Hypertriglyceridemia and transient corneal lipidosis in a cat following intravenous lipid therapy for permethrin toxicosis.

An 8-year-old male neutered domestic shorthair cat developed corneal lipidosis and marked hypertriglyceridemia approximately 36 hours after intravenous lipid therapy (IVLT) for the treatment of permethrin toxicosis. The cat's ocular changes resolved approximately 72 hours after IVLT without treatment. This study reports a rare complication of IVLT.

Hypertriglycéridémie et lipidose cornéenne transitoire chez un chat après une lipidothérapie intraveineuse pour une toxicose à la perméthrine. Un chat commun mâle stérilisé âgé de 8 ans a développé une lipidose cornéenne et une hypertriglycéridémie marquée environ 36 heures après une lipidothérapie intraveineuse (LTI) pour le traitement de la toxicose à la perméthrine. Les changements oculaires du chat se sont résorbés sans traitement environ 72 heures près la LTI. Cette étude signale une complication rare de la LTI.(Traduit par Isabelle Vallières).

Glomerular Lesions in Proteinuric Miniature Schnauzer Dogs.

Miniature Schnauzer dogs are predisposed to idiopathic hypertriglyerceridemia, which increases risk for diseases such as pancreatitis and gallbladder mucocele. Recently, elevated triglyceride concentrations have been associated with proteinuria in this breed, although it is difficult to determine which abnormality is primary. Retrospective review of renal tissue from 27 proteinuric Miniature Schnauzers revealed that 20 dogs had ultrastructural evidence of osmophilic globules consistent with lipid in glomerular tufts. Seven of these dogs had lipid thromboemboli in glomerular capillary loops that distorted their shape and compressed circulating erythrocytes. Triglyceride concentrations were reported in 6 of these 7 dogs, and all were hypertriglyceridemic. In addition, glomerular lipidosis (defined as accumulation of foam cells within peripheral capillary loops) was identified in a single dog. The remaining 12 dogs had smaller amounts of lipid that could only be identified ultrastructurally. Neither signalment data nor clinicopathologic parameters (serum albumin, serum creatinine, urine protein-to-creatinine ratio, and blood pressure) differed among the various types of lipid lesions. During the time course of this study, all dogs diagnosed with glomerular lipid thromboemboli were Miniature Schnauzers, underscoring the importance of recognizing these clear spaces within capillary loops as lipid.

Mucopolysaccharidosis type VI in a juvenile miniature schnauzer dog with concurrent hypertriglyceridemia, necrotizing pancreatitis, and diabetic ketoacidosis.

A 7-month-old, neutered male miniature schnauzer dog with a history of cryptorchidism and umbilical hernia was referred for diabetic ketoacidosis. Clinical evaluation revealed stunted growth, skeletal abnormalities, hypertriglyceridemia, diabetic ketoacidosis, and acute necrotizing pancreatitis. Further testing was diagnostic for mucopolysaccharidosis type VI causing the stunted growth and skeletal deformities, but no connection between mucopolysaccharidosis type VI, hypertriglyceridemia, and pancreatic diseases was found.

Mucopolysaccharidose de type VI chez un jeune chien Schnauzer miniature atteint d'hypertriglycéridémie, de pancréatite nécrosante et d'acidocétose diabétique concomitantes. Un chien Schnauzer miniature castré âgé de 7 mois avec une anamnèse de cryptorchidie et d'hernie ombilicale a été référé pour une acidocétose diabétique. L'évaluation clinique a révélé une croissance arrêtée, des anomalies squelettiques, l'hypertriglycéridemie, l'acidocétose diabétique et une pancréatite nécrosante aiguë. Des tests supplémentaires ont permis de diagnostiquer une mucopolysaccharidose de type VI causant une croissance arrêtée et des difformités squelettiques, mais aucun lien avec la mucopolysaccharidose de type VI, l'hypertriglycéridémie et les maladies pancréatiques n'a été trouvé.(Traduit par Isabelle Vallières).

Lipoprotein profiles in Miniature Schnauzer dogs with idiopathic hypertriglyceridemia and hypercortisolism.

Miniature Schnauzer dogs (MSs) are predisposed to both idiopathic hypertriglyceridemia (iHTG) and hypercortisolism (HCort). To our knowledge, the lipoprotein profiles of MSs with iHTG have not been compared to those with HCort. We analyzed cholesterol and triglyceride concentrations and lipoprotein fractions in 4 groups of MSs: normotriglyceridemia (NTG) without concurrent disease (Healthy-NTG), HCort and NTG (HCort-NTG), HCort and HTG (HCort-HTG), and iHTG. Lipoprotein fractions were assessed by lipoprotein electrophoresis and compared between groups. Fifty-one plasma samples were analyzed. Twenty-five dogs had NTG (16 Healthy-NTG, 9 HCort-NTG) and 26 dogs had HTG (7 iHTG, 19 HCort-HTG). Dogs with iHTG or HCort-HTG had significantly higher cholesterol concentrations than Healthy-NTG dogs. Dogs with HCort-HTG had higher cholesterol than HCort-NTG dogs. There was a significantly higher low-density lipoprotein (LDL) percentage in iHTG and HCort-HTG dogs than HCort-NTG dogs. HCort-HTG dogs also had lower high-density lipoproteins (HDL) than HCort-NTG dogs. It was not possible to readily distinguish MSs with iHTG from MSs with HCort-HTG or Healthy-NTG using lipoprotein electrophoresis fractions. The diagnosis of iHTG remains a diagnosis by exclusion.

Clustering analysis of lipoprotein profiles to identify subtypes of hypertriglyceridemia in Miniature Schnauzers.

BACKGROUND: Hypertriglyceridemia (HTG) is prevalent in Miniature Schnauzers, predisposing them to life-threatening diseases. Varied responses to management strategies suggest the possibility of multiple subtypes. HYPOTHESIS/OBJECTIVE: To identify and characterize HTG subtypes in Miniature Schnauzers through cluster analysis of lipoprotein profiles. We hypothesize that multiple phenotypes of primary HTG exist in this breed. ANIMALS: Twenty Miniature Schnauzers with normal serum triglyceride concentration (NTG), 25 with primary HTG, and 5 with secondary HTG. METHODS: Cross-sectional study using archived samples. Lipoprotein profiles, generated using continuous lipoprotein density profiling, were clustered with hierarchical cluster analysis. Clinical data (age, sex, body condition score, and dietary fat content) was compared between clusters. RESULTS: Six clusters were identified. Dogs with primary HTG were dispersed among 4 clusters. One cluster showed the highest intensities for triglyceride-rich lipoprotein (TRL) and low-density lipoprotein (LDL) fractions and also included 4 dogs with secondary HTG. Two clusters had moderately high TRL fraction intensities and low-to-intermediate LDL intensities. The fourth cluster had high LDL but variable TRL fraction intensities with equal numbers of NTG and mild HTG dogs. The final 2 clusters comprised only NTG dogs with low TRL intensities and low-to-intermediate LDL intensities. The clusters did not appear to be driven by differences in the clinical data. CONCLUSIONS AND CLINICAL IMPORTANCE: The results of this study support a spectrum of lipoprotein phenotypes within Miniature Schnauzers that cannot be predicted by triglyceride concentration alone. Lipoprotein profiling might be useful to determine if subtypes have different origins, clinical consequences, and response to treatment.

Sequence Analysis of Six Candidate Genes in Miniature Schnauzers with Primary Hypertriglyceridemia.

Miniature Schnauzers are predisposed to primary hypertriglyceridemia (HTG). In this study, we performed whole genome sequencing (WGS) of eight Miniature Schnauzers with primary HTG and screened for risk variants in six HTG candidate genes: LPL, APOC2, APOA5, GPIHBP1, LMF1, and APOE. Variants were filtered to identify those present in ≥2 Miniature Schnauzers with primary HTG and uncommon (<10% allele frequency) in a WGS variant database including 613 dogs from 61 other breeds. Three variants passed filtering: an APOE TATA box deletion, an LMF1 intronic SNP, and a GPIHBP1 missense variant. The APOE and GPIHBP1 variants were genotyped in a cohort of 108 Miniature Schnauzers, including 68 with primary HTG and 40 controls. A multivariable regression model, including age and sex, did not identify an effect of APOE (estimate = 0.18, std. error = 0.14; p = 0.20) or GPIHBP1 genotypes (estimate = -0.26, std. error = 0.42; p = 0.54) on triglyceride concentration. In conclusion, we did not identify a monogenic cause for primary HTG in Miniature Schnauzers in the six genes evaluated. However, if HTG in Miniature Schnauzers is a complex disease resulting from the cumulative effects of multiple variants and environment, the identified variants cannot be ruled out as contributing factors.

Successful multimodal treatment of extreme hypertriglyceridemia in a juvenile diabetic dog.

OBJECTIVE: To describe the therapeutic protocol used to normalize severe hypertriglyceridemia in a dog. CASE SUMMARY: A 7-month-old, 1.2-kg female Pomeranian presented with acute polyuria, polydipsia, and ocular discoloration. Diagnoses included diabetic ketosis, severe hypertriglyceridemia (>225 mmol/L [>20,000 mg/dl]), lipemia retinalis, and bilateral uveitis. The triglyceride concentration was near normal within 2 days of initiating treatment with fenofibrate, regular insulin constant rate infusion (CRI), manual therapeutic plasma exchange (TPE), and a low-fat diet. All clinical signs resolved. The dog has had no relapse of hypertriglyceridemia at the time of writing the manuscript, 6 months later, with continued treatment of diabetes mellitus. NEW OR UNIQUE INFORMATION PROVIDED: This is the first case report documenting the combination of fenofibrate, insulin CRI, and manual TPE for treatment of severe hyperlipidemia in a dog. Detailed protocols for manual TPE and a novel insulin CRI are provided. A discussion of multiple spurious biochemical and hematologic errors associated with the severe hypertriglyceridemia is also provided.

Hypertriglyceridemia in equines with refractory hyperinsulinemia treated with SGLT2 inhibitors.

Background: Sodium-Glucose CoTransporter-2 (SGLT2) inhibitors, the -flozin group of drugs, which block glucose reuptake in the renal proximal tubule, are being increasingly used off-label to treat horses with refractory hyperinsulinemia. After 2 years of use by animals in our group, a horse on canagliflozin was incidentally noted to be hyperlipemic. Case Description: We have been following a cohort of equines (n = 20) treated with SGLT2 inhibitors due to refractory hyperinsulinemia. The animals are owned by members of the Equine Cushing's and Insulin Resistance Group and treated by their attending veterinarians. The index case was a 23 years old gelding with a 2 years history of recurring laminitis that began canagliflozin therapy to control hyperinsulinemia which was no longer responsive to metformin. Between 6 and 10 weeks post start of therapy, significant weight loss was noticed. Two days later he was hospitalized with colic symptoms and hyperlipemia but was bright, alert, and eating well throughout. Canagliflozin was discontinued and triglycerides returned to normal reference values within 10 days. A subsequent study of 19 other horses on SGLT2 inhibitors revealed varying degrees of hypertriglyceridemia, all asymptomatic. Conclusion: While this class of drugs holds great promise for cases of refractory hyperinsulinemia and laminitis that do not respond to diet or metformin therapy, hypertriglyceridemia is a potential side effect. In our experience, animals remained asymptomatic and eating well. Further study of hypertriglyceridemia in horses on SGLT2 inhibitors and the possible mitigating effect of diet is indicated. To our knowledge, this is the first report of hypertriglyceridemia with canagliflozin treatment in equines.

Associations among serum insulin, calprotectin, and C-reactive protein concentrations in Miniature Schnauzers with idiopathic hyperlipidemia before and after feeding an ultra-low-fat diet.

BACKGROUND: Miniature Schnauzers (MS) commonly have idiopathic hypertriglyceridemia (HTGL), which is associated with insulin resistance (IR) and a subclinical inflammatory phenotype. OBJECTIVES: Determine the association between indicators of IR and inflammatory biomarkers in MS with and without HTGL and identify how indicators of IR are affected by dietary intervention in MS with HTGL. ANIMALS: Seventy MS with HTGL and 79 MS without HTGL. In addition, 15 MS with HTGL were placed on a low-fat diet. METHODS: Serum concentrations of triglycerides, cholesterol, calprotectin, insulin, and glucose were compared between groups. RESULTS: Serum glucose and calprotectin concentrations (shown to be higher in MS with HTGL than in MS without HTGL) were inversely correlated (ρ = -.28; P < .001). After dietary intervention, median serum insulin concentrations were 8.1 mU/L compared to 20.8 mU/L before dietary intervention (P = .06). Dogs with complete resolution of HTGL after dietary intervention (5 dogs) had significantly lower serum insulin concentrations compared to baseline (P = .03). CONCLUSION AND CLINICAL IMPORTANCE: The subclinical inflammatory phenotype in MS with HTGL appears to be associated with IR. Resolution of HTGL by dietary intervention is associated with a decrease in serum insulin concentrations. The implication of the increase in serum calprotectin concentrations after resolution of HTGL warrants further study.

Therapy for feline secondary hypertriglyceridemia with fenofibrate.

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.

Association of hypertriglyceridemia with insulin resistance in healthy Miniature Schnauzers.

OBJECTIVE: To determine whether hypertriglyceridemia in Miniature Schnauzers is associated with insulin resistance. DESIGN: Case-control study. ANIMALS: 28 Miniature Schnauzers with hypertriglyceridemia and 31 Miniature Schnauzers for which serum triglyceride concentrations were within the reference range (control dogs). PROCEDURES: All dogs had no history of chronic disease, were free of clinical signs for at least 3 months prior to blood collection, and were not receiving any medications known to affect lipid metabolism or serum insulin concentration. Food was withheld from each dog for ≥ 12 hours; a 5- to 10-mL blood sample was collected and allowed to clot to obtain serum. Serum insulin and glucose concentrations were measured, and the homeostasis model assessment (HOMA) score was calculated (ie, [basal serum insulin concentration {mU/L} × basal serum glucose concentration {mmol/L}]/22.5). RESULTS: Median serum insulin concentration was significantly higher in hypertriglyceridemic Miniature Schnauzers (21.3 mU/L) than it was in control dogs (12.5 mU/L). The percentage of dogs with high serum insulin concentrations was significantly greater in the hypertriglyceridemic group (28.6%) than it was in the control group (6.5%; odds ratio, 5.8; 95% confidence interval, 1.1 to 30.2). Median HOMA score for hypertriglyceridemic Miniature Schnauzers (4.9) was significantly higher than that for control dogs (2.8). CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that hypertriglyceridemia in Miniature Schnauzers is often associated with insulin resistance. Further studies are needed to determine the prevalence and clinical importance of insulin resistance in hypertriglyceridemic Miniature Schnauzers.

Fenofibrate treatment for severe hypertriglyceridemia in dogs.

Lipid disorders are relatively common in dogs. Hyperlipidemia can be primary or secondary to other diseases. In humans, fenofibrate is used to control hypertriglyceridemia. In dogs, there are no studies evaluating fenofibrate in hypertriglyceridemia. The aim of the study was to evaluate the safety and efficacy of fenofibrate to control severe hypertriglyceridemia in dogs. A total of 124 dogs (n = 124) with severe hypertriglyceridemia (>300 mg/dL, 3.39 mmol/L) were randomly distributed in the fenofibrate group (n = 64) and the diet group (n = 60). Dogs of the fenofibrate group were treated with fenofibrate (10 mg/Kg) once daily. Dogs of the diet group were treated with low-fat diet (10%). Serum triglycerides (TGs), total cholesterol (TC), liver enzymes, and creatine kinase concentrations were evaluated, before and after 1 mo of medical or dietary treatment. Triglyceride concentrations were reduced with fenofibrate (P < 0.001), and 85.93% of the dogs normalized their levels. Triglyceride concentrations also decreased with low-fat diet (P < 0.001), but only 26.6% of the dogs normalized their levels. Triglyceride concentrations were reduced with fenofibrate (P < 0.01) and with low-fat diet (P < 0.01). Of the cases with hypercholesterolemia, 53.7% and 50% of the dogs normalized their TC concentrations, with fenofibrate and diet, respectively. No significant adverse effects were observed (3% showed diarrhea). Fenofibrate was safe and effective in reducing and normalizing TG concentrations in dogs with severe hypertriglyceridemia, regardless of the cause of hyperlipidemia. The low-fat diet was effective in reducing, but not normalizing, TG concentrations. Fenofibrate and low-fat diet were effective in reducing TC concentrations. This is the first study evaluating fibrates in dogs with severe hypertriglyceridemia and comparing results with a low-fat diet.

Association between serum triglyceride and canine pancreatic lipase immunoreactivity concentrations in miniature schnauzers.

The objective of this study was to investigate possible associations between serum triglyceride and canine pancreatic lipase immunoreactivity (cPLI) concentrations in miniature schnauzers. One hundred and ninety-five miniature schnauzers were enrolled and divided into two groups based on whether they had normal (group 1) or increased (group 2) serum triglyceride concentrations. Serum cPLI concentrations were measured and compared between groups. A significant positive correlation was seen between serum triglyceride and cPLI concentrations (Spearman r=0.321; P<0.0001). Miniature schnauzers with hypertriglyceridemia had a significantly higher median serum cPLI concentration (99.5 microg/L) than miniature schnauzers with normal serum triglyceride concentrations (median cPLI concentration 39.3 microg/L; P=0.0001). A cutoff value of 862 mg/dL was selected for serum triglyceride concentrations based on receiver operator characteristic analysis. Miniature schnauzers with severe hypertriglyceridemia (> or =862 mg/dL) were 4.5 times more likely to have a serum cPLI concentration consistent with pancreatitis (> or =200 microg/L) than miniature schnauzers with a normal serum triglyceride concentration. The present study supports an association between hypertriglyceridemia (especially when severe [> or =862 mg/dL]) and high cPLI concentrations in miniature schnauzers.

Effect of a low-fat diet on serum triglyceride and cholesterol concentrations and lipoprotein profiles in Miniature Schnauzers with hypertriglyceridemia.

BACKGROUND: Hypertriglyceridemia is common in Miniature Schnauzer (MS). Dietary management of hypertriglyceridemia is important, but no studies are available. HYPOTHESIS/OBJECTIVES: To evaluate the effect of a commercially available low-fat diet on serum triglyceride and cholesterol concentrations and lipoprotein profiles in MS with hypertriglyceridemia. ANIMALS: Sixteen MS with hypertriglyceridemia and 28 MS without hypertriglyceridemia. METHODS: Prospective clinical trial. Four blood samples (1-2 months before and 1 day before diet change and 2 and 3 months after the dogs were fed the low-fat diet) were collected from the MS with hypertriglyceridemia. RESULTS: Serum triglyceride concentrations for the 2 samples after the diet change (median of sample 3 = 177 mg/dL; range, 48-498; median of sample 4 = 168 mg/dL; range, 77-745) were significantly lower than the 2 samples before the diet change (median of sample 1 = 480 mg/dL; range, 181-1320; median of sample 2 = 493 mg/dL; range, 114-1395; P < .001). Serum cholesterol concentrations for the 2 samples after the diet change (mean for sample 3 = 257 mg/dL, SD = 82.2; mean for sample 4 = 178 mg/dL, SD = 87.4) were also significantly lower than the 2 samples before the diet change (mean for sample 1 = 381 mg/dL, SD = 146.1; mean for sample 2 = 380 mg/dL, SD = 134.7; P < .001). Before the diet change, 15/16 (94%) of hyperlipidemic MS were classified as hyperlipidemic based on their lipoprotein profiles alone. After the diet change, significantly fewer MS (7/16; 44%; odds ratio = 19.3; 95% CI = 2.0-184.0; P = .006) were classified as hyperlipidemic based on lipoprotein profile analysis. CONCLUSIONS AND CLINICAL IMPORTANCE: The study diet was effective in reducing serum triglyceride and cholesterol concentrations and correcting lipoprotein profiles in MS with hypertriglyceridemia.

Sequence analysis of the coding regions of the apolipoprotein C2 (APOC2) gene in Miniature Schnauzers with idiopathic hypertriglyceridemia.

It has been hypothesized that idiopathic hypertriglyceridemia in Miniature Schnauzers is hereditary, but the gene responsible has yet to be identified. The objective of this study was to determine if there were coding variants in the apolipoprotein C2 (APOC2) gene in Miniature Schnauzers with idiopathic hypertriglyceridemia. Blood samples from 12 Miniature Schnauzers with idiopathic hypertriglyceridemia were analyzed. Genomic DNA was extracted from whole blood, and the three coding exons of APOC2 were amplified by PCR. The PCR amplicons were sequenced and analyzed for variants relative to the canine reference genome (CanFam3.1 assembly). A second objective was to determine the extent of variation in coding exons of APOC2 in a large and diverse canine population using the Dog Biomedical Variant Database Consortium variant catalog, comprised of whole genome sequencing variant calls from 582 dogs of 126 breeds and eight wolves. There were no variants detected in the coding exons of APOC2 for any of the 12 Miniature Schnauzers with idiopathic hypertriglyceridemia. Variants in the coding exons of APOC2 were also rare in the Dog Biomedical Variant Database Consortium variant catalog; a single synonymous variant was identified in a heterozygous state in a Tibetan Mastiff. Thus, we concluded that coding variants in APOC2 are unlikely to be a major cause of idiopathic hypertriglyceridemia in North American Miniature Schnauzers and furthermore, that such coding variants are rare in the canine population.

Parenteral nutrition in neonatal foals: clinical description, complications and outcome in 53 foals (1995-2005).

This retrospective study describes the use of and complications associated with parenteral nutrition (PN) administration to 53 equine neonates at the University of California Veterinary Medical Teaching Hospital. Medical records were examined and information obtained on signalment, physical examination, clinical diagnosis, outcome, total hospitalization time, insulin administration, microbiology culture results, other complications (i.e. thrombophlebitis) and necropsy findings. Complete blood count and serum biochemistry analytes, venous blood gas, serum electrolyte and glucose concentrations, and blood lactate concentration results were compared before and during PN administration in all foals. Seventeen foals (32%) developed hypertriglyceridemia (>200mg/dL). Triglyceride concentrations >200mg/dL were significantly (P=0.049) associated with non-survival. Forty-seven foals (89%) developed hyperglycemia (blood glucose >120mg/dL) and eight (15%) developed catheter-related complications (thrombosis or local sepsis). Packed cell volume, total protein, creatinine, blood urea nitrogen, and sorbitol dehydrogenase concentrations decreased while foals were on PN, while serum chloride concentration increased. This study highlighted that hypertriglyceridemia during the acute phase of neonatal illness may be detrimental to outcome, and that the safety of lipid-containing solutions in foals warrants further study.

Triglyceride response following an oral fat tolerance test in Burmese cats, other pedigree cats and domestic crossbred cats.

Primary lipid disorders causing fasting triglyceridaemia have been documented infrequently in Burmese cats. Due to the known increased risk of diabetes mellitus and sporadic reports of lipid aqueous in this breed, the aim of this study was to determine whether healthy Burmese cats displayed a more pronounced pre- or post-prandial triglyceridaemia compared to other cats. Serum triglyceride (TG) concentrations were determined at baseline and variably at 2, 4 and 6h after ingestion of a high-fat meal (ie, an oral fat tolerance test) in a representative sample of Burmese and non-Burmese cats. The median 4 and 6h serum TG concentrations were significantly higher in Burmese cats (4h - 2.8mmol/l; 6h - 8.2mmol/l) than in other pedigree and domestic crossbred cats (4h - 1.5mmol/l; 6h - 1.0mmol/l). The non-Burmese group had post-prandial TG concentrations ranging from 0.6 to 3.9mmol/l. Seven Burmese cats had post-prandial TG concentrations between 6.6 and 19.0mmol/l, five had concentrations between 4.2 and 4.7mmol/l, while the remaining 15 had post-prandial concentrations between 0.5 and 2.8mmol/l. None of these Burmese cats had fasting triglyceridaemia. Most Burmese cats with a 4 h TG > 6.0 mmol/l had elevated fasting very low density lipoprotein (VLDL) concentrations. This study demonstrates that a proportion of Burmese cats in Australia have delayed TG clearance compared to other cats. The potential repercussions of this observation with reference to lipid aqueous, pancreatitis and diabetes mellitus in Burmese cats are discussed.

Characterization of hypertriglyceridemia and response to treatment with insulin in horses, ponies, and donkeys: 44 cases (1995-2005).

OBJECTIVE: To characterize signalment, clinical signs of disease, and clinical response to insulin in equids with hypertriglyceridemia. DESIGN: Retrospective case series. ANIMALS: 20 horses, 17 ponies, and 7 donkeys with hypertriglyceridemia. PROCEDURES: For analysis of medical record data, horses, donkeys, and ponies with multiple serum or plasma triglycerides measurements were separated into groups. Hypertriglyceridemic equids that were (HT-I; n = 14) or were not (HT-N; 10) treated with insulin consisted of equids with an initial triglycerides concentration > 44 mg/dL but < 500 mg/dL. Equids with an initial triglycerides concentration > 500 mg/dL, all of which were treated with insulin, constituted the lipemic group (LIP-I; 20). Each group included a full range of ages. Pretreatment and posttreatment values from serum or plasma biochemical analyses were compared among groups. RESULTS: No age predilection for hypertriglyceridemia was apparent. Of the 29 female equids, only 7 (24%) were lactating or pregnant. Multiple illnesses were diagnosed in hypertriglyceridemic equids, including colitis (14/44; 32%) and colic (9/44; 20%). Many breeds were affected, including 16 (36%) American Miniature Horses and 9 (20%) Arabians or Arabian crossbreds. The mean posttreatment triglycerides concentration was not significantly different from the initial value in HT-N equids (175 vs 125 mg/dL) but was significantly lower than the pretreatment triglycerides concentration in HT-I (252 vs 55 mg/dL) and LIP-I (872 vs 87 mg/dL) equids. CONCLUSIONS AND CLINICAL RELEVANCE: Equids of all ages and sexes with various diseases had hypertriglyceridemia. Insulin treatment decreased the triglycerides concentrations in affected equids.

Effects of marked hypertriglyceridemia and lipid clearance techniques on canine biochemistry testing.

Triglyceride concentrations in dogs with hyperlipidemic disorders can exceed concentrations used by assay manufacturers for interference testing. High-speed centrifugation or the polar solvent LipoClear reduce triglyceride concentrations, but efficacy requires evaluation in veterinary species. We determined the effect of marked hypertriglyceridemia on canine biochemistry testing; assessed the ability of high-speed centrifugation or LipoClear to correct lipemic interferences; and determined if LipoClear introduces inaccuracy into biochemistry assays. Fifteen pooled canine serum samples were aliquoted and spiked with equal volumes of water or Intralipid [triglyceride concentration 33.9 mmol/L (3,000 mg/dL)]. Intralipid aliquots underwent lipid removal by high-speed centrifugation or LipoClear treatment, and a water-spiked aliquot underwent LipoClear treatment. Biochemistry panels were performed using a Vitros 4600 chemistry analyzer. Results were compared by paired t-test or Wilcoxon test. Total observed errors were considered clinically acceptable if below veterinary allowable total error (TEa) guidelines. Statistically significant (p ≤ 0.05) interferences were introduced by Intralipid for 15 of 15 analytes. Median observed error exceeded TEa for potassium and enzymatic carbon dioxide, neither of which were identified by the manufacturer as susceptible to lipemic interference. After centrifugation, median observed error exceeded TEa for potassium and chloride. LipoClear treatment resulted in median errors that exceeded TEa for total protein, chloride, and phosphorus. Given that severe lipemia can occur in dogs with primary or secondary hyperlipidemia, veterinary laboratories should perform their own interference testing at triglyceride concentrations relevant to their patient population and provide this information to clinicians to ensure optimal case management.

Evaluation of Hypertriglyceridemia as a Mediator Between Endocrine Diseases and Pancreatitis in Dogs.

The role of hypertriglyceridemia (HTG) secondary to endocrine diseases in the occurrence of pancreatitis in dogs has not been fully investigated. The objective of the present study was to evaluate HTG as a mediator between endocrine diseases and pancreatitis in dogs. The study design was a retrospective case-control study. Medical records of dogs newly diagnosed with acutely presenting pancreatitis between 2012 and 2014 were reviewed for the presence or absence of hyperadrenocorticism (HAC), diabetes mellitus (DM), and hypothyroidism. A matched case-control analysis was performed, and the association between endocrine diseases and pancreatitis was evaluated using multiple logistic regression analysis. In dogs with pancreatitis, the odds of HAC (P < .001) and DM (P < .001) were 4.5 and 12.4 times that of dogs without pancreatitis, respectively. HTG significantly mediated the association between DM and pancreatitis but not between HAC and pancreatitis. Additional studies will be necessary to confirm these findings and to further elucidate the associations between endocrine diseases and pancreatitis.