Identification of a novel kisspeptin with high gonadotrophin stimulatory activity in the dog

Kisspeptin (KISS1) and its receptor (KISS1r) are essential for normal reproductive function in many species, but the role of kiss1/kiss1r signalling in the dog has not yet been elucidated. The aims of this study were to identify the canine kiss1 and kiss1r genes and to determine gonadotrophin and oestradiol stimulatory activity of KP-10, the shortest biologically active form of KISS1. Canine kiss1 and kiss1r genes were localized by comparing the reference dog genome with relevant human cDNA sequences, using BLASTn software. The amino acid sequence of canine KP-10 (YNWN V FGLR Y ) differs at two positions from human KP-10 (YNWN S FGLR F ). A single bolus of canine KP-10 was administered intravenously to anoestrous Beagle bitches in dosages of 0, 0.1, 0.2, 0.3, 0.5, 1, 5, 10, and 30 μg/kg. Blood samples were collected before and after canine KP-10 administration for the measurement of plasma luteinizing hormone (LH, all doses), follicle-stimulating hormone (FSH) and oestradiol (1-30 μg/kg). From 0.2 μg/kg onwards, canine KP-10 resulted in a rapid and robust rise in plasma LH concentration (max. at 10 min). KP-10 also resulted in a rapid and robust rise in plasma FSH concentration (max. at 10-20 min). Plasma oestradiol concentration increased significantly after dosages of 1, 5, and 10 μg/kg and reached a maximum at 60-90 min. In conclusion, canine KP-10 is a potent kisspeptin which elicits robust gonadotrophin and oestradiol responses in anoestrous bitches, suggesting that canine kiss1/kiss1r are cogent targets for modulating reproduction in dogs.Medical Research Council, the National Research Foundation, the Technology Innovation Agency and the University of Pretoria.http://www.karger.com/Journal/Home/223855hb201

Recent advances in the diagnosis of Cushing’s syndrome in dogs

Vet Clin North Am Small Anim Pract. 2010 Mar;40(2):259-67. Recent advances in the diagnosis of Cushing's syndrome in dogs. Kooistra HS, Galac S. Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 108, 3584 CM Utrecht, The Netherlands. [email protected] Abstract There are several recent advances in the diagnosis of Cushing's syndrome, or spontaneous hypercortisolism, in dogs. Diagnostic procedures are being reshaped by the recognition of new causes of the disease and advances in imaging procedures. This article reviews the clinical manifestations, diagnostic procedures, and the forms and causes of the syndrome. Copyright 2010 Elsevier Inc. All rights reserved. PMID: 20219487 [PubMed - indexed for MEDLINE

Creatinine Ratios in Dogs with Pituitary-Dependent Hypercortisolism during Trilostane Treatment

J Vet Intern Med. 2009 Nov-Dec;23(6):1214-9. Epub 2009 Aug 26. Urinary Corticoid : Creatinine Ratios in Dogs with Pituitary-Dependent Hypercortisolism during Trilostane Treatment. Galac S, Buijtels JJ, Kooistra HS. Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Utrecht, the Netherlands. Background: The adrenocorticotropic hormone (ACTH) stimulation test is used to evaluate trilostane treatment in dogs with hypercortisolism. Hypothesis: The urinary corticoid : creatinine ratio (UCCR) is a good alternative to the ACTH stimulation test to determine optimal trilostane dose. Animals: Eighteen dogs with pituitary-dependent hypercortisolism. Methods: In this prospective study, the dose of trilostane was judged to be optimal on the basis of resolution of clinical signs of hypercortisolism and results of an ACTH stimulation test. The owners collected urine for determination of UCCR at 2-week intervals for at least 8 weeks after achieving the optimal trilostane dose. Results: The UCCRs were significantly higher before treatment (11.5-202.0 x 10(-6); median, 42.0 x 10(-6)) than at rechecks 2 months after optimal dosing, but they did not decrease below the upper limit of the reference range in the majority of dogs. The UCCRs of 11 dogs that initially were dosed insufficiently (range, 7.5-79.0 x 10(-6); median, 31.0 x 10(-6)) did not differ significantly from UCCRs when the dosage was optimal (8.2-72.0 x 10(-6); median, 33.0 x 10(-6)). Post-ACTH cortisol concentrations did not correlate significantly with UCCRs at rechecks during trilostane treatment. Long-term follow-up indicated that the decrease in UCCR below the upper limit of the reference was associated with hypocortisolism. Conclusion and Clinical Importance: The UCCR cannot be used as an alternative to the ACTH stimulation test to determine the optimal dose of trilostane, but might be helpful in detecting dogs at risk for developing hypocortisolism during trilostane treatment. PMID: 19709356 [PubMed - in process

Neurological signs due to hypoadrenocorticism in two dogs

Primary hypoadrenocorticism, also known as Addison’s disease and nicknamed ‘the great pretender’, is a rare disease in dogs and has been sporadically documented in cats. Documented cases of confirmed hypoadrenocorticism as a cause of neurological signs are limited. This report describes two cases of hypoadrenocorticism primarily referred for neurological signs. In case 1, neurological signs consisted of generalised neuromuscular weakness/paresis. The very noticeable tetraparesis (paraparesis most apparent) in case 2 is an example of the generalised paresis that may be a consequence of hypoadrenocorticism. Both cases responded to treatment for hypoadrenocorticism with resolution of neurological signs. In conclusion, hypoadrenocorticism should be considered a differential diagnosis for dogs presented with neurological signs of (generalised neuromuscular) weakness/paresis (manifesting as a ‘wobbly gait’ which is easily confused with ataxia), especially when signs are long-standing or vaguely defined

Neurological signs due to hypoadrenocorticism in two dogs

Primary hypoadrenocorticism, also known as Addison’s disease and nicknamed ‘the great pretender’, is a rare disease in dogs and has been sporadically documented in cats. Documented cases of confirmed hypoadrenocorticism as a cause of neurological signs are limited. This report describes two cases of hypoadrenocorticism primarily referred for neurological signs. In case 1, neurological signs consisted of generalised neuromuscular weakness/paresis. The very noticeable tetraparesis (paraparesis most apparent) in case 2 is an example of the generalised paresis that may be a consequence of hypoadrenocorticism. Both cases responded to treatment for hypoadrenocorticism with resolution of neurological signs. In conclusion, hypoadrenocorticism should be considered a differential diagnosis for dogs presented with neurological signs of (generalised neuromuscular) weakness/paresis (manifesting as a ‘wobbly gait’ which is easily confused with ataxia), especially when signs are long-standing or vaguely defined

Effects of trilostane treatment on the pituitary-adrenocortical and renin-aldosterone axis in dogs with pituitary-dependent hypercortisolism

Vet J. 2010 Jan;183(1):75-80. Epub 2008 Nov 29. Effects of trilostane on the pituitary-adrenocortical and renin-aldosterone axis in dogs with pituitary-dependent hypercortisolism. Galac S, Buijtels JJ, Mol JA, Kooistra HS. Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands. [email protected] Abstract The medical records of 63 dogs with pituitary-dependent hypercortisolism (PDH) before and during treatment with trilostane were reviewed retrospectively. The correct trilostane dosage in dogs with PDH was based on the resolution of clinical signs and the results of an adrenocorticotropic hormone (ACTH) stimulation test. The mean (+/-SD) dose rate of trilostane to achieve good clinical control was 2.8+/-1.0mg/kg bodyweight. Trilostane treatment resulted in a significant decline in basal plasma cortisol concentrations. The median plasma ACTH concentration (39 pmol/L, range 7-132 pmol/L; n=60) at the optimal trilostane dosage time was significantly higher (

Questionnaire-based survey of parturition in the queen

The lack of scientific data concerning whether parturition in the queen proceeds normally or not may prevent veterinarians and cat owners from recognizing parturition problems in time. A questionnaire-based study of parturition in 197 queens was performed to determine several parameters of parturition and their influence on its progress. The mean length of gestation was 65.3 days (range 57 to 72 days) and it decreased with increasing litter size (P = 0.02). The median litter size was 4.5 kittens (range 1 to 9), with more males (53%) than females (46%) (P = 0.05). Sixty-nine percent of the kittens were born in anterior presentation and 31% in posterior presentation, indicating that either can be considered normal in the cat. Males were born in posterior position (34%) more often than females (26%) (P = 0.03). The mean birth weight was 98 g (range of 35 to 167 g) and decreased with increasing litter size (P <0.01). Mean birth weight was higher in males and kittens born in posterior presentation (P <0.01). Forty-four (5%) of the 887 kittens were stillborn. This was not correlated with the presentation at expulsion but stillborn kittens were more often female (P = 0.02) and weighed less than those born alive (P = 0.04). The median interkitten time was 30 min (range 2 to 343 min) and 95% were born within 100 min after expulsion of the preceding kitten. The interkitten time as a measure of the progress of parturition was not influenced by the kitten's gender, presentation at expulsion, birth weight, or stillbirth, or by the parity of the queen. The results of this study can be used to develop reference values for parturition parameters in the queen, both to determine whether a given parturition is abnormal and as the basis for a parturition protocol. © 2011 Elsevier Inc