Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When larvae of C. sinensis reach the biliary system and mature, the flukes provoke pathological changes, both as a result of local trauma and of toxic irritation. The appearances vary with duration and severity of the infestation, but they are sufficiently distinctive and characteristic to allow a classification into four phases as follows; 1st phase, desquamation of epithelial cells, 2nd phase, hyperplasia and desquamation of epithelial cells, 3rd phase, hyperplasia and desquamation of epithelial cells, and adenomatous tissue formation, and 4th phase, marked proliferation of the periductal connective tissue with scattered abortive acini of epithelial cells and fibrosis of the wall of the bile duct. The onset of symptoms and signs is at times gradual, at times sudden. Chill and fever up to 40 degrees C occur during the acute stage, i.e. the period less than a month after parasite invasion. And a few weeks later, the chronic stage follows with the classical clinical features. In general, symptoms and signs can be classified as follows: mild, essentially symptomless, progressive, with irregular appetite, gastrointestinal disturbances, oedema, hepatomegaly, etc., and severe, with a syndrome associated with portal cirrhosis and hypertension. Pathogenic changes and complications are generally restricted to foci, but may eventually affect the whole liver. Calculi, acute suppurative cholangitis, recurrent pyogenic cholangitis, cholecystitis, hepatitis, and acute pancreatitis are important complications. Carcinoma of the liver is often found in association with clonorchiasis, too.
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PMID:Clonorchis sinensis: pathogenesis and clinical features of infection. 639 2

A Doberman with jaundice, hepatomegaly and cranial abdominal pain had evidence of centrilobular necrosis on liver biopsy. Therapy with fluids, ampicillin and rest resulted in recovery. A Collie hit by a car developed traumatic hepatopathy and myopathy. The animal recovered with rest as the only treatment. A mongrel with hepatic lymphosarcoma benefited from chemotherapy for 5 months before euthanasia was necessary. A cat became lethargic and anorectic 9 days after an oral dose of piperazine. Liver biopsy revealed fatty change, vacuolation and mononuclear infiltration. Supportive care with amoxicillin, fluids and a high caloric intake resulted in recovery. Laparotomy in a jaundiced, anorectic cat revealed an obstructed common bile duct. Cholecystoduodenostomy and supportive care resulted in recovery. A vomiting, lethargic, jaundiced cat had evidence of chronic cholangitis on liver biopsy. The animal recovered after treatment with amoxicillin, fluids, prednisolone and forced feeding.
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PMID:Management of liver disease in dogs and cats. 654 4

Between 1978 and 1982 14 patients were treated for bile-duct cysts. The predominant clinical signs were obstructive jaundice and hepatomegaly in the younger patients, while pain was the most common symptom in the older patients. Ultrasonography was a valuable diagnostic technic but percutaneous transhepatic cholangiography (PTC) and endoscopic retrograde cholangiopancreatography (ERCP) were associated with septic complications; as an alternative, routine preoperative cholangiography is recommended to visualize the type of bile-duct cyst. Excision of the bile-duct cyst was considered the treatment of choice. Excision was performed in 11, and internal drainage in three patients. Cholangitis developed in four children after excision of the cyst. In our series the prognosis was good following surgical treatment, even in younger patients.
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PMID:Bile-duct cysts--diagnosis and treatment in 14 patients. 663 26

The hepatic morphological findings in 3 patients treated with amiodarone, a potent and effective antiarrhythmic drug, are reported. An enlarged liver and mild elevation of hepatic enzymes were the most important clinical findings. Fibrosis, cholangitis, mixed inflammatory infiltrate, and cytoplasmic granularity of the hepatocytes were the main histologic changes common to all cases. In 2 of the cases the presence of Mallory bodies was confirmed by electron microscopy. In 1 of these 2 cases, Mallory bodies were also confirmed by immunostaining. Ultrastructurally, numerous cytoplasmic inclusions with a membranous or lamellar structure identical to those described in phospholipidosis were the most striking features seen in hepatocytes, biliary epithelial cells, Kupffer cells, and endothelial cells.
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PMID:Amiodarone-associated phospholipidosis and fibrosis of the liver. Light, immunohistochemical, and electron microscopic studies. 670 74

Wedge biopsy of the liver during episodic clinical illness in three male cats showed lymphocytic cholangitis. Principal clinical findings were increased serum alkaline phosphatase activity and hepatomegaly (two cats) associated with anorexia, pyrexia. and weight loss; these signs of illness were intermittent with asymptomatic periods. The hepatic lesions were characterized by lymphoid aggregate or follicle formation, diffusely dispersed lymphocytes and plasma cells, and abnormal bile ducts and ductules. Lymphoid aggregates and diffusely scattered lymphocytes were seen in the pancreas also. The spectrum of hepatic lesions in three cats seemed to represent a progression in the development of the disease. Similarities and dissimilarities between the findings in the three cats and human primary biliary cirrhosis or chronic nonsuppurative destruction cholangitis are discussed. During a prospective search for cats with this disease, other hepatis lesions were found, and it was concluded that cats may be affected by more than one pathogenic mechanism culminating in chronic cholangitis or cholangiohepatitis.
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PMID:Chronic lymphocytic cholangitis in three cats. 707 97

From 1978 to 1992, 62 patients were diagnosed as having extrahepatic biliary atresia (EHBA) at Childrens Hospital Los Angeles. The patients presented with either persistent jaundice, alcoholic stools, and/or hepatomegaly. Hepatobiliary IDA scans were performed in 47 of the patients; 46 had results typical of EHBA. Fifty-nine of the 62 patients underwent a Kasai portoenterostomy; three patients were more than 4 months of age at initial presentation and were referred directly for liver transplantation. The preoperative total bilirubin level for all patients averaged 8.6 mg/dL (range, 4.1 to 18.1). All patients underwent a standardized Kasai procedure using a 40-cm Roux-en-Y intestinal segment performed in the end-to-side fashion. Postoperative management included oral antibiotics and fat-soluble vitamins for at least 9 months. Long-term complications included cholangitis in 20 cases and portal hypertension in 25, which led to variceal hemorrhage in 12 cases. Growth rates were at or above the 50th percentile for age in 59% of the Kasai patients. Forty-one of the 59 Kasai patients survived (69.5%); six deaths occurred within 2 years after the Kasai procedure. Twelve patients were lost to follow-up within 2 years after surgery, and for calculation of mortality were presumed dead. Seventeen patients had follow-up for 5 or more years, 13 had follow-up for 2 to 5 years, and 29 had follow-up for less than 2 years. The average total bilirubin level for the patients with less than 2 years of follow-up was 7.9 mg/dL (0.3 to 20.8), and that for the patients with more than 2 years of follow-up was 1.6 mg/dL (0.3 to 18.1). Orthotopic liver transplantation was performed in 11 Kasai patients, in whom chronic liver failure eventually developed. Rejection occurred in one of these patients, which required retransplantation. Based on these results, the Kasai portoenterostomy procedure continues to offer palliation, if not long-term success, in a large percentage of patients with EHBA.
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PMID:The Kasai procedure in the treatment of biliary atresia. 747 36

Focal and multilobular biliary cirrhosis are considered pathognomonic of cystic fibrosis (CF) and almost invariably have been reported in patients with steatorrhea. In contrast, patients with pancreatic sufficiency and normal absorption are considered less likely to develop liver or biliary tract problems. The authors report three patients with CF and pancreatic sufficiency, presenting with recurrent abdominal pain (unrelated to pancreatitis). All had common bile duct disease, one with multilobular cirrhosis and portal hypertension. Pancreatic sufficiency was proven by quantitative pancreatic stimulation tests, 3-day fecal fat analyses, and serum pancreatic isoamylases. All three patients had mild lung disease. Two were homozygous for the common delta F508 mutation, and the other, a delta F508 compound heterozygote. Hepatobiliary structure and function were determined by serial hepatobiliary scintigraphy, percutaneous transhepatic cholecystography, and biochemical liver function tests. Patients 1 and 3 had mild hepatomegaly, normal liver biochemistry, and distal common bile duct strictures. Patient 2 had a firm nodular liver with splenomegaly, abnormal liver biochemistry, and a cholangiographic appearance of sclerosing cholangitis. All have undergone operative treatment for persistent abdominal pain. These cases confirm the occurrence of common bile duct pathology and liver disease in patients with CF and pancreatic sufficiency. They demonstrate that liver and biliary tract disease can occur independently of the underlying disease severity and the presence of steatorrhea. Further, they suggest that obstruction of the biliary tract may be an additional factor in the evolution of liver disease in CF.
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PMID:Hepatobiliary disease in cystic fibrosis patients with pancreatic sufficiency. 753 38

Hepatomegaly and abnormalities of serum liver tests are common problems in patients with acquired immune deficiency syndrome. Opportunist infections (Mycobacterium avium-intracellulare and cytomegalovirus) and neoplasms (lymphoma, Kaposi's sarcoma) are among the most prevalent hepatic lesions in AIDS. Although Kupffer cells and endothelial cells are potential sites of human immunodeficiency virus 1 (HIV-1) infection, current studies do not indicate that the liver is a major reservoir for this virus. Drug hepatotoxicity, multimicrobial infections of the biliary tree resembling sclerosing cholangitis and a variety of nonspecific hepatic changes should be considered in evaluating AIDS patients or HIV-1-infected patients with evidence of liver dysfunction.
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PMID:Pathology of AIDS-related liver disease. 771 15

Cases of human infestation by Fasciola hepatica are not uncommon in Spain and other European countries. We report our experience with 20 patients diagnosed from 1982 to 1991 and present a critical review of published cases from western countries. Because F. hepatica has a special tropism for the liver, abdominal pain, hepatomegaly, and constitutional symptoms are among the most common manifestations of acute-stage fascioliasis. However, in the chronic stage, biliary colic and cholangitis are the predominant manifestations. The clinical spectrum of fascioliasis is variable, and patients may present with extrahepatic abnormalities, such as pulmonary infiltrates, pleuropericarditis, meningitis, or lymphadenopathy. Therefore, a high index of suspicion is required to establish a correct diagnosis. Eosinophilia is the most frequent laboratory abnormality. The CT scan has become a useful technique in the diagnostic work-up. A definitive diagnosis may be established by the observation of parasite ova in the feces, but most cases may be diagnosed by serologic methods. Triclabendazole and bithionol are the most effective drugs against F. hepatica. The efficacy of praziquantel is controversial.
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PMID:Fascioliasis in developed countries: a review of classic and aberrant forms of the disease. 783 67

We report on 56 children with sclerosing cholangitis (SC) seen between 1972 and 1992. The first symptoms occurred at a mean age of 3.7 years; 15 infants had neonatal cholestatic jaundice. At diagnosis, cholestatic jaundice was present in 25 children, hepatomegaly in 54, splenomegaly in 41, and ascites in 12. Serum alkaline phosphatase activity was increased in 49 patients and gamma-glutamyltransferase activity in all patients tested. Most often the histopathologic findings were extensive portal fibrosis and neoductular proliferation. Cholangiography showed abnormal intrahepatic bile ducts in all children and abnormal extrahepatic bile ducts in 35 (63%). The children were separated into three groups: (1) those with SC of neonatal onset (27%); (2) those with SC of postneonatal onset associated with another disease (55%)--histiocytosis X in 14 children, immunodeficiency syndromes in 8, chronic inflammatory bowel disease or autoimmune hepatitis in 8, and congenital psoriasis in 1; and (3) those with SC of postneonatal onset without an associated disease (18%). Biliary cirrhosis was present in all but three children after 6 months to 19.3 years of follow-up. Eleven children died of portal hypertension or liver failure, and six died of a complication related to the associated disease. Fifteen children had liver transplantation; 11 of these are alive 6 months to 6 1/2 years later without recurrence of SC. The overall estimated median survival time of children with SC was 10 years from clinical onset. These results indicate that SC should be suspected in all children with a chronic cholestatic disease and increased serum gamma-glutamyl transferase activity, especially when diseases known to be associated with SC are present. The prognosis is poor, but liver transplantation should be considered except in those with severe immunodeficiency syndromes.
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PMID:Sclerosing cholangitis in children. 828 75


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