limiting step in cholesterol synthesis.18 Statins, by inhibiting HMG-CoA reductase, reduce hepatic cholesterol synthesis. A decreased hepatic cholesterol concentration
results in the upregulation of hepatic LDL receptors and increased removal of LDLs from the blood.18 The statins also decrease the hepatic production of VLDLs and are modestly effective in the treatment of hypertriglyceridemia.18 Lovastatin (10 mg orally once a day) is effective for persistent hypercholesterolemia in dogs.3 Potential adverse effects include hepatotoxicity, vomiting, diarrhea, myopathy, and hyperesthesia.18 Perform a serum chemistry profile, including creatine kinase activity, before administering any statin, and frequent monitoring
for hepatotoxicosis and myopathy is a must. Serum alanine aminotransferase and alkaline phosphatase activities along with
serum creatine kinase activities (myopathy) should be measured after one month and then, if normal, at six-month intervals.
The combination of a statin plus a fibric acid derivative (gemfibrozil) may increase the risk of skeletal myopathy. These
drugs should not be used or should be discontinued in any patient with hepatic disease or that develops evidence of hepatic
disease or myopathy during use. The benefit of statins in dogs and cats to reduce LDL is unproven because most of their total
cholesterol is transported as HDL.
PROGNOSIS
The prognosis for patients with secondary hyperlipidemia is favorable with effective treatment of the underlying disorder.
For patients with primary hyperlipidemia, a lifelong commitment by the owner and veterinarian is required. In our experience,
most patients respond favorably to diet modification alone or in combination with pharmacologic agents. The pharmacologic
intervention in patients with hyperlipidemia should not be taken lightly. All drugs are potentially toxic, and patients should
be monitored carefully. With a committed owner and a veterinarian's thorough understanding of pharmacologic agents used, treating
hyperlipidemia can be rewarding.
Justin D. Thomason, DVM, DACVIM (internal medicine)*
Department of Small Animal Medicine and Surgery
College of Veterinary Medicine
University of Georgia
Athens, GA 30602
Bente Flatland, DVM, DACVIM (internal medicine)
Department of Pathobiology
College of Veterinary Medicine
The University of Tennessee
Knoxville, TN 37996
Clay A. Calvert, DVM, DACVIM (internal medicine)
Department of Small Animal Medicine and Surgery
College of Veterinary Medicine
University of Georgia
Athens, GA 30602
*Dr. Thomason's current address is Department of Veterinary Clinical Sciences, Center for Veterinary Health Scieces, Oklahoma
State University, Stillwater, OK 74078.
REFERENCES
1. Whitney MS. Evaluation of hyperlipidemias in dogs and cats. Semin Vet Med Surg (Small Anim) 1992;7:292-300.
2. Ford RB. Clinical management of lipemic patients. Compend Contin Educ Pract Vet 1996;18:1053-1065.
3. Nelson RW, Elliot DA. Disorders of metabolism. In: Nelson RW, Couto CG, eds. Small animal internal medicine. 3rd ed. St. Louis, Mo: Mosby, 2003;822-827.
4. Ganong WF. Energy balance, metabolism, and nutrition. In: Review of medical physiology. 20th ed. New York: McGraw-Hill Company, 2001;271-306.
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