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Background Folate and cobalamin are essential cofactors for homocysteine ( HCY) metabolism. Hyperhomocysteinemia, a multifactorial condition, may reflect B vitamin deficiency and is associated with increased risk of cardiovascular disease, thrombosis, and neurodegenerative and chronic gastrointestinal diseases in humans. Hyperhomocysteinemia has been reported in Greyhounds with suspected chronic enteropathy. Objectives To evaluate the frequencies of and the association between hypofolatemia and hyperhomocysteinemia in Greyhounds. Animals Data and serum samples from 559 Greyhounds. Methods Nested case-control study. The frequency of hypofolatemia in Greyhounds was determined by a laboratory database search. The relationship between hyperhomocysteinemia (measured by gas chromatography-mass spectrometry) and hypocobalaminemia and hypofolatemia was evaluated, and its frequency compared between healthy Greyhounds and Greyhounds with thrombosis or chronic diarrhea. Results Hypofolatemia was identified in 172 of 423 (41%) Greyhounds and was more common in hypo- than in normocobalaminemic dogs (49% vs. 35%; P = .0064). Hyperhomocysteinemia was detected in 53 of 78 (68%) of Greyhounds, being more common in hypo- than in normofolatemic dogs (88% vs. 59%; P = .0175). All healthy Greyhounds, 21 of 30 (70%) of dogs with chronic diarrhea and 6 of 8 (75%) of those with thrombosis, were hyperhomocysteinemic. Serum HCY concentrations were inversely correlated with serum folate concentration (ρ = −0.28; P = .0386) and were positively associated with serum albumin concentration (ρ = 0.66; P = .0022). Conclusions and Clinical Relevance Hyperhomocysteinemia occurs frequently in the Greyhound population. Its association with hypofolatemia suggests decreased intracellular availability of B vitamins, but the functional implications warrant further investigation. Hyperhomocysteinemia in Greyhounds potentially may serve as a spontaneous canine model to further investigate hyperhomocysteinemia in humans. [ABSTRACT FROM AUTHOR]

Background Famotidine is an acid suppressant commonly administered to dogs. Prolonged famotidine use in people results in decreased efficacy, but the effect in dogs is unknown. Hypothesis/Objectives To compare the effect of repeated oral administration of famotidine or placebo on intragastric pH and serum gastrin in dogs. We hypothesized that famotidine would have a diminished effect on intragastric pH on day 13 compared to day 1. Animals Six healthy adult colony Beagles. Methods Randomized, 2-factor repeated-measures crossover design. All dogs received oral placebo or 1.0 mg/kg famotidine q12h for 14 consecutive days. Intragastric pH monitoring was used to continuously record intragastric pH on treatment days 1-2 and 12-13. Mean pH as well as mean percentage time ( MPT) that intragastric pH was ≥3 or ≥4 were compared between and within groups by analysis of variance. Serum gastrin was measured on days 0, 3, and 12 for each treatment. Results Continued administration of famotidine resulted in a significant decrease in mean pH, MPT ≥3, and MPT ≥4 ( P < .0001) on day 12 and 13. This resulted in a mean decrease in pH by 1.63 on days 12 and 13 compared to days 1 and 2. Furthermore, a mean decrease of MPT ≥3 and MPT ≥4 by 33 and 45% was observed for the same time period, respectively. Conclusions and Clinical Importance Continued administration of famotidine results in a diminished effect on intragastric pH in dogs. Caution is advised when recommending long-term, daily oral administration of famotidine to dogs. [ABSTRACT FROM AUTHOR]

Background Cavalier King Charles spaniels ( CKCSs) are predisposed to degenerative mitral valve disease (DMVD) and studies have indicated a genetic cause. Animals A total of 8,860 CKCSs were examined at shows or private clinics from 1991 to 2010. Objectives To analyze the effects of a breed scheme for CKCS on the age at which a murmur consistent with DMVD was first detected. Methods The presence or absence of a murmur consistent with mitral regurgitation was noted and age a murmur was first detected recorded. Results A total of 16,887 examinations were performed on 8,860 dogs. The median age dogs developed a murmur were slightly younger in male than female dogs (7.8 versus 8.3 years, 95% confidence interval [ CI] 7.4-8.1 versus 8.0-8.4, P < .001) and cardiologists detected murmurs in younger dogs than did general practitioner ( GP) veterinary surgeons (7.2 versus 8.6 years, 95% CI 7.0-7.4 versus 8.3-8.7 P < .001). In bitches examined by GP vets during the study, there was a significantly increased age of detection of murmurs over time (8.6-9.2 years, 95% CI 8.3-9.1 and 8.5-10.9, P = .001) but not for male dogs examined by GP vets or dogs of either sex examined by cardiologists. Conclusions and Clinical Importance This study suggests that the age incidence of murmurs associated with DMVD might be increased by application of breeding guidelines based on auscultation alone. This benefit was only seen in a subgroup and compliance of breeders with this voluntary scheme was poor. [ABSTRACT FROM AUTHOR]

Management of persistent lower urinary tract dysfunction resulting from severe thoracolumbar spinal cord injury can be challenging. Severe suprasacral spinal cord injury releases the spinal cord segmental micturition reflex from supraspinal modulation and increases nerve growth factor concentration in the bladder wall, lumbosacral spinal cord, and dorsal root ganglion, which subsequently activates hypermechanosensitive C-fiber bladder wall afferents. Hyperexcitability of bladder afferents and detrusor overactivity can cause urine leaking during the storage phase. During urine voiding, the loss of supraspinal control that normally coordinates detrusor contraction with sphincter relaxation can lead to spinal cord segmental reflex-mediated simultaneous detrusor and sphincter contractions or detrusor-sphincter dyssynergia, resulting in inefficient urine voiding and high residual volume. These disease-associated changes can impact on the quality of life and life expectancy of spinal-injured animals. Here, we discuss the pathophysiology and management considerations of lower urinary tract dysfunction as the result of severe, acute, suprasacral spinal cord injury. In addition, drawing from experimental, preclinical, and clinical medicine, we introduce some treatment options for neurogenic lower urinary tract dysfunction that are designed to: (1) prevent urine leakage arising because of detrusor overactivity during bladder filling, (2) preserve upper urinary tract integrity and function by reducing intravesical pressure and subsequent vesicoureteral reflux, and (3) prevent urinary tract and systemic complications by treating and preventing urinary tract infections. [ABSTRACT FROM AUTHOR]