Background: Copper-associated chronic hepatitis (CACH) recently has been recognized in the Labrador Retriever as an inherited disorder with a late onset of clinical signs. No studies have investigated dietary management for the long-term treatment of this disease or for its potential in delaying the onset of clinical signs in subclinical cases.Objectives: To investigate the effects of a low-copper diet and zinc gluconate on hepatic copper concentrations in Labrador Retrievers with abnormal hepatic copper concentrations.Animals: Twenty-four client-owned Labradors that were related to patients affected with CACH and that had been diagnosed with increased hepatic copper concentrations.Methods: Hepatic copper concentrations were assessed before and after an average of 8 and 16 months of treatment. During this time, all dogs were fed exclusively a low-copper diet. In addition, dogs were assigned to 1 of 2 groups in a randomized double-blind manner to receive a supplement of zinc gluconate or placebo.Results: Twenty-one dogs completed the study. Hepatic copper concentrations decreased in both groups at recheck 1 (n 5 21; group 1, P o .001; group 2, P 5 .001) and at recheck 2 (n5 16; group 1, P 5 .03; group 2, P 5 .04). No difference in hepatic copper concentrations was found between the 2 groups before treatment (P 5 .65), at recheck 1 or at recheck 2 (P 5 .52-.79).Conclusions and Clinical Relevance: Feeding low-copper diets to Labradors is effective in decreasing hepatic copper concentrations. Adjunctive treatment with zinc does not appear to increase the copper-lowering effects of dietary management.
Nineteen dogs with vesico-urethral reflex dyssynergia (VURD) were treated with prazosin or terazosin 0.5 mg/kg twice daily to compare efficacy and side effects. Dogs were referred because of signs of (partial) urethral obstruction. Physical examination, abdominal ultrasonography, urinalysis and a radiographic contrast study of bladder and urethra (urethrocystography) were routinely performed. If no mechanical causes of obstruction or disease of the distal urinary tract were observed, the diagnosis VURD was presumed and the dogs were included in our study. Follow-up information was obtained from owners or referring veterinarians. Significantly more side effects were seen in the dogs treated with terazosin (n=14; 93 per cent) compared with the dogs treated with prazosin (n=5; 20 per cent; P=0.002). Effects of the treatment were comparable between prazosin and terazosin. Labradors and dogs that were castrated surgically had a significant better survival (P<0.01) compared with other breeds and animals that were castrated chemically. There was a moderate to good effect in 60 per cent of the dogs treated with prazosin, and in 64 per cent of the dogs treated with terazosin.
Urea cycle enzyme deficiency (UCED) patients with hyperammonemia are treated with sodium benzoate (SB) and sodium phenylacetate (SPA) to induce alternative pathways of nitrogen excretion. The suggested guidelines supporting their use in the management of hyperammonemia are primarily based on non-analytic studies such as case reports and case series. Canine congenital portosystemic shunting (CPSS) is a naturally occurring model for hyperammonemia. Here, we performed cross-over, randomized, placebo-controlled studies in healthy dogs to assess safety and pharmacokinetics of SB and SPA (phase I). As follow-up safety and efficacy of SB was evaluated in CPSS-dogs with hyperammonemia (phase II). Pharmacokinetics of SB and SPA were comparable to those reported in humans. Treatment with SB and SPA was safe and both nitrogen scavengers were converted into their respective metabolites hippuric acid and phenylacetylglutamine or phenylacetylglycine, with a preference for phenylacetylglycine. In CPSS-dogs, treatment with SB resulted in the same effect on plasma ammonia as the control treatment (i.e. saline infusion) suggesting that the decrease is a result of volume expansion and/or forced diuresis rather than increased production of nitrogenous waste. Consequentially, treatment of hyperammonemia justifies additional/placebo-controlled trials in human medicine.
Background Hyperammonemia can result in hepatic encephalopathy, which in severe cases eventually can lead to coma and death. In dogs, congenital portosystemic shunts (CPSS) are the most common cause for hyperammonemia. Conservative treatment consists of a protein modified diet, nonabsorbable disaccharides, antibiotics, or some combinations of these. Sodium benzoate (SB) and sodium phenylbutyrate (SPB) both are used in the acute and long‐term treatment of humans with hyperammonemia caused by urea cycle enzyme deficiencies. Both treatments are believed to lower blood ammonia concentrations by promoting excretion of excess nitrogen via alternative pathways. Objectives To evaluate the efficacy and safety of PO treatment with SB and SPB on hyperammonemia and clinical signs in CPSS dogs. Methods Randomized, double‐blind, placebo‐controlled crossover trial. Concentrations of blood ammonia and bile acids were measured in CPSS dogs before and after a 5‐day treatment with SB, SPB, and placebo. A wash‐out period of 3 days was used between treatments. A standard questionnaire was developed and distributed to owners to evaluate clinical signs before and after each treatment. Results Blood ammonia concentrations were not influenced by any of the treatments and were comparable to those observed during placebo treatment. In addition, SB and SPB treatment did not result in improvement of clinical signs. Adverse effects during treatment included anorexia, vomiting, and lethargy. Conclusions and Clinical Importance Based on our results, we conclude that SB or SPB are not useful in the conservative treatment of hyperammonemia in dogs with CPSS.
Headshaking is a threat to the welfare of affected horses. As seasonal headshaking may be triggered by allergic conditions, this clinical trial investigated whether the second-generation antihistamine cetirizine decreased headshaking. The objective was to assess the clinical effect of cetirizine versus placebo on seasonal headshaking. The hypothesis was that it would reduce headshaking by 50 % in 50 % of the horses. Thirty client-owned horses with seasonal headshaking were selected on the basis of information from the owner and a general clinical examination. In this crossover randomised double-blind placebo-controlled clinical trial, horses were given cetirizine (0.4 mg/kg twice daily PO for 7 days) or placebo (same number of tablets twice daily PO for 7 days) in a randomised order, with a washout period of 1 week in between. A 9-minute lunge protocol was recorded on video at the start and after both treatment weeks, and the number of headshakes in this 9-minute period was scored by two assessors in a blinded manner. Data of 29 horses were analysed. The number of headshakes decreased by more than 50 % in 10 horses when they were given cetirizine and in 8 horses when they were given placebo. This difference was not significant (p = 0.73). In a mixed linear model incorporating weather conditions no significant treatment effect was found either. In conclusion: no significant effect of cetirizine on seasonal headshaking was found in the group of horses included in this study.
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