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Abstract

Objectives

The aim of this study was to assess the short-term safety and efficacy of fenofibrate in controlling secondary hypertriglyceridemia in cats.

Methods

This was a prospective cohort study. Seventeen adult cats with hypertriglyceridemia (serum triglycerides [TG] >160 mg/dl) were enrolled. Cats received a median dose of 5 mg/kg (range 3.2–6) fenofibrate (q24h PO) for 1 month. Serum TG, total cholesterol (TC), creatine kinase and liver enzymes (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) were evaluated before (t0) and after 1 month (t1) of fenofibrate treatment.

Results

The causes of secondary hypertriglyceridemia were diabetes mellitus (DM; 29.4%), obesity (29.4%), hyperadrenocorticism (HAC) and DM (11.7%), HAC without DM (5.9%), hypersomatotropism (HST) and DM (5.9%), hypothyroidism (5.9%), long-term treatment with glucocorticoids (5.9%) and chylothorax (5.9%). Serum TG (t0 median 920 mg/dl [range 237–1780]; t1 median 51 mg/dl [range 21–1001]; P = 0.0002) and TC (t0 median 278 mg/dl [range 103–502]; t1 median 156 mg/dl [range 66–244]; P = 0.0001) concentrations showed a significant decrease after 1 month of fenofibrate treatment. Fifteen cats normalized their TG concentration at t1 (88.2%). Of the eight cats that were hypercholesterolemic at t0, six (75%) normalized their TC concentrations at t1. One of 17 cats (5.9 %) presented with diarrhea; the remaining 16 did not show any adverse effects.

Conclusions and relevance

DM and obesity are the most common endocrine causes of secondary hyperlipidemia, although it can also be found in cats with HAC, HST or hypothyroidism. This study suggests that fenofibrate treatment was associated with reduction and normalization of TG and TC concentrations in cats with moderate and severe hypertriglyceridemia, regardless of the cause of secondary hypertriglyceridemia. Further work should focus on controlled studies with a greater number of cases.

Keywords

Fenofibrate hypertriglyceridemia hyperlipidemia peroxisome proliferator-activated receptor

Introduction

Hypertriglyceridemia refers to an increase in serum triglyceride (TG) concentration, which leads to a milky appearance of serum or plasma.^1,2 This condition is frequently seen in dogs, but it is not commonly observed in cats.^3,4

Hypertriglyceridemia can be classified as primary or secondary according to its origin. Primary causes are associated with genetic or family disorders of lipid metabolism, while secondary causes are due to other pathologies such as hypothyroidism, diabetes mellitus (DM), hyperadrenocorticism (HAC), pancreatitis, obesity, protein-losing nephropathy, cholestasis and hepatic lipidosis, among others.^5–7 Few reports refer to primary hypertriglyceridemia in cats, but they all describe this condition as being a consequence of genetic mutations.^8–10

Hypertriglyceridemia not only affects the measurement of different serum analytes, but is also related to severe clinical conditions, such as pancreatitis and neurological signs in dogs.⁶ In cats, hyperlipidemia is potentially associated with development of ocular disease (lipemia retinalis, lipid aqueous, lipid keratopathy), peripheral neuropathy, cutaneous xanthomatosis, anemia and, possibly, insulin resistance.^5,11–13

Fenofibrate is a drug used in humans and dogs to control hypertriglyceridemia.^14–16 It is a derivative of fibric acid, which, after being metabolized, originates feno-fibric acid (an active pharmaceutical ingredient).¹⁵ It exerts its effect through the peroxisome proliferator-activated receptor alpha, which modifies the expression of genes related to lipid metabolism and insulin sensitivity.¹⁷ In humans, it has been described that fenofibrate increases extrahepatic activity of lipoprotein lipase (LPL) and reduces very-low-density lipoprotein (VLDL) synthesis, leading to a decrease in TG-rich lipoprotein concentrations, such as VLDL.¹⁸ Moreover, it reduces total cholesterol (TC) and slightly increases high-density lipoprotein (HDL) cholesterol concentrations.¹⁹

Our research group has previously studied the efficacy of fenofibrate in controlling hypertriglyceridemia in dogs;¹⁴ however, there are no reports on the use of this drug to control this condition in cats. Therefore, the aim of this study was to evaluate the short-term safety and efficacy of fenofibrate to control secondary hypertriglyceridemia in cats.

Materials and methods

This study was approved by the Institutional Committee on the Care and Use of Experimental Animals of the Veterinary Science Center (VSC) in accordance with the laws on animal testing in Argentina and the recommendations of the World Health Organization. Informed written consent was obtained from all owners before enrollment. Client-owned cats with hypertriglyceridemia admitted to the VSC, Maimonides University, were enrolled in the study between 1 November 2019 and 30 January 2022.

Inclusion criteria were cats with lipemic serum (TG >160 mg/dl [1.8 mmol/l]; laboratory reference interval [RI] <160 mg/dl) whose primary disease could wait 1 month until starting treatment for the corresponding disease (HAC, hypersomatotropism [HST], obesity and hypothyroidism), with the exception of DM. Inclusion criteria also included indoor lifestyle and good owner compliance. On the day of admission, all cats received a physical examination, routine blood tests (complete blood count and serum biochemistry), urinalysis with urine protein to creatinine (UPC) ratio, abdominal ultrasonography and echocardiography (1 month after treatment, the same blood and urine tests were repeated). Exclusion criteria were poor patient tolerance of veterinary procedures, kidney or liver failure (combination of history and clinical signs, liver function tests [liver enzymes, bilirubin, albumin] and abdominal ultrasonography)^20,21 or any severe illnesses with poor prognosis that could exacerbate the condition, precipitate adverse effects of fenofibrate or affect successful study completion. None of these cats was treated for the underlying disease during the study, except for diabetic cats that continued insulin therapy (glargine 100 IU/ml [Lantus; Sanofi-Aventis]). At the end of the study, the non-diabetic cats started with pharmacological treatment for their underlying disease (trilostane, levothyroxine or cabergoline).

The owners of eligible cats were offered free fenofibrate treatment during the study period, and they did not have to pay the costs of the blood, urine and ultrasound studies. Owners were instructed to monitor their cats for any potential adverse effects. In diabetic cats, owners were encouraged to perform intensive glucose monitoring to detect possible variations in insulin sensitivity. Owners were instructed to contact the investigator if their cats presented any possible adverse effect or if they had any questions about the research protocol. No owner declined to enroll on the trial after receiving this information.

Cats suspected of endocrine concurrent diseases were tested with hormonal evaluations. A diagnosis of DM was made according to clinical signs, persistent fasting hyperglycemia, glycosuria and increased serum fructosamine concentrations. All diabetic cats had adequate metabolic control of DM at enrollment. Diagnosis of obesity was made according to the body condition score (BCS 8/9 or 9/9).^22,23 Diagnosis of HAC was made according to clinical signs and the following hormonal findings: increased urinary cortisol:creatinine ratio (>36 ×10^–6; RI <36 ×10^–6) and lack of suppression on the low-dose dexamethasone suppression test, 0.1 mg/kg dexamethasone (cortisol at 8 h >1.4 μg/dl). None of the cats with HAC was diagnosed with urinary cortisol:creatinine ratio alone. A diagnosis of HST was made according to clinical signs (acromegalic features), serum insulin-like growth factor 1 (IGF-1) concentration and pituitary images (CT). Cats were considered compatible with HST based on serum IGF-1 concentration >1000 ng/ml and the presence of pituitary enlargement on CT (>4 mm dorsoventral height).^24,25 Diagnosis of hypothyroidism was made according to clinical signs, increased serum thyroid stimulating hormone (RI <0.3 ng/ml) and reduced total thyroxine concentration (RI 1–3.2 µg/dl).

All cats were treated with fenofibrate non-micronized tablets (5 mg/kg PO q24h [Procetoken; Bernabo]; median dose 5 mg/kg [range 3.2–6]), immediately after the first meal, as the single and total administration, for 1 month. All diabetic cats received the same commercial diet for diabetic cats (Royal Canin Diabetic, fat content 12%) and all non-diabetic cats received the same standard commercial diet for adults (Royal Canin indoor, fat content 13%). All cats had received the same diet at least 2 months prior to enrollment.

All blood tests were performed after 12 h of solid fasting, before treatment (t0) and 1 month after treatment (t1). Serum TG, TC, creatine kinase (CK), liver enzymes (alanine aminotransferase [ALT], aspartate aminotransferase and alkaline phosphatase), creatinine, blood urea nitrogen (BUN) and UPC were evaluated (to assess possible liver, renal or muscle damage), at both times. All determinations were analyzed with an automated laboratory method (Metrolab Autoanalyzer; Merck), in accordance with the manufacturer’s instructions.

Cats were monitored weekly in VSC (Maimonides University) to detect possible adverse drug effects, variations in glycemia in diabetic cats or eventual clinical changes in body weight or BCS. Cats were monitored for any clinical signs that might develop. Owners were asked via a questionnaire about any clinical signs that might have appeared (diarrhea, vomiting, anorexia, changes in food/water intake, diuresis, behavior, mood, physical activity, etc.; see questionnaire in the supplementary material). BCS and body weight were also monitored at t0 and t1.

Statistical analysis

Statistical analysis was performed with GraphPad Prism 6. Data were analyzed for normal distribution (Shapiro–Wilk tests). The pre- and post-treatment results were analyzed using the Wilcoxon signed-rank test. Comparison between total TG and TC concentrations in diabetic and non-diabetic cats was performed using the Mann–Whitney U-test. Serum TG concentrations >1000 mg/dl that could not be diluted were analyzed as 1001 mg/dl. Values were expressed as mean ± SD or median (range), as applicable, with a statistical significance level set at P <0.05.

Results

Twenty cats with hypertriglyceridemia were recruited during the study period; of these 20, one case did not meet inclusion criteria and two owners declined to participate. Seventeen cats were therefore enrolled in the study and all cats completed the trial. Thirteen cats were domestic shorthairs, three were Siamese and one was a Burmese. Nine were female and eight were male (all castrated); mean age was 9.1 ± 4 years and mean body weight was 6 ± 2.5 kg. All diabetic cats had at least 6 weeks of insulin therapy (median 7 weeks [range 6–24]) at the time of enrollment. No cats changed insulin type during the study period. No owner reported any difficulties with the oral administration of fenofibrate. All owners reported that the medication had been handled as per the manufacturer’s instructions.

Causes of hypertriglyceridemia

All causes of hypertriglyceridemia were secondary: five cats had solely DM (29.4%), five were obese (29.4%), two had HAC and DM (11.7%), one had HAC without DM (5.9%), one had HST and DM (5.9%), one had acquired hypothyroidism (5.9%), one was receiving long-term treatment with glucocorticoids (prednisolone 1 mg/kg q24h; 5.9%) and one had chylothorax (5.9%).

Serum TG concentrations

All cats showed severe hypertriglyceridemia (>300 mg/dl), except for one case (hypothyroid cat) that manifested milder dyslipidemia (TG at t0: 237 mg/dl). Moreover, 8/17 cats (47%) presented TG concentrations >1000 mg/dl. Serum TG concentration showed a statistically significant decrease after 1 month of fenofibrate treatment in cats with secondary hypertriglyceridemia (P = 0.0002; Table 1). The appearance of the serum was clarified in 15/17 cats (88.2%), allowing the measurement of the analytes that could not be performed previously by lipemia. A total of 15 cats had normal TG concentration at the end of the study (88.2%). Comparing t0 with t1, cats treated with fenofibrate expressed a median decrease of 93.5% (range 12–99%) in TG concentrations.

Table 1

Triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), creatine kinase (CK), creatinine, blood urea nitrogen concentrations (BUN) and urine protein:creatinine ratio (UPC) in 17 cats treated with fenofibrate, before (t0) and after 1 month of treatment (t1)

	t0	t1	P value
TG (mg/dl)*	920 (237–1780)	51 (21–1001)	0.0002
TC (mg/dl)^†	278 (103–502)	156 (66–244)	0.0001
ALT (U/l)^‡	68 (25–198)	48 (21–105)	0.12
AST (U/l)^§	32 (5–73)	25 (2–51)	0.18
ALP (U/l)^¶	91 (40–123)	91 (36–195)	0.13
CK (U/l)^∞	110 (65–716)	110 (71–710)	0.75
Creatinine (mg/dl)^#	1.1 (0.7–1.2)	1.08 (0.6–1.2)	0.9
BUN (mg/dl)**	34 (17–44)	34 (19–42)	0.64
UPC^††	0.15 (0.05–0.39)	0.14 (0.06–0.37)	0.73

Data are presented as median (range)

Reference interval (RI) <160 mg/dl

†

RI <220 mg/dl

‡

RI <80 U/l

RI <100 U/l

∞

RI <250 U/l

RI <1.4 mg/dl

RI <45 mg/dl

††

RI <0.4

All cats reduced and normalized TG concentrations at t1, except in two cases. One, which had DM, also had a nodular lesion in the liver and a polypoid lesion in the gallbladder found by ultrasonography. The other cat, which had HAC, was unable to receive the prescribed dose due to adverse effects (see below) and therefore the dose had to be reduced. The two cats that did not respond favorably to fenofibrate treatment registered TG concentrations >1000 mg/dl at both times. No significant differences were observed when comparing TG concentrations in cats with DM (t0 median 967 mg/dl [range 504–1780]; t1 median 52 mg/dl [range 23–1001]) or without DM (t0 median 650 mg/dl [range 237–1273]; t1 median 50 mg/dl [range 21–1001]) at any time (t0 P = 0.19; t1 P = 0.7).

Serum TC concentrations

Serum TC concentrations showed a significant decrease after 1 month of fenofibrate treatment (P = 0.0001; Table 1). Of the eight cats that were hypercholesterolemic at t0 (TC >220 mg/dl, 5.6 mmol/l), six (75%) normalized their TC concentrations at the end of the study. One of 17 cats (5.9%) showed a slight increase in TC concentrations from 310 mg/dl at t0 to 341 mg/dl at t1 (the same cat that received a lower dose for adverse effects). Comparing t0 with t1, cats treated with fenofibrate showed a median decrease of 39% (range 5–78%) in TC concentrations. No significant differences were observed when comparing TC concentrations in cats with DM (t0 median 295 mg/dl [range 150–502]; t1 median 177 mg/dl [range 140–221]) or without DM (t0 median 247 mg/dl [range 135–402]; t1 median 135 mg/dl [range 66–244]) at any time (t0 P = 0.61; t1 P = 0.16).

Liver enzymes, CK, adverse effects and clinical outcomes

There were no significant changes in any of the liver enzymes analyzed or CK concentrations in any cat during the studied period (Table 1). In addition, there were no significant changes in serum creatinine, BUN or UPC in any cat during the studied period (Table 1). Furthermore, no significant weight loss or changes in BCS or alterations in food intake were observed in either diabetic or non-diabetic cats. In diabetic cats, the same insulin dose (median insulin dose 0.55 IU/kg [range 0.2–1.1]) was maintained during the study period and no significant improvement in DM control (intense glucose monitoring and serum fructosamine concentration [data not shown]) was seen.

One of 17 cats (5.9%) had severe diarrhea with a dosage of 5 mg/kg q24h. The dosage was reduced to 2.5 mg/kgq24h and the diarrhea improved but did not normalize during the study period. This cat had adrenal-dependent HAC and did not experience reductions in TG and TC concentrations at t1. The remaining 16 cats (94.1%) showed no adverse effects. No owner requested withdrawal from the trial owing to concerns over possible adverse effects of fenofibrate.

Discussion

This is the first study to date to have evaluated the use of fenofibrate in hypertriglyceridemic cats due to different secondary causes of hyperlipidemia. The results of this study suggest that fenofibrate was associated with a reduction in and normalization of TG and TC concentrations in cats with moderate and severe hypertriglyceridemia, regardless of the cause of secondary hypertriglyceridemia.

Studies of medical treatments for hyperlipidemia in cats are lacking. In a previous report, cats with dietary-induced hyperlipidemia showed a decrease in both TG and TC after treatment with atorvastatin and/or ezetimibe, as well as with chitosan.^7,26 However, the potential effect in natural (not-induced) patients was not assessed. The mechanism of action of these drugs is different from that of fenofibrate. Ezetimibe inhibits the intestinal absorption of cholesterol, atorvastatin is a HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitor, which reduces cholesterol synthesis, and chitosan is a natural compound that binds fats in the digestive tract and shows antioxidant properties, although its mechanism of action has not been completely studied.^7,26 In dogs, the use of fibrates (fenofibrate and bezafibrate) has been shown to be highly effective in reducing TG and TC, regardless of the cause of hyperlipidemia.^14,27

The clinical importance of fenofibrate in the management of hyperlipidemia in cats, dogs and humans is multiple. By normalizing TG concentrations, the biochemical analysis, which was previously prevented by lipemia, was allowed. At the same time, it could be hypothesized that by reducing TG and cholesterol concentrations, the risks of suffering from complications of hyperlipidemia are reduced.^14,28

Hyperlipidemia can be classified as either primary or secondary to other diseases or drug administration. In cats, primary hyperlipidemia is rare and is associated with several degrees of suppression of the activity of LPL and with a familiar form of a lipoprotein metabolism disorder (Burmese cats).^8–11 The most common expressions of feline hyperlipidemia are related to causes secondary to endocrinopathies, among which the most frequent is DM. It is estimated that 30–50% of diabetic cats have some degree of hyperlipidemia.^29–31 In this study, 47% (n = 8/17) of cats had DM, some of them secondary to HAC (n = 2/17) or HST (n = 1/17). All diabetic cats, with or without concurrent endocrine diseases, had experienced severe hypertriglyceridemia since the diagnosis of DM. None of these cats had reduced TG and TC concentrations with insulin therapy and dietary management, despite having ‘good diabetic control’ at enrollment (no clinical signs of DM, and fructosamine concentrations and glycemia within the therapeutic goal [5.5–16.6 mmol/l]). After treatment with fenofibrate, 7/8 (87.5%) diabetic cats reduced and normalized their TG concentrations. It is important to highlight that secondary hyperlipidemia in these cases had not been resolved with insulin and dietary management alone (median time on insulin and dietary treatment before enrollment: 7 weeks [range 6–24]), reinforcing the necessity of implementing lipid-lowering therapies, such as fenofibrate, in diabetic cats with hyperlipidemia that is not controlled with insulin therapy and dietary management. In addition, it is necessary to clarify that this study did not evaluate the use of fenofibrate in cats with primary hyperlipidemia or in cats in which hyperlipidemia does not resolve with treatment of the underlying disease (with the exception of DM). Therefore, the findings of this study may not necessarily be extrapolated to these groups.

The second most frequent cause of hyperlipidemia was obesity, seen in 29.4% of cases.^32,33 In obese cats there is a decrease in LPL activity and an elevated concentration of LDL particles.³⁴ HAC and hypothyroidism are also described as secondary causes of feline hyperlipidemia, although they are less prevalent than DM and obesity. In many cats with HAC, DM is a concomitant disease; therefore, the dyslipidemia could result from a combination of both conditions. However, hyperlipidemia may be an independent abnormality of HAC, as observed in this study in a cat with HAC and without DM, which had TGs >1000 mg/dl. In this trial, we added HST as a secondary cause of hyperlipidemia, although it should be noted that this cat had concurrent DM. We did not register cases of hepatic lipidosis (a common cause of hyperlipidemia in cats), protein-losing nephropathy or cholestasis. This could be due to the fact that these types of pathologies may not be referred to the endocrinology unit. Finally, this study reported a case of hypertriglyceridemia associated with chylothorax. There have been no reports of such a correlation in feline medicine. In children, chylothorax should raise the suspicion of LPL deficiency.³⁵

The dose of fenofibrate used in this study was arbitrary, based on half the dose compared with the dog (10 mg/kg q24h),¹⁴ as there have been no previous studies on the use of fibrates in cats. The non-micronized presentation (standard tablets) was chosen because micronized fenofibrate is only available in capsules in Argentina, and cannot be fractionated according to body weight. The adverse effects of fenofibrate are observed in approximately 2–15% of humans and 3–10% in dogs.^14,16,36 The most common side effects in humans include liver and muscle damage and digestive disorders.³⁷ Digestive disorders (vomiting, diarrhea, risk of gallstones, nausea, constipation), increases in creatinine and cystatin C, dermatological reactions, abdominal pain, headache, back pain, rhinitis, respiratory disorder and decreased libido have also been described.^36,37 In dogs, diarrhea, a quiet demeanor, firm stools and an increase in ALT activity have been reported.^14,16 Fibrates are contraindicated in liver dysfunction, kidney failure and gallstones.²⁸ In this study, we did not observe significant adverse effects after 1 month of fenofibrate treatment, except in one cat in which diarrhea was reported. We found no clinical muscle disorders or detectable biochemical abnormalities on the hepatogram for serum creatinine, UPC or CK values. One of the cats had a mild polypoid lesion in the gallbladder, and although the use of fenofibrate in cholelithiasis is contraindicated in humans, the inclusion of this cat in the trial was considered as it had persistent severe hypertriglyceridemia. The pharmacokinetics, and safety and toxicity profiles of fenofibrate in cats are currently unknown and require future studies in order to establish the optimum dosing protocol for fenofibrate as a treatment for secondary hypertriglyceridemia in cats. It is not appropriate to draw conclusions about the safety of fenofibrate in this study, considering the small cohort of cats followed over a short time period. However, according to the results of the present study, fenofibrate (5 mg/kg q24h) seems to be a relatively safe drug for cats with secondary hypertriglyceridemia, at least in the short term.

This study had several limitations: the inability to assess cholesterol fractions (HDL and LDL) because of hypertriglyceridemia, the short follow-up to assess adverse effects and the time frame of sampling. The inclusion of a control group would have helped support that the observed changes in TG and TC concentrations were directly due to fenofibrate treatment, especially in non-diabetic cats. The improvement in lipid profile could be due to fenofibrate treatment, but an effect of time cannot be ruled out (eg, effects of dietary therapy with possible weight loss). In the same way, it cannot be ruled out that dyslipidemia can be controlled with the establishment of treatment for the underlying disease. In this study, only diabetic cats (8/17 cases; five diabetic cases without concurrent endocrine disease and three diabetic cases with concurrent endocrine disease) received their insulin and dietary treatment. In these cases, all cats had persistence of severe hypertriglyceridemia at enrollment, despite insulin therapy and dietary management. Therefore, it is likely that the changes observed in the lipidogram of diabetic cats were associated with the use of fenofibrate. Also, another important limitation of the study was the impossibility of suspending insulin therapy in diabetic cats and thus evaluating the effect of fenofibrate as monotherapy in these cases. The study might not have been powered to detect differences between liver enzymes or CK and report adverse effects properly as this trial used a convenience sample formed from cats with hypertriglyceridemia at VSC (Maimonides University) over 2 years and no sample size calculation was performed. Further studies are needed with greater numbers of cats. One more limitation was that samples were not diluted to obtain the exact concentration of TG >1000 ng/dl in three samples (two at t0 and one at t1). Finally, another limitation of the study was that we were unable to offer the same diet to all cats.

Conclusions

This is the first study to date that has evaluated the use of fenofibrate in cats with secondary hypertriglyceridemia. DM and obesity are the most common endocrine causes of secondary hyperlipidemia in cats, although it can also be found in cats with HAC, HST or hypothyroidism. This study suggests that fenofibrate treatment was associated with reduction and normalization of TG concentrations in cats with moderate and severe hypertriglyceridemia, regardless of the cause of secondary hypertriglyceridemia. Likewise, fenofibrate was associated with a reduction in and normalization of TC concentrations. Further controlled studies are necessary to support the hypothesis that the observed changes on the lipid profile of cats with secondary hypertriglyceridemia were directly due to fenofibrate treatment. In addition, it remains for further studies to evaluate the long-term safety and efficacy of fenofibrate with more cats and other types of hyperlipidemia.

Supplemental Material

Owner questionnaire: fenofibrate protocol in cats.

Footnotes

Acknowledgements

We are grateful to Dr Mariana Gambarotta (University of Buenos Aires, Argentina) for statistical advice.

Accepted: 5 May 2022

Supplementary material

The following file is available online:

Owner questionnaire: fenofibrate protocol in cats.

Conflict of interest

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Ethical approval

The work described in this manuscript involved the use of non-experimental (owned or unowned) animals and procedures that differed from established internationally recognized high standards (‘best practice’) of veterinary clinical care for the individual patient. The study therefore had prior ethical approval from an established (or ad hoc) committee as stated in the manuscript.

Informed consent

Informed consent (verbal or written) was obtained from the owner or legal custodian of all animal(s) described in this work (experimental or non-experimental animals, including cadavers) for all procedure(s) undertaken (prospective or retrospective studies). No animals or people are identifiable within this publication, and therefore additional informed consent for publication was not required.

ORCID iD

Diego D Miceli

Juan M Guevara

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Therapy for feline secondary hypertriglyceridemia with fenofibrate

Abstract

Objectives

Methods

Results

Conclusions and relevance

Keywords

Introduction

Materials and methods

Statistical analysis

Results

Causes of hypertriglyceridemia

Serum TG concentrations

Serum TC concentrations

Liver enzymes, CK, adverse effects and clinical outcomes

Discussion

Conclusions

Supplemental Material

Supplemental Material

Footnotes

Acknowledgements

Supplementary material

Conflict of interest

Funding

Ethical approval

Informed consent

ORCID iD

References

Supplementary Material