Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is a hepatitis of dogs which occurs in acute, persistent and chronic forms. Histological studies of spontaneous cases suggested that several apparently diverse hepatic diseases might be stages of one process. This was also implied by follow up studies and case histories: acute non-lethal episodes were followed later by the development of chronic hepatitis, cirrhosis and liver failure. Serum was taken and homogenates of liver were made from three field cases representing different putative temporal stages of the complex. These were injected into experimental dogs and a hepatitis was induced in all. The cytopathological and histological changes were the same in all animals and were identical to field cases. Acute lethal disease and persistent infections were produced. Two second passages were carried out and an identical condition was induced, characterised by recurrent episodes of subclinical hepatitis and persistent infection. It is suggested that the disease might be named canine acidophil cell hepatitis in view of the pathognomonic cytopathology. Specific morphological criteria have been established for this hepatitis.
Vet Rec 1985 Jun 15
PMID:A new transmissible agent causing acute hepatitis, chronic hepatitis and cirrhosis in dogs. 402 28

An outbreak of hepatic cirrhosis in a flock of young geese was investigated. The affected geese were cyanotic with purple beaks, shanks and footwebs. On post mortem examination severe atrophy of the liver was seen and, histologically, extensive areas of necrosis, cirrhosis and bile duct proliferation were prominent. Liver function tests and serum enzyme levels confirmed that the liver damage was extensive. The findings are compared with those found in aflatoxicosis of other avian species.
Vet Rec 1982 Jan 30
PMID:Hepatic cirrhosis suggesting aflatoxicosis in a flock of geese. 718 88

Two dogs with metabolic epidermal necrosis had hyperkeratosis of the footpads accompanied by erythematous, erosive and crusting lesions affecting the muzzle, external genitalia, perineum and periocular regions. Histopathological examination of skin biopsies revealed a superficial hydropic dermatitis with marked parakeratosis. Both dogs had high plasma activities of alkaline phosphatase and alanine aminotransferase and high concentrations of glucose, and also a marked hypoaminoacidaemia. Despite these similarities, the cutaneous eruptions were associated with different underlying diseases. One dog had a pancreatic carcinoma which had metastasised widely; the primary tumour and the metastases showed glucagon immunoreactivity on immunocytochemical staining, and the dog's plasma glucagon concentration was markedly greater than that of control dogs. The other dog had diffuse hepatic disease; its plasma glucagon concentration was similar to that of control samples and cirrhosis was identified post mortem. Metabolic epidermal necrosis in dogs is a distinct cutaneous reaction pattern which may be associated with different underlying systemic diseases; however, the pathogenesis of the skin lesions remains unclear.
Vet Rec 1995 May 06
PMID:Metabolic epidermal necrosis in two dogs with different underlying diseases. 763 36

Liver samples from four groups of calves were analysed chemically and histologically for copper and iron levels. Milk replacer-fed 'yellow' calves were compared with milk replacer-fed 'white' calves, concentrate and silage-fed 'pink' calves and concentrate and silage-fed young 'red' fattening bulls. In the milk replacer-fed calves high copper and low iron levels were measured in the liver, whereas in the concentrate and silage fed pink calves and fattening bulls lower copper and higher iron levels were found. The yellow calves appeared to be icteric and had chronic hepatitis. Their hepatic histopathology was characterised by fibrosis, cirrhosis, fatty change, increased amounts of stainable copper, necrobiosis and prominent cholestasis; some animals had intranuclear inclusion bodies in the hepatocytes. They had similar or lower hepatic copper levels than the white calves and varying iron levels, indicating that copper toxicity was not the primary cause of the hepatic damage.
Vet Rec 1993 Feb 13
PMID:Yellow discoloration in veal calves: the role of hepatic copper. 845 46

In a previous study in dogs with chronic liver disease it was found that a combination of clinical features and laboratory findings was useful in differentiating liver diseases but could not be used to evaluate a dog's prognosis. When an electrophoretic analysis of the serum proteins was included, marked decreases in the concentrations of albumin and the alpha-globulins alpha-1-antitrypsin and haptoglobin were observed in terminal liver cirrhosis, indicating impaired liver function. However, low albumin concentrations, together with normal or increased concentrations of alpha-1-antitrypsin and haptoglobin, were observed in dogs which, although severely depressed when examined, often recovered and survived for a year or more.
Vet Rec
PMID:Serum protein electrophoresis as a prognostic marker of chronic liver disease in dogs. 896 72

Immunocytochemical localization of big endothelin-1 (big ET-1), ET-1, and ET receptor A and B (ET(A) and ET(B)), and gene expression of prepro ET-1 mRNA were examined on the rat liver vasculature. Immunoreactivities for big ET-1 and ET-1 were preferentially seen along the endothelium of interlobular veins (IV) and artery (IA), although the staining intensity was more pronounced in IV. Expression of preproET-1 mRNA was detected in both vascular endothelia and the signal intensity was more prevalent in IV. Immunoelectron microscopy showed that rough endoplasmic cisterns were immunoreactive for big ET-1, while Weibel-Palade (WP) bodies, a storage site for ET-1, were immunoreactive for ET-1 in endothelial cells of IV. These results indicate that endothelial cells of IV are the major site of synthesis of ET-1, which is extracellularly secreted by degranulation and/or exocytosis of WP bodies. Hepatic stellate cells (HSCs), especially of the plasma membrane of perisinusoidal and interhepatocellular processes, were immunoreactive for both ET(A) and ET(B) receptor antibodies. These findings suggest that ET-1 receptor-mediated HSC contraction is involved in the regulation of hepatic sinusoidal blood flow as previously cited in mammalian liver cirrhosis. We also showed that sarcolemma and caveoles in the smooth muscle cells of the media of IV, and its branches before reaching the hepatic sinusoids, were immunoreactive for ET(A) receptor antibody. The results suggest that such vessels, which contains a large amount of hepatic blood inflow, participate in pump mechanism toward hepatic sinusoidal circulation in a receptor-mediated paracrine fashion.
Anat Rec 2000 08 01
PMID:Synthesis and receptor sites of endothelin-1 in the rat liver vasculature. 1090 35

Liver progenitor cells as well as hepatic stellate cells have neuroendocrine features. Progenitor cells express chromogranin-A and neural cell adhesion molecule, parathyroid hormone-related peptide, S-100 protein, neurotrophins, and neurotrophin receptors, while hepatic stellate cells express synaptophysin, glial fibrillary acidic protein, neural cell adhesion molecule, nestin, neurotrophins, and their receptors. This phenotype suggests that these cell types form a neuroendocrine compartment of the liver, which could be under the control of the central nervous system. We recently showed that the parasympathetic nervous system promotes progenitor cell expansion after liver injury, since selective vagotomy reduces the number of progenitor cells after chemical injury in the rat. Similarly, after transplantation, which surgically denervates the liver, human livers that develop hepatitis have fewer progenitor cells than native, fully innervated livers with similar degrees of liver injury. There is also accumulating experimental evidence linking the autonomic system, in particular the sympathetic nervous system (SNS), with the pathogenesis of cirrhosis and its complications. Recently, it has been shown that hepatic stellate cells themselves respond to neurotransmitters. Moreover, inhibition of the SNS reduced fibrosis in carbon tetrachloride-induced liver injury. In view of the denervated state of transplanted livers, it is very important to unravel the neural control mechanisms of regeneration and fibrogenesis. Moreover, since there is a shortage of donor organs, a better understanding of the mechanisms of regeneration could have therapeutic possibilities, which could even obviate the need for orthotopic liver transplantation.
Anat Rec A Discov Mol Cell Evol Biol 2004 Sep
PMID:Neuroregulation of the neuroendocrine compartment of the liver. 1538 10

This chapter reviews recent evidence that the sympathetic nervous system (SNS) regulates liver repair by modulating the phenotypes of hepatic stellate cells (HSCs), the liver's principal fibrogenic cells, and hepatic epithelial progenitors, i.e., oval cells. SNS nerve fibers touch HSCs and these cells express adrenoceptors, suggesting that HSCs may be targets for SNS neurotransmitters. HSCs also contain catecholamine biosynthetic enzymes, release norepinephrine (NE), and are growth-inhibited by adrenoceptor antagonists. In addition, HSCs from mice with reduced levels of NE grow poorly in culture and exhibit inhibited activation during liver injury. Finally, growth and injury-related fibrogenic responses are rescued by adrenoceptor agonists. Thus, certain SNS inhibitors (SNSIs) protect experimental animals from cirrhosis. Conversely, SNSIs enhance the hepatic accumulation of oval cells (OCs) in injured livers. This response is associated with improved liver injury. Because SNSIs do not affect the expression of cytokines, growth factors, or growth factor receptors that are known to regulate OCs, and OCs express adrenoceptors, it is conceivable that catecholamines influence OCs by direct interaction with OC adrenoceptors. Given evidence that the SNS regulates the viability and activation of HSCs and OCs differentially, SNSIs may be novel therapies to improve the repair of damaged livers.
Anat Rec A Discov Mol Cell Evol Biol 2004 Sep
PMID:Sympathetic nervous system regulation of liver repair. 1538 23

Over the course of one year, slight jaundice and ascites suggestive of chronic liver disease occurred in 17 German shepherd dogs from one breeding colony. Blood analyses, performed twice with a six-month interval, revealed elevated serum activities of liver enzymes in 13 dogs. In addition, four young adult German shepherd dogs that showed severe ascites, slight jaundice and increased serum liver enzyme activities were referred for further evaluation. Because of their poor prognosis these four dogs were euthanased. There were no signs of photosensitivity. Postmortem examinations revealed macronodular darkened livers, which were characterised histopathologically by cirrhosis associated with aggregates of brown pigments showing a striking orange birefringence in polarised light. Ultrastructurally, the crystalline pigments were typical of protoporphyrins. High-performance liquid chromatographic analysis of liver samples revealed very high levels of protoporphyrins (mean 9550 nmol/g wet liver, reference value 0.41 nmol/g wet liver) and low activities of ferrochelatase (mean 0.274 mmol/mg protein/hour, reference value 0.684 nmol/mg protein/hour). Twenty-six months after the onset of the hepatopathies, the clinical condition of the 13 surviving dogs had improved and their serum liver enzyme activities were normal. The clinical histories and pedigree analyses were not in concordance with an inherited form of protoporphyria. There was no known history of exposure to toxic substances or drugs. The findings are in accordance with a transient erythropoietic protoporphyria associated with hepatic complications, presumably caused by exposure to a porphyrinogenic, ferrochelatase-inhibitory substance of unknown origin.
Vet Rec 2006 Jan 28
PMID:Transient erythropoietic protoporphyria associated with chronic hepatitis and cirrhosis in a cohort of German shepherd dogs. 1644 37

The liver produces a large amount of lymph, which is estimated to be 25 to 50 % of lymph flowing through the thoracic duct. The hepatic lymphatic system falls into three categories depending on their locations: portal, sublobular, and superficial lymphatic vessels. It is suggested that 80 % or more of hepatic lymph drains into portal lymphatic vessels, while the remainder drains through sublobular and capsular lymphatic vessels. The hepatic lymph primarily comes from the hepatic sinusoids. Our tracer studies, together with electron microscopy, show many channels with collagen fibers traversing through the limiting plate and connecting the space of Disse with the interstitial space either in the portal tracts, or around the sublobular veins. Fluid filtered out of the sinusoids into the space of Disse flows through the channels traversing the limiting plate either independently of blood vessels or along blood vessels and enters the interstitial space of either portal tract or sublobular veins. Fluid in the space of Disse also flows through similar channels traversing the hepatocytes intervening between the space of Disse and the hepatic capsule and drains into the interstitial space of the capsule. Fluid and migrating cells in the interstitial space pass through prelymphatic vessels to finally enter the lymphatic vessels. The area of the portal lymphatic vessels increases in liver fibrosis and cirrhosis and in idiopathic portal hypertension. Lymphatic vessels are abundant in the immediate vicinity of the hepatocellular carcinoma (HCC) and liver metastasis. HCCs expressing vascular endothelial growth factor-C are more liable to metastasize, indicating that lymphangiogenesis is associated with their enhanced metastasis.
Anat Rec (Hoboken) 2008 Jun
PMID:Lymph circulation in the liver. 1848 10


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