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Idiopathic hepatic fibrosis was diagnosed by liver biopsy in 15 young dogs, of which nine were German shepherds. Clinical signs included ascites, anorexia, weight loss and hepatic encephalopathy. Erythrocyte microcytosis was a consistent clinical feature, and clinical chemistry generally revealed hypoproteinaemia and high serum activities of alkaline phosphatase and, to a smaller extent, alanine aminotransferase. Fasting blood ammonia and serum bile acid concentrations were increased in most dogs examined, and all the dogs tested had prolonged retention of sulfobromophthalein at 30 minutes. Multiple acquired portosystemic shunts were revealed by laparotomy and/or portography. Non-inflammatory fibrosis was present to different degrees in all the dogs' livers, and on the basis of its predominant location these were classified as having central perivenous fibrosis, diffuse pericellular fibrosis or periportal fibrosis. The response to symptomatic treatment and anti-fibrotic therapy with glucocorticosteroids or colchicine was variable. Seven dogs died or were euthanased shortly after diagnosis, but one dog survived two-and-a-half years, and three dogs were still alive more than four years after the initial diagnosis.
Vet Rec 1993 Jul 31
PMID:Idiopathic hepatic fibrosis in 15 dogs. 821 1

A three-month-old native pony foal had a history of recurrent episodes of bizarre neurological behaviour. The results of clinical examinations were non-specific but clinicopathological investigations indicated hepatic encephalopathy. A percutaneous, needle liver biopsy revealed histopathological changes consistent with a portosystemic shunt, which was later identified by operative mesenteric portovenography, and confirmed at post mortem.
Vet Rec 1993 May 01
PMID:Clinical signs and radiographic diagnosis of a portosystemic shunt in a foal. 851 6

Inherited portosystemic shunts occur in 2 to 3 per cent of Irish wolfhounds and are associated with high venous ammonia concentrations and signs of hepatic encephalopathy. Moreover, the vast majority of Irish wolfhound pups without signs of hepatic encephalopathy have moderate hyperammonaemia. The aim of this study was to investigate whether the increased ammonia levels in these clinically healthy dogs are caused by low-grade portosystemic shunting, and whether the hyperammonaemia persists in adulthood. The fasting venous ammonia concentration and the fraction of portal blood by-passing the liver, expressed as the shunt index (SI) were measured in 42 Irish wolfhound pups, and the dogs with high SI values were examined post mortem. The ammonia concentration was also measured in 25 adult Irish wolfhounds in which it had been measured when they were seven to eight weeks old. Eleven of the 42 pups had a portosystemic shunt, as evidenced by a high SI (mean 0.82, range 0.12 to 1.00, normal range 0.01 to 0.05) and by post mortem examination. Their mean ammonia concentration was 249 mumol/litre (range 121 to 350). The 31 pups with a normal SI (mean 0.025, range 0.00 to 0.05) had a mean ammonia concentration of 93 mumol/litre (range 51 to 125). In the 25 dogs in which the ammonia concentration was measured twice, the mean concentration at seven to eight weeks of age was 77 mumol/litre (range 47 to 115) and in the adults it was 17 mumol/litre (range 6 to 27) at a mean age of 3.1 years (range 1.0 to 8.9). These results show that Irish wolfhounds with ammonia concentrations > 125 mumol/litre had a portosystemic shunt, whereas the hyperammonaemia in dogs with ammonia concentrations < 120 mumol/litre was transient and of metabolic origin.
Vet Rec 1996 Feb 03
PMID:Transient metabolic hyperammonaemia in young Irish wolfhounds. 871 92

Hepatic lipodystrophy has been recognised in pedigree Galloway calves since 1965. Between 1975 and 1984 15 cases from five farms were examined. The calves initially appear normal and in good bodily condition but invariably die by five months of age. The characteristic clinical and neurological changes lead to body tremors, opisthotonus, and dyspnoea before the animals become recumbent and die. On postmortem examination the most significant finding in all cases was an enlarged, pale and mottled liver weighing up to 2.75 kg. Limited histopathological examinations of the brain and liver revealed changes suggestive of hepatic encephalopathy. Exhaustive investigations of the farms failed to reveal any significant findings and the small number of cases made it impossible to determine whether the disease was genetically determined; limited evidence suggests that a 'storage disease' cannot be excluded.
Vet Rec 1999 Feb 06
PMID:Hepatic lipodystrophy of pedigree Galloway calves. 1007 61

The measurement of ammonia in biological fluids is the only way to diagnose and evaluate hepatic encephalopathy, but samples for ammonia measurement cannot be stored or sent by post. Two analysers for use in veterinary practice have recently become available, the VetTest and the Blood Ammonia Checker II; the reliability of ammonia measurements in canine blood with these two analysers has been evaluated by comparing the results with a standard automated enzymatic assay. Blood samples from 39 dogs, with a range of ammonia concentrations from 5 to 589 microM, were used simultaneously in the three assays. The blood samples were placed immediately on ice, and the measurements were made in duplicate. The intra-assay coefficients of variation were 13.7 per cent for the VetTest, 4.7 per cent for the Blood Ammonia Checker, and 2.8 per cent for the enzymatic assay. The correlation coefficients over the entire range of concentrations were 0.79 between the VetTest and the enzymatic assay, and 0.98 between the Ammonia Checker and the enzymatic assay. The ammonia concentrations recorded in the enzymatic assay were divided into 12 samples within the normal range (0 to 50 microM), 18 samples with moderately increased concentrations (51 to 150 microM), and nine samples with concentrations above 150 microM. No correlation or a poor correlation was found between the results from the VetTest and those from the enzymatic assay from 0 to 50 microM (R = 0.27) and from 50 to 150 microM (R = 0.51; P = 0.05). The results from the VetTest were only reliable in samples with the highest concentrations (R = 0.93; P < 0.05). In contrast, the results from the Ammonia Checker correlated well with the results from the enzymatic assay over all the ranges: R = 0.79 (P < 0.05) from 0 to 50 microM, R = 0.86 (P < 0.05) from 50 to 150 microM, and R = 1.00 (P < 0.05) in samples exceeding 150 microM.
Vet Rec 1999 May 08
PMID:Evaluation of ammonia measurements in dogs with two analysers for use in veterinary practice. 1037 79

The clinicopathological features of 50 cases of equine hepatic disease were reviewed. There was a wide range of clinical signs and at least 50 per cent of the animals exhibited either dull demeanour, anorexia, abdominal pain, cerebral dysfunction and/or weight loss. Life-threatening complications of hepatic failure recorded were: gastric impaction in 10 cases, bilateral laryngeal paralysis in seven cases and coagulopathy in five cases. All the cases had high activities of gamma-glutamyl transferase (GGT) and most had high activities of glutamate dehydrogenase (GLDH) and high concentrations of bile acids. Fewer of the horses had abnormal concentrations of bilirubin, albumin and globulin. The horses that were euthanased or died had significantly higher concentrations of GGT, GLDH and bile acids than the survivors. There were biochemical data for 18 cases with signs of hepatic encephalopathy, all of them had plasma ammonia levels greater than 90 micromol/litre but this was not significantly correlated with the clinical severity of the condition. Half of the cases with hepatic encephalopathy were hyperglycaemic, none was hypoglycaemic, and none had abnormally low levels of plasma urea.
Vet Rec 1999 Jul 31
PMID:Clinicopathological features of equine primary hepatic disease: a review of 50 cases. 1046 31

In hepatic encephalopathy the brain lesions are usually characterised by polymicrocavitation, preferentially in the white matter, and the occurrence of Alzheimer type II cells. This paper describes an unusual manifestation of hepatic encephalopathy in two Irish wolfhound siblings in which the white matter was not involved predominantly. Both puppies had developed progressive neurological disturbances and signs of blindness. Histologically, there were widespread spongiform changes in the neuropil and fibre bundles interspersed within the grey matter, and there were some neuronal vacuoles. In both animals, the regions of the brain mainly affected were the nucleus caudatus, amygdala, cerebellar nuclei, mesencephalon, thalamus, hypothalamus and medulla oblongata. An astrogliosis characterised by Alzheimer type II-like cells was also observed. Electron microscopy revealed a splitting of the myelin sheath. No infectious agents such as rabies virus, canine distemper virus or prion proteins were detected. The main findings in the portal regions of the liver consisted of a dilatation of the lymphatic vessels and increased numbers of small arteries, indicating that a portosystemic shunt was the probable cause of the spongiform brain lesions.
Vet Rec 2003 Nov 29
PMID:Unusual manifestation of hepatic encephalopathy in two Irish wolfhound siblings. 1468 42

Doppler ultrasonography was used to evaluate the portal vein in 14 dogs before, immediately after and four weeks after a partial ligation of a congenital extrahepatic portocaval shunt. By four weeks after the operation, the hepatofugal or zero flow in the portal vein segment cranial to the shunt origin had become a hepatopetal flow in 13 of the dogs, which became clinically healthy. The other dog continued to have a hepatofugal flow in the portal vein cranial to the origin of the shunt and continued to show clinical signs of hepatic encephalopathy. The shunt remained functional in six of the dogs, and three of them developed portosystemic collaterals in addition. In the other eight dogs the patent shunt was non-functional, because a hepatopetal flow was detected in the shunt adjacent to the portal vein. This flow was the result of the splenic vein entering the shunt, and the splenic blood dividing; some flowed via the shunt towards the portal vein, preventing the portal blood from shunting, and the rest flowed via the attenuated shunt segment to the caudal vena cava. Shunting of the splenic venous blood was clinically insignificant.
Vet Rec 2004 Oct 09
PMID:Ultrasonographic evaluation of partially attenuated congenital extrahepatic portosystemic shunts in 14 dogs. 1551 5

Six ponies and four horses with a mean (sd) age of 15.9 (6.0) years developed sudden-onset bilateral laryngeal paralysis (BLP) in association with hepatic dysfunction. Nine of them had been referred for the investigation of respiratory distress, and one pony had been referred for weight loss before BLP developed. Nine of the animals had clinicopathological evidence of liver disease, and nine had histological evidence of liver disease. All of the animals had one or more of the following: hepatic encephalopathy (in eight), hyperammonaemia (in six) and endoscopic evidence of BLP (in nine). Three of the animals had signs of pituitary pars intermedia dysfunction, a diagnosis supported in two by endocrine function testing, and in two by histopathological examination. Histopathological examination of the intrinsic laryngeal musculature and recurrent laryngeal nerves of four of the horses and of the region of the nucleus ambiguus of two did not reveal any abnormalities. Three of the animals were euthanased after they had first been examined, and one improved temporarily before the condition recurred. A temporary tracheostomy was performed in six of the animals, five of which subsequently died or were euthanased; one pony recovered.
Vet Rec 2009 Jan 31
PMID:Bilateral laryngeal paralysis associated with hepatic dysfunction and hepatic encephalopathy in six ponies and four horses. 1918 45

Dogs with liver disease have been shown to have increased serum C-reactive protein (CRP) concentrations. However, it is unclear whether dogs with liver disease also have increased serum haptoglobin concentrations. The aim of the study was to measure serum haptoglobin concentrations in healthy dogs, hospitalised dogs and dogs with liver diseases. Haptoglobin concentrations were measured in 30 healthy dogs, 47 hospitalised dogs with non-hepatic illness, 46 dogs with congenital portosystemic shunt (cPSS) and 11 dogs with primary hepatopathy. Haptoglobin concentrations were not significantly different between cPSS dogs with and without hepatic encephalopathy (HE), thus all cPSS dogs were considered as one group. Haptoglobin concentrations were significantly different between the remaining groups (P<0.0001). Hospitalised ill dogs had significantly higher haptoglobin concentrations than healthy dogs (P<0.001), dogs with cPSS (P<0.001) and dogs with primary hepatopathy (P<0.05). There was no significant difference between haptoglobin concentrations in healthy dogs, dogs with cPSS and dogs with primary hepatopathy. Haptoglobin concentrations were not significantly increased in dogs with liver diseases or in dogs with cPSS and HE. This is in contrast with the previously reported CRP results. This study demonstrates that liver function should be considered when interpreting haptoglobin concentrations in dogs.
Vet Rec 2013 Dec 14
PMID:Serum haptoglobin concentrations in dogs with liver disease. 2415 22


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