Treatment and outcomes of dogs with hepatocutaneous syndrome or hepatocutaneous-associated hepatopathy.

BACKGROUND: Superficial necrolytic dermatitis (SND) in dogs is a rare disorder most commonly associated with hepatocutaneous syndrome. Although often reported as fatal, sporadically reported long-term remissions might be more common than previously believed and linked to treatment regimens. HYPOTHESIS/OBJECTIVES: Evaluate treatments and associated outcomes in dogs with hepatocutaneous-associated hepatopathy (HCH) with or without SND, designated collectively aminoaciduric canine hypoaminoacidemic hepatopathy syndrome (ACHES). ANIMALS: Forty-one dogs of various breeds and ages diagnosed with ACHES. METHODS: Retrospective study. Electronic surveys, medical records (2014-2019), and communication with veterinarians provided data. Three treatment categories were each dichotomized: IV amino acid (IV-AA) infusions (≥2 vs <2), supplements including S-adenosylmethionine (SAMe), arginine with ornithine, glutathione, lysine, proline, omega-3 fatty acids, or zinc (≥3 vs <3), and diet type (home-cooked vs commercial). Optimal treatment was defined as receiving ≥2 IV-AA treatments, ≥3 nutritional supplements, and a home-cooked diet. RESULTS: Most dogs (29/41, 71%) received IV-AA infusions (23/29, ≥2 infusions). Twenty-one dogs (51%) were fed commercial diets; 17/41 (41%) were fed home-cooked diets. Most dogs received SAMe (32/41, 78%) and a median of 3 supplements. In 4 dogs, HCH remission occurred. Overall all-cause median survival time (MST) was 359 days, and disease-specific MST was 557 days (range, 1-1783 days). Optimally treated dogs (n = 9) lived significantly longer (MST, >1783 days, P = .02) than variably treated dogs (MST, 214 days). CONCLUSIONS AND CLINICAL IMPORTANCE: Optimized ACHES management can resolve SND and HCH and confer long-term survival.

Enhancement of Campylobacter hepaticus culturing to facilitate downstream applications.

Campylobacter hepaticus causes Spotty Liver Disease (SLD) in chickens. C. hepaticus is fastidious and slow-growing, presenting difficulties when growing this bacterium for the preparation of bacterin vaccines and experimental disease challenge trials. This study applied genomic analysis and in vitro experiments to develop an enhanced C. hepaticus liquid culture method. In silico analysis of the anabolic pathways encoded by C. hepaticus revealed that the bacterium is unable to biosynthesise L-cysteine, L-lysine and L-arginine. It was found that L-cysteine added to Brucella broth, significantly enhanced the growth of C. hepaticus, but L-lysine or L-arginine addition did not enhance growth. Brucella broth supplemented with L-cysteine (0.4 mM), L-glutamine (4 mM), and sodium pyruvate (10 mM) gave high-density growth of C. hepaticus and resulted in an almost tenfold increase in culture density compared to the growth in Brucella broth alone (log10 = 9.3 vs 8.4 CFU/mL). The type of culture flask used also significantly affected C. hepaticus culture density. An SLD challenge trial demonstrated that C. hepaticus grown in the enhanced culture conditions retained full virulence. The enhanced liquid culture method developed in this study enables the efficient production of bacterial biomass and therefore facilitates further studies of SLD biology and vaccine development.

Isoquinoline alkaloids induce partial protection of laying hens from the impact of Campylobacter hepaticus (spotty liver disease) challenge.

Spotty liver disease (SLD) is a serious condition affecting extensively housed laying hens. The causative bacterium was described in 2015 and characterized in 2016 and named Campylobacter hepaticus. Antibiotics are the only tool currently available to combat SLD. However, antimicrobial resistance has already been detected, so finding therapeutic alternatives is imperative. Isoquinoline alkaloids (IQA), such as sanguinarine and chelerythrine, have been shown to have immunomodulatory effects. It has been hypothesized that IQA could ameliorate some of the deleterious effects of SLD. This study aimed to address that hypothesis in an experimental disease induction model. Birds were fed with diets containing 2 different doses of an IQA containing product, 100 mg of product/kg of feed (0.5 ppm of sanguinarine) and 200 mg of product/kg of feed (1.0 ppm of sanguinarine). Two additional groups remained untreated (a challenged positive control and an unchallenged negative control). After 4 wk of treatment, birds from all groups except the negative control group were exposed to C. hepaticus strain HV10. The IQA treated groups showed a reduction in the number of miliary lesions on the liver surface and reduced lesion scores compared with untreated hens. A significant reduction of egg mass was detected 6 d after exposure to C. hepaticus in the untreated group (P = 0.02). However, there was not a significant drop in egg-mass in the IQA groups, especially those fed with a high dose of IQA (P = 0.93). IQA supplementation did not produce significant changes in intestinal villus height and crypt depth but did result in a significant reduction in the proinflammatory cytokine, interleukin-8, in the blood (P < 0.01). Microbiota analysis showed that IQA treatment did not alter the alpha diversity of the cecal microbiota but did produce changes in the phylogenetic structure, with the higher dose of IQA increasing the Firmicutes/Bacteroidetes ratio. Other minor changes in production indicators included an increase in feed consumption (P < 0.01) and an increase in body weight of the treated hens (P < 0.0001). The present study has demonstrated that IQA confers some protection of chickens from the impact of SLD.

Hepatotoxicity in Cattle Associated with Salvia reflexa Diterpenes, including 7-Hydroxyrhyacophiline, a New Seco-Clerodane Diterpene.

A case of baled alfalfa hay contaminated with multiple weeds induced hepatotoxicity and death in cattle. The hepatotoxic compounds were isolated by bioassay-guided fractionation using a mouse model and identified as salviarin, salvianduline D, rhyacophiline, and 7-hydroxyrhyacophiline. The structure of 7-hydroxyrhyacophiline has not been previously reported. All compounds were found to induce severe acute hepatic necrosis within 24-48 h after a single oral dosage (260-280 mg/kg). The identified diterpenes are known to be found among different Salvia species which led to finding dried plant parts of Salvia reflexa within bales of weedy hay and subsequently a population of S. reflexa was found along the field edges and irrigation ditch banks of the alfalfa hay field. It was thus determined that S. reflexa was responsible for the hepatotoxicity observed in cattle fed the contaminated hay.

Mulberry Heart Disease and Hepatosis Dietetica in Farm Pigs (Sus scrofa domesticus) in a Research Setting.

Perioperative complications and deaths occurred while developing a novel surgical model of pediatric kyphosis in 10 to 12 kg male farm-raised Yorkshire piglets. All piglets appeared clinically normal preoperatively. Intraoperative complications included tachycardia, respiratory acidosis, and death. Postoperatively, clinical signs included posterior paresis, head pressing, prolonged anesthetic recovery, difficulty rising, and sudden death. Necropsies were performed on all piglets. Some morbidity and mortality were accurately attributed to the spinal surgery. However, the index piglet for this report died suddenly approximately 16 to 18 h after surgery. Necropsy of this animal revealed clear, serosanguineous pleural and pericardial effusions along with myocardial hemorrhage and hepatic lesions, consistent with mulberry heart disease and hepatosis dietetica, respectively. Serum vitamin E and selenium levels from this animal were below age-specific lab reference ranges. Clinical signs of vitamin E and selenium deficiency are most common in fast-growing weaner piglets. The added stress of major surgery may exacerbate the condition in young piglets. Resolution of morbidity and mortality in both juvenile and adult pigs occurred upon the use of an alternate vendor able to provide feed analyses meeting industry standards, although serum levels of vitamin E and selenium in similar ages and breed of swine were still occasionally slightly below reference ranges.

Serum vitamin D status in sick cats with and without cholestatic liver disease.

OBJECTIVES: Vitamin D deficiency accompanies chronic cholestatic liver disease (CLD) in humans. The vitamin D status of cats with CLD is unknown. The objectives of this study were to describe serum vitamin D concentrations in cats with CLD and to determine if they correlated with indices of liver disease severity. METHODS: Thirty-six cats with CLD, defined by increases in serum bilirubin and serum alanine aminotransferase, and 23 sick cats with non-hepatobiliary diseases were prospectively enrolled. Serum 25-hydroxyvitamin D (25[OH]D), parathyroid hormone (PTH) and ionized calcium were measured. Signalment, clinical signs, comorbidities, diet history, serum bilirubin, liver enzyme activity, albumin, phosphorus, white blood cell count, prothrombin time and final hepatic cytologic/histopathologic diagnosis, when available, were recorded. RESULTS: Median serum 25(OH)D levels were similar in cats with CLD (89.5 nmol/l; range 21-112 nmol/l) and sick cats (89.0 nmol/l; range 49-115 nmol/l). Overall 12/36 (33%) cats with CLD and 4/23 (17%) sick cats had 25(OH)D levels below the lower limit of the reference interval (<65 nmol/l). Median PTH concentrations in cats with CLD were significantly higher (0.95 pmol/l; range 0-11.3 pmol/l) than in sick cats (0.70 pmol/l; range 0.5-6 pmol/l). In cats with CLD, 6/36 (17%) had high PTH levels in contrast to only 1/23 (4%) sick cats. In cats with CLD, 25(OH)D concentrations did not correlate with serum bilirubin, albumin or serum liver enzymes but were moderately negatively correlated with white blood cell count (r = - 0.402, P = 0.013). Cats with hepatic lipidosis had the highest prevalence of 25(OH)D concentrations that fell below the reference interval. CONCLUSIONS AND RELEVANCE: Many cats with CLD have serum 25(OH)D concentrations below the lower limit of the reference interval. Further study is warranted to determine the clinical relevance and whether supplementation would provide benefits.

Remarkable frequency of a history of liver disease in dogs fed homemade diets with buckwheat.

OBJECTIVE: In our nutrition consultation service we observed liver disease in 2 dogs of one owner who was feeding buckwheat. This led to the hypothesis that buckwheat may cause problems. The present retrospective study in a German and a Russian nutrition consultation service was carried out to see whether there is an increased incidence of liver disease in dogs fed buckwheat. MATERIALS AND METHODS: A retrospective study was carried out on the nutrition consultation cases of the Chair of Animal Nutrition and Dietetics, LMU Munich and a Russian nutrition consultant. All cases of dogs with buckwheat in their nutritional history were evaluated and compared with randomly selected dogs that had not been fed buckwheat from the same case set. Two German and 1 Russian buckwheat samples were compared (appearance, nutrient content, starch gelatinization, flavonoids, fagopyrin) as well as cooking methods. RESULTS: In the years 2007-2017, 34 cases of dogs fed buckwheat were identified in Germany and 57 in Russia. Eighty-five control cases in Germany and 48 in Russia were evaluated. In Germany, the incidence of liver disease in dogs fed buckwheat was 32 %, while that of the control group was 3.5 %. However, in Russia there was no significant difference between dogs fed buckwheat and control dogs. The appearance of the German and Russian buckwheat differed, with smaller seeds and more greenish colour in the German specimens while the Russian buckwheat presented larger and more brownish seeds. There was no difference in the analyses of the 3 buckwheat samples in crude nutrient and rutin content. Quercetin, quercitrin and fagopyrin were not detectable in all three samples. The degree of starch gelatinization in the Russian sample was higher than in the German. In Russia it is recommended to remove the reddish scum during boiling whereas this is rarely mentioned in Germany. CONCLUSION AND CLINICAL SIGNIFICANCE: German buckwheat may represent a risk in canine diets. With the difference remaining unclear, it is recommended to refrain from feeding buckwheat to dogs. In dogs fed homemade diets and suffering from liver disease, buckwheat should be considered in the nutrition history.

Dietary N-Carbamylglutamate (NCG) alleviates liver metabolic disease and hepatocyte apoptosis by suppressing ERK1/2-mTOR-S6K1 signal pathway via promoting endogenous arginine synthesis in Japanese seabass (Lateolabrax japonicus).

N-Carbamylglutamate (NCG), an analogue of N-acetylglutamate (NAG), can promote the synthesis of endogenous Arginine (Arg) in mammals, but not well studied in fish. This study was conducted to investigate the capacity of Arg endogenous synthesis by NCG, and the effects of various dietary NCG doses on growth performance, hepatic health and underlying nutrient regulation metabolism on ERK1/2-mTOR-S6K1 signaling pathway in Japanese seabass (Lateolabrax japonicus). Four experimental diets were prepared with NCG supplement levels of 0 (N0), 360 (N360), 720 (N720) and 3600 (N3600) mg/kg, in which N360 was at the maximum recommended level authorized by MOA, China in fish feed, and the N720 and N3600 levels were 2 and 10-fold of N360, respectively. Each diet was fed to 6 replicates with 30 Japanese seabass (initial body weight, IBW = 11.67 ±â€¯0.02 g) in each tank. The results showed that the dietary NCG supplementation had no significant effects on the SGR and morphometric parameters of Japanese seabass, but 360-720 mg/kg NCG inclusion promoted PPV, while the 10-fold (3600 mg/kg) overdose of NCG had remarkably negative effects with significantly reduced feed efficiency, PPV and LPV. We found that Japanese seabass can utilize 360-720 mg/kg NCG to synthesis Arg to improve the amino acid metabolism by increasing plasma Arg and up-regulating intestinal ASL gene expression. Increased plasma GST and decreased MDA indicated the improved antioxidant response. Dietary NCG inclusion decreased plasma IgM and down-regulated the mRNA levels of inflammation (TNF-α and IL8), apoptosis (caspase family) and fibrosis (TGF-ß1) related genes in the liver. The immunofluorescence examination revealed significantly decreased hepatic apoptosis and necrosis signals in the NCG groups. The ameliorated liver function and histological structure were closely related to the improved lipid metabolism parameters with decreased plasma VLDL and hepatic TG and NEFA accumulation, down-regulated fatty acid and cholesterol synthesis and simultaneously increased lipolysis gene mRNA levels, which regulated by inhibiting phosphorylation of ERK1/2-mTOR-S6K1 signaling pathway. Consuming 3600 mg/kg of dietary NCG is not safe for Japanese seabass culturing with the significantly increased FCR and decreased protein and lipid retention, and reduced plasma ALB. Accordingly, the observed efficacy and safety level of dietary NCG in the diet of Japanese seabass is 720 mg/kg.

Feed supplementation with biochar may reduce poultry pathogens, including Campylobacter hepaticus, the causative agent of Spotty Liver Disease.

Increased global regulation and restrictions on the non-therapeutic use of antibiotics in the poultry industry means that there is a need to identify alternatives that prevent infection while still conveying the growth and performance benefits afforded by their use. Biochars are produced by the incomplete pyrolysis of organic materials, with reports of use as a feed supplement and activity against pathogenic bacteria. In the current study the dose-dependent effects of biochar dietary inclusion in layer diets at 1%, 2% and 4% w/w were investigated to determine a) the efficacy of biochar as an anti-pathogenic additive on the intestinal microbiota and b) the optimal inclusion level. Biochar inclusion for anti-pathogenic effects was found to be most beneficial at 2% w/w. Poultry pathogens such as Gallibacterium anatis and campylobacters, including Campylobacter hepaticus, were found to be significantly lower in biochar fed birds. A shift in microbiota was also associated with the incorporation of 2% w/w biochar in the feed in two large scale trials on two commercial layer farms. Biochar inclusion for anti-pathogenic effects was found to be most beneficial at 2% w/w. Differential effects of the timing of biochar administration (supplementation beginning at hatch or at point of lay) were also evident, with greater impact on community microbial structure at 48 weeks of age when birds were fed from hatch rather than supplemented at point of lay.

Grape pomace flour alleviates Pseudomonas aeruginosa-induced hepatic oxidative stress in grass carp by improving antioxidant defense.

Pseudomonas aeruginosa is a Gram-negative opportunistic bacterial pathogen in aquaculture systems being associated to extensive liver damage caused by oxidative stress in both marine and freshwater fish. Dietary supplementation with natural antioxidants is considered a rational strategy to prevent hepatic diseases involved with oxidative stress. Bio-residues resulting from the wine industry, such as grape pomace, are potential sources of bioactive phenolic compounds that can be applied as supplement for animal production. Thus, the aim of this study was to evaluate whether dietary supplementation with grape pomace flour (GPF) was able to prevent or reduce the hepatic oxidative damage of grass carp, Ctenopharyngodon idella, experimentally infected by P. aeruginosa. Hepatic reactive oxygen species (ROS), metabolites of nitric oxide (NOx), thiobarbituric acid reactive substances, and protein carbonylation levels were higher in fish experimentally infected by P. aeruginosa compared to the control group. Hepatic superoxide dismutase and catalase activities and antioxidant capacity against peroxyl radical levels were also higher in fish experimentally infected by P. aeruginosa compared to the control group. Dietary supplementation with 300 mg/kg GPF prevented all alterations elicited by P. aeruginosa, with the exception of protein carbonylation levels. The dietary supplementation with 150 mg/kg GPF was not able to avoid alteration of the analyzed variables, being results similar to those infected (positive control). Based on these results, dietary supplementation with 300 mg/kg GPF prevented P. aeruginosa-induced liver damage in grass carp, and this protective effect occurred through prevention on excessive ROS and NOx production, as well as via prevention of lipid damage. Moreover, 300 mg/kg GPF exerted its hepatoprotective effects by improving enzymatic and non-enzymatic antioxidant defense system. In summary, this supplementation can be an interesting approach to prevent P. aeruginosa-induced liver damage.

A caffeine-supplemented diet modulates oxidative stress markers and prevents oxidative damage in the livers of Nile tilapia (Oreochromis niloticus) exposed to hypoxia.

Recent evidence has revealed the involvement of oxidative stress and oxidative damage with health impairment and mortality in fish exposed to hypoxia. Thus, natural compounds with antioxidant and free-radical-scavenging properties, such as caffeine, might help to prevent or reduce hepatic damage elicited by hypoxia. Thus, the aim of this study was to evaluate whether dietary supplementation with caffeine could prevent or reduce oxidative damage in the livers of Nile tilapia (Oreochromis niloticus) exposed to hypoxia. Hepatic reactive oxygen species, lipid peroxidation levels, and xanthine oxidase (XO) activity were higher in fish exposed to hypoxia compared with normoxia. Hepatic catalase, glutathione peroxidase, and glutathione S-transferase activities, as well as the antioxidant capacity against peroxyl radical levels, were lower in fish exposed to hypoxia compared with normoxia. No significant difference between groups was observed regarding hepatic superoxide dismutase activity. Dietary supplementation with 8% caffeine prevented all alterations elicited by hypoxia. Based on this evidence, the use of dietary supplementation with 8% caffeine can be an interesting approach to preventing hepatic lipid damage and impairment of the antioxidant defense system elicited by hypoxia, and this effect can be mediated by protective effects on XO activity.

Serum biochemistry, histology and transcriptomic profile analysis reflect liver inflammation and damage following dietary histamine supplementation in yellow catfish (Pelteobagrus fulvidraco).

Previous studies suggested that diets containing high levels of histamine influenced digestive system of aquatic animals. In addition, the exogenous histamine was first detoxified by diamine oxidase in the intestine, while the rest of histamine was further detoxified in the liver. Thus, based on the evidence from the previous studies, we hypothesized that high levels of histamine may lead to damage on liver of the aquatic animals. Here, in current attempt, we sought to investigate the toxic effect of histamine on yellow catfish (Pelteobagrus fulvidraco) liver physiology and pathogenesis. In the present study, yellow catfish were fed for 56 days on diets supplemented with 1000 mg kg-1 histamine (His) or a basal diet as the control group (Con). A significant change on the morphology of the intestine and liver was observed, followed with an induction of serum activity of aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Furthermore, the transcriptomic analysis was performed to gain an overview of the gene expression profile in liver between control and histamine supplemented groups. Through the bioinformatics analysis, 431 differentially expressed genes were identified. Among these genes, Gene Ontology enrichment analysis (GO) suggests that immune-related genes are significantly dysregulated. In addition, TNF signaling pathway is enriched in Kyoto Encyclopedia of Genes and Genomes analysis (KEGG), and is also the dominant pathway in immune system, suggesting that the inflammatory response and apoptosis of hepatocytes are induced by exogenous histamine.

Utilização de sal mineral rico em molibdênio na prevenção da intoxicação cúprica acumulativa em ovinos - microminerais hepáticos / Use of molybdenum rich mineral mix in the prevention of cumulative cooper poisoning in sheep - hepatic microminerals

Este estudo avaliou a capacidade de um sal mineral rico em molibdênio (Mo) em prevenir a intoxicação cúprica acumulativa (ICA), mediante a análise das variáveis clínicas e dos teores de cobre (Cu) e Mo hepático. Foram utilizados 25 ovinos cruzados da raça Ile-de-France, aleatoriamente distribuídos igualmente em cinco grupos, em que o grupo 1 recebia dieta contendo 80% de volumoso e 20% de concentrado, os grupos 2 e 3 recebiam 50% de volumoso e 50% de concentrado, e os grupos 4 e 5 recebiam a mesma dieta dos grupos 2 e 3, com a adição diária de 150mg de sulfato de Cu. Os grupos 1, 3 e 5 recebiam sal mineral contendo 300ppm de Mo. Foram realizadas três biópsias hepáticas para determinação de Cu, Mo e Zn. Três ovinos do grupo 4 e um do grupo 5 manifestaram ICA. Não houve diferença na frequência de mortalidade entre os grupos (P=0,56). Os teores de Cu hepático nos ovinos com ICA (2450ppm) foram superiores aos que não intoxicaram (1518ppm). Quanto maior a ingestão de Mo na dieta, menor foi o acúmulo de Cu hepático ao término do experimento (r = -0,72).(AU)

The aim of this project is to evaluate the capacity of a molybdenum-rich mineral salt in the prevention of cumulative cooper poisoning (CCP) in sheep, through clinical and hepatic copper and molybdenum concentrations. Twenty five crossbreed Ile-de-France sheep were randomly distributed equally into five groups. Group 1 received a 80% forage and 20% concentrate diet, groups 2 and 3 received a 50% forage and 50% concentrate diet, and groups 4 and 5 received the same diet as groups 2 and 3 with a daily supplementation of 150 mg of copper sulfate. Groups 1, 3 and 5 received a mineral salt with 300 ppm of molybdenum. Three times during the experiment a liver biopsy was carried out to evaluate the degree of copper accumulation. Three sheep from group 4 and one sheep from group 5 showed a clinical picture of CCP. There was no difference in the frequency of mortality between groups 4 and 5 (P=0.56). The liver copper concentration was higher in sheep with CCP (2450 ppm) compared to sheep that did not present CCP (1518 ppm). The higher the ingestion of molybdenum in the diet the lower the liver copper concentration at the end of the experiment (r=-0.72).(AU)

Polioencephalomalacia and Heart Failure Secondary to Presumptive Thiamine Deficiency, Hepatic Lipidosis, and Starvation in 2 Abandoned Siamese Cats.

Two 4-year-old spayed female Siamese cats were seized by the British Columbia Society for the Prevention of Cruelty to Animals after confinement to an abandoned housing unit without food for 9 weeks. One cat was found dead, and the second was euthanized within 24 hours due to neurologic deterioration despite therapy. Polioencephalomalacia of the caudal colliculus, hepatic lipidosis, cachexia, and congestive heart failure with cardiomyocyte atrophy were identified in both cats through postmortem examination and attributed to a prolonged period of starvation. Brain lesions were likely the result of thiamine deficiency (Chastek paralysis), which can be associated with both malnutrition and liver disease. This case highlights the importance of thiamine supplementation during realimentation of cats with hepatic lipidosis. Heart failure resulting from cachexia may have contributed to the death of the first cat and the morbidity of the second cat.

Nutritional Considerations for Dogs and Cats with Liver Disease.

The goals of nutritional management of liver disease in the dog and cat are directed at treating the clinical manifestations as opposed to treating the underlying cause. Specifically, the clinician strives to avoid overwhelming the remaining metabolic capacities of the damaged liver while providing sufficient nutrients for regeneration. A brief overview of liver diseases and associated clinical signs encountered in the dog and cat and a review of specific nutrients are discussed as well as amounts and sources of nutrients recommended to meet nutritional goals in the diseased liver.

Canine hyperlipidaemia.

Hyperlipidaemia refers to an increased concentration of lipids in the blood. Hyperlipidaemia is common in dogs and has recently emerged as an important clinical condition that requires a systematic diagnostic approach and appropriate treatment. Hyperlipidaemia can be either primary or secondary to other diseases. Secondary hyperlipidaemia is the most common form in dogs, and it can be a result of endocrine disorders, pancreatitis, cholestasis, protein-losing nephropathy, obesity, as well as other conditions and the use of certain drugs. Primary hyperlipidaemia is less common in the general canine population but it can be very common within certain breeds. Hypertriglyceridaemia of Miniature Schnauzers is the most common form of primary hyperlipidaemia in dogs but other breeds are also affected. Possible complications of hyperlipidaemia in dogs include pancreatitis, liver disease, atherosclerosis, ocular disease and seizures. Management of primary hyperlipidaemia in dogs is achieved by administration of ultra low-fat diets with or without the administration of lipid lowering drugs such as omega-3 fatty acids, fibrates, niacin and statins.

Effects of a 6-wk intraduodenal supplementation with quercetin on energy metabolism and indicators of liver damage in periparturient dairy cows.

Periparturient dairy cows experience metabolic challenges that result in a negative energy balance (EB) and a range of postpartum health problems. To compensate for the negative EB, cows mobilize fatty acids from adipose tissues, which can lead to fatty liver disease, a periparturient metabolic disorder. Flavonoids, such as quercetin (Q), are polyphenolic substances found in all higher plants and have hepatoprotective potential and the ability to prevent or reduce lipid accumulation in the liver. In ruminants, few studies on the metabolic effects of Q are available, and thus this study was conducted to determine whether Q has beneficial effects on EB, lipid metabolism, and hepatoprotective effects in periparturient dairy cows. Quercetin was supplemented intraduodenally to circumvent Q degradation in the rumen. Cows (n=10) with duodenal fistulas were monitored for 7wk. Beginning 3wk before expected calving, 5 cows were treated with 100mg of quercetin dihydrate per kilogram of body weight daily in a 0.9% sodium chloride solution for a total period of 6wk, whereas the control cows received only the sodium chloride solution. The plasma flavonoid levels were higher in the Q-treated cows than in the control cows. A tendency for higher postpartum (pp) than antepartum (ap) plasma flavonoid levels was observed in the Q-treated cows than in the controls, which was potentially caused by a reduced capacity to metabolize Q. However, the metabolic status of the Q-treated cows did not differ from that of the control cows. The pp increases in plasma aspartate aminotransferase and glutamate dehydrogenase activities were less in the Q-treated cows than in the control cows. The Q had no effect on energy expenditures, but from ap to pp the cows had a slight decline in respiratory quotients. Irrespective of the treatment group, the oxidation of fat peaked after calving, suggesting that the increase occurred because of an increased supply of fatty acids from lipomobilization. In conclusion, supplementation with Q resulted in lower pp plasma aminotransferase and glutamate dehydrogenase, which indicated reduced liver damage. However, the direct effects of Q on the liver and the implications for animal performance remain to be investigated.

Hypercobalaminaemia is associated with hepatic and neoplastic disease in cats: a cross sectional study.

BACKGROUND: When increased serum cobalamin concentrations are encountered clinically they are usually attributed to parenteral supplementation, dietary factors, or otherwise ignored. However, recently, hypercobalaminaemia has been associated with numerous diseases in humans, most notably neoplastic and hepatic disorders. The aim of this retrospective, observational, cross-sectional study was to determine the significance of increased cobalamin in cats. RESULTS: In total, 237 records were retrieved and 174 cats, of various ages and sexes met the inclusion criteria. A total of 42 cats had increased serum cobalamin concentration, and had not received prior supplementation. Multiple logistic regression analysis revealed that increased serum cobalamin concentration was positively related to pedigree breed (pedigree breeds more likely to have increased cobalamin concentration, odds ratio [OR] 4.24, 95% CI 1.78-10.15, P = 0.001), to having liver disease (OR 9.91, 95% CI 3.54-27.68), and to having a solid neoplasm (OR 8.54, 95% CI 1.10-66.45). CONCLUSIONS: The results of the current study suggest that increased serum cobalamin concentrations should not be ignored in cats with no history of supplementation, and investigation for underlying hepatic or neoplastic disease is warranted.

Nutraceuticals for canine liver disease: assessing the evidence.

Nutraceuticals, or nutritional supplements, have been promoted for the ancillary treatment of liver disease in dogs. However, minimal information is available in the scientific literature about commonly used nutraceuticals, such as S-adenosylmethionine, silymarin, and vitamin E. No strong clinical evidence exists regarding the efficacy of these compounds as hepatoprotectants in canine liver disease. Until this evidence exists, individual veterinarians must assume responsibility for their decision to use nutritional supplements in their canine patients with liver disease.