Background: The epidemiology of Equine Metabolic Syndrome (EMS) is poorly described.

Background: Many diagnostic tests for insulin dysregulation use reference intervals established with an insulin radioimmunoassay (RIA) that is no longer available. A chemiluminescent immunoassay (CLIA) is commonly used for the measurement of serum insulin concentration in clinical practice but requires further validation, especially at clinically relevant reference intervals.Objectives: To evaluate the CLIA for measurement of equine insulin and compare it to the previously validated, but now unavailable RIA.Samples: Equine serum samples (n = 78) from clinical and experimental studies. Methods: In this experimental study, performance of the CLIA was evaluated using standard variables, including comparison with the RIA. Continuous and binary outcomes were analyzed.Results: The CLIA showed good intra-assay (coefficient of variation [CV], 1.8-2.4%) and interassay (CV, 3-7.1%) precision. Acceptable recovery on dilution (100 AE 10%) was achieved only at dilutions <1:1. Recovery on addition was acceptable.Comparison of the CLIA and RIA showed strong positive correlation (r = 0.91-0.98), with fixed and proportional bias. At 3 diagnostic cutoffs, sensitivity of CLIA compared with RIA ranged from 67 to 100% and specificity from 96 to 100%.Conclusions and Clinical Importance: The CLIA is a highly repeatable assay which is suitable for within-and betweenhorse comparisons. Dilution of high concentration samples should be performed with charcoal-stripped serum (CSS) and at the lowest dilution factor possible. At concentrations commonly used for diagnosis of insulin dysregulation (≤100 lIU/mL), results from the CLIA tend to be lower than from the RIA and should be interpreted accordingly. Further standardization of equine insulin assays is required.

and splits his time between leading the internal medicine and critical care services and running the referral laboratory. Since graduating from The University of Bristol in 2001 he has worked in universities in both the UK and Australia but has spent most of his career in private equine practice in the UK. He is actively involved in all fields of equine medicine and has published on a range of topics, but has particular interests in endocrinology, gastroenterology and respiratory disease. He holds the RCVS certificate in equine medicine and was awarded a masters degree from The University of Glasgow.

Summary Background Primary hyperparathyroidism is uncommon in equids. Objectives To describe the diagnostic findings and efficacy of treatment in equids with primary hyperparathyroidism. Study design Retrospective case series describing 16 horses and one mule. Methods Cases were identified by retrospective review of records at Cornell University and via an ACVIM listserv query. Inclusion criteria were an equid with hypercalcemia, normal renal function and high parathyroid hormone (PTH) or histopathological diagnosis of a parathyroid adenoma. Equids with normal PTH and PTH‐related protein (PTHrP) in the face of hypercalcemia were included as suspect cases. Results The most common presenting complaints were weight loss (12/17) and hypercalcemia (10/17). PTH was above reference range in 12/17 cases. Suspected parathyroid tumours were localised in 12/14 equids imaged using ultrasonography alone (2/3), technetium 99m Tc sestamibi scintigraphy alone (1/1) or both modalities (9/10). Three horses did not have imaging performed. Surgical exploration successfully excised tumours in six of 10 cases. Five were located at the thoracic inlet, and surgery resulted in complete cure. One tumour was excised from the thyroid lobe, and the horse remained hypercalcemic. Four other cases explored surgically, four treated medically and three that were not treated also remained hypercalcemic. Main limitations The small study size prohibited statistical analysis. Conclusions Parathyroid adenomas in equids can be successfully localised with ultrasonography and scintigraphy. Surgical excision appears more likely to be successful for single gland disease at the thoracic inlet.

No abstract