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 Concentration of lipid in the blood of a fasted (>12 h) patient that exceeds the upper range of normal for that species; includes both hypercholesterolemia and hypertriglyceridemia  Lipemic serum or plasma separated from blood that contains an excess concentration of  Lactescence opaque, milklike appearance of serum or plasma that contains an even higher concentration of triglycerides (>1000 mg/dL) than lipemic serum PATHOPHYSIOLOGY
Primary Hyperlipidemia
 Idiopathic hyperchylomicronemia defect in lipid metabolism causing hypertriglyceridemia and hyperchylomicronemia; possibly caused by a defect in lipoprotein lipase activity or the absence of the surface apoprotein CII; familial disorder in the miniature schnauzer  Hyperchylomicronemia in cats familial, autosomal recessive defect in lipoprotein lipase activity  Idiopathic hypercholesterolemia occurs in some families of Doberman pinschers and Rottweilers; Secondary Hyperlipidemia
 Postprandial absorption of chylomicrons from the gastrointestinal tract occurs 30–60 min after ingestion of a meal containing fat; may increase serum triglycerides for 3–10 hours  Diabetes mellitus low lipoprotein lipase (LPL) activity; high synthesis of very-low-density  Hypothyroidism low LPL activity and lipolytic activity by other hormones (e.g., catecholamines); reduced hepatic degradation of cholesterol to bile acids  Hyperadrenocorticism increased synthesis of VLDL by the liver and low LPL activity causes both hypercholesterolemia and hypertriglyceridemia.  Liver disease hypercholesterolemia caused by reduced excretion of cholesterol in the bile  Nephrotic syndrome common synthetic pathway for albumin and cholesterol and possibly low oncotic pressure lead to increased cholesterol synthesis.  Obesity excessive hepatic synthesis of VLDL SYSTEMS AFFECTED
 Ophthalmic  Nervous  Endocrine/Metabolism  Gastrointestinal  Hepatobiliary SIGNALMENT
 Dog and cat  Variable, depending on the cause  Hereditary hyperlipidemias age of onset is >8 months in cats and >4 years in predisposed breeds Historical Findings
 Recent ingestion of a meal  Seizures  Abdominal pain and distress  Neuropathies Physical Examination Findings
 Lipemia retinalis  Lipemic aqueous  Neuropathy  Cutaneous xanthomata  Lipid granulomas in abdominal organs Increased Absorption of Triglycerides or Cholesterol
Increased Production of Triglycerides or Cholesterol
 Nephrotic syndrome  Pregnancy  Defects in lipid clearance enzymes or lipid carrier proteins  Idiopathic hyperchylomicronemia  Hyperchylomicronemia in cats  Idiopathic hypercholesterolemia Decreased Clearance of Triglycerides or Cholesterol
 Hypothyroidism  Hyperadrenocorticism  Diabetes mellitus  Pancreatitis  Cholestasis RISK FACTORS
 Obesity  High dietary intake of fats  Genetic predisposition in miniature schnauzer and Himalayan cat  Idiopathic hypercholesterolemia observed in families of Doberman pinschers and rottweilers Diagnosis
Fasting Hyperlipidemia
Rule out postprandial lipemia with a 12-hour fast. Primary Hyperlipoproteinemia
 Idiopathic hyperchylomicronemia is observed most commonly in the miniature schnauzer breed.  Hyperchylomicronemia in cats often manifests as polyneuropathies and lipogranulomas.  Idiopathic hypercholesterolemia is observed most frequently in the Doberman pinscher and rottweiler breeds; animals are often asymptomatic. Secondary Hyperlipidemia
 Diabetes mellitus signs include polyphagia, weight loss, polydypsia, and polyuria; glycosuria and fasting hyperglycemia confirm the diagnosis.  Hypothyroidism signs include lethargy, hypothermia, heat seeking, and dermatologic changes  Pancreatitis signs include abdominal pain, vomiting, diarrhea, and anorexia; often hyperlipidemia is accompanied by high liver enzyme activities and high lipase and amylase.  Hyperadrenocorticism signs include polydypsia, polyuria, polyphagia, dermatologic changes (e.g., alopecia and thin skin), and hepatomegaly; hypercholesterolemia often is attended by high ALP isoenzyme.  Hepatic disease and cholestatic disorders—signs include anorexia, weight loss, and icterus.  Nephrotic syndrome signs include ascites and peripheral edema; hypercholesterolemia is observed in conjunction with hypoproteinemia and proteinuria. LABORATORY FINDINGS
Sample Handling
 Submit serum.  Lipemia causes hemolysis if serum remains on RBC for a long time; inquire about the laboratory method of clearing lipemic samples before submission.  Two samples may be submitted: one for biochemical analysis, which may be cleared, and one for triglycerides and cholesterol concentrations. Drugs That May Alter Laboratory Results
 Corticosteroids  Phenytoin  Prochlorperazine  Thiazides  Phenothiazines Disorders That May Alter Laboratory Results
 Nonfasted samples (<12 hours)  Icterus spectrophotometric techniques  Fluoride and oxalate anticoagulants enzymatic techniques  Lipemia Valid If Run in Human Laboratory?
 Results of hemogram usually normal  Hyperadrenocorticism polycythemia and nucleated RBCs  Hypothyroidism mild normocytic, normochromic anemia  High triglycerides dogs, >150 mg/dL; cats, >100 mg/dL  High cholesterol dogs, >300 mg/dL; cats, >200 mg/dL  Nephrotic syndrome low albumin  Diabetes mellitus high serum glucose  Hyperadrenocorticism high ALP activity  Pancreatitis high serum lipase  Results of urinalysis often normal  Nephrotic syndrome—proteinuria OTHER LABORATORY TESTS
 HDL and LDL determinations used in human medicine; values reported for HDL and LDL in dogs and cats cannot be assumed to be reliable.  Chylomicron test obtain serum sample after a 12-hour fast and refrigerate for 12–14 hours; do not freeze; chylomicrons rise to the surface and form a creamy layer.  Lipoprotein electrophoresis separates LDL, VLDL, HDL1, and HDL2  LPL activity collect serum for triglycerides and cholesterol concentrations and lipoprotein electrophoresis before and 15 min after IV administration of heparin (90 IU/kg); if there is no change in values before and after heparin administration, a defective LPL enzyme system should be suspected.  T and T determinations indicated if hypothyroidism is suspected  Adrenocorticotropic hormone (ACTH) stimulation test indicated if hyperadrenocorticism is DIAGNOSTIC PROCEDURES
Diet should contain <10% fat (e.g., Hill's r/d, Iams restricted calorie). Medications
 Initial management is dietary.  See Alternative Drugs if diet fails to control hyperlipidemia. CONTRAINDICATIONS
 Gemfibrozil 7.5 mg/kg PO q12h  Fish oils linolenic acid (omega-3 polyunsaturated fat), 10–30 mg/kg PO q24h  Clofibrate and niacin not currently recommended in cats or dogs Follow-Up
 Keep triglyceride concentrations < 500 mg/dL to avoid possibly fatal episodes of acute  Checking cholesterol often is not necessary because hypercholesterolemia is not associated with POSSIBLE COMPLICATIONS
 Pancreatitis and seizures are common complications of hyperlipidemia in the miniature schnauzer.  In cats with hereditary chylomicronemia, xanthoma formation, lipemia retinalis, and neuropathies have been reported; peripheral neuropathies usually resolve 2–3 months after institution of a low-fat diet. Miscellaneous
 Pancreatitis  Seizures  Neuropathies AGE-RELATED FACTORS
 ALP = alkaline phosphatase  HDL = high-density lipoprotein  LDL = low-density lipoprotein  LPL = lipoprotein lipase  T = thyroxine Suggested Readings
 Barrie J, Watson TOG. Hyperlipidemia. In: Bonagura JD, ed. Kirk's Current veterinary therapy XII. Philadelphia: Saunders, 1995:430–434.  Ford R. Canine hyperlipidemias. In: Ettinger ST, Feldman EC, eds. Textbook of veterinary internal medicine. 4th ed. Philadelphia: Saunders, 1994:1414–1418.  Jones B. Feline hyperlipidemias. In: Ettinger ST, Feldman EC, eds. Textbook of veterinary internal medicine. 4th ed. Philadelphia: Saunders, 1994:1410–1413.
Author: Deborah S. Greco
Consulting Editor: Editor Deborah S. Greco


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