A veterinary-calibrated point-of-care glucometer accurately measures blood glucose concentration in dogs and cats.

OBJECTIVE: To determine the clinical and analytical accuracy of a new veterinary-calibrated portable blood glucose monitor (PBGM) compared to a reference laboratory analyzer. ANIMALS: Client-owned dogs (n = 77) and cats (n = 64). METHODS: Peripheral and paired capillary whole-blood glucose concentrations measured via PBGM were compared to plasma glucose concentrations measured via a Cobas c501 reference analyzer (Roche). Analytical accuracy was evaluated with the Spearman rank correlation coefficient, Bland-Altman difference plot analysis, and Deming regression. Clinical accuracy was evaluated with Parkes error grid analysis. Paired peripheral and capillary blood samples were compared with the Wilcoxon matched-pairs signed-rank test. RESULTS: There was a high correlation between PBGM and reference analyzer readings in dogs and cats. Human quality assurance standards (International Organization for Standardization 15197:2013 guidelines) for analytical accuracy were met for 95% of feline peripheral blood samples and 89% of canine samples. Similar veterinary standards (American Society of Veterinary Clinical Pathology guidelines) were met for 89% of canine and 92% of feline peripheral blood glucose measurements. Error grid analysis showed that all peripheral canine and 97% of feline measurements were clinically accurate (zone A). Any altered clinical decision for the remaining feline measurements was expected to minimally impact outcome (zone B). No significant difference was found between peripheral and capillary blood glucose measurements in either species. CLINICAL RELEVANCE: The PBGM produced clinically accurate results and is suitable for use in veterinary and home settings to measure blood glucose.

Serum metabolome analysis in hyperthyroid cats before and after radioactive iodine therapy.

Hyperthyroidism is the most common feline endocrinopathy. In hyperthyroid humans, untargeted metabolomic analysis identified persistent metabolic derangements despite achieving a euthyroid state. Therefore, we sought to define the metabolome of hyperthyroid cats and identify ongoing metabolic changes after treatment. We prospectively compared privately-owned hyperthyroid cats (n = 7) admitted for radioactive iodine (I-131) treatment and euthyroid privately-owned control (CON) cats (n = 12). Serum samples were collected before (T0), 1-month (T1), and three months after (T3) I-131 therapy for untargeted metabolomic analysis by MS/MS. Hyperthyroid cats (T0) had a distinct metabolic signature with 277 significantly different metabolites than controls (70 increased, 207 decreased). After treatment, 66 (T1 vs. CON) and 64 (T3 vs. CON) metabolite differences persisted. Clustering and data reduction analysis revealed separate clustering of hyperthyroid (T0) and CON cats with intermediate phenotypes after treatment (T1 & T3). Mevalonate/mevalonolactone and creatine phosphate were candidate biomarkers with excellent discrimination between hyperthyroid and healthy cats. We found several metabolic derangements (e.g., decreased carnitine and α-tocopherol) do not entirely resolve after achieving a euthyroid state after treating hyperthyroid cats with I-131. Further investigation is warranted to determine diagnostic and therapeutic implications for candidate biomarkers and persistent metabolic abnormalities.

Glucagon infusion alters the circulating metabolome and urine amino acid excretion in dogs.

Glucagon plays a central role in amino acid (AA) homeostasis. The dog is an established model of glucagon biology, and recently, metabolomic changes in people associated with glucagon infusions have been reported. Glucagon also has effects on the kidney; however, changes in urinary AA concentrations associated with glucagon remain under investigation. Therefore, we aimed to fill these gaps in the canine model by determining the effects of glucagon on the canine plasma metabolome and measuring urine AA concentrations. Employing two constant rate glucagon infusions (CRI) - low-dose (CRI-LO: 3 ng/kg/min) and high-dose (CRI-HI: 50 ng/kg/min) on five research beagles, we monitored interstitial glucose and conducted untargeted liquid chromatography-tandem mass spectrometry (LC-MS/MS) on plasma samples and urine AA concentrations collected pre- and post-infusion. The CRI-HI induced a transient glucose peak (90-120 min), returning near baseline by infusion end, while only the CRI-LO resulted in 372 significantly altered plasma metabolites, primarily reductions (333). Similarly, CRI-HI affected 414 metabolites, with 369 reductions, evidenced by distinct clustering post-infusion via data reduction (PCA and sPLS-DA). CRI-HI notably decreased circulating AA levels, impacting various AA-related and energy-generating metabolic pathways. Urine analysis revealed increased 3-methyl-l-histidine and glutamine, and decreased alanine concentrations post-infusion. These findings demonstrate glucagon's glucose-independent modulation of the canine plasma metabolome and highlight the dog's relevance as a translational model for glucagon biology. Understanding these effects contributes to managing dysregulated glucagon conditions and informs treatments impacting glucagon homeostasis.

Serum vitamin D metabolite and acute-phase protein concentrations are frequently abnormal in a cohort of hospitalized dogs and cats.

OBJECTIVE: To determine whether serum 25-hydroxyvitamin D (25[OH]D) and 1,25-dihydroxyvitamin D (1,25[OH]2D) concentrations are associated with survival and negatively correlate with acute-phase protein (APP) concentrations in ill dogs and cats admitted to nursing care units. ANIMALS: Client-owned dogs (n = 79) and cats (16) admitted to 2 academic veterinary hospital nursing care units. METHODS: A prospective cohort study was conducted between August 12, 2019, and October 26, 2021. A diagnostic laboratory measured 25(OH)D, 1,25(OH)2D, and haptoglobin (HPT) in dogs and cats; C-reactive protein (CRP) in dogs; and serum amyloid A (SAA) in cats. Serum was collected within 12 hours of admission. Illness severity (acute patient physiologic and laboratory evaluation [APPLEfast]) scores and survival data were recorded. RESULTS: Serum 25(OH)D concentrations were in the deficient range for 22 of 79 dogs and 2 of 16 cats. There were no associations between serum analyte concentrations (25[OH]D, 1,25[OH]2D, and APP) or APPLEfast score and survival in dogs or cats. In dogs, HPT was negatively correlated with 25(OH)D (P = .002; r = -0.34) and 1,25(OH)2D (P = .012; r = -0.28), while CRP was positively correlated with HPT (P = .001; r = 0.32) and APPLEfast score (P = .014; r = 0.16). In cats, 1,25(OH)2D was negatively correlated with APPLEfast scores (P = .055; r = -0.49) and SAA was positively correlated with HPT (P = .002; r = 0.73). CLINICAL RELEVANCE: Serum 25(OH)D or 1,25(OH)2D was not associated with survival in our hospitalized patient population. Relationships between APP and serum vitamin D metabolites with APPLEfast scores in cats warrant further investigation as illness severity biomarkers.

Short-term parenteral infusions with high-osmolality amino acid solutions can be safely administered through peripheral catheters in dogs treated for hypoaminoacidemia-related conditions.

OBJECTIVE: To compare complications between central and peripheral administration of high-osmolarity (approx 700 to 1,000 mOsm/L) amino acid (± lipid) infusions. ANIMALS: 18 client-owned dogs diagnosed with aminoaciduric canine hypoaminoacidemic hepatopathy syndrome or superficial necrolytic dermatitis receiving parenteral amino acid ± lipid infusions. METHODS: In this retrospective case series, medical records were reviewed for administration route (central vs peripheral), catheter details and infusion characteristics (product osmolarity, concurrent lipid administration, infusion volume, duration, and rate), and complications for each infusion. RESULTS: 18 dogs received 277 infusions (median, 8.5; range, 1 to 84). Effective infusion osmolarities were 683 mOsm/L in 22% of infusions, 791 mOsm/L in 8%, 802 mOsm/L in 2%, 837 mOsm/L in 45%, and 998 mOsm/L in 23% (65% peripheral, 35% central). Most (n = 230 [83%]) infusions were given peripherally. The osmolarities of solutions administered by each route (P = .53), the infusion rate indexed to body weight (P = .17), or the lipid infusion rates indexed to body weight (P = .89) did not differ. One dog suffered 2 complications in 63 infusions-1 mild, 1 severe-both occurring with peripheral infusions. Thus, the overall complication rate was 2 of 277 (0.9%) infusions. CLINICAL RELEVANCE: Short-term peripherally administered amino acid ± lipid infusions < 1,000 mOsm/L confer little risk compared to centrally administered infusions. Additional studies are needed to determine the safety of infusions with longer durations. Due to the relative ease of peripheral catheterization, clinicians should consider this route for medically managing aminoaciduric canine hypoaminoacidemic hepatopathy syndrome and superficial necrolytic dermatitis in dogs.

A prospective cohort study to identify clinical diagnostic and prognostic markers of primary immune thrombocytopenia in dogs.

BACKGROUND: Primary immune thrombocytopenia (pITP) in dogs presents a diagnostic challenge, and clinical markers of severity are lacking. OBJECTIVES: Identify clinicopathologic features that differentiate pITP from secondary ITP (sITP) and markers related to bleeding severity, transfusion, and survival of dogs with pITP. ANIMALS: Ninety-eight thrombocytopenic dogs (58 pITP and 40 sITP). METHODS: Client-owned dogs with platelet counts <50 000/µL were enrolled in a prospective, multi-institution cohort study. History and treatment information, through a maximum of 7 days, was recorded on standard data forms. Bleeding severity was scored daily using a bleeding assessment tool (DOGiBAT). At-admission blood samples were collected for CBC, biochemistry, C-reactive protein concentration, and coagulation panels, and to measure platelet surface-associated immunoglobulin G (PSAIg) and expression of platelet membrane proteins and phospholipids. Dogs with evidence of coincident disease were classified as sITP. RESULTS: No definitive pITP diagnostic test was found. However, pITP cases were characterized by lower platelet counts, D dimer concentrations, and platelet membrane protein expression than sITP cases. Differentiation between pITP and sITP was further enhanced using logistic regression modeling combining patient sex, coagulation profile, platelet count, D dimer, and PSAIg. A second model of pITP severity indicated that low hematocrit and high BUN concentration were associated with non-survival. Low hematocrit at admission, but not platelet count or DOGiBAT score, was associated with transfusion. CONCLUSIONS AND CLINICAL IMPORTANCE: Pending validation studies, models constructed from at-admission clinicopathologic findings may improve differentiation of pITP from sITP and identify the most severe pITP cases at the time of presentation.