ttp://www.bsava.

com REVIEW

Canine hyperlipidaemia
P. G. Xenoulis and J. M. Steiner†

Clinic of Medicine, Faculty of Veterinary Medicine, University of Thessally, Trikalon 224, Karditsa 43100, Greece and Animal Medical
Center of Athens, Mesogeion 267, 15451 Athens, Greece
†Gastrointestinal Laboratory, Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences,
Texas A&M University, College Station, TX 77843, USA

Hyperlipidaemia refers to an increased concentration of lipids in the blood. Hyperlipidaemia is com-

mon in dogs and has recently emerged as an important clinical condition that requires a systematic
diagnostic approach and appropriate treatment. Hyperlipidaemia can be either primary or second-
ary to other diseases. Secondary hyperlipidaemia is the most common form in dogs, and it can be a
result of endocrine disorders, pancreatitis, cholestasis, protein-losing nephropathy, obesity, as well as
other conditions and the use of certain drugs. Primary hyperlipidaemia is less common in the general
canine population but it can be very common within certain breeds. Hypertriglyceridaemia of Miniature
Schnauzers is the most common form of primary hyperlipidaemia in dogs but other breeds are also
affected. Possible complications of hyperlipidaemia in dogs include pancreatitis, liver disease, athero-
sclerosis, ocular disease and seizures. Management of primary hyperlipidaemia in dogs is achieved by
administration of ultra low-fat diets with or without the administration of lipid lowering drugs such as
omega-3 fatty acids, fibrates, niacin and statins.

Journal of Small Animal Practice (2015) 56, 595–605

DOI: 10.1111/jsap.12396
Accepted: 25 June 2015

INTRODUCTION of triglycerides is referred to as hypertriglyceridaemia, while an

increased blood concentration of cholesterol is referred to as
hypercholesterolaemia. Because both triglycerides and choles-
Hyperlipidaemia is an important emergent condition in dogs
terol are transported in the blood combined with specific pro-
(Comazzi et al. 2004). However, in contrast to humans, hyperlipi-
teins called apoproteins or apolipoproteins (the lipid–protein
daemia has been traditionally considered a relatively benign condi-
complex is referred to as lipoprotein), the term hyperlipoprotein-
tion in dogs and, therefore, clinical experience with, and research
aemia is often used interchangeably with the term hyperlipidae-
regarding, canine hyperlipidaemia have been limited (Xenoulis &
mia. The term lipaemia is used to describe a grossly visible turbid
Steiner 2010). In the last decade, several studies in both humans
or lactescent appearance of serum or plasma. Lipaemia is a result
and dogs have associated specific forms of hyperlipidaemia with a
of moderate and severe hypertriglyceridaemia (typically >2·26 to
much wider range of diseases than previously thought. Therefore,
3·39 mmol/L), but not hypercholesterolaemia or mild hypertri-
canine hyperlipidaemia is emerging as an important clinical con-
glyceridaemia. Finally, the term dyslipidaemia is a more general
dition that requires a systematic diagnostic approach and appro-
term that describes not only increases in blood lipid concentra-
priate treatment (Fleeman 2009, Xenoulis & Steiner 2010). The
tions, but any kind of disturbance in the characteristics of the
aim of the present review is to provide the small animal clinician
lipids and/or lipoproteins.
with the most up-to-date information on lipoprotein metabolism,
the clinical consequences of hyperlipidaemia, as well as the diag-
nostic and therapeutic approach of hyperlipidaemic dogs.
OVERVIEW OF CANINE LIPOPROTEIN
METABOLISM
DEFINITIONS
A detailed review of canine lipoprotein metabolism is beyond the
The term hyperlipidaemia refers to an increased concentration of scope of this article and the interested reader is referred to other
lipids (i.e. triglycerides, cholesterol or both) in the blood (serum sources for a more detailed discussion on this topic (Xenoulis
or plasma). More specifically, an increased blood concentration & Steiner 2010). Canine lipoproteins can be divided into four

Journal of Small Animal Practice • Vol 56 • October 2015 • © 2015 British Small Animal Veterinary Association 595
 P. G. Xenoulis & J. M. Steiner

major classes based on their hydrated density after ultracentri-
fugation: chylomicrons, very low-density lipoproteins (VLDL),
low-density lipoproteins (LDL) and high-density lipoproteins
(HDL). Clinically, it is important to note that chylomicrons and
VLDL are the main carriers of serum triglycerides and are often
referred to as triglyceride-rich lipoproteins (TRL), while HDL
and LDL (to a lesser degree in dogs) contain mainly cholesterol
(Xenoulis & Steiner 2010). As in humans, several subclasses of
the above-mentioned major classes of lipoproteins exist in dogs,
but their nature and clinical significance in the dog have not been
fully elucidated to date (Xenoulis et al. 2013).
Lipid metabolism can be divided into two basic pathways
(Fig 1): the exogenous pathway, which is associated with the metab-
olism of exogenous (dietary) lipids, and the endogenous pathway,
which is associated with the metabolism of endogenously pro-
duced lipids (Xenoulis & Steiner 2010). Chylomicrons, which
are formed in the enterocytes of the small intestine, are the lipo-
protein class mainly involved in the exogenous pathway and are
responsible for transporting dietary lipids. In contrast, VLDL,
LDL and HDL are mainly involved in the metabolism of endog-
enously produced lipids (endogenous pathway). TRL (i.e. chy-
lomicrons and VLDL) contain an apoprotein called apoprotein
C-II (apo C-II) that acts as an activator of the enzyme lipoprotein
lipase located on the lining of capillary beds, which in turn leads
to hydrolysis of triglycerides. Increased production or decreased
clearance (e.g. due to deficiency of apo C-II or lipoprotein lipase)
of TRL can lead to hypertriglyceridaemia; such causes of hyper-
lipidaemia have been confirmed in humans, but not yet in dogs.
On the other hand, changes in serum cholesterol concentration
are mainly associated with changes in the concentration or com-
position of HDL and/or LDL.
CAUSES OF CANINE HYPERLIPIDAEMIA
A list of the most important causes of canine hyperlipidaemia
is shown in Table 1 (Xenoulis & Steiner 2010). Postprandial
hyperlipidaemia is physiologic and typically resolves within 7
to 12 hours after a meal (Whitney 1992, Downs et al. 1997).
Therefore, determination of serum lipid concentrations should
always follow a fast of at least 12 hours. However, recent evi-
dence suggests that food might need to be withheld more than
12 hours when assessing fasting concentrations of serum triglyc-
erides (Elliott et al. 2011) and the author typically implements a
15-hour fast before evaluating dogs for hyperlipidaemia.
Persistent fasting hyperlipidaemia is abnormal and can be
either primary or secondary to other diseases or drug adminis-
tration. Secondary hyperlipidaemia is the most common form
of hyperlipidaemia in dogs. Most commonly, secondary canine
hyperlipidaemia is the result of an endocrine disorder, such as
hypothyroidism, diabetes mellitus or hyperadrenocorticism
(Rogers et al. 1975b, Rogers 1977, Ling et al. 1979, Wilson
et al. 1986, Barrie et al. 1993, Panciera 1994, Dixon et al. 1999,
Huang et al. 1999). Hyperlipidaemia (hypertriglyceridaemia and/
or hypercholesterolaemia) has also been traditionally thought to
be the result of naturally occurring pancreatitis in dogs (Rogers
et al. 1975b, Rogers 1977, Cook et al. 1993, Hess et al. 1998).
However, data from experimental studies suggest that hyperlipi-
daemia is not a feature of experimentally induced pancreatitis in
dogs (Bass et al. 1976, Whitney et al. 1987, Chikamune et al.
1998). In addition, results of a recent unpublished study in dogs
with naturally occurring pancreatitis indicate that when concur-
rent diseases (e.g. diabetes mellitus, hypothyroidism) and use
of certain drugs that can cause hyperlipidaemia are excluded,

Exogenous pathway Endogenous pathway

Dietary fat Bile acids and LDL

cholesterol
ApoB-100 LDL
Endogenous cholesterol receptors
Liver
Intestine
Dietary Extra hepatic tissue
Remnant cholesterol
receptor
VLDL
remnants
Chylomicrons Remnants VLDL HDL
ApoE ApoE ApoE
Apo C-II ApoB-48 Apo C-II Cholesterol
ApoB-48 ApoB-100
ApoB-48 HDL3

Capillaries Capillaries LCAT

HDL2
Lipoprotein lipase Lipoprotein lipase CETP
Free fatty acids Free fatty acids
Adipose tissue, muscle Adipose tissue, muscle HDL1

FIG 1. Simplified cartoon illustrating the basics of lipoprotein metabolism in dogs. (CEPT is crossed out because, in contrast to humans, it does
not exist in dogs). Apo Apoprotein, LDL low-density lipoproteins, VLDL very low-density lipoproteins, HDL high-density lipoproteins, LCAT Lecithin—
cholesterol acyltransferase, CEPT cholesteryl-ester transfer protein. CEPT does not exist in dogs and in its absence HDL2 is transformed into HDL1.
Figure adapted and modified by authors from e-Learning Unit, St George’s, University of London, http://www.elu.sgul.ac.uk/rehash/guest/
scorm/294/package/content/liver_lipoprotein.html. Accessed on 7 April 2015. Copyright 2006 St George’s, University of London

596 Journal of Small Animal Practice • Vol 56 • October 2015 • © 2015 British Small Animal Veterinary Association
 Canine hyperlipidaemia

Table 1. Causes of hyperlipidaemia in dogs

Type of lipid abnormality Comments
Postprandial Increases are typically mild and last <15 hours
hyperlipidaemia* HTG (rarely HCH) Most common cause of hyperlipidaemia
High-fat diets HTG and/or HCH Fat content must be very high (typically >50%) to cause hyperlipidaemia
Secondary hyperlipidaemia
Endocrine disease
Diabetes mellitus* HTG (mainly) and/or HCH HTG and HCH can range from mild to marked; present in >50% of cases
Hypothyroidism* HTG and/or HCH HTG and HCH can range from mild to marked; present in >75% of cases
Hyperadrenocorticism* HTG and/or HCH HTG and HCH can range from mild to marked
Pancreatitis* HTG and/or HCH Both HTG and HCH are typically mild if other causes of hyperlipidemia are not present;
present in ~30% of cases
Obesity* HTG and/or HCH HTG and HCH can range from mild to marked; present in >25% of cases
Protein-losing nephropathy* HCH HCH is part of the nephrotic syndrome; HCH is usually mild
Cholestasis* HTG and/or HCH Increases are usually mild
Hepatic insufficiency* HTG and/or HCH Increases are usually mild
Lymphoma HTG with or without HCH Hyperlipidaemia might persist despite treatment
Leishmania infantum infection HTG and HCH Increases are typically mild if present
Parvoviral enteritis HTG HTG is typically mild if present
Hypernatraemia? HTG and HCH Based on a case report and evidence from human medicine
Drugs*
Glucocorticoids HTG and/or HCH Increases can range from mild to marked
Phenobarbital HTG HTG can range from mild to marked; present in >30% of cases
Estrogen/progesterone? HTG and/or HCH Anecdotal
Primary hyperlipidaemia It is usually breed specific but can appear in any dog
Miniature Schnauzer* HTG with or without HCH HTG can range from mild to marked; HCH may be mild to moderate; present in >30% of
all dogs in the USA; prevalence increases with age
Beagle* HTG and/or HCH Increases are usually mild to moderate
Shetland sheepdog* HCH with or without HTG HCH might be marked; HTG is typically mild; present in >40% of dogs in Japan
Dobermann HCH HCH is usually mild
Rottweiler HCH HCH is usually mild
Briard HCH HCH in Briards has only been reported in the UK
Rough-coated Collie HCH Reported in a single family in the UK
Pyrenees Mountain dogs HCH HCH is usually mild
HTG hypertriglyceridemia, HCH hypercholesterolaemia
*Indicates common causes

hypertriglyceridemia and hypercholesterolaemia occur infre-
quently (18 and 24%, respectively) as a possible result of pancre-
atitis and are typically mild (Xenoulis et al. 2011a,b). Therefore,
fasting hyperlipidaemia (especially when severe) in dogs with
pancreatitis likely reflects concurrent primary hyperlipidaemia
or hyperlipidaemia secondary to other causes (e.g. an endocrine
disease), and warrants further diagnostic investigation.
Several other causes of hyperlipidaemia have been reported
or suspected in dogs. These include obesity (Chikamune et al.
1995, Bailhache et al. 2003, Jeusette et al. 2005), protein-losing
nephropathy (Center et al. 1987, DiBartola et al. 1989, 1990,
Cook & Cowgill 1996, Littman et al. 2000), cholestasis (Dan-
ielsson et al. 1977, Chuang et al. 1995), high-fat diets (Downs
et al. 1997), lymphoma (Ogilvie et al. 1994), infection with
Leishmania infantum (Nieto et al. 1992), congestive heart failure
due to dilated cardiomyopathy (Tidholm & Jonsson 1997), par-
voviral enteritis (Yilmaz & Senturk 2007), and administration of
certain drugs (e.g. glucocorticoids, estrogen, phenobarbital and
potassium bromide) (Kluger et al. 2008).
Primary lipid abnormalities are usually, but not always, associ-
ated with certain breeds (Table 1). Depending on the breed, the
prevalence of a primary lipid abnormality can vary widely. Also,
the geographic region of the canine population tested seems
to play an important role due to genetic differences. Primary
hyperlipidaemia is very common in Miniature Schnauzers in
the USA (>30% of Miniature Schnauzers are affected based on
one study) and was the first breed-related primary lipid disor-
der described in the dog (Rogers et al. 1975a, Whitney et al.
1993, Xenoulis et al. 2007). Miniature Schnauzers from Japan
have also been described with this condition (Mori et al. 2010).
Although studies are lacking, based on anecdotal evidence,
hyperlipidaemia may not be as common in this breed in Europe,
although this is controversial. Primary hyperlipidaemia in the
Miniature Schnauzer is typically characterised by hypertriglyc-
eridaemia resulting from an abnormal accumulation of VLDL
or a combination of VLDL and chylomicrons (Whitney et al.
1993, Xenoulis et al. 2013). Although hypercholesterolaemia
may also be present, it is not found in all affected dogs and is
always present in association with hypertriglyceridaemia (Whit-
ney et al. 1993, Xenoulis et al. 2007, 2013). Hyperlipidaemia in
Miniature Schnauzers is an age-related condition and both its
prevalence and severity increase with age (Xenoulis et al. 2007).
The cause of primary hyperlipidaemia in Miniature Schnauzers
is currently unknown.
Primary hyperlipidaemia (mainly hypercholesterolaemia but
in some cases with concurrent hypertriglyceridemia) has also been
reported in Shetland sheepdogs in Japan, and likely also exists in
other countries (Sato et al. 2000, Aguirre et al. 2007, Mori et al.

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 P. G. Xenoulis & J. M. Steiner

2010). Primary hyperlipidaemia with hypercholesterolaemia and
hypertriglyceridaemia has also been reported in Beagles (Wada
et al. 1977). Primary hypercholesterolaemia without hyper-
triglyceridaemia has been described in Briards and a family of
rough-coated Collies from the UK (Watson et al. 1993, Jeusette
et al. 2004). In addition, primary hypercholesterolaemia has been
reported anecdotally in Dobermann and Rottweilers but no spe-
cific studies have yet been carried out.
severe hypertriglyceridaemia in Miniature Schnauzers should be
treated even when clinical signs are not present, due to the risk of
developing pancreatitis. In addition, in dogs with severe hyper-
triglyceridaemia and pancreatitis, the first should be considered
the cause of the latter rather than vice versa and treatment of pan-
creatitis in those cases should always include measures to control
hypertriglyceridaemia. It is currently not certain, but likely, that
hypertriglyceridaemia is also a risk factor for pancreatitis in dogs
of other breeds.

CLINICAL IMPORTANCE OF Hepatobiliary disease

HYPERLIPIDAEMIA IN DOGS Clinical studies and anecdotal observations suggest that two hepatic
disorders are associated with hypertriglyceridaemia in dogs: diffuse
As mentioned previously, canine hyperlipidaemia has emerged as vacuolar hepatopathy and gallbladder mucocele (Xenoulis & Steiner
an important clinical condition that requires a systematic diag- 2010). Hyperlipidaemia-associated vacuolar hepatopathy has been
nostic approach and appropriate treatment. Although hyperlipi- anecdotally reported and associated with primary hyperlipidaemia
daemia itself does not seem to lead directly to the development in dogs. It is characterised by hepatocellular accumulation of tri-
of major clinical signs, it has been reported to be associated with glycerides and glycogen, and it is often referred to as hepatic lipido-
other diseases that are clinically important and potentially life sis or steatosis (Xenoulis & Steiner 2010). Gallbladder mucoceles
threatening (Table 2). have been commonly reported in dog breeds that are predisposed
to primary hyperlipidaemia (e.g. Miniature Schnauzers and
Pancreatitis Shetland sheepdogs) (Aguirre et al. 2007) and may also potentially
Hyperlipidaemia, and more specifically hypertriglyceridaemia, develop in association with secondary hyperlipidaemia. In asymp-
has long been suspected as a risk factor for canine pancreatitis tomatic dogs, vacuolar hepatopathy and gall bladder mucoceles are
(Cook et al. 1993, Hess et al. 1998, Xenoulis & Steiner 2010). only associated with increased hepatic enzyme activities. In a recent
Also, the high prevalence of pancreatitis in Miniature Schnauzers study, primary hypertriglyceridaemia was found to be associated
has been attributed to the fact that dogs of this breed com- with increased serum hepatic enzyme activities in clinically healthy
monly develop primary hypertriglyceridaemia (Williams 1996). Miniature Schnauzers (Xenoulis et al. 2008). In that study, 60 and
However, little evidence to support this notion was available 45% of the Miniature Schnauzers with serum triglyceride concen-
until recently. Two recent clinical studies, each using a differ- trations 4·52 mmol/L and greater had increased serum ALP and
ent methodological approach, provided stronger evidence that ALT activities, respectively.
hypertriglyceridaemia, especially severe hypertriglyceridae-
mia (10 mmol/L), is a risk factor for pancreatitis in Miniature Insulin resistance
Schnauzers (Xenoulis et al. 2010, 2011b). In one of those stud- Another potential complication of hypertriglyceridaemia in dogs
ies, Miniature Schnauzers that developed pancreatitis were is insulin resistance. In a recent study, almost 30% of Miniature
five times more likely to have hypertriglyceridaemia before the Schnauzers with primary hypertriglyceridaemia had evidence of
development of pancreatitis than dogs of the same breed that insulin resistance as determined by serum insulin concentration
did not develop pancreatitis (Xenoulis et al. 2011c,d). Therefore, (Xenoulis et al. 2011a,b). This might have an implication on gly-
caemic control in dogs with hypertriglyceridaemia and concurrent
diabetes mellitus. However, the clinical importance of hypertriglyc-
Table 2. Possible consequences and complications of eridaemia-associated insulin resistance remains to be determined.
hyperlipidaemia
Disorder Type of lipid abnormality responsible Atherosclerosis
Pancreatitis HTG Although dogs appear to be resistant to atherosclerosis due to
Hepatobiliary disease
Vacuolar hepatopathy HTG
their lipoprotein composition and metabolism, they have been
Lipidosis HTG reported to develop atherosclerosis in both experimental and
Biliary mucocele HTG/HCH clinical studies (Mahley et al. 1977, Liu et al. 1986, Kagawa et al.
Insulin resistance HTG 1998, Hess et al. 2003). Spontaneous atherosclerosis has been
Ocular disease
Lipaemia retinalis HTG
reported in dogs mainly in association with secondary hypercho-
Lipaemic aqueous HTG lesterolaemia due to endocrinopathies. In one study, 60% of 30
Lipid keratopathy HTG dogs with atherosclerosis had hypothyroidism and 20% had dia-
Intraocular xanthogranuloma HTG betes mellitus (Hess et al. 2003).
Arcus lipoides corneae HTG/HCH
Seizures HTG
Lipomas HTG Ocular disease
Atherosclerosis HCH Several ocular manifestations of hyperlipidaemia, such as
HTG hypertriglyceridaemia, HCH hypercholesterolaemia lipaemia retinalis, lipaemic aqueous and lipid keratopathy have

598 Journal of Small Animal Practice • Vol 56 • October 2015 • © 2015 British Small Animal Veterinary Association

been reported in dogs (Crispin 1993). Recently, solid intra-
ocular xanthogranuloma formation was reported as a unique
disorder of hyperlipidaemic Miniature Schnauzers (Zafross &
Dubielzig 2007).
Other conditions
Seizures and other neurologic signs have been reported to poten-
tially occur as a result of severe hyperlipidaemia in dogs (Bodkin
1992, Vitale & Olby 2007). Some clinicians associate hyper-
lipidaemia with the development of cutaneous xanthomata or
lipomas. Finally, some authors report that hyperlipidaemia can
cause clinical signs of abdominal pain, lethargy, vomiting and/
or diarrhoea without evidence of pancreatitis or other diseases
(Ford 1993). This is highly speculative, however, because pub-
lished reports are lacking and, given the difficulty in diagnosing
pancreatitis, especially in past decades, pancreatitis could have
easily been missed in these patients.
EFFECT OF LIPAEMIA ON THE MEASUREMENT
OF OTHER ANALYTES
Depending on the methods and instruments used, lipaemia
might affect the measurement of several other analytes in serum
or plasma, potentially leading to inaccurate results. Laboratory
staff should be aware of which analytes are affected by lipaemia
and make sure that lipaemia does not interfere with their mea-
surement. Analytes that are known to be affected by lipaemia
could be measured after centrifugation of the sample to remove
the excess lipids or by adding clearing agents to the sample.
DIAGNOSTIC APPROACH TO DOGS WITH
HYPERLIPIDAEMIA
Hyperlipidaemia is typically diagnosed by measurement of fast-
ing serum triglyceride and/or cholesterol concentrations. Because
hyperlipidaemia is most commonly the result of other diseases it
can serve as an important diagnostic clue for dogs with other pri-
mary conditions. In addition, hyperlipidaemia is often the only
abnormality in dogs with primary hyperlipidaemia. In order not
to miss existing hyperlipidaemia, the authors believe that mea-
surement of serum cholesterol and triglyceride concentrations
should be part of every routine chemistry profile. Measurement
of serum triglyceride concentration is often not included in a
typical chemistry profile and has to be specifically requested by
the clinician. Moderate and severe hypertriglyceridaemia (but
not mild hypertriglyceridaemia or hypercholesterolaemia) can be
suspected based on inspection of serum or plasma that has a tur-
bid or lactescent appearance. However, even in those cases, mea-
surement of serum triglyceride and cholesterol concentrations is
mandatory in order to reach an accurate assessment of the sever-
ity and spectrum of hyperlipidaemia. In some cases, use of a meal
challenge to diagnose postprandial hyperlipidaemia might be
necessary, although experience with such a test is limited (Elliott
et al. 2011).
Journal of Small Animal Practice • Vol 56 • October 2015
Canine hyperlipidaemia
The general diagnostic approach when evaluating dogs with
hyperlipidaemia is presented in Fig 2. After hyperlipidaemia has
been diagnosed, the next step is to determine whether the patient
has a primary or a secondary lipid disorder. If hyperlipidaemia is
secondary, the condition responsible for causing hyperlipidaemia
should be diagnosed and treated. Thus, specific diagnostic inves-
tigations should be performed in order to diagnose or rule out
diseases that can cause secondary hyperlipidaemia. If secondary
hyperlipidaemia is excluded, a tentative diagnosis of a primary
lipid disorder can be made.
A detailed history should be obtained and physical examina-
tion performed first. This is crucial because dogs with secondary
hyperlipidaemia typically show clinical signs of the primary dis-
ease (e.g. obesity, polyuria and polydipsia in dogs with diabetes
mellitus or hyperadrenocorticism, hypoactivity and hair loss in
dogs with hypothyroidism), which can help prioritise the selec-
tion of diagnostic tests and lead the way towards an appropri-
ate diagnostic plan. Dogs with primary hyperlipidaemia may or
may not have clinical signs. Dogs with hyperlipidaemia should
have at least a Complete Blood Count (CBC), chemistry panel
and urinalysis performed. Additional tests that may be useful
for the diagnostic investigation of dogs with hyperlipidaemia
include but are not limited to measurement of serum total and
free thyroxine concentrations, serum TSH concentration, serum
pancreatic-lipase immunoreactivity concentration, serum bile-
acid concentrations, urine protein:creatinine ratio, and low-dose
dexamethasone suppression test or another test to rule-in or rule-
out hyperadrenocorticism. The selection of tests to be performed
is based on information from the history, physical examination
and clinicopathologic findings, and is tailored to each individual
case. A more general and wide selection of tests might be nec-
essary for patients that have vague or no clinical signs or other
findings. It should be noted that often there are dogs with hyper-
lipidaemia that are clinically healthy and have no evidence of a
primary condition that causes secondary hyperlipidaemia. It is
likely that at least some of these dogs have some form of primary
hyperlipidaemia. In such cases, and if hyperlipidaemia is mild or
moderate, there may be no need for detailed diagnostic investiga-
tions, although periodic monitoring is recommended.
Ideally, an appropriate selection of the above-mentioned tests
should be used in every dog with hyperlipidaemia as part of the
diagnostic investigation. One possible exception is the Minia-
ture Schnauzer, in which primary hyperlipidaemia is common.
A detailed diagnostic investigation of hyperlipidaemia might not
be necessary in this breed in the absence of clinical signs sug-
gesting an underlying cause. However, if hypercholesterolaemia
is the main abnormality (without or with only mild hypertriglyc-
eridaemia), then it is more likely that the dog has some form of
secondary hyperlipidaemia and further diagnostic investigation is
required. It can also be recommended that all Miniature Schnau-
zers (and potentially other dog of breeds that commonly develop
primary hyperlipidaemia) should be evaluated for hypertriglycer-
idaemia while they are healthy, because this information may be
useful for the avoidance of misinterpretation of increased serum
triglyceride concentrations when the dogs are presented for a
clinical illness. In addition, by knowing the serum triglyceride
• © 2015 British Small Animal Veterinary Association 599
 P. G. Xenoulis & J. M. Steiner

Increased serum triglyceride and/or cholesterol concentrations

If not fasted, possibly postprandial

Confirm animal is fasted
hyperliipidaemia consider fasting and retesting

If fasted, complete history and physical examination (including recording

breeds that are known to develop primary hyperlipidaemia)

Identify findings that might suggest

secondary hyperliipidaemia (e.g. obesity,
PU/PD (diabetes mellitus, If the dog belongs to a
hyperadrenocorticism), hypoactivity breed known to
(hypothyroidism), symmetrical commonly develop
alopecia (hyperadrenocorticism, primary
hypothyroidism), vomiting and hyperliipidaemia and
abdominal pain (pandreatitis), other clinical and Treat
clinicopathological
Run CBC, chemistry profile, urinalysis evidence does not
suggest a secondary
Prioritize selection of further diagnostic Tentative diagnosis of primary
cause
tests based on history, clinical and hyperliipidaemia
clinicopathologicalfindings If a cause of
secondary
Run diagnostic tests as needed to
hyperliipidaemia is not
identify the cause of secondary
identified
hyperliipidaemia (serum total T4, free T4,
TSH, cPLI, bile-acids, UPC, LDDST, Diagnosis of primary hyperlipidemia
abdominal ultrasound, other)

Treat primary Perform additional diagnostics if needed (potentially including lipid ultracentrifugation,
disease electrophoresis, chylomicron test, etc)

FIG 2. Algorithm showing the basic steps of the diagnostic approach in dogs with hyperliipidaemia. PU/PD polyuria/polydipsia, UPC protein:creatinine
ratio, LDDST Low-dose dexamethasone suppression test

status of the dog, the veterinarian might consider switching the
affected dog to a low-fat diet to avoid possible complications of
hypertriglyceridaemia.
When based on an appropriate diagnostic investigation, a pri-
mary lipid disorder leading to hyperlipidaemia is suspected, there
is little more that can be done to identify the cause of hyperlipi-
daemia in a given patient. Tests that have occasionally been used to
further characterise or investigate the cause of primary hyperlipi-
daemia in dogs include the chylomicron test (i.e. lipemic serum is
left for 12 hours undisturbed at 4°C; if chylomicrons are present,
a cream layer will form; the remaining serum can be clear or turbid
indicating an excess of VLDL), lipoprotein electrophoresis, ultra-
centrifugation, measurement of specific apoproteins and indirect
measurement of lipoprotein lipase activity with a heparin response
test (i.e. measurement of serum triglyceride concentrations before
and after intravenous administration of 90 IU/kg heparin; heparin
activates lipoprotein lipase). None of these tests are used routinely
in clinical cases and their availability is limited. Genetic testing for
specific lipid disorders related to mutations of genes involved in
lipid metabolism is currently not available.
TREATMENT OF CANINE HYPERLIPIDAEMIA
Treatment of secondary hyperlipidaemia relies on the successful
treatment of the underlying disorder after which hyperlipidaemia
usually resolves. Resolution of secondary hyperlipidaemia after
treatment of the cause should always be confirmed by laboratory
testing (typically 4 to 6 weeks after initiation of treatment of the
primary disease and periodically thereafter). If hyperlipidaemia
has not resolved, another underlying cause, alternative or addi-
tional therapy, or concurrent primary hyperlipidaemia should
be considered. In some dogs with secondary hyperlipidaemia,
especially those with hyperlipidaemia due to diabetes mellitus,
it might be difficult to optimally control their primary disease,
and therefore, hyperlipidaemia might persist despite treatment.
If hyperlipidaemia in those cases is severe, it might be necessary
to take measures for its control. The management of persistent
secondary hyperlipidaemia relies on the same principles as for
primary hyperlipidaemia (see below).
As mentioned above, hypertriglyceridemia can potentially
predispose to several disorders in dogs. Therefore, treatment of
primary or persistent secondary hypertriglyceridemia is clini-
cally important. Some clinicians recommend that hypertriglyc-
eridemia should be treated only when exceeding 5·5 mmol/L.
However, recent studies have shown that insulin resistance,
hepatobiliary disease and possibly other complications of hyper-
triglyceridaemia can exist even with serum triglyceride concen-
trations below 5·5 mmol/L. Therefore, treatment (at least with
dietary management) should be considered even in patients with
less severe hypertriglyceridaemia in order to keep serum triglyc-
eride concentrations as low as possible and lower the risk for

600 Journal of Small Animal Practice • Vol 56 • October 2015 • © 2015 British Small Animal Veterinary Association
 Canine hyperlipidaemia
complications. It should be noted that there are no universally
accepted definitions and cut-offs regarding the severity of hyper-
triglyceridaemia in dogs. In addition, variation in the reference
intervals for triglycerides does exist between laboratories (owing
to differences in dog populations and methods used) and there-
fore mild, moderate and severe hypertriglyceridaemia might be
defined using different cut-offs for different laboratories.
The initial treatment goal for severe hypertriglyceridaemia
should be to keep fasting serum triglyceride concentration below
5·5 mmol/L. This goal should initially be pursued with dietary
management, while drug therapy can be initiated later if deemed
necessary. After this initial goal has been achieved, further reduc-
tion or even normalisation of serum triglyceride concentrations
(typically with the addition of lipid-lowering drugs) should be
decided on the basis of a risk-to-benefit ratio for each individual
case. Dogs with hyperlipidaemia in which additional treatment is
not deemed necessary or has been declined by the owner should
be at least monitored periodically for potential worsening of
hyperlipidaemia.
Although the management of hypercholesterolaemia seems to
be of less clinical importance than that of hypertriglyceridaemia
in dogs and there are no studies evaluating the need for treatment
of hypercholesterolaemia in dogs, severe hypercholesterolaemia
may be treated at least with dietary management. As for triglyc-
erides, reference intervals for serum cholesterol concentrations
may differ significantly between laboratories, and therefore the
severity of hypercholesterolaemia might be defined using dif-
ferent cut-offs for different laboratories. Drug therapy may be
considered in cases where hypercholesterolaemia is resistant to
dietary therapy and exceeds 13 mmol/L. The following sections
focus mainly on the treatment of hypertriglyceridaemia unless
otherwise indicated. However, the general treatment principles
of hypercholesterolaemia are similar to the ones described for
hypertriglyceridaemia.
Dietary management
The first step in the management of primary or persistent second-
ary hyperlipidaemia is dietary modification. Dogs with primary
hyperlipidaemia should be offered an ultra low-fat diet through-
out their lives, while dogs with persistent secondary hyperlipi-
daemia should be offered low-fat diets on the basis of repeated
testing and the effectiveness of control of the primary disease.
Although there are currently no studies in the peer-reviewed lit-
erature that have evaluated the amount of fat that a diet should
contain in order to effectively manage dogs with hyperlipidae-
mia, the authors generally recommend diets that contain less
than 25 grams of total fat per 1000 Kcal (metabolisable energy).
Many commercially available diets are labelled as “low-fat” but
their fat content can vary widely. In addition, although many
diets have low total fat content, several other factors (e.g. type of
fat, fibre content) that might potentially affect the effectiveness
of those diets in the management of hyperlipidaemia are usually
unknown. Published studies investigating the efficacy of low-fat
diets in dogs with hyperlipidaemia are lacking. Therefore, the
selection of the most effective low-fat diet for the treatment of
hyperlipidaemia is uncertain and quite challenging. In a recent
Journal of Small Animal Practice • Vol 56 • October 2015 • © 2015 British Small Animal Veterinary Association
unpublished study, Miniature Schnauzers with primary hyper-
lipidaemia were put on the Royal Canin Gastrointestinal Low
Fat® diet for 8 weeks (Xenoulis et al. 2011c,d). By the end of
the treatment period, there was a significant reduction in both
serum triglyceride and cholesterol concentrations. Serum choles-
terol concentrations returned to normal in all dogs, while serum
triglyceride concentrations returned to normal in about 30% of
dogs. Further, all dogs that had serum triglyceride concentrations
more than 5·5 mmol/L at the beginning of the study had serum
triglyceride concentrations less than 5·5 mmol/L by the end of
the trial.
Home-made ultra low-fat diets have not been systematically
evaluated for the management of hyperlipidaemia in dogs, but
clinical experience suggests that they are suitable. However, care
should be taken to make sure that these diets are balanced, espe-
cially when intended for long-term feeding, and that the mini-
mum nutrient requirements are met for all nutrients, including
lipids. Some of these diets (e.g. rice and boiled lean turkey breast
without the skin) may have an even lower fat content than some
commercially available low-fat diets and may be more effective
in lowering serum lipid concentrations in dogs. Treats and table
scraps should be avoided unless they are ultra-low in fat. Fruits
and vegetables typically constitute ideal treats for hyperlipidae-
mic dogs.
Serum lipid concentrations should be re-evaluated after feed-
ing a low-fat diet for about 3 to 4 weeks. If the serum triglyceride
concentration in hypertriglyceridaemic dogs has decreased to less
than 5·5 mmol/L, dietary therapy should be continued and serum
triglyceride concentrations should be re-evaluated periodically.
If serum triglyceride concentration remains above 5·5 mmol/L
or if additional reduction of serum triglyceride concentration is
desired, additional dietary modifications (if possible) or medical
treatment should be considered.
Medical management
Some dogs with primary hyperlipidaemia will not sufficiently
respond to feeding an ultra low-fat diet alone. In these cases,
medical treatment is required. A plethora of lipid-lowering drugs
are available and some of them have been widely used in human
medicine for decades. It needs to be pointed out, however, that
no studies have evaluated the efficacy and safety of lipid-lowering
drugs in dogs, and therefore, evidence-based recommendations
cannot be made. Instead, recommendations in this manuscript
are based on clinical experience and extrapolation from humans.
Therefore, the drugs described below should be used with cau-
tion and only when it is deemed necessary by the clinician. It
also needs to be noted that lipid-lowering drugs are not approved
for use in dogs and therefore owner consent is recommended
when these drugs are being used. Drugs that are more commonly
used in the management of canine hyperlipidaemia are shown in
Table 3.
Omega-3 fatty acids (fish oils)
Polyunsaturated fatty acids of the n-3 series [omega-3 fatty acids;
eicosapentanoic acid (EPA), and docosahexaenoic acid (DHA)]
601

Table 3. Drugs used for the medical management of hyperlipidaemia in dogsa
Drug Dosage regimen
Omega-3 fatty acids 200 to 300 mg/kg, every 24 hours, orally
Fibrates
Gemfibrozil 10 mg/kg every 12 hours, orally
Bezafibrate 4 to 10 mg/kg, every 24 hours, orally
Niacin 50 to 200 mg/day (total dose)
Statins Not established for dogs
a
It should be noted that at the time of this writing no clinical trials have assessed the efficacy and safety of any of the listed substances in dogs with hyperlipidaemia and that
recommendations are based on anecdotal evidence and clinical experience
are abundant in marine fish. Omega-3 fatty acid supplementa-
tion has been shown to lower serum triglyceride concentrations in
experimental animals, normal humans and humans with primary
hypertriglyceridaemia. Specifically, omega-3 fatty acids have been
shown to reduce serum triglyceride concentrations by up to 50%
when used at high doses in humans with hypertriglyceridaemia
(Toth et al. 2009). The mechanisms of the lipid-lowering action of
omega-3 fatty acids are complex and include regulation of several
transcription factors that lead to reduced lipogenesis, increased
β-oxidation and activation of lipoprotein lipase (Toth et al. 2009,
Watts & Karpe 2011). In a study of healthy dogs, fish-oil sup-
plementation led to a significant reduction of serum triglyceride
concentrations, suggesting that this supplement may be helpful
in the treatment of canine hypertriglyceridaemia (LeBlanc et al.
2005). No major side effects have been observed in humans or in
dogs receiving omega-3 fatty acids. However, studies evaluating
the efficacy and safety of omega-3 fatty acid supplementation in
dogs with hyperlipidaemia are lacking. A “fishy” odour is often
noted in dogs receiving high doses of omega-3 fatty acids and it
might be unacceptable for some owners.
Because serious side effects are rarely reported and because
omega-3 fatty acids are likely effective in lowering serum tri-
glyceride concentrations, fish oils could be tried as a second-line
therapy in dogs with primary hypertriglyceridaemia that do not
respond to a low-fat diet alone. The formulation of omega-3
fatty acids with the highest purity currently is Lovaza (Glaxo-
SmithKline) and it is FDA approved for use in humans as a
lipid-lowering agent (Toth et al. 2009). However, there are many
other human and veterinary formulations of omega-3 fatty acids
depending on the country. Omega-3 fatty acids are used in dogs
at doses ranging from 200 to 300 mg/kg (total dose), orally, once
a day, and their effect on serum triglyceride concentrations is
dose-dependent (Bauer 1995, LeBlanc et al. 2005). Their lipid-
lowering effect typically requires doses at the high end of the rec-
ommended dose for dogs. An upper daily limit of 4 to 5 grams
might be recommended. Periodic retesting of serum triglyceride
concentrations is recommended during the treatment period.
Fibrates (fabric acid derivatives)
Fibrates are weak agonists of peroxisome proliferator-activated
receptor-α, a nuclear transcription factor that regulates lipid and
lipoprotein synthesis and catabolism (Tenenbaum & Fisman
2012). Fibrates suppress fatty acid synthesis, stimulate fatty acid
602
P. G. Xenoulis & J. M. Steiner
Side effects Comments
Fishy odour, GI signs Questionable efficacy in severe cases
Myotoxicity, hepatotoxicity Questionable efficacy
Myotoxicity, hepatotoxicity Likely more efficacious that gemfibrozil
Erythema, pruritus, myotoxicity, Questionable efficacy
hepatotoxicity
Unknown; hepatotoxicity Very limited clinical experience; use only if other
medications have proven uneffective
oxidation, activate lipoprotein lipase and inhibit noncompeti-
tively the enzyme diacylglycerol acyl transferase 2 (the enzyme
that catalyses the conversion of diglycerides to triglycerides),
therefore leading to an overall reduction in serum triglycer-
ide concentration (Toth et al. 2009, Watts & Karpe 2011). In
humans, fibrates typically reduce serum triglyceride concentra-
tions by 25 to 50% (Toth et al. 2009, Watts & Karpe 2011).
It is of interest that fibrates have been shown to be particularly
useful in the management of humans with diabetic dyslipidaemia
that is resistant to other drugs (Toth et al. 2009). Fibrate use
in humans is associated with low incidence of myotoxicity and
increases in serum liver enzyme activities. Gemfibrozil (Lopid,
Pfizer and generics) is one of the most commonly used fibrate in
humans, and has also been used anecdotally in dogs with hyper-
triglyceridaemia. In dogs, it can be administered at 10 mg/kg
every 12 hours, orally. No side effects have been observed in dogs,
although no studies have evaluated its safety in this species. It is
the authors’ experience that, similar to what has been reported in
humans (Beggs et al. 1999), some canine patients with primary
hyperlipidaemia do not respond well to treatment with gemfibro-
zil. Bezafibrate (Bezalip, Actavis and generics), another fibric acid
derivative, may be both more effective and associated with less
adverse effects in the treatment of humans with hyperlipidaemia
(Beggs et al. 1999). Recently, bezafibrate was evaluated in a study
published in abstract form and was found to be highly effective in
reducing serum triglyceride and cholesterol concentrations in 15
dogs with primary and 31 dogs with secondary hyperlipidaemia
(De Marco et al. 2013). In that study, bezafibrate was used at a
dose ranging from 4 to 10 mg/kg, every 24 hours, for 30 days.
Normalisation of serum triglyceride and cholesterol concentra-
tions was achieved in 91 and 68% of cases, respectively. No side
effects were observed. Fibrates may be recommended in dogs
where dietary modification with or without omega-3 fatty acids
have failed to effectively reduce serum triglyceride concentra-
tions. Periodic testing of serum triglyceride concentration and
liver enzyme activities is recommended.
Niacin (nicotinic acid)
Niacin is a form of vitamin B3 that has been used successfully
for the treatment of hyperlipidaemia in humans for many
years (Kashyap et al. 2002). When used in pharmacological
doses, niacin is a broad-spectrum lipid modifying drug and, in
humans, reduces both LDL-cholesterol and serum triglyceride
Journal of Small Animal Practice • Vol 56 • October 2015 • © 2015 British Small Animal Veterinary Association
 Canine hyperlipidaemia
concentrations (Watts & Karpe 2011). The mechanism of action
of niacin is complex and incompletely understood but includes
inhibition of hormone-sensitive lipase activity and the enzyme
diacylglycerol acyltransferase, both of which actions eventually
lead to reduced triglyceride biosynthesis (Watts & Karpe 2011).
In dogs, niacin treatment has been reported in very few patients
with primary hypertriglyceridaemia. In these patients, niacin
reduced serum triglyceride concentrations for several months
without causing any side effects (Bauer 1995). However, large
clinical trials regarding the efficacy and safety of niacin in dogs
with primary hypertriglyceridaemia are lacking. As is often the
case in humans, niacin administration in dogs is potentially asso-
ciated with side effects such as erythema and pruritus, which may
require discontinuation of therapy. Long-term risk for myotoxic-
ity and hepatotoxicity may also exist (Watts & Karpe 2011).
Niacin is usually administered to dogs at a dose of 50 to
200 mg/day. Both the therapeutic and side effects of niacin are
dose dependent and it is therefore recommended that niacin is
started at a low dose and slowly titered upwards (every 4 weeks)
based on the results of follow-up serum cholesterol and triglyc-
eride concentrations. It should be used with caution in diabetic
patients because it can increase blood glucose concentration,
especially when used at higher doses. Serum liver enzyme activi-
ties should be monitored with long-term use of niacin.
Statins
Statins (HMG-CoA reductase inhibitors) are among the most
potent and commonly used lipid-lowering drugs and constitute
first-line therapy for the treatment of hypercholesterolaemia in
humans (Watts & Karpe 2011). They are reversible inhibitors
of the enzyme HMG-CoA reductase, which is the rate-limiting
step for cholesterol biosynthesis. Therefore, statins are mainly
cholesterol-lowering drugs (in humans they specifically lower
LDL-cholesterol) with less potent effects on triglyceride metab-
olism (Watts & Karpe 2011). This makes them less than ideal
for both human and canine patients with hypertriglyceridaemia
as the main lipid abnormality (Tenenbaum & Fisman 2012).
Statin use has been associated with myopathy, rhabdomyolysis
and hepatotoxicity in humans, and there are anecdotal reports of
hepatotoxicity in dogs. The potential for hepatotoxicity is prob-
ably higher when concurrent hepatic steatosis is present, a condi-
tion that likely occurs in at least a portion of dogs with severe
hypertriglyceridaemia (especially Miniature Schnauzers). When
collectively considering the potential side effects of statins, the
fact that hypercholesterolaemia rarely needs to be treated medi-
cally in dogs, and that statins are unlikely to be very effective in
the treatment of canine hypertriglyceridaemia, the routine use of
statins is not recommended in hyperlipidemic dogs. In cases of
persistent severe hypercholesterolaemia statins may be used, but
it needs to be pointed out that the pharmacokinetic profiles of
the various statins for dogs are unknown and therefore, the dose
and frequency of administration of these drugs can currently only
be extrapolated from human medicine. In dogs in which statins
are used, serum hepatic enzyme activities should be periodically
monitored for potential hepatotoxicity. In humans, concurrent
Journal of Small Animal Practice • Vol 56 • October 2015 • © 2015 British Small Animal Veterinary Association
administration of statins and fibrates (especially gemfibrozil) is
not recommended, because the latter has been shown to affect
the pharmacokinetics of statins leading to increased risk for
toxicity (Tenenbaum & Fisman 2012). However, other fibrates
(e.g. bezafibrate) appear to be safer and better tolerated than
gemfibrozil when combined with statins (Watts & Karpe 2011,
Tenenbaum & Fisman 2012). There is no similar information
available for dogs.
Combination drug therapy
Some dogs, especially those with primary hypertriglyceridaemia,
can manifest extremely high serum triglyceride concentrations.
Serum triglyceride concentrations in many of these dogs cannot
be controlled with diet alone or monotherapy with lipid-low-
ering drugs, and require combinations of more than one lipid-
lowering medication and ultra low-fat diets. Experience with
combination therapy is very limited in dogs. The authors’ pre-
ferred order of treatment trials in dogs with severe hypertriglyc-
eridaemia is the administration of an ultra low-fat diet, followed
by the addition of omega-3 fatty acids (typically at high doses),
followed by bezafibrate, and finally the addition of niacin if nec-
essary. Patients with very severe primary hypertriglyceridaemia
may alternatively be immediately started on both ultra low-fat
diets and medical treatment(s) in order to more rapidly reduce
their serum triglyceride concentrations and decrease the risk for
the development of diseases such as pancreatitis.
CONCLUDING REMARKS
Canine hyperlipidaemia is an important clinical condition.
Hypertriglyceridaemia is likely of greater clinical importance
than hypercholesterolaemia. In the majority of cases (especially
when clinical signs are present) a detailed diagnostic investiga-
tion of the cause of hyperlipidaemia is required. Secondary
hyperlipidaemia typically resolves with treatment of the primary
disease. Primary hyperlipidaemia or severe persistent secondary
hyperlipidaemia (especially hypertriglyceridaemia) typically need
to be treated. The authors typically begin with dietary therapy
alone and assess the effectiveness of the diet 4 to 6 weeks later,
unless a more rapid reduction in serum triglyceride or choles-
terol concentrations is required. In that case, medical treatment
is started typically with fish oils or bezafibrate first (depending on
the severity of hyperlipidaemia). Statins are typically reserved for
cases that do not respond to other treatments.
Conflict of interest
None of the authors of this article has a financial or personal
relationship with other people or organisations that could inap-
propriately influence or bias the content of the paper.
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