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)

From 1994 to 2002, tissues from 61 prairie dogs were submitted to Northwest ZooPath for histopathology. Of these, 12 (20%) had hepatocellular carcinoma (HCC). Three were pets submitted from private veterinary practices. The others were submitted from zoos in the United States. All were adults, ranging from young adult to 7 years of age, with average age of 5.1 years. The most common clinical signs were weight loss, lethargy, palpable abdominal mass, and respiratory difficulty. All tumors were well-differentiated HCCs in which four histologic patterns were recognized. The trabecular pattern was predominant in nine tumors, and the pseudoglandular pattern was predominant in two tumors. The pelioid pattern was also represented in eight tumors. A papillary pattern was present in one case. In seven cases vacuolar change resembling lipidosis was present in the neoplastic hepatocytes of both primary and metastatic tumors. Anaplasia was mild to moderate in most tumors, but a marked degree of anaplasia was noted in the metastatic foci of the case with papillary differentiation. Metastasis to lung was noted in five cases. One of these also had metastasis to the spleen, and another had metastasis to heart and mediastinum. In two cases there was concurrent hepatitis and in two cases, cirrhosis. All tumors and nonneoplastic liver stained negatively for woodchuck hepatitis virus surface and core antigens, and orcein and Victoria blue positive staining of hepatocytes typical of hepadnavirus infection in humans and woodchucks was not present. HCC is apparently common in captive prairie dogs. The hepatic neoplasia observed in prairie dogs was similar to that associated with hepadnaviral infection in humans, woodchucks, and ground squirrels, but no direct evidence of hepadnaviral infection was detected. The rate of metastasis in captive prairie dogs was higher than that reported in woodchucks.
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PMID:Hepatocellular carcinoma in black-tailed prairie dogs (Cynomys ludivicianus): tumor morphology and immunohistochemistry for hepadnavirus core and surface antigens. 1523 35

The purpose of this study was to characterize light and electron microscopic findings from 9 dogs that had consumed aflatoxin-contaminated commercial dog food from recalled batches. Four dogs died and 5 were euthanized after signs of liver failure. Analysis of feed and liver samples confirmed exposure to aflatoxin. Of the 9 dogs, 8 had classic signs of liver failure, and 1 had signs of liver failure. Enlarged, pale yellow livers were seen macroscopically at necropsy in the dogs with subacute hepatopathy, and cirrhosis was noted in the dog with chronic hepatopathy. Histopathologic findings included hepatic lipidosis, portal fibroplasia, and biliary hyperplasia, which supported a diagnosis of subacute toxic hepatopathy in the 8 symptomatic animals. Marked lobular atrophy, bridging portal fibrosis, and regenerative hepatocellular nodules characterized the dog with chronic hepatopathy. Electron microscopy revealed marked hepatocellular lipid vacuolation and early fibroplasia in the dogs with acute hepatopathy and marked fibrosis and regeneration in the dog with chronic hepatopathy. Analysis of feed for aflatoxin consistently revealed high levels of aflatoxin B1 (range of 223-579 ppb), and hepatic tissue contained elevated levels of aflatoxin B1 metabolite M1 (0.6-4.4 ppb). Although dogs are not commonly affected by aflatoxicosis, they are highly susceptible and can present with classic signs of acute or chronic hepatopathy. Characteristic gross, histologic, and electron microscopic changes help pathologists determine a presumptive toxic insult. Detecting aflatoxins or their metabolites in feed or liver specimens can help confirm the diagnosis of aflatoxicosis.
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PMID:Aflatoxicosis in nine dogs after exposure to contaminated commercial dog food. 1740 11

The diagnosis of drug-induced liver injury (DILI) is a challenging problem, often confounded by incomplete clinical information and the difficulty of eliciting exposure to herbal products, over-the-counter agents and toxins. The task is further rendered difficult on biopsy, as drugs can mimic all the patterns found in primary liver disease. Acute hepatitis, with or without cholestasis, is the most common histological pattern of DILI, and drugs such as acetaminophen are the leading causes of acute liver failure. Most cases of DILI resolve on discontinuation of the drug, but recovery can take months or rarely the disease can progress despite drug withdrawal. Drugs such as methotrexate can lead to chronic hepatitis and cirrhosis, while others such as minocycline, nitrofurantoin and methyldopa are implicated in autoimmune hepatitis. Prolonged cholestasis and ductopenia resembling primary chronic biliary disease can occur. Drug-induced steatohepatitis is also an uncommon pattern, but is well described with drugs such as amiodarone and irinotecan. In the presence of risk factors such as obesity and diabetes, some drugs such as tamoxifen, oestrogens and nifedipine can precipitate or exacerbate steatohepatitis. Other observed patterns include granulomatous hepatitis, vascular injury (eg, sinusoidal obstruction syndrome), Ito cell lipidosis and neoplasms (eg, adenomas).
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PMID:Histological patterns in drug-induced liver disease. 1947 52

In camels, hepatic diseases are relatively common and most of them are misdiagnosed as a cause of illness because signs may be subtle. In addition, diagnostic laboratory methods are insufficient as hepatic enzymes can also be elevated in camels with cardiac or skeletal muscle damage. Examples of liver diseases in camels are hepatic lipidosis, hepatitis, cirrhosis, hepatic necrosis, choleostasis, hyperplasia of biliary epithelium, hydatid cysts, glycogen deposition, cholangitis, cholangiohepatitis, calcified hydatid cyst and hepatic abscesses. When the liver is examined by ultrasonography, the clinician gets sufficient information about the size, position, echopatterns of the hepatic parenchyma, bile ducts and outlines of the hepatic blood vessels. Ultrasonography has been used previously in camels only for reproductive purposes. However, during the past decade, it has been used for scanning of the healthy organs as well as evaluation and determining the diagnosis and prognosis of non-reproductive disorders. Examples of diseases evaluated by ultrasonography in camels are paratuberculosis, trypanosomiasis, abdominal and urinary disorders, thoracic diseases, renal tumors, pyelonephritis, renal abscessation, gastrointestinal tumors, chronic peritonitis and splenic abscessation. Ultrasound-guidance in biopsy of hepatic lesions and in portocentesis has also been reported in camels. This mini review article is written to shed light on ultrasonography of the liver and its blood vessels in healthy camels as well as finding in camels with hepatic disorders such as fatty infiltration of the liver, hepatic abscesses and calcification of the bile ducts.
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PMID:Ultrasonography of the liver in healthy and diseased camels (Camelus dromedaries). 3210 26

Non-alcoholic fatty liver disease (NAFLD) affects 30 to 40% of adults and 10% of children in the US. About 20% of people with NAFLD develop non-alcoholic steatohepatitis (NASH), which may lead to cirrhosis and liver cancer, and is projected to be a leading cause of liver transplantation in the near future. Human induced pluripotent stem cells (iPSC) from NASH patients are useful for generating a large number of hepatocytes for NASH modeling applications and identification of potential drug targets. We developed a novel defined in vitro differentiation process to generate cryopreservable hepatocytes using an iPSC panel of NASH donors and apparently healthy normal (AHN) controls. iPSC-derived hepatocytes displayed stage specific phenotypic markers, hepatocyte morphology, with bile canaliculi. Importantly, both fresh and cryopreserved Definitive Endoderm and Hepatoblasts successfully differentiated to pure and functional hepatocytes with increased CYP3A4 activity in response to rifampicin and lipid accumulation upon fatty acid (FA) treatment. End stage hepatocytes integrated into three dimensional liver organoids and demonstrated increased levels of albumin secretion compared to aggregates consisting of hepatocytes alone. End stage hepatocytes derived from NASH donors demonstrated spontaneous lipidosis without fatty acid supplementation, recapitulating a feature of NASH hepatocytes in vivo. Cryopreserved hepatocytes generated by this protocol across multiple donors will provide a critical cell source to facilitate the fundamental understanding of NAFLD/NASH biology and potential high throughput screening applications for preclinical evaluation of therapeutic targets.
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PMID:iPSC-derived hepatocytes generated from NASH donors provide a valuable platform for disease modeling and drug discovery. 3326 31


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