Tests for secondary hyperlipidemia
Once hyperlipidemia is confirmed and recognizing that lipemia is usually secondary, additional testing aimed at identifying
the primary cause is recommended. Additional testing (including a complete blood count, serum chemistry profile, and urinalysis)
may include a low-dose dexamethasone suppression test, thyroid function testing (serum T4 and thyroid-stimulating hormone concentrations), and serum pancreatic lipase immunoreactivity.
Tests for primary hyperlipidemia
If secondary hyperlipidemia is ruled out, primary hyperlipidemia is likely, and additional testing may include lipoprotein
electrophoresis and lipoprotein lipase activity. However, lipoprotein electrophoresis has limited value in the clinical evaluation
of lipid disorders in dogs and cats because validation of lipoprotein classes by electrophoresis is incomplete.2 Furthermore, it is unlikely that electrophoretic patterns are disease-specific.2
The absence or decreased activity of lipoprotein lipase can be evaluated by determining the plasma activity of this enzyme.
Indirect activity can be determined by collecting serum samples both before and 15 minutes after an intravenous injection
of heparin (90 IU/kg) in dogs.1 In cats, samples should be collected before and 10 minutes after an intravenous injection of heparin (45 IU/kg).1 Heparin causes lipoprotein lipase release from vascular endothelium, stimulating the hydrolysis of chylomicrons and VLDLs.7 Cholesterol and triglyceride concentrations are measured in pre- and post-heparin samples. A post-heparin decrease in triglyceride
and cholesterol concentrations confirms lipoprotein lipase activity. Similar pre- and post-heparin triglyceride and cholesterol
concentrations are compatible with decreased or absent lipoprotein lipase activity.1 Molecular polymerase chain reaction analysis is available for lipoprotein lipase deficiency in cats with hyperchylomicronemia.16
Treatment options for hyperlipidemia include treatment of inciting diseases, diet modification, and pharmacologic intervention.
The importance of testing for inciting causes of hyperlipidemia cannot be overemphasized. Hyperlipidemia secondary to an underlying
disorder will probably resolve or improve after the metabolic disturbance is corrected.
In cases of familial or idiopathic hyperlipidemia with elevated triglyceride concentrations, combined dietary and pharmacologic
intervention may be necessary. We recommend treating patients with moderate to severe hyperlipidemia. Dogs that require cataract
surgery (diabetic patients) should ideally have a fasted triglyceride concentration < 500 mg/dl. In our experience, triglyceride
enters the aqueous chamber at an approximate serum concentration of 500 mg/dl and causes severe uveitis. So we treat patients
with fasting triglyceride concentrations > 500 mg/dl aggressively before cataract surgery. The goal of therapy is not to reduce
triglyceride and cholesterol concentrations to the normal range. Instead, triglyceride and cholesterol concentrations should
be reduced so that clinical signs are ameliorated while avoiding drug-induced side effects.
Dietary modification. In some patients, switching the patient to a low-fat diet may be the only therapy needed. It is generally recommended that
diets should contain less than 20% fat on a metabolizable energy basis for dogs and less than 25% for cats (Table 6).3,17 However, obtaining a good diet history to estimate the level of consumed fat is important before deciding the degree of
fat restriction. The patient should be fed a diet with a fat level lower than the previous diet. Treats should be restricted
to 5% of the daily caloric intake and changed to low-fat varieties (carrots or brown rice crackers).3,17
Table 6: Selected Low-Fat Commercial Diets for Dogs and Cats*