BackgroundApolipoprotein B100 (apoB) is a superior indicator of CV risk than total or LDL-C. Non-HDL-C represents a simple surrogate for apoB in hypertriglyceridemic and/or T2DM patients. ApoB and non-HDL-C show high correlation, although the degree of mutual concordance remains debated in CV risk evaluation.ObjectivesWe used the Discriminant Ratio (DR) methodology to compare the performance of non-HDL-C with that of apoB to rank diabetic patients according to dyslipidemia and to establish the underlying relationship between these variables taking measurement noise and intra-/intersubject variation into account, and to derive an unbiased equivalence equation.MethodsFasting total C, HDL-C, apoB and triglycerides were measured in 45 diabetic patients. The DR of the underlying between-subject standard deviation (SD) to the within-subject SD was calculated from duplicates. Correlation coefficients between pairs were adjusted to include an estimate of the underlying correlation.ResultsMean values [day 1 (1SD)] were 143 (36) mg/dl (non-HDL-C) and 98 (24) mg/dl (apoB). The DR's of both parameters were similar (1.76 and 1.83) (p = 0.83). Pearson's product-moment correlation coefficient between tests was very high (0.94), reaching unity (1.00) after attenuation adjustment. The unbiased equation of equivalence relating apoB to non-HDL-C had a slope of 0.65 and an intercept of 6.3 mg/dl.ConclusionsThe discrimination power of non-HDL-C is similar to that of apoB to rank diabetic patients according to atherogenic cholesterol and lipoprotein burden. Since true correlation between variables reached unity, non-HDL-C may provide not only a metabolic surrogate but also a candidate biometrical equivalent to apoB, as non-HDL-C calculation is readily available.
A seven‐year‐old Miniature Schnauzer and a 16‐month‐old Domestic shorthair with clinical features of disproportionate dwarfism, presented with progressive thoracolumbar and cervical myelopathies, respectively. CT and MR imaging were performed in both patients revealing multiple thoracolumbar intervertebral disc protrusions located between T10 and L3 in the dog, and a cervical spinal arachnoid diverticulum at C2 in the cat as the cause for their myelopathic signs. Additionally, epiphysial dysgenesis of the vertebral column and shortened vertebrae were noticed. The history of hypothyroidism in the dog and the low serum thyroxine and elevated thyroid stimulating hormone concentration in the cat, together with the clinical presentations and the skeletal deformities, resulted in the diagnosis of congenital hypothyroidism in both patients. Congenital hypothyroidism is known to cause vertebral deformities and joint laxity, which possibly contributed in both cases to the development of the myelopathic disorders. Surgical treatment, combined with levothyroxine therapy, resulted in successful outcomes.
Objectives Phenobarbital (PB) is the most common antiseizure drug (ASD) used for the management of feline epilepsy. In dogs, PB is known to cause serum liver enzyme induction and hepatotoxicity, especially after administration long term or in high concentrations. In cats, insufficient evidence is available to draw similar conclusions. The aim of this study was to evaluate the effect of PB administration on the serum biochemistry profile of epileptic cats. As an additional objective, other adverse effects arising, related to PB treatment, were recorded. Methods Medical records of four veterinary centres were retrospectively reviewed for epileptic cats receiving PB treatment. Cats were included if they had a diagnosis of idiopathic epilepsy or structural epilepsy; a normal baseline serum biochemistry profile; at least one follow-up serum biochemistry profile; no concurrent disease or had not received medication that could possibly influence liver function or lead to serum liver enzyme induction. Alkaline phosphatase, alanine aminotransferase (ALT), aspartate transaminase and gamma-glutamyl transferase activities, and total bilirubin, bile acids, glucose, albumin, total protein, urea and creatinine concentrations before and during PB administration were recorded. PB serum concentration was also recorded, when available. Results Thirty-three cats (24 males, nine females) with a median age of 3 years (range 2 months to 12 years) met the inclusion criteria. Idiopathic or structural epilepsy was diagnosed in 25 (76%) and eight (24%) cats, respectively. The follow-up period ranged from 9 to 62 months. This study found an increase in ALT in three cats, possibly related to a PB serum concentration >30 µg/ml. No statistically significant increase in serum liver enzymes or other evaluated biochemistry parameters was found by comparing pre- and post-treatment parameters. Conclusions and relevance PB administration did not result in hepatic enzyme induction or other biochemical abnormalities in cats. This strengthens the safety profile of PB as an ASD in cats.
BackgroundTo our knowledge, this is the first description of long-term nutritional management in a dog with paroxysmal dyskinesia.Case summaryAn obese 9-year-old, male entire, German Spitz was presented for dietary management after being diagnosed with calcium oxalate urolithiasis and suspected pancreatitis. Since he was seven years old, the dog has had a history of neurological signs, which were thought to be epileptic seizures. He was treated with phenobarbital and potassium bromide and was clinically controlled. For his nutritional advice, aiming to minimize one of the most important risk factors for the diseases, a weight loss program was started and successfully executed. However, 10 months later, the dog restarted presenting neurological episodes at a high frequency (3x/week). Based on videos and the characteristics of the neurological signs, the dog was diagnosed with paroxysmal dyskinesia. To investigate the role of gluten intake on this patient's neurological signs, a dietary trial with a commercial hypoallergenic diet (gluten-free; hydrolyzed protein) was followed. During the 3 months of the dietary trial, four neurologic episodes related to food indiscretion occurred. Upon the decrease in neurological episodes, the anti-seizure drugs were slowly discontinued. During this period, the dog presented only two neurologic episodes that were related to the days that the anti-seizure drugs were decreased. For 4 months the dog remained episode-free. However, a change in the dog's diet to another gluten-free diet (higher fat) led the dog to vomit and experience another neurologic episode. Once the dog was back to the previous gluten-free diet, it clinically improved, and no other clinical signs were reported by the client during the next 5 months.ConclusionAlthough a relationship between gluten and paroxysmal dyskinesia cannot be confirmed, the dog's improvement after the nutritional management and the removal of the anti-seizure therapy is supportive of dietary association.
Disclaimer: This paper should not be reported as representing the views of the European Central Bank (ECB). The views expressed are those of the authors and do not necessarily reflect those of the ECB.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.