Hyperlipidemia quiz

Hyperlipidemia - what vet techs need to know

By Ann Wortinger, BIS, LVT, VTS (ECC,SAIM, Nutrition)

Hyperlipidemia is a disturbance of lipid metabolism that results in an increased concentration of lipoproteins in the blood, particularly triglycerides and cholesterol. In a fasted sample (typically 12 hours), the presence of increased lipids represent either increased synthesis of lipids within the body, or decreased degradation of lipoproteins by the body.  
Triglycerides are the most abundant dietary lipid, and the primary fat found in pet foods.  Triglycerides are used as a source of stored energy in adipocytes or metabolized for tissue demand. Cholesterol is a major component of cellular membranes and an essential precursor of steroid hormones, vitamins, and bile acids.

Triglycerides and cholesterol are hydrophobic molecules that are unable to circulate in the blood without being incorporated into a complex molecule called a lipoprotein.  The water-soluble outer layer of this molecule is composed of phospholipids, free cholesterol, and apolipoproteins. Cholesterol in the form of cholesterol esters and triglycerides are carried within the non-polar core with lipoprotein macromolecules.                     

Classification of fats

Fats are classified into one of four groups based on their buoyant density upon ultracentrifugation: chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL).

Chylomicrons are the largest and least dense of the lipoproteins, and contain the highest amount of triglycerides (~90%).  They are derived from dietary fat and are formed in the intestinal mucosa.  Chylomicrons are responsible for delivery of dietary triglyceride to the body tissues and cholesterol to the liver. When acted on by lipoprotein lipase, the chylomicrons are hydrolyzed into glycerol, cholesterol, and free fatty acids. Hyperchylomicronemia is the most common lipid disorder in companion animals.

VLDLs are produced in the liver from endogenously derived triglycerides. When transported to the tissue capillaries, they are catabolized by lipoprotein lipase, as are the chylomicrons.

LDLs are responsible for transporting endogenously synthesized lipids, especially cholesterol, from the liver to the target tissues. After hydrolysis of the VLDL molecule and removal of triglyceride from the core, a short-lived intermediate density lipoprotein is formed that ultimately is processed by hepatic lipase into LDL. In humans ~70% of the cholesterol is carried within the LDL molecule; in companion animals most of the cholesterol is carried in the HDL molecule.

HDLs are produced in the liver, and are recognized for their ability to remove excess cholesterol from the tissues and transport it back to the liver. Newly formed HDL molecules are secreted by the liver and intestine and bind with unesterified cholesterol released from the peripheral tissue during normal cellular turnover.

Clinical importance of hyperlipidemia

Lipemic serum may positively or negatively interfere with quantitative analysis of other serum analytes. It can falsely increase serum values for total bilirubin, conjugated bilirubin, and phosphorus.  At very high levels it can cause interference with alkaline phosphatase and glucose. Total protein can be affected when measured using a refractometer. False decreases can be seen with creatinine and total CO2. Red blood cells are more fragile in lipemic plasma and tend to lyse in vitro, so hemolysis is often seen with lipemia. On a differential blood smear, the red blood cells can appear fuzzy with a blue foamy background.

Hyperlipidemia places an animal at increase risk for development of pancreatitis in dogs. Hyperlipidemia can also cause seizures, blindness, abdominal pain, anorexia, vomiting, behavioural changes, lipemia retinalis, uveitis, and peripheral neuropathies.

Classifications of hyperlipidemia

Causes of hyperlipidemia can be classified as postprandial, familial, and acquired.


With familial, also called primary or idiopathic hyperlipidemia, defects in lipoprotein metabolism are known or suspected to be inherited. Idiopathic hyperlipidemia of schnauzers typically affects middle- to older-aged miniature schnauzers, though other purebred and mixed-breed dogs can be affected.  An increased serum triglyceride is seen, with a mild increase in cholesterol, VLDL, and visible lipemia.  Etiology is unknown but lipoprotein lipase deficiency is believed to be the cause.


Acquired or secondary hyperlipidemia refers to excess concentrations of lipids in the blood stream resulting from underlying disease in which normal lipoprotein metabolism is markedly altered. Several endocrine diseases alter lipid metabolism.  An insulin deficient state as seen with diabetes mellitus alters carbohydrate and lipid metabolism, and can present with either increased triglycerides or increased cholesterol.  Cushing’s disease, protein-losing nephropathy, pancreatitis (in both dogs and cats), and hypothyroidism are variably associated with secondary hyperlipidemia.  Hyperlipidemia secondary to an underlying disease will typically resolve or improve with correction of the metabolic disturbance.


In normal dogs and cats postprandial hyperlipidemia usually persists from 6-12 hours post meal, and even with a high fat diet, the serum triglyceride levels would not be expected to exceed 500 mg/dl. Hyperlipidemia is diagnosed after a 12 hour fast if blood levels exceed those listed.

Diagnostic levels for hyperlipidemia





>300 mg/dl

>200 mg/dl


>150 mg/dl

>100 mg/dl



The first step in treating hyperlipidemia is to determine whether the condition is postprandial, familial, or acquired. The blood sample should be taken after a 12-18 hour fast to rule out postprandial hyperlipidemia. If the hyperlipidemia is still present, and secondary causes have been ruled out, dietary management is the primary means of control. Restriction of dietary fat in the diet, and strict owner compliance of this restriction, are essential.


The addition of drugs should only be done when the animal is not responding adequately to diet alone (i.e. triglycerides persistently above 750mg/dl or showing clinical signs caused by increased triglyceride levels).  The dose and efficacy of hypolipidemic drugs have not been critically evaluated in dogs and cats. The fibric acid derivatives (clofibrate, bezafibrate, gemfibrozil, ciprofibrate, fenofibrate) lower plasma triglyceride levels by stimulating lipoprotein lipase activity, in addition to reducing the free fatty acid concentration that decreases the substrate for VLDL synthesis.  In humans, fibrates generally lower the plasma triglyceride concentration by only 20-40%. Reported adverse effects include abdominal pain, vomiting, diarrhea, liver enzyme elevations, and liver failure. The statins (lovostatin, simvastatin, pravastatin, fluvastatin, cerivastatin, atorvastatin) are HMG CoA (3-hydroxy 3-methyl glutaryl coenzyme A) reductase inhibitors and therefore primarily suppress cholesterol metabolism and would be of lesser value in treating dogs and cats. In addition, the statins decrease hepative production of VLDL.  In humans, the statins can lower triglyceride concentrations by 10-15%. Adverse effects include lethargy, diarrhea, muscle pain, and hepatotoxicity.

Hyperlipidemia is a problem that many of us see on a daily basis, with hypertriglyceridemia being the most common lipid metabolism disorder seen in dogs and cats.  The major clinical importance is its association with pancreatitis and the effect lipids can have on routine blood work.  A 12-hour fast is required to confirm whether the cause is post-prandial or familial/acquired.  Restriction of dietary fat and recognition and treatment of acquired causes are the mainstays of medical therapy.

This article is based on an article presented by Ms. Wortinger at the North America Veterinary Conference in Orlando, FL.CVT