Clinic Management If Lipemic Patients

Vol.18, No. 10

October 1996

V

Continuing Education Article

FOCAL POINT ★ Fasting lipemia represents a familial or acquired disorder of lipid metabolism; affected dogs and cats are at risk of developing clinical signs attributable to the underlying metabolic defect and resulting lipemia.

KEY FACTS ■ Fasting lipemia is an abnormal laboratory finding in dogs and cats that defines the presence of an excess concentration of triglyceride in the blood. ■ Retention of chylomicrons is the most common cause of fasting hypertriglyceridemia in dogs and cats. ■ Dogs with fasting lipemia are most often presented for intermittent vomiting, diarrhea, and abdominal pain. ■ In dogs and cats, dietary therapy is the most effective means of managing diseases associated with lipemia.

Clinical Management of Lipemic Patients North Carolina State University

Richard B. Ford, DVM, MS

L

ipemia describes the appearance of blood, serum, or plasma that contains an excess concentration of triglyceride. It is a common, visible manifestation of the most common disorder of lipid metabolism encountered in companion animals: hyperchylomicronemia. In fasted patients, lipemia represents a significant clinical finding that is variably associated with the development of clinical signs referring to the gastrointestinal tract or nervous system. Although the precise role of dietary therapy has not been elucidated, clinically affected patients may derive significant, long-term health benefits from eating commercially prepared diets that are high in complex carbohydrates and restricted in fat (7% to 12% on a dry matter basis).

HYPERLIPIDEMIA The term hyperlipidemia refers to a disturbance of lipid metabolism that results in an elevated concentration of blood lipids, particularly triglyceride (TG) and/or cholesterol.1 In the fasted state, hyperlipidemia is an abnormal laboratory finding that represents accelerated synthesis or retarded degradation of lipoproteins. Lipoproteins are complex, spherical macromolecules that are responsible for transporting lipids from sites of absorption or synthesis to sites of storage or catabolism. Each lipoprotein consists of a nonpolar lipid core, predominantly triglycerides and cholesteryl esters, and a thin outer shell that contains numerous specialized proteins known as apolipoproteins. The apolipoproteins bind to specific enzymes or transport proteins on cell membranes, thereby directing the lipoprotein to various sites of metabolism.1–5 Among dogs and cats, the most common and clinically important type of hyperlipidemia is characterized by an excess concentration of triglyceride in blood, a condition referred to as hypertriglyceridemia.2 The serum and plasma of affected animals typically appear milky white and turbid (lipemic). In cases of extreme hypertriglyceridemia, the patient’s serum can be so lipemic that it is opaque (lactescent).1,2 Patients with lipemic serum present two important clinical challenges to the clinician. First, lipemic serum may induce laboratory interference (positive or negative) during quantitative analyses of serum analytes. Second, lipemia can cause significant, even life-threatening, clinical disease (e.g., acute pancreatitis). Persistent lipemia is an important clinical finding that represents a potential

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health risk for the affected blood (hyperchylomicronepatient. Although not all mia) is characterized by prolipemic patients manifest found lipemia and serum clinical signs, dogs typically triglyceride concentrations present with vomiting, diarthat are often in excess of rhea, and/or abdominal dis1000 mg/dl. comfort; cats may present Because chylomicrons with signs of peripheral neualso transport a small amount ropathy or superficial cutaof cholesteryl esters, lipemic neous lesions. Regardless of patients are expected to have whether signs are evident on slight to moderate elevations presentation, dietary inin serum cholesterol. If the tervention is justified as a lipemic serum is allowed means of preventing clinical Figure 1—The appearance of a 6-year-old male, mixed-breed to stand undisturbed for signs. approximately 12 hours, a dog with unilateral lipemic aqueous humor. Hyperlipidemic states reclear infranatant of serum sult from a familial (or priwill form below an opaque, mary) defect in lipoprotein creamlike layer of chylomimetabolism or from an accrons. quired disorder that develHypertriglyceridemia, ops secondary to a disease particularly that associain which lipid metabolism ted with the retention of is significantly altered (e.g., chylomicrons, is the most insulin-dependent diabetes prevalent lipid disorder recmellitus or hyperadrenocorognized in dogs and cats ticism).3,4 In either case, the and is associated with the presence of lipemia implies greatest health risk.2,10–13 Although the precise mechathe risk of significant illness. nism has not been elucidatIn dogs and cats, four major lipoprotein classes have Figure 2—The right eye of the patient in Figure 1. It is not ed, it is probably caused by been recognized: chylomi- known whether the unilateral uveitis preceded the infiltration the lack of lipoprotein lipase crons, very low–density lipo- of lipid into the anterior chamber or was caused by the activity or the absence of the surface apoprotein C-II.1,3,8,14 proteins (VLDL), low–densi- lipemia. Several reports have suggestty lipoproteins (LDL), and ed that miniature schnauzers are predisposed to primary, high-density lipoproteins (HDL).2,6,7 Chylomicrons, the largest and least-dense lipoproteins, are predomior familial, hyperlipidemia. 10–12 Although it is not definitively known that hyperlipidemia is an inherited nantly responsible for the transport of dietary fat disorder of miniature schnauzers, there apparently is a (triglyceride) from the intestine after a meal. Chylomihigher-than-expected incidence of hypertriglyceridemia crons become apparent in plasma within 1 to 2 hours in the breed in North America.12,15 A similar miniature after ingestion of a fat-containing meal; their presence schnauzer predilection has not been observed in the is indicated by transient (6 to 10 hours) plasma or United Kingdom. serum turbidity in normal dogs and cats. Very low–density lipoproteins, which are produced Chylomicrons transport fat to the capillaries of adiin the liver and contain a predominance of triglycpose tissue and skeletal muscle, where they are exposed erides, are transported to tissue capillaries, where they to the enzyme lipoprotein lipase. Once activated by the are catabolized by lipoprotein lipase in the same manapoprotein C-II, the enzyme hydrolyzes the triglycner that chylomicrons are.1,9 Retention of VLDLs, and erides into fatty acids (which enter adipocytes and musthe resulting hypertriglyceridemia, occurs frequently in cle) and glycerol. What remains of the chylomicron is a dogs with insulin-dependent diabetes mellitus. Alremnant particle, rich in cholesteryl esters, that subthough serum turbidity and hypertriglyceridemia can sequently delivers cholesterol to the liver.3,4,8,9 Chylomicron hydrolysis is normally complete within 6 to 10 be associated with an accumulation of VLDLs, a dishours after a meal; the plasma then becomes clear tinct creamlike layer does not develop. again. The persistence of excessive chylomicrons in In dogs and cats, HDLs and LDLs are predomiNONPOLAR LIPID CORE ■ LIPOPROTEIN CLASSES ■ HYPERTRIGLYCERIDEMIA

The Compendium October 1996

nantly responsible for transporting cholesterol. Only trace quantities of triglycerides are carried by these lipoproteins. 2 Even in patients with extreme elevations of cholesterol, the serum does not appear lipemic because these lipoproteins are so small that they do not refract light. Although hypercholesterolemia occurs in dogs and cats, specific clinical disease has not been associated with sustained elevations of LDLs or HDLs.

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In humans and animals, sustained hypertriglyceridemia is a principal risk factor for the development of acute pancreatitis.1,6,12,13,16–18 Dogs presented with clinical signs consistent with acute abdominal pain and vomiting should be evaluated for evidence of hyperchylomicronemia at the time of presentation and during recovery, when normal diet and caloric intake are restored. Palliative therapy with a commercial diet intended for gastrointestinal disorders CLINICAL SIGNS may contribute to increased In Dogs frequency and/or severity of The presenting comclinical signs in dogs. The plaints most often associated moderate fat content of the with hyperchylomicronemia diet (>13% dry matter bain dogs are vomiting and/or Figure 3—Samples of whole blood (5 minutes after collec- sis) may induce sustained diarrhea. Accompanying tion) from an 8-year-old miniature schnauzer presented for lipemia in dogs that are unsigns include nonlocalized intermittent vomiting, lethargy, anorexia, and abdominal able to metabolize chylomiabdominal pain or discom- discomfort. The patient had been fasted for 36 hours. The crons normally.15 Hypertriglyceridemia fort accompanied by de- results of hematologic evaluation and a biochemical profile should be considered in creased appetite. Abdominal (including amylase and lipase) were normal. dogs that present with a hisdistention is occasionally retory of seizures. A few patients, some of them miniaported. Complicating the clinical history is the fact that ture schnauzers, diagnosed with idiopathic epilepsy clinical signs are intermittent, may persist for months have fasting hypertriglyceridemia and lipemic seor years, and are associated with spontaneous resolution rum.10,11 In some patients, dietary therapy has been suc(usually related to decreased appetite or anorexia). cessful in reducing triglyceride concentration and Signs that are reported less often include lethargy, eliminating seizures without concomitant use of antiseizures (not attributable to idiopathic epilepsy), convulsant drugs.18 lipemia retinalis, and lipemic aqueous humor (Figures 1 and 2). In Cats There apparently is no sex predilection. Although In dogs and cats, persistent fasting lipemia results miniature schnauzers evidently have a higher-thanfrom hypertriglyceridemia caused by the retention of expected incidence of fasting lipemia and hypertrichylomicrons; however, clinical signs reported in cats glyceridemia, several purebred and mixed canine breeds differ from those reported in dogs. In affected cats, the are similarly affected. Dogs are typically at least 4 years most common clinical finding is cutaneous xanthoma, of age, but dogs as young as 2 years of age may have a painless raised lesion caused by an accumulation of fasting lipemia. lipid-laden macrophages or foam cells in the skin.19 ArOn physical examination, dogs may exhibit lethargy eas of skin that are subject to trauma and small blood and abdominal pain. Clinical signs and history may be vessel injury are most likely to be affected. Peripheral compatible with acute pancreatitis; however, abdominal neuropathy reportedly develops in cats. Although sites radiographs, ultrasonography, and laboratory evidence to of nerve involvement vary, Horner’s syndrome, tibial support a diagnosis of pancreatitis are typically lacking. nerve paralysis, and radial nerve paralysis are comThe term pseudopancreatitis has been suggested to demon.19 The xanthomas and the neurologic signs are exscribe this pattern of clinical manifestations associated 2 pected to resolve within 2 to 3 months after institution with persistent lipemia. HYPERCHYLOMICRONEMIA ■ SPONTANEOUS RESOLUTION ■ PALLIATIVE THERAPY

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Postprandial of a fat-restricted diet.19 Hyperlipidemia In dogs and cats, the paChylomicrons normally tient’s blood (particularly the appear in the serum of dogs serum) often appears lipemic and cats 30 minutes to 1 and may remain so after a hour after the ingestion of a 24-hour (or longer) fast. meal that contains fat. This Serum lipid determinations is associated with a transient demonstrate extreme con(6 to 10 hours) increase in centrations of total triglycserum triglycerides, after erides and moderate elevawhich triglyceride rapidly tions in total cholesterol. returns to baseline levels. Lactescent serum is usually Physiologic hyperlipidemia associated with triglyceride is easily excluded from conconcentrations in excess of sideration if the patient is 2000 mg/dl (the canine norknown to have been fasted mal is 50 to 150 mg/dl; the throughout the 12-hour pefeline normal is 50 to 100 riod before blood collection. mg/dl). Although a correIn normal animals, postlation between triglyceride prandial serum turbidity is concentration and the severassociated with a modest ity of clinical signs has not (150 to 400 mg/dl) serum been observed, dogs with a triglyceride elevation that triglyceride concentration of typically returns to normal at least 1000 mg/dl are conwithin 10 hours. sidered to be at risk of developing clinical signs and thus are candidates for dietary in- Figure 4—The blood samples in Figure 3 after clot retraction. Laboratory tervention.2,6,12 The samples are profoundly lipemic; serum triglyceride ex- Considerations A diagnosis of hyperSignificant hyperlipi- ceeded 3000 mg/dl (normal is 50 to 150 mg/dl). triglyceridemia should be demia characterized by based on laboratory deterlipemic serum and hypermination of serum triglycerides in uncleared serum. By triglyceridemia has been observed as an incidental findlaboratory methods used in North America, serum ing in fasted, adult dogs and cats. The absence of clinitriglyceride concentrations higher than 500 mg/dl are cal signs at the time of presentation does not justify significantly beyond the high range of normal for fasted ignoring the significance of the lipemia. Because of the dogs and cats. Clinical signs are most likely when risk associated with hypertriglyceridemia, patients with triglyceride concentrations exceed 1000 mg/dl.2,6,12 persistent lipemia should be managed in the same manner as those that present with clinical signs. Lipoprotein Electrophoresis Lipoprotein electrophoresis (LPE) has been used DIAGNOSTIC CONSIDERATIONS as a means of characterizing abnormalities in lipid Disturbances of lipid transport that culminate in exmetabolism. 13,16,20 The value of lipoprotein electrocess concentrations of triglyceride are the most impor2,6,12 phoresis has been questioned in human medicine for tant form of hyperlipidemia in veterinary medicine. several years and is justifiably questioned in veterinary Fasting triglyceride concentrations in excess of 1000 medicine. Compared with the quantitative assays that mg/dl in dogs or cats justifies therapeutic intervention are currently available, lipoprotein electrophoresis has and an attempt to lower the triglyceride concentration limited value in the clinical evaluation of lipid disorders below 500 mg/dl. in dogs and cats. Visual inspection of the patient’s serum provides valuable physical evidence concerning the absence or Sample Handling presence of an excess concentration of triglyceride (FigA veterinarian attempting to assess a dog or cat for ures 3 and 4). In fasted patients, lipemia denotes hyperhyperlipidemia should submit serum rather than plastriglyceride associated with retention of VLDLs and/or ma or whole blood. Serum for cholesterol and triglycchylomicrons. LACTESCENT SERUM ■ TRIGLYCERIDE CONCENTRATION ■ ELECTROPHORESIS

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eride determinations can be concentration was deterrefrigerated or frozen for mined is critical in making several days without signifireasonable interpretations. cant effect. The presence of Although clearing a lipemic excess triglyceride, particusample does eliminate inlarly if associated with retenterference associated with tion of chylomicrons, is an chylomicrons, it effectively important source of positive eliminates a critical element (falsely increased) or negaof clinical information: that tive (falsely decreased) inthe patient is hypertriglycterf e re n c e f o r a n a l y t e s eridemic. determined by colorimetIdeally, two aliquots of a ric methods.21 The effect of serum sample from a lipelipemia on individual anamic patient are submitted lytes varies and depends on simultaneously. One samthe degree of lipemia, the ple, if effectively cleared, analyte being measured, and can be used to perform routhe analytic method used. tine biochemical testing, Lipemia also causes in viincluding testing for triglyctro hemolysis (a phenomerides. Determining trienon induced by the effect g l y c erides in the second, of lipid on erythrocyte memlipemic (uncleared) sample brane fragility), which may documents the true extent interfere with certain bioof triglyceride excess, serves chemical tests. The extent as an important baseline to which in vitro hemolysis value for assessing response affects determination of to therapy, and can (when hemoglobin and hematocrit compared with the triglychas not been established. eride value in the cleared The amount of red blood Figure 5—The positive chylomicron test. The lactescent sample) help in characterizcell hemolysis is evidently serum in both test tubes was taken from a 4-year-old dog ing the nature of the hyperproportional to the length with hypertriglyceridemia. The sample on the left depicts the lipidemia. of time red blood cells are in appearance of the serum immediately after separation from contact with the lipemic the red blood cells. The sample on the right is an aliquot of The Chylomicron Test Knowing that the patient serum and to the degree of the patient’s serum that has been allowed to stand undislipemia. The type and ex- turbed for 10 hours. The so-called cream layer on top con- has fasting lipemia provides tent of interference induced sists of triglyceride-rich chylomicrons. (From Ford RB: immediate evidence of hyby lipemia varies among Canine hyperlipidemia, in Ettinger SJ, Feldman EC [eds]: pertriglyceridemia. The Textbook of Veterinary Internal Medicine, ed 4. Philadelphia, laboratories, depending on WB Saunders Co, 1995, p 1414. Reproduced with permis- lipid disorder can be further characterized by performing the analytical instrumenta- sion.) a simple, in-hospital test for tion and methods used. the presence of chylomiSubmission of lipemic crons. The lipemic serum, separated from red blood blood to a commercial laboratory necessitates knowing cells, is allowed to stand refrigerated and undisturbed how the sample will be processed. Because of the interfor 6 to 10 hours. Chylomicrons, if present, will float ference induced by lipemia, some laboratories simply to the surface of the sample and form an opaque soreject lipemic samples. called cream layer over a clear infranatant (Figure 5). Many laboratories attempt to clear lipemic serum (by This finding suggests a disorder of chylomicron caremoving chylomicrons) before performing biochemitabolism, the most common form of hyperlipidemia in cal assays. There is no standardized method of clearing dogs. If the sample remains turbid but does not form a lipemic serum, and commercial laboratories do not cream layer, retention of VLDLs rather than chylomiconsistently report whether an attempt was made to crons is suggested. This also indicates that the hyperclear the sample. For the clinician, however, knowing lipidemia may be secondary to an underlying disorder. that a lipemic sample was cleared before the triglyceride LIPEMIC BLOOD ■ TRIGLYCERIDE EXCESS ■ CREAM LAYER

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TABLE I Representative Commercial Dog Food Products Used in Dietary Management of Lipemic Patients Product Name (Manufacturer)

Formulation

Percentage Fat (dry matter basis)

Rx or OTC a

Caloric Density (kcal/g)

Prescription Diet® w/d® (Hill’s Pet Nutrition) Prescription Diet® w/d® (Hill’s Pet Nutrition)

Canned

12.1

Rx

0.87

Dry

6.9

Rx

2.98

Prescription Diet® r/d® (Hill’s Pet Nutrition) Prescription Diet® r/d® (Hill’s Pet Nutrition)

Canned

7.0

Rx

0.58

Dry

7.0

Rx

2.70

Science Diet® Canine Light Formula (Hill’s Pet Nutrition) Science Diet® Canine Light Formula (Hill’s Pet Nutrition)

Canned

9.6

OTC

0.85

Dry

6.8

OTC

2.78

Eukanuba® Low-Residue FormulaTM (Iams Company)

Dry

9.0

Rx

3.9

Eukanuba® Restricted-Calorie Formula® (Iams Company)

Dry

4.0

Rx

3.65

Eukanuba® Light (Iams Company)

Dry

9.7

OTC

3.87

Purina Senior® (Ralston Purina)

Dry

8.5

OTC

pending

Purina Fit & Trim® (Ralston Purina)

Dry

10.8

OTC

pending

CNM OM-Formula® for Dogs (Ralston Purina)

Dry

5.98

Rx

pending

CNM OM-Formula® for Dogs (Ralston Purina)

Canned

8.38

Rx

pending

aRx

= available from a veterinarian or with a veterinarian’s prescription, OTC = available from pet stores or grocery stores.

In some dogs (particularly poorly regulated diabetics), a cream layer may form over turbid, lipemic serum, suggesting retention of chylomicrons and VLDLs.2,6

MANAGEMENT Before initiating treatment of a patient with fasting lipemia, the clinician should attempt to determine whether the lipemia is primary or secondary to an underlying disorder that has altered triglyceride metabolism. Fasting lipemia is an important clinical sign that justifies performing (at a minimum) routine hemato-

logic evaluation, urinalysis, and biochemical profile in affected patients. To avoid lipid interference, an effort should be made to perform biochemical analysis on serum that has been cleared. By contrast, total triglyceride concentration should be determined from an aliquot of uncleared, lipemic serum.

Primary Hypertriglyceridemia Because chylomicrons are exclusively of dietary origin, restriction of dietary fat is the first and most important form of therapy for dogs and cats with primary hypertriglyceridemia. Before treatment is instituted, the

PRIMARY OR SECONDARY LIPEMIA ■ BIOCHEMICAL PROFILE

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TABLE II Representative Commercial Cat Food Products Used in Dietary Management of Lipemic Patients Product Name (Manufacturer)

Formulation

Percentage Fat (dry matter basis)

Rx or OTC a

Caloric Density (kcal/g)

Prescription Diet® Feline w/d® (Hill’s Pet Nutrition) Prescription Diet® Feline w/d® (Hill’s Pet Nutrition)

Canned

17.1

Rx

0.91

Dry

9.4

Rx

3.25

Prescription Diet® Feline r/d® (Hill’s Pet Nutrition) Prescription Diet® Feline r/d® (Hill’s Pet Nutrition)

Canned

7.2

Rx

0.63

Dry

8.2

Rx

2.95

Dry

9.1

OTC

3.27

Eukanuba® Restricted-Calorie Formula FelineTM Dry (Iams Company)

8.0

Rx

3.9

Purina Cat Chow Mature® (Ralston Purina)

Dry

9.7

OTC

pending

CNM OM-Formula® for Cats (Ralston Purina)

Dry

7.68

Rx

pending

Pro Plan® Cat Lite Formula (Ralston Purina)

Dry

9.4

OTC

pending

Science Diet® Feline Maintenance Light® (Hill’s Pet Nutrition)

aRx

= available from a veterinarian or with a veterinarian’s prescription, OTC = available from pet stores or grocery stores.

patient’s weight is recorded. A diet that contains 7% to 12% fat (dry matter basis) is recommended (Tables I and II). After eating only the fat-restricted diet for a minimum of 3 to 4 weeks, the patient is weighed again; blood is submitted for serum triglyceride determination after a 12-hour fast. The goal is a triglyceride level, in uncleared serum, less than 500 mg/dl and no weight loss. If the goal is reached, this diet becomes the recommended diet for life. The client should be counseled concerning the risks associated with allowing a patient, especially a dog, to consume a large quantity of fat (e.g., meat scraps) in a single meal. Two facts remain at issue for clinicians attempting to manage patients with primary hypertriglyceridemia via fat-restricted diets. First, most low-fat diets are intended to promote weight loss. Most dogs and cats with fasting lipemia are not overweight and thus may actual-

ly lose an unacceptable amount of weight as a result of consuming a hypocaloric diet for an extended period. A normocaloric low-fat diet is preferred in patients that are not overweight. Dietary supplementation with complex carbohydrates (e.g., pasta or potatoes) has been useful in selected cases. Also of concern is the fact that a minority of patients may experience resolution of clinical signs yet continue to have fasting lipemia despite strict feeding of a diet with less than 9% fat (dry matter basis). Drug therapy for patients with primary hypertriglyceridemia has included clofibrate, niacin, and gemfibrozil as well as dietary supplementation with n-3 polyunsaturated fatty acids from fish oils.19,22–24 Only anecdotal reports are available of successes and failures associated with these products in clinical patients. Therapeutic guidelines and documented benefits have not been substantiated for these products; their indis-

TRIGLYCERIDE LEVEL ■ FAT-RESTRICTED DIETS ■ DRUG THERAPY

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criminate use in dogs and cats cannot be recommended until dosage and efficacy are determined.

Secondary Hypertriglyceridemia Long-term dietary management of a dog or cat with lipemia caused by primary hypertriglyceridemia is indicated only after secondary causes of hypertriglyceridemia have been ruled out. Several metabolic diseases, particularly endocrinopathies, may be associated with persistent or fasting lipemia.1,2,4,6,12 Diagnostic differentials that should be considered include diabetes mellitus, hyperadrenocorticism, and hypothyroidism. Although lipemia is commonly reported in dogs with acute pancreatitis, hypertriglyceridemia is considered to be a cause, not a result, of pancreatitis. The approach to treating a patient with secondary hypertriglyceridemia is based on managing the underlying disease; an appropriate response to the medication includes resolution of the lipemia. Diabetic dogs with excess serum triglyceride concentrations are apparently at risk of developing acute pancreatitis or pseudopancreatitis. Diabetic dogs and cats may derive significant benefit from long-term dietary fat restriction. Many commercially prepared low-fat diets contain high amounts of insoluble fiber. Reducing daily fat intake decreases the risks associated with lipemia; diets that contain increased insoluble fiber evidently enhance glycemic control compared with diets that lack added fiber.25 Regardless of whether the cause is a primary or secondary disorder of lipid metabolism, lowering the triglyceride concentration below 500 mg/dl has been associated with increased activity, playfulness, and physical endurance in hypertriglyceridemic dogs. This unexpected response to therapy, as reported by owners and veterinarians, corresponds with a decrease in serum triglyceride concentration. Such observations are significant and suggest that hypertriglyceridemia may alter behavior and/or activity in some dogs. I have not observed similar responses among hyperlipidemic cats that experienced significant reductions in triglycerides after institution of dietary therapy. CONCLUSION The clinical importance of hyperlipidemia in veterinary medicine focuses on three principal facts. First, fasting lipemia in dogs or cats is abnormal and represents a significant clinical finding. Second, lipemic patients are at risk of developing significant clinical illness, including at least one potentially fatal disease— acute pancreatitis. Third, specific dietary intervention and possibly drug therapy are indicated to eliminate or at least diminish associated morbidity.

About the Author Dr. Ford, who is a Diplomate of the American College of Veterinary Internal Medicine, is a Professor of Medicine in the Department of Companion Animal and Special Species Medicine, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina.

REFERENCES 1. Brown MS, Goldstein JL: The hyperlipoproteinemias and other disorders of lipid metabolism, in Braunwald E, Isselbacher KJ, Petersdorf RG, et al (eds): Harrison’s Principles of Internal Medicine, ed 11. New York, McGraw-Hill Book Co, 1987, pp 1650–1661. 2. Ford RB: Canine hyperlipidemia, in Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine, ed 4. Philadelphia, WB Saunders Co, 1995, pp 1414–1419. 3. Schaefer EJ, Levy RI: Pathogenesis and management of lipoprotein disorders. New Engl J Med 312:1300–1310, 1985. 4. Weinberg RB: Lipoprotein metabolism: Hormonal regulation. Hosp Pract 22:223–243, 1987. 5. Naito HK: The clinical significance of apolipoprotein measurements. J Clin Immunoassay 9:11–20, 1986. 6. Armstrong PJ, Ford RB: Hyperlipidemia, in Kirk RW (ed): Current Veterinary Therapy. X. Philadelphia, WB Saunders Co, 1989, pp 1046–1050. 7. Mahley RW, Weisgraber KH: Canine lipoproteins and atherosclerosis. I. Isolation and characterization of plasma lipoproteins from control dogs. Circ Res 35:713–721, 1974. 8. Gotto AM: Lipoprotein metabolism and the etiology of hyperlipidemia. An update: Pharmacologic approaches to the hyperlipidemias. Hosp Pract 23(Suppl 1):4–13, 1988. 9. Eckel RH: Lipoprotein lipase. New Engl J Med 16:1060– 1068, 1989. 10. Rogers WA, Donovan EF, Kociba GJ: Idiopathic hyperlipoproteinemia in dogs. JAVMA 166:1087–1099, 1975. 11. Rogers WA, Donovan EF, Kociba GJ: Lipids and lipoproteins in normal dogs and dogs with secondary hyperlipoproteinemia. JAVMA 166:1092–1097, 1975. 12. Ford RB: Idiopathic hyperchylomicronemia in miniature schnauzers. J Small Anim Pract 34:488–492, 1993. 13. DeBowes LJ: Lipid metabolism and hyperlipoproteinemia in dogs. Compend Contin Educ Pract Vet 9(7):727–731, 1987. 14. Zerbe CA: Canine hyperlipidemias, in Kirk RW (ed): Current Veterinary Therapy. IX. Philadelphia, WB Saunders Co, 1986, pp 1045–1053. 15. Ford RB: Unpublished data, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, 1995. 16. Whitney MS: Evaluation of hyperlipidemias in dogs and cats. Semin Vet Med Surg 7:292–300, 1992. 17. Sanfey H, Cameron JL: Pancreatitis and hyperlipemia, in Berk JE (ed): Gastroenterology, ed 4. Philadelphia, WB Saunders Co, 1985, pp 4055–4071. 18. Whitney MS, Boon GD, Rebar AH, et al: Effects of acute pancreatitis on circulating lipids in dogs. Am J Vet Res 48: 1492–1497, 1987. 19. Jones B: Feline hyperlipidemia, in Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine, ed 4.

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Philadelphia, WB Saunders Co, 1995, pp 1410–1414. 20. Rogers WA: Lipemia in the dog. Vet Clin North Am Small Anim Pract 7:637–640, 1977. 21. Allerman AR: The effects of hemolysis and lipemia on serum biochemical constituents. Vet Med 85:1272–1284, 1990. 22. Logas D, Beale KM, Bauer JE: Potential clinical benefits of dietary supplementation with marine-life oil. JAVMA 199: 1631–1636, 1991.

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23. Levy RI: Currently available lipid-lowering agents. An update: Pharmacologic approaches to the hyperlipidemias. Hosp Pract 23(Suppl 1):14–21, 1988. 24. Schaefer EJ: When and how to treat the dyslipidemias. Hosp Pract 23:69–84, 1988. 25. Feldman EC, Nelson RW: Diabetes mellitus, in Canine and Feline Endocrinology and Reproduction, ed 2. Philadelphia, WB Saunders Co, 1996, pp 339–391.