Use of bee venom in preventive medicine: An experimental hepatic encephalopathy study in rats.

OBJECTIVES: Bee venom is used for medicinal purposes, including the treatment of neurological and liver diseases, but its use as a primary health care approach for preventive purposes requires further exploration. The aim of this study was to provide the first investigation into the possible protective effects of bee venom against hepatic encephalopathy, a serious neurodegenerative disease. MATERIALS AND METHODS: An experimental animal study was conducted in which healthy albino Sprague-Dawley rats were randomized into three groups: healthy, control and bee venom groups. All rats were tested for locomotor activity at the beginning and end of the study. No intervention was made in the healthy group, whereas hepatic encephalopathy was induced in the control and bee venom groups by the administration of thioacetamide (TAA) (200 mg/kg/day). The bee venom group also received bee venom (5 mg/kg/day) subcutaneously every day for 14 days prior to the TAA administration. RESULTS: The results for the final locomotor activity tests were statistically better in the bee venom group than in the control group, supporting a beneficial effect of prophylactic bee venom application. Blood ammonia levels and liver weights, determined as indicators of inflammation, were lower in the bee venom group than in the control group and were close to levels in the healthy group, but not statistically significant. CONCLUSIONS: Bee venom administration has protective effects against the development of hepatic encephalopathy and offers a promising therapeutic opportunity in preventive medicine.

Computed tomographic features of portal vein thrombosis in two cats with splenosystemic shunts.

Two spayed female cats presented with hepatic encephalopathy due to hyperammonaemia. On abdominal ultrasound, concurrent portal vein thrombosis and splenosystemic shunts were suspected in both cats. Computed tomographic angiography clearly detected thrombi as non-contrast enhancing intraluminal structures in the main portal vein of both cats. Additionally, splenorenal shunts were revealed in both cats. Follow-up computed tomographic angiography for portal vein thrombosis was performed in both cats, only one of whom received anticoagulant therapy. In the untreated cat, portal vein thrombosis had progressed with the development of an aberrant tortuous vessel. In the cat treated with low-molecular-weight heparin, the thrombus progressively decreased in size and disappeared on follow-up diagnostic imaging. Computed tomographic angiography might be useful for the diagnosis and follow-up of portal vein thrombosis in cats.

Astrocyte lesions in cerebral cortex and cerebellum of dogs with congenital ortosystemic shunting.

BACKGROUND: Congenital portosystemic shunt (cPSS) is one of the most common congenital disorders diagnosed in dogs. Hepatic encephalopathy (HE) is a frequent complication in dogs with a cPSS and is a major cause of morbidity and mortality. Despite HE been a major cause of morbidity in dogs with a cPSS, little is known about the cellular changes that occur in the central nervous system of dogs with a cPSS. OBJECTIVES: The objective of this study was to characterise the histological changes in the cerebral cortex and cerebellum of dogs with cPSS with particular emphasis on astrocyte morphology. METHODS: Eight dogs with a confirmed cPSS were included in the study. RESULTS: Six dogs had substantial numbers of Alzheimer type II astrocytes and all cases had increased immunoreactivity for glial fibrillary acidic protein in the cerebral cortex, even if there were minimal other morphological changes. CONCLUSIONS: This study demonstrates that dogs with a cPSS have marked cellular changes in the cerebral cortex and cerebellum. The cellular changes that occur in the cerebral cortex and cerebellum of dogs with spontaneously arising HE are similar to changes which occur in humans with HE, further validating dogs with a cPSS as a good model for human HE.

Outcome of non-surgical dietary treatment with or without lactulose in dogs with congenital portosystemic shunts.

Background: Congenital portosystemic shunts (CPSS) are vascular anomalies, allowing portal blood to bypass the hepatic parenchyma, thereby accumulating toxic substances such as ammonia in the systemic circulation resulting in hepatic encephalopathy.Aim: To evaluate the outcome of non-surgically treated dogs with a CPSS.Methods: Case records of 78 dogs with a single congenital CPSS confirmed by ultrasound and/or computed tomography between September 2003 and February 2015 were reviewed. Median age at diagnosis of CPSS in dogs was 10.8 months (range 2-133 months). Non-surgical treatment was started as an adjusted diet (a diet restricted in protein) with or without lactulose. Owners were contacted by telephone to determine survival time and presumed cause of death, if applicable. In addition, a questionnaire was used to retrospectively assess quality of life (QoL) and CPSS scores in 37 dogs before and during non-surgical treatment. Differences between Kaplan-Meier curves were tested by a Log rank test.Results: Overall estimated median survival time (EMST) was 38.5 months (range 1 day - 91 months; 78 dogs). No significant differences between EMSTs were found between dogs with extra- (n = 48) or intrahepatic (n = 29) shunts, nor between treatment with only an adjusted diet, or an adjusted diet combined with lactulose. During non-surgical treatment, significant improvement in perceived QoL and CPSS scores were found (P < 0.01).Conclusion: Our study demonstrated that an overall median EMST of 3.2 years was reached and that owners retrospectively perceived that non-surgical treatment resulted in an improved QoL and clinical performance, irrespective of intrahepatic or extrahepatic CPSS location.

Successful management of clinical signs associated with hepatic encephalopathy with manual therapeutic plasma exchange in a dog.

OBJECTIVE: To describe the use of manual therapeutic plasma exchange (TPE) to manage hepatic encephalopathy (HE) in a dog. CASE SUMMARY: A 9-year-old neutered female Dachshund presented for HE secondary to a previously diagnosed portosystemic shunt. The hyperammonemia and severe clinical signs of HE persisted despite extensive medical management. Therapeutic plasma exchange was performed for stabilization prior to surgical shunt ligation. A total of 1 plasma volume was processed during a single manual TPE session. The ammonia immediately prior to TPE was 235 µmol/L (reference interval, 10-30 µmol/L) and decreased to 117 µmol/L by the end of the session. The dog showed significant improvement in clinical signs shortly after the session and remained stable thereafter. Shunt ligation was performed 5 days later with no complications observed with TPE or postoperatively. The dog was discharged 3 days after surgery with no neurological signs and was doing well 100 days after surgery. NEW OR UNIQUE INFORMATION PROVIDED: To the authors' knowledge, this is the first published report of manual TPE to manage HE in veterinary medicine. Therapeutic plasma exchange should be further investigated as a possible strategy to manage clinical signs of HE in patients that are refractory to medical management. Achieving this with manual TPE may be considered in patients that are too small for conventional TPE due to extracorporeal volume or in situations where conventional TPE is not available.

Serum melatonin in dogs with congenital portosystemic shunting, with and without hepatic encephalopathy.

BACKGROUND: Melatonin is a hormone produced and secreted primarily by the pineal gland and mainly metabolised in the liver. Increased melatonin concentrations have been reported in human cirrhosis and hepatic encephalopathy (HE), a syndrome of neurological dysfunction. The pathogenesis of canine HE is incompletely understood. Melatonin has been hypothesised as a contributor to the development of HE. The aim of this study was to investigate whether serum melatonin concentrations are increased in canine congenital portosystemic shunting (cPSS), with and without HE. METHODS: Medical records were retrospectively reviewed, for which archived (-80°C) serum samples were available. A canine competitive ELISA was used to measure melatonin in two cohorts: dogs with a final diagnosis of cPSS (n=23) with and without clinical signs of HE, and healthy dogs (n=15). RESULTS: Melatonin concentrations were not significantly different (P=0.81) between healthy controls (median 27.2 pg/mL, range 19.8-161.5 pg/mL) and dogs with cPSS (median 25.7 pg/mL, range 18.5-244.9 pg/mL). Serum melatonin did not differ between cPSS patients with and without clinical signs of HE (P>0.99). No correlation was found between serum melatonin and blood ammonia (Spearman rank correlation coefficient, rs =-0.41, P=0.08). CONCLUSION: Serum melatonin is not increased in canine cPSS with and without HE. We found no evidence that altered melatonin metabolism plays a role in the pathogenesis of cPSS-associated HE.

Comparative accuracy and precision of two commercial laboratory analyzers for the quantification of ammonia in cerebrospinal fluid.

BACKGROUND: Hyperammonemia is one of the contributing factors of hepatic encephalopathy (HE). Although blood ammonia concentrations are frequently measured in patients suspected of HE, systemic levels do not necessarily reflect the amount of ammonia in the central nervous system. Measuring ammonia in cerebrospinal fluid (CSF) can help to understand HE better and potentially improve the diagnosis and follow-up of patients with HE. OBJECTIVES: The objectives of this technical report were to evaluate the accuracy and precision of two commercial blood ammonia analyzers (Catalyst Dx, CatDX and Pocket Chem BA, PocBA) to measure CSF ammonia concentrations. METHODS: A pool of normal equine CSF was spiked with concentrated ammonia, and a series of six spiked samples were measured in parallel with both CatDx and PocBA. RESULTS: CatDx and PocBA data correlated excellently with but differed significantly from the spiked ammonia concentrations. These differences were smaller when ammonia CSF concentrations were measured with the PocBA than with the CatDx. In addition, values obtained with the PocBA were more precise than those measured with the CatDx, especially for low ammonia concentrations. CONCLUSION: This in-house comparative study shows that ammonia concentrations in spiked equine CSF correlate well with those measured by two commercial blood ammonia analyzers. Nevertheless, concentrations obtained with the PocBA are more accurate and more precise than those obtained with the CatDx, making the former device the preferred choice for clinical veterinary applications.

Computed Tomography of Lobular Dissecting Hepatitis in a Young Golden Retriever.

A 9 mo old female intact golden retriever presented for evaluation of chronic lethargy and decreased appetite. The serum biochemistry profile revealed increased liver enzymes consistent with a mixed hepatocellular and cholestatic pattern. A multiphase computed tomography angiography was performed to evaluate for a portosystemic shunt. Numerous hyperattenuating nodules were identified throughout the liver on the noncontrast-enhanced series. Histologic evaluation of percutaneous needle biopsy samples of a liver nodule showed a rare form of hepatitis called lobular dissecting hepatitis. Lobular dissecting hepatitis should be considered as a differential in young dogs with precontrast hyperattenuating hepatic nodules on noncontrast-enhanced computed tomography.

Protective role of chrysin on thioacetamide-induced hepatic encephalopathy in rats.

Hepatic encephalopathy (HE) is a serious neuropsychiatric syndrome due to either acute or chronic hepatic failure. This study aimed to investigate the possible neuroprotective effect of chrysin, a natural flavenoid on thioacetamide (TAA)-induced hepatic encephalopathy in rats. Also the effect of chrysin on motor impairment, cognitive deficits, oxidative stress, neuroinflammation, apoptosis and histopathological damage was assessed. HE was induced in Wistar rats by intraperitoneal (i.p.) injection of TAA (200 mg/kg) for three alternative days. Normal and control groups received the vehicle for 21 days. Chrysin was administered orally for 21 days (25, 50, 100 mg/kg) and starting from day 17, rats received i.p. dose of TAA (200 mg/kg) at three alternative days. Then behavioral, biochemical, histopathological and immunohistochemical analyses were conducted. Chrysin improved TAA-induced motor incoordination as it reduced final falling latency time in rotarod test, ameliorated cognitive deficits in object recognition test (ORT) and attenuated serum ammonia, hepatic liver enzymes namely, aspartate aminotransferase (AST) and alanine aminotransferase (ALT), reduced malondialdehyde (MDA), elevated reduced glutathione (GSH), reduced nuclear factor kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) brain contents. Chrysin administration also reduced Toll-4 receptor (TLR-4) gene expression, caspase-3 protein expression, hepatic necrosis and astrocyte swelling. This study depicts that chrysin exerted neuroprotective effect in TAA-induced HE rats, evidenced by improvement of cognitive deficits, motor incoordination and histopathological changes such as astrocyte swelling and vacuolization; hallmarks in HE, via reducing hyperammonia, ameliorating hepatic function, in addition to its anti-oxidant, inactivation of TLR-4/NF-κB inflammatory pathway, and anti-apoptotic effects.

Spongiform encephalomyelopathy in a calf with a congenital portosystemic shunt.

A 3-month-old Holstein heifer calf was presented because of an abnormal gait. Further examination revealed cranial nerve deficits, including a severely delayed corneal reflex. The calf was not ataxic and maintained an appetite, but was considerably stunted for her age. A postmortem examination resulted in a diagnosis of a congenital portosystemic shunt.

Encéphalomyélopathie spongiforme chez un veau atteint d'un shunt portosystémique congénital. Une génisse Holstein âgée de 3 mois a été présentée en raison d'une démarche anormale. Un examen a révélé des déficits nerveux crâniens, y compris un réflexe cornéen gravement retardé. Le veau n'était pas ataxique et avait conservé un appétit, mais avait une croissance ralentie pour son âge. Un shunt portosystémique congénital a été diagnostiqué à l'examen post mortem.(Traduit par Isabelle Vallières).

Multiple acquired portosystemic shunts secondary to primary hypoplasia of the portal vein in a cat.

A 6-year 5-month-old spayed female Scottish Fold cat presented with a one-month history of gait abnormalities, increased salivation, and decreased activity. A blood test showed hyperammonemia and increased serum bile acids. Imaging tests revealed multiple shunt vessels indicating acquired portosystemic shunt. Histopathologic analysis of liver biopsy showed features consistent with liver hypoperfusion, such as a barely recognizable portal vein, increased numbers of small arterioles, and diffuse vacuolar degeneration of hepatocytes. These findings supported the diagnosis of primary hypoplasia of the portal vein/microvascular dysplasia, (PHPV/MVD). To our knowledge, this is the first case of feline PHPV/MVD that developed multiple acquired portosystemic shunts and presented with hepatic encephalopathy.

Encefalopatia hepática secundária à intoxicação por Tephrosia cinerea em ovinos / Hepatic encephalopathy secondary to poisoning by Tephrosia cinerea in sheep

A intoxicação por Tephrosia cinerea causa fibrose hepática periacinar em ovinos na região semiárida do Nordeste, com quadro clínico de ascite acentuada, e, ocasionalmente, com sinais neurológicos. Neste trabalho foram estudadas 16 ovinos em 6 surtos de intoxicação por T. cinerea. Todos os ovinos apresentaram lesões histológicas de fibrose periacinar e seis apresentaram, no encéfalo, vacuolização da substância branca e da junção entre a substância branca e a cinzenta com presença de astrócitos de Alzheimer tipo II na substância cinzenta. A doença foi reproduzida experimentalmente em dois ovinos que apresentaram ascite, desvios vasculares (shunts) porto-sistêmicos e sinais nervosos com lesões histológicas semelhantes a dos casos espontâneos. Na técnica de imuno-histoquímica houve marcação fraca ou ausente do citoplasma astrocitário para o anticorpo anti-GFAP em seis ovinos evidenciando uma alteração degenerativa, em que os astrócitos acumulam corpos densos e reduzem o volume de GFAP. Houve marcação positiva para o anticorpo anti-S100 em oito ovinos, incluindo os dois ovinos experimentais o que sugere reatividade celular, com proliferação mitocondrial e de retículo endoplasmático liso. Estas alterações são caraterísticas dos efeitos da amônia nos astrócitos. Conclui-se que na intoxicação por T. cinerea em alguns ovinos ocorrem sinais nervosos em consequência da encefalopatia hepática.(AU)

In the semiarid region of northeastern Brazil, Tephrosia cinerea causes periacinar hepatic fibrosis in sheep with severe ascites and, occasionally, nervous signs. Sixteen sheep from six outbreaks of T. cinerea poisoning were studied. All sheep had histologic lesion of periacinar fibrosis and six showed, in the brain, vacuolization (spongy degeneration) of the white matter and junction between grey and white matter and presence of Alzheimer type II astrocytes in the grey matter. The disease was produced experimentally in two sheep, that presented porto-sistemic shunts and similar histologic lesions as those observed in the spontaneous cases. Immunohistochemistry revealed weak labelling with anti-GFAP antibodies suggesting a degenerative alteration of astrocytes with accumulation of dense bodies and reduction of the GFAP. There was strong labelling with anti-S100 antibodies suggesting cellular reactivity with proliferation of mitochondria and endoplasmatic reticulum. Such alterations are characteristic of the effects caused by ammonia on the astrocytes. It is concluded that in poisoning by T. cinerea nervous signs due to hepatic encephalopathy occur in some sheep.(AU)

Ammonia concentrations in arterial blood, venous blood, and cerebrospinal fluid of dogs with and without congenital extrahepatic portosystemic shunts.

OBJECTIVE To compare ammonia concentrations in arterial blood, venous blood, and CSF samples of dogs with and without extrahepatic portosystemic shunts (EHPSS). ANIMALS 19 dogs with congenital EHPSS and 6 healthy control dogs. PROCEDURES All dogs underwent a physical examination and then were anesthetized for transsplenic portal scintigraphy to confirm the presence or absence of EHPSS. While dogs were anesthetized, arterial and venous blood samples and a CSF sample were simultaneously collected for determination of ammonia concentration, which was measured by use of a portable blood ammonia analyzer (device A) and a nonportable biochemical analyzer (device B). Results were compared between dogs with EHPSS and control dogs. RESULTS Arterial, venous, and CSF ammonia concentrations for dogs with EHPSS were significantly greater than those for control dogs. For dogs with EHPSS, ammonia concentrations in both arterial and venous blood samples were markedly increased from the reference range. There was a strong positive correlation between arterial and venous ammonia concentrations and between blood (arterial or venous) and CSF ammonia concentrations. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that blood and CSF ammonia concentrations in dogs with EHPSS were greater than those for healthy dogs and were strongly and positively correlated, albeit in a nonlinear manner. This suggested that the permeability of the blood-brain barrier to ammonia may be abnormally increased in dogs with EHPSS, but further investigation of the relationship between blood or CSF ammonia concentration and clinical signs of hepatic encephalopathy or the surgical outcome for dogs with EHPSS is warranted.

Regional cerebral blood flow assessed by single photon emission computed tomography (SPECT) in dogs with congenital portosystemic shunt and hepatic encephalopathy.

Regional cerebral blood flow (rCBF) in eight dogs with congenital portosystemic shunt (PSS) and hepatic encephalopathy (HE) was compared with rCBF in eight healthy control dogs using single photon emission computed tomography (SPECT) with a 99mtechnetium-hexamethylpropylene amine oxime (99mTc-HMPAO) tracer. SPECT scans were abnormal in all PSS dogs. Compared to the control group, rCBF in PSS dogs was significantly decreased in the temporal lobes and increased in the subcortical (thalamic and striatal) area. Brain perfusion imaging alterations observed in the dogs with PSS and HE are similar to those in human patients with HE. These findings suggest that dogs with HE and PSS have altered perfusion of mainly the subcortical and the temporal regions of the brain.

Hepatic Lipodystrophy in Galloway Calves.

Hepatic lipodystrophy in Galloway calves is a fatal liver disease affecting a small proportion of the Galloway breed described in different parts of Europe and North America during the past decades. The clinical findings include a diversity of neurological signs. Clinical pathology findings frequently indicate hepatobiliary disease. Postmortem examination reveals an enlarged, pale yellow, and firm liver. Histologic lesions include hepatic fibrosis, hepatic lipidosis, and bile duct hyperplasia. To date, the etiopathogenesis remains obscure. Infectious causes, intoxications, and a hereditary origin have been considered. We describe hepatic lipodystrophy in Galloway calves from an extensively farmed cow-calf operation in southern Germany. Main clinical findings in 6 calves were consistent with hepatic encephalopathy. Clinical pathology findings in 5 of 6 tested animals revealed increased concentration of total bilirubin (maximum value [MV], 54 µmol/l; reference range [RR], <8.5 µmol/l), direct bilirubin (MV, 20 µmol/l; RR, <3.4 µmol/l), increased activity of gamma glutamyl transferase (MV, 162 U/l; RR, <36 U/l) and glutamate dehydrogenase (MV, 420 U/l; RR, <16 U/l). In addition, activity of glutathione peroxidase was decreased in all tested ( n = 5) animals (MV, 61 U/g hemoglobin [Hb]; RR, >250 U/g Hb). Postmortem examination in 6 calves revealed a firm, diffusely enlarged yellow liver with a finely nodular surface. Histologic lesions included hepatic fibrosis, hepatic lipidosis, and bile duct hyperplasia. Our findings add to the existing data on hepatic lipodystrophy in the Galloway breed and outline a protocol to aid in the diagnosis of this disorder.

Hepatic Encephalopathy.

This article reviews hepatic encephalopathy (HE) in companion animals. Clinical signs and categories of hepatic disease likely to cause HE are discussed. Ammonia has a key role in pathogenesis and current concepts in body ammonia metabolism are reviewed. Inflammation and manganese accumulation are also thought to be important in pathogenesis. Treatment of HE in acute and chronic cases is discussed along with the rationale for current treatment recommendations. Potential avenues for new treatments and human treatments, which may be transferable to companion animals, are reviewed.

Hepatic encephalopathy in dogs and cats.

OBJECTIVE: To comparatively review the pathogenesis, clinical presentation, diagnosis, and management of hepatic encephalopathy (HE) in dogs and cats. DATA SOURCES: The Medline database was searched for articles related to HE in people, dogs, and cats. Articles published within the last 5 years were given special importance. HUMAN DATA SYNTHESIS: The pathogenesis of HE is complex and incompletely understood, but ammonia appears to play a central role. Hyperammonemia leads to accumulation of glutamine in astrocytes, with subsequent astrocyte swelling and neurological dysfunction. The development of HE in patients with hepatic cirrhosis is a poor prognostic indicator. The fermentable disaccharide lactulose and the antimicrobial rifaximin are US Food and Drug Administration approved treatments for human HE. Severe protein restriction is no longer recommended for patients with this condition. VETERINARY DATA SYNTHESIS: HE is often associated with portosystemic shunting in dogs and cats. Ammonia plays a central role in the pathogenesis of HE in dogs and cats, but other factors such as manganese and endogenous benzodiazepines may also contribute. Recently, a soy protein-based diet was found to be beneficial in treating canine HE. Severe dietary protein restriction is likely to be detrimental in affected animals. There have been no clinical trials of drugs routinely used in the management HE in veterinary medicine, but lactulose and antimicrobials such as metronidazole are well-established treatments. CONCLUSIONS: HE is a potentially life-threatening condition that is probably underdiagnosed in companion animals. Although various treatment recommendations have been proposed, there is a lack of evidence in the veterinary literature regarding optimal strategies for the management of this condition. As our understanding of the pathogenesis of HE in dogs and cats evolves, novel diagnostic tests and therapeutic agents may become available.

Hyperammonemic hepatic encephalopathy management through L-ornithin-L-aspartate administration in dogs.

Seventeen dogs were treated with L-ornithin-L-aspartate (LOLA; experimental group). Three dogs were treated with lactulose recognized therapy (control group). Following LOLA administration, 15 dogs experienced a significant decrease in ammonia level (p ＜ 0.05) and showed clinical signs of improvement. However, there were no clinical signs of improvement in two dogs, even though the ammonia level decreased. Conversely, the clinical signs of the control group also improved and the ammonia level decreased, although these changes were not significant (p ＞ 0.05). These results suggest that LOLA is an effective drug to treat hyperammonemia in veterinary medicine.

Putative precipitating factors for hepatic encephalopathy in dogs: 118 cases (1991-2014).

OBJECTIVE: To elucidate the relationship between plasma ammonia concentration and severity of hepatic encephalopathy and determine whether factors that precipitate hepatic encephalopathy in humans are associated with the presence of clinical signs of hepatic encephalopathy in dogs previously treated for the disease. DESIGN: Retrospective case series. ANIMALS: 118 dogs with hepatic encephalopathy. PROCEDURES: The medical records database of a veterinary teaching hospital was searched for records of dogs in which hepatic encephalopathy was diagnosed between October 1, 1991, and September 1, 2014. Hepatic encephalopathy severity was graded on a 5-point scale, and the correlation between disease severity and plasma ammonia concentration was determined. Respective associations between hepatic encephalopathy and systemic inflammatory response syndrome, gastrointestinal hemorrhage, dietary indiscretion, constipation, furosemide treatment, azotemia, hypokalemia, hyponatremia, alkalosis, and hyperammonemia were assessed by Fisher exact tests followed by multivariable logistic regression. RESULTS: Severity of hepatic encephalopathy at hospital admission was not significantly correlated with plasma ammonia concentration. Dogs treated for hepatic encephalopathy prior to hospital admission were significantly less likely to have clinical signs of the disease at hospital admission, compared with dogs that were not treated for the disease (OR, 0.36; 95% confidence interval, 0.17 to 0.78). None of the putative precipitating factors for hepatic encephalopathy were significantly associated with the presence of clinical signs of the disease at hospital admission. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that hepatic encephalopathy treatment alleviated clinical signs of the disease. Further investigation is necessary to identify precipitating factors for hepatic encephalopathy in dogs.

Magnetic resonance imaging of the lentiform nuclei in dogs with portosystemic shunts.

OBJECTIVES: To develop and evaluate a method to quantify the T1-weighted magnetic resonance imaging signal intensity of the lentiform nuclei in dogs, and to determine if there is any significant difference in this signal intensity between dogs with portosystemic shunts and a control group. MATERIALS AND METHODS: A retrospective blinded study was performed to investigate the reliability and use of a quantitative method for assessing the T1-weighted magnetic resonance imaging signal intensity of the lentiform nuclei in dogs with and without portosystemic shunts. The lentiform nuclei index (mean lentiform nucleus signal intensity/mean white matter signal intensity) was calculated for nine dogs with portosystemic shunts and a control group of 14 dogs. RESULTS: The intra- and inter-observer intraclass correlation coefficients were considered excellent (>0 · 75), suggesting that the lentiform nuclei index is a reliable method. The dogs with portosystemic shunts had a higher lentiform nuclei index than the control group (P = 0 · 0127). CLINICAL SIGNIFICANCE: This method of quantifying the T1-weighted magnetic resonance imaging signal intensity of the lentiform nuclei was reliable and showed that dogs with portosystemic shunts tend to have increased signal intensity. Further prospective studies are necessary to investigate the clinical significance and applications of these findings.