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Compendium May 2005 (Vol 27, No 5)

Hyperlipidemia Disorders in Dogs

by Mark C. Johnson, DVM, DACVP (Clinical Pathology)


    Lipid disorders are common in dogs, with most arising from secondary causes such as endocrine imbalances, cholestatic liver disease, or protein-losing nephropathies. Two primary lipid disorders—idiopathic hyperlipidemia in miniature schnauzers and hypercholesterolemia in briards—are also recognized. Visualization of a lipemic fasted blood sample or elevated plasma cholesterol or triglyceride in combination with clinical assessment is the method by which most lipid disorders are diagnosed. Cholesterol and triglyceride are components of larger molecules called lipoproteins, which have a complex and highly regulated metabolism that is important to understand when altered by lipid disorders.

    Lipid disorders are relatively common in veterinary medicine, particularly in dogs. The presence of a lipid disorder provides clues regarding underlying disease and presents a risk factor for other problems. In dogs, lipid disorders are either primary or secondary, of which the latter is by far the most common.1-4 Primary disorders are con­sidered hereditary in some breeds of dogs.1,3-6 Secondary disorders can be dietary related or more often of endocrine origin, resulting from an imbalance of homeostatic mechanisms that normally regulate plasma lipids1-4 (see box). Unfortunately, it is not always easy to separate these two based on clinical assessment or biochemical analysis. Therefore, it is imperative that signalment, clinical presentation, and biochemical information for each animal be analyzed collectively when suspecting one of these disorders. This article discusses basic concepts of lipid metabolism, addresses laboratory evaluation of plasma lipids, and examines the causes of hyperlipidemia disorders in dogs.

    Lipid Metabolism

    Cholesterol and triglyceride are clinically relevant plasma lipids (Figure 1 and Figure 2). Free cholesterol and triglyceride are water insoluble in plasma, so they are transported via water-soluble lipoproteins in plasma. There are four general types of lipoproteins: chylomicrons, very-low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL). Intermediate-density lipoprotein is also recognized but is considered less important. Humans have two HDL molecules: HDL2 and HDL3. Dogs have HDL2 and HDL3 but are unique in that they have HDL1, which is recognized by a distinct a2 band on lipoprotein electrophoresis.1,3,7

    Lipoproteins exist in plasma as spherical structures composed of an outer shell and an inner core (Figure 1). The outer shell has both hydrophilic and hydrophobic properties containing free cholesterol, apoproteins, and phospholipids.3,7 Apoproteins serve as cofactors for cholesterol-shuttling enzymes, receptors for uptake and delivery of tissue cholesterol and triglyceride, and receptors for removal of remnant lipoproteins by the liver. The inner core consists of hydrophobic lipids, primarily cholesterol esters and triglyceride.3,7

    Chylomicrons are created by intestinal epithelial cells following fatty meal ingestion. They are large molecules composed primarily of triglyceride with smaller amounts of cholesterol. Chylomicrons transport triglyceride to tissue, such as muscle or fat. A critical enzyme called lipoprotein lipase, which is located on the endothelium in many tissues, mediates this transport.3,7,8 Lipoprotein lipase hydrolyzes triglyceride within chylomicrons to long-chain fatty acids and glycerol for active uptake by cells.8 Insulin and thyroxine are known to enhance the activity of this enzyme.8 After triglyceride is delivered to tissue, remnant chylomicron particles are removed from circulation by the liver.

    VLDL is produced by hepatocytes and is smaller than chylomicrons but also contains similar cholesterol and triglyceride proportions. Lipoprotein lipase also hydrolyzes triglyceride within VLDL, subsequently forming remnant VLDL. Remnant VLDL particles may be removed from circulation by the liver or may undergo further triglyceride depletion by lipoprotein lipase or a second enzyme called hepatic triglyceride lipase, forming smaller and denser LDL.3,7

    There are notable differences in how dogs and hu­mans process LDL and form HDL. LDL, the "bad lipoprotein," primarily transports cholesterol with smaller amounts of triglyceride for delivery to tissues. Subsequently, remnant LDL particles can be removed from circulation by the liver in both species, similar to remnant VLDL. In humans, a process called cholesterol shuttling, which is mediated by cholesterol ester transfer protein, enables triglyceride to be transported directly from LDL or VLDL to HDL3 in plasma in exchange for cholesterol esters, consequently forming cholesterol ester-rich LDL and triglyceride-rich HDL2, respectively.3,7 Cholesterol ester-rich LDL is removed from the bloodstream by the liver but can also be actively removed from circulation by macrophages lining large arteries, potentially leading to atherosclerosis. Unlike humans, dogs have no documented activity of cholesterol ester transfer protein, which likely contributes to their general resistance to this detrimental phenomenon.3,7,9

    Native HDL, the "good lipoprotein," is produced by the liver and transports cholesterol from tissue back to the liver (i.e., the so-called "reverse cholesterol transport" mechanism). Lecithin-cholesterol acyltransferase (LCAT), which is an enzyme bound to native HDL in circulation, converts free cholesterol from tissue to cholesterol esters for incorporation into HDL molecules.3,7 These cholesterol ester-rich molecules are called HDL3 in both species. Because dogs do not have cholesterol ester transfer protein activity, most HDL3 continues to acquire cholesterol esters and results in formation of the unique HDL1 molecule. Consequently, HDL1 is usually increased with hypercholesterolemia in dogs.3,7 Cholesterol ester-rich HDL can be removed from the blood by receptor-mediated endocytosis in the liver for possible reuse. Recent evidence in cultured mouse adrenal cells also shows that cholesterol esters can be removed from cholesterol ester-rich HDL by scavenger receptors (class B, type 1) without endocytosis of the HDL molecule.10 This receptor has been characterized in humans, but a canine counterpart has not been identified in the literature.11

    Laboratory Features of Lipid Disorders

    Increased plasma lipids are often discovered in dogs only serendipitously following biochemical testing for a clinically suspected disease that is subsequently known to elicit increased plasma lipids. However, dogs may not exhibit overt clinical signs of such a disease, and laboratory testing may be the only route by which lipid disorders are initially identified. Therefore, routine health screening blood work can be important in early detection of lipid disorders. Dogs should be fasted for 12 hours before blood samples are collected in clot or heparinized glass tubes.1,12,13

    When plasma levels of either cholesterol or triglyceride are increased, an assumption is made that one or more of the lipoproteins carrying these lipids are also increased. Clinically speaking, however, abnormalities in laboratory data are typically defined by alterations in cholesterol or triglyceride and not in lipoproteins. An increase in plasma lipid is called hyperlipidemia and results from increased triglyceride, cholesterol, or both.13 Hyperlipoproteinemia is often used synonymously with hyperlipidemia but is best used when plasma lipoprotein analysis is actually conducted.13

    One of the first indications of hyperlipidemia is observation of turbid (i.e., cloudy) or lactescent (i.e., white) plasma, which suggests that lipemia and a lipid disorder may be present.1,12,13 From a laboratory perspective, lipemia can interfere with certain biochemical tests that use endpoint or kinetic assays and can falsely increase tests using refractometry or spectrophotometry, such as plasma protein and hemoglobin testing, respectively.14 Spurious biochemical results reported in patients with lipemia are increased total bilirubin, total protein, albumin, globulin, glucose, calcium, phosphorus and bile acid levels.3,14 Falsely decreased assays can be seen with electrolyte levels and serum activity of amylase, lipase, alanine aminotransferase, aspartate transaminase, and alkaline phosphatase.3,14

    Lipemia is always associated with elevated plasma triglycerides. However, hyperlipidemia does not always induce lipemia because hypercholesterolemia by itself does not cause lipemia.13 Consumption of fatty diets can induce transient lipemia for up to 12 hours after eating.1,3,15 Therefore, it is vital to differentiate chylomicron-induced, postprandial lipemia from VLDL-generated hypertriglyceridemia because the former is usually short-lived and does not typically indicate the presence of a lipid disorder. These disorders can often be differentiated by placing lipemic samples in a refrigerator (i.e., a chylomicron or refrigeration test) for 12 hours. Chylomicrons are larger and less dense than VLDL and tend to form a "cream" layer on top of plasma when refrigerated.1,13 VLDL often remains suspended in plasma following refrigeration.1,13 When both chylomicrons and VLDL are present, the sample is turbid with a creamy layer.1,13

    Lipid biochemical analysis is often needed to identify a potential lipid disorder. In human medicine, detailed lipoprotein analysis is conducted by ultracentrifugation and electrophoresis of plasma. Although many veterinary diagnostic laboratories can conduct this evaluation, this type of testing for veterinary patients is often im­practical. Most veterinary chemistry analyzers can quantify plasma cholesterol and triglyceride, which is an indirect reflection of plasma lipoprotein. Serum cholesterol is a usual component of canine chemistry panels, so more attention is initially focused on increased cholesterol values when suspecting a lipid disorder. Triglyceride measurement is not standard to every canine chemistry panel but can be requested as an additional test.

    In general, plasma cholesterol exceeding 300 mg/dl is considered increased.1,13 The magnitude of cholesterol increase may reflect the seriousness of the clinical disorder, especially with extreme elevations. Cholesterol values of 300 to 500 mg/dl are considered mildly increased, values of 500 to 750 mg/dl moderately increased, and those over 750 mg/dl severely increased.1 Hypertriglyceridemia follows similar trends used for clinical assessment. Values of 150 to 400 mg/dl are generally considered mildly elevated, results of 400 to 1,000 mg/dl moderately elevated, and those greater than 1,000 mg/dl seriously elevated.1 Plasma turbidity is often grossly visible with triglyceride values above 300 mg/dl and lactescent with values greater than 1,000 mg/dl.3

    Clinical Significance of Hyperlipidemia

    The consequences of persistent hyperlipidemia can be clinically relevant in dogs. Plasma cholesterol values greater than 750 mg/dl predispose dogs to atherosclerosis despite their natural resistance.1,7 A recent citation re­ported that dogs with atherosclerosis are 53 times more likely to have diabetes mellitus (DM) and 51 times more likely to have hypothyroidism, both of which are known secondary causes of hyperlipidemia.16 Xanthomas (i.e., yellowish raised skin nodules or plaques composed of foamy macrophages laden with lipid) are often seen in cats with hyperlipidemia but are rarely present with hyperlipidemia in dogs.15,17,18 Al­though a cause-and-effect relationship between hypertriglyceridemia and pancreatitis and DM has not been established in dogs, a direct correlation between them has been suggested. In humans, elevated plasma lipids associated with type 2 DM have been linked with pancreatic b-cell toxicity and decreased function likely due to accumulation of lipid metabolites in these cells.19 Hyper­triglyceridemia can be associated with abdominal pain, vomiting and diarrhea, lipemia retinalis and clouding of the aqueous humor, lethargy, hepatomegaly, and seizures.1,12,15

    Primary Lipid Disorders

    Primary lipid disorders are rare in dogs, and the mechanisms inducing them are often unknown. Idiopathic hyperlipidemia in miniature schnauzers and hypercholesterolemia in briards are the two recognized primary lipid disorders in dogs, although references also describe familial hyperlipoproteinemia in beagles, hypertriglyceridemia in two related Brittanys, and congenital lipoprotein lipase deficiency in a mixed-breed puppy.1,3,5,6,20-23

    Idiopathic hyperlipidemia in miniature schnauzers is by far the most common primary disorder. Although this complex metabolic syndrome is considered to have familial tendencies, no defined genetic defect has been characterized. Lipemia and thus hypertriglyceridemia are commonly reported; hypercholesterolemia is also documented but is less consistent.1,5 Lipoprotein evaluations in one study revealed increased VLDL with variable chylomicron results.5 Miniature schnauzers may have concurrent acute pancreatitis. This poses the question of which came first—pancreatitis or hyperlipidemia—because acute pancreatitis is a common secondary cause of hyperlipidemia.1,3-5 Although not proved, it is conceivable that patients with idiopathic hyperlipidemia may have an increased risk of developing DM, especially if they have concurrent acute pancreatitis.5 Some of the clinical features documented with idiopathic hyperlipidemia are abdominal pain, seizures, and vomiting.5,15,20

    Hypercholesterolemia in briards has been reported primarily in the United Kingdom.6 It was initially discovered because of an association with retinal pigment epithelial dystrophy (also called briard lipid retinopathy), which is a degenerative disorder affecting the retina. A genetic defect for hypercholesterolemia has not been defined in the literature. This condition is characterized by deposition of lipid droplets within the cells of the retinal-pigmented epithelium. Further studies of the disorder noted that briards had significantly higher plasma cholesterol than did control dogs.24 Hypertriglyceridemia is not a documented feature of this disorder.

    Secondary Lipid Disorders

    Frequent causes of secondary lipid disorders include high-fat diets, DM, hyperadrenocorticism, hypothyroidism, acute pancreatitis, protein-losing nephropathy (PLN), and cholestatic liver disease. Other reports describing hyperlipidemia include glycogen storage disease type 1a in a crossbreed colony of Maltese and beagles with a defective glucose-6-phosphatase gene, dogs with dilated cardiomyopathy, and dogs with chronic Leishmania infantum infections.25-27

    As stated previously, high-fat diets can induce hyperlipidemia that is often transient and causes lipemia 6 to 12 hours after ingestion.1,15 However, if these diets induce more persistent hyperlipidemia, dogs may be at risk for some of the clinical problems described previously.15 Interestingly, unlike in humans, cholesterol-enriched diets have not been shown to elevate LDL cholesterol in normal dogs.28 This is thought to be due to the ability of the canine body to switch classes of VLDL-associated apoprotein made in the liver from apo B100 to apo B48, which is normally found in chylomicrons produced by intestinal epithelial cells.28 This switch enhances VLDL uptake and clearance from the circulation by the liver so that less VLDL is available for subsequent LDL generation.28

    Hyperlipidemia is reported in both insulin-dependent (type 1) and non-insulin-dependent DM (type 2) in humans. Dogs almost exclusively have type 1 DM.1-4,29,30 Lack of insulin or insulin resistance causes hyperlipidemia because of impaired insulin interaction with lipoprotein lipase.13,29 Studies show insulin increases lipoprotein lipase activity levels in human adipocytes without changing transcription of the gene or increasing lipoprotein lipase mRNA levels, suggesting that insulin has posttranscriptional or posttranslational control of lipoprotein lipase.31 Other mechanisms are also possible, such as increased VLDL production after tissue mobilization of fat to the liver.29,30 Diabetic dogs often have hypertriglyceridemia and sometimes hypercholesterolemia, which if present may not be as notable as hypertriglyceridemia.15

    Hyperadrenocorticism, whether primary or from iatrogenic corticosteroid administration, is a documented cause of hyperlipidemia in dogs.1-4,30,32,33 One reference suggests that hyperlipidemia associated with hyperadrenocorticism may result from down-regulation of LDL receptors and decreased liver uptake of plasma LDL that can develop as a consequence of reduced biliary excretion of steroid that may accompany hyperadrenocorticism.4 Alternatively, insulin resistance can develop with hyperadrenocorticism, leading to impairment of lipoprotein lipase as in DM.29 Hypercholesterolemia is more commonly reported than hyper­-triglyceridemia in dogs and cats with hyperadrenocorticism, and lipemia is not a typical finding.1,3

    Adult-onset hypothyroidism and congenital hypothyroidism in a family of giant schnauzers with hypothyroid dwarfism are associated with hyperlipidemia.34,35 Thyroxine is thought to enhance the activity of lipoprotein lipase similar to insulin, although the exact mechanism remains unknown.8 Hypercholesterolemia is the abnormal lipid value that is typically reported. Cholesterol elevations are usually moderate, but values greater than 1,000 mg/dl are sometimes documented.34 Hypertriglyceridemia is less common in dogs with hypothyroidism. A further indication of the association of hyperlipidemia with hypothyroidism was illustrated in a recent retrospective study that showed dogs with chronic hyperlipidemia were 3.2 times more likely to have hypo­thyroidism than those without chronic hyperlipidemia.36

    Acute pancreatitis is multifaceted and complex and may result in hyperlipidemia, primarily hypertriglyceridemia. Although the explanation for this is unknown, a plausible theory for hyperlipidemia is that in addition to exocrine pancreatic damage, simultaneous islet cell destruction occurs, leading to decreased secretion of insulin and resulting in impaired activity of lipoprotein lipase.29 Another possibility is impairment of lipoprotein lipase activity by inflammatory cytokines liberated in acute pancreatitis.29 Lipid abnormalities include moderate to marked hypertriglyceridemia and mild to moderate hypercholesterolemia.37 Elevated chylomicron and VLDL levels were detected via lipoprotein electro­phoresis in one study.38

    PLN and cholestatic liver diseases are recognized initiators of hyperlipidemia.1,3,39-43 Hereditary PLN with hyperlipidemia has been documented in familial protein-losing enteropathy and PLN in soft-coated wheaten terriers, familial renal amyloidosis in Chinese shar-peis, juvenile renal disease in golden retrievers and Doberman pinschers, and familial glomerulonephropathy in Bernese mountain dogs.39-43 Acquired PLN results from any glomerular disease leading to protein loss. PLN can result in a condition called nephrotic syndrome, which is characterized by hypercholesterolemia, severe hypoalbuminemia, ascites, and proteinuria. Mild hypertriglyceridemia is also reported in dogs and cats with nephrotic syndrome.3 The derivation of hypercholesterolemia in PLN is not fully understood but may be related to a generalized increase in protein production, including lipoproteins, by the liver in response to hypoalbuminemia.13 Diet may also contribute to hyper­cholesterolemia because patients with PLN are often fed diets higher in fat.

    Cholestatic liver disease, regardless of the cause, can lead to mild or moderate hypercholesterolemia.1,4,13,29 Lipoprotein X (i.e., an abnormal lipoprotein rich in cholesterol esters and ineffective in cholesterol delivery to the liver) has been identified in experimental induction of cholestasis in rats, dogs, and pigs.44 Lipoprotein X is also present in humans with cholestasis and is thought to contribute to hypercholesterolemia associated with cholestasis.44 The mechanisms for increased cholesterol and formation of lipoprotein X are complex and still largely unknown. It is speculated that they occur in cholestasis from a combination of reduced excretion of biliary lipids and bile acids and increased cholesterol synthesis by the liver occurring as a result of lack of normal regulatory suppression of cholesterol production by hepatocytes.29,44 Alleviation of cholestasis typically resolves hypercholesterolemia.


    Because most lipid disorders in dogs arise from secondary causes, correcting or managing the secondary cause is the aim of many therapeutic regimens, which in turn should lower plasma lipid levels. However, dietary intervention is considered the most practical and efficacious treatment of hyperlipidemia, primarily hypertriglyceridemia. Placing dogs on balanced low-fat diets is the aim of this regimen.28 Many reduced-fat diets for dogs are available on the market; however, what is most important in managing hyperlipidemia in dogs is feeding a high-quality, balanced ration that maintains dietary fat below 12% based on dry-weight matter.15

    In human medicine, hyperlipidemia is often reduced through various "cholesterol-lowering" medications. Although these medications are not approved for use in dogs, niacin at 25 to 100 mg/day and gemfibrozil at 200 mg/day have reportedly been used in dogs.15,28 Pruritus and erythema are two reported side effects of niacin in dogs, whereas minimal side effects of gemfibrozil have been reported.15,28 Other lipid-reducing strategies for dogs include dietary supplementation of marine-life oil, omega-3 fatty acids, and fish oil.28 Menhaden fish-oil capsules (which are omega-3 fatty acid rich) at a dose of 1 g/4.55 kg along with reduced dietary fat have reportedly been effective in controlling hypertriglyceridemia.28 Interestingly, one study of the effects of fatty acid supplementation in canine renal insufficiency induced by nephrectomy showed that addition of omega-3 fatty acids lessened associated hypercholesterolemia in dogs and minimized or protected further renal impairment compared with omega-6 fatty acid supplementation.45


    Lipid disorders are frequently reported in dogs, with most being the secondary type. A combination of clinical findings and laboratory data is often needed to diagnose such disorders, and the first indication that a problem exists is often the finding of hypercholesterolemia on a biochemical panel or lipemia in a blood sample from a fasted patient. Diagnosing lipid disorders initially involves ruling in or out known causes of secondary lipid disorders. Primary disorders should be considered after excluding secondary lipid disorders, especially in miniature schnauzers.

    Downloadable PDF

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    2. Rogers WA, Donovan EF, Kociba GJ: Lipids and lipoproteins in normal dogs and in dogs with secondary hyperlipoproteinemia. JAVMA 166(11):1092-1099, 1975.

    3. Bauer JE: Lipoprotein-mediated transport of dietary and synthesized lipids and lipid abnormalities of dogs and cats. JAVMA 224(5):668-675, 2004.

    4. Barrie J, Watson TG, Stear MJ, Nash AS: Plasma cholesterol and lipoprotein concentrations in the dog: The effects of age, breed, gender, and endocrine disease. J Small Anim Pract 34:507-512, 1993.

    5. Whitney MS, Boon DG, Rebar AH, et al: Ultracentrifugal and electrophoretic characteristics of the plasma lipoproteins of miniature schnauzer dogs with idiopathic hyperlipoproteinemia. J Vet Intern Med 7(4):253-260, 1993.

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    9. Liu S-K, Tilley LP, Tappe JP, Fox PR: Clinical and pathologic findings in dogs with atherosclerosis: 21 cases (1970-1983). JAVMA 189(2):227-232, 1986.

    10. Temel RE, Trigatti B, DeMattos RB, et al: Scavenger receptor class B, type I (SR-BI) is the major route for the delivery of high-density lipoprotein cholesterol to the steroidogenic pathway in cultured mouse adrenocortical cells. Proc Natl Acad Sci 94:13600-13605, 1997.

    11. Murao K, Terpstra V, Green SR, et al: Characterization of CLA-1, a human homologue of rodent scavenger receptor BI, as a receptor for high-density lipoprotein and apoptotic thymocytes. J Biol Chem 272:17551-17557, 1997.

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    13. Evans EW, Duncan RJ: Proteins, lipids, and carbohydrates, in Latimer KS, Mahaffey EA, Prasse KW (eds): Duncan & Prasse's Veterinary Laboratory Medicine, Clinical Pathology, ed 4. Ames, Iowa State University Press, 2003, pp 171-179.

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    17. Goldschmidt MH, Hendrick MJ: Tumors of the skin and soft tissues, in Meuten DJ (ed): Tumors in Domestic Animals, ed 4. Ames, Iowa State University Press, 2002, pp 111-113.

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    19. Robertson RP, Harmon J, Tran PT, Poitout V: b-cell glucose toxicity, lipotoxicity, and chronic oxidative stress in type 2 diabetes. Diabetes 53(suppl)1:119-124, 2004.

    20. Rogers WA, Donovan EF, Kociba GJ: Idiopathic hyperlipoproteinemia in dogs. JAVMA 166:1087-1091, 1975.

    21. Wada M, Minamisono T, Ehrhart LA, et al: Familial hyperlipoproteinaemia in beagles. Life Sci 20:999-1008, 1977.

    22. Hubert B, Braun JP, de la Farge F, Magnol JP: Hypertriglyceridemia in two related dogs. Comp Anim Pract 1:33-35, 1987.

    23. Baum D, Schweid AI, Porte D, Bierman EL: Congenital lipoprotein lipase deficiency and hyperlipidemia in a young puppy. Proc Soc Exp Biol Med 131:183-185, 1969.

    24. Bedford PG: Retinal pigment epithelial dystrophy (cPRA): A study of the disease in the briard. J Small Anim Pract 25:129-138, 1984.

    25. Kishnani PS, Faulkner E, VanCamp S, et al: Canine model and genomic structural organization of glycogen storage disease type Ia (GSD Ia). Vet Pathol 38:83-91, 2001.

    26. Tidholm A, Jönsson L: A retrospective study of canine dilated cardiomyopathy. JAAHA 33:544-550, 1997.

    27. Nieto CG, Barrera R, Habela MA, et al: Changes in the plasma concentrations of lipids and lipoprotein fractions in dogs infected with Leishmania infantum. Vet Parasitol 44:175-182, 1992.

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    43. Autran de Morais HS, DiBartola SP, Chew DJ: Juvenile renal disease in golden retrievers: 12 cases (1984-1994). JAVMA 209(4):792-797, 1996.

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    References »

    NEXT: Lateral Approach to Subtotal Bulla Osteotomy in Dogs: Pertinent Anatomy and Procedural Details


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