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)

2-Deoxy-D-galactose, in a dose of 3 mmol/kg, was administered intraperitoneally twice daily to young rats for periods up to 12 weeks. This dosage schedule resulted in recurrent phosphate trapping predominantly in liver. UTP deficiency was excluded by simultaneous uridine injections. Phosphate trapping was caused by the rapid accumulation of 2-deoxy-D-galactose 1-phosphate and was most pronounced in liver but also demonstrated in small intestine, brain, spleen, and thymus. The marked, although transient, drop in the hepatic content of inorganic phosphate triggered the catabolism of adenine nucleotides and a loss of ATP. Other metabolic pathways affected by phosphate deficiency include glycogenolysis and glycolysis. Increasing with time, repeated doses of the galactose analog led to retardation and arrest of growth, hepatomegaly, and splenomegaly. The average relative liver and spleen weights were elevated 2.5- and 4.5-fold, respectively, after 12 weeks of treatment. Liver damage was indicated by hyperbilirubinaemia and a progressive rise in the activity in plasma of sorbitol dehydrogenase, alkaline phosphatase, and gamma-glutamyltransferase. Examination by light and electron microscopy showed increasing numbers of vacuoles, surrounded by a single membrane, in hepatocytes, sinusoidal endothelial cells, and Kupffer cells. Focal cytoplasmic degeneration in hepatocytes was occasionally indicated by formation of autophagic vacuoles and finger print lysosomes. Hepatocytes of 2-deoxy-D-galactose-treated rats showed a dissociation and fragmentation of the rough endoplasmic reticulum. Sinusoidal endothelial cells and Kupffer cells were markedly enlarged, the latter contained a PAS-positive but amylase resistant substance. Extrahepatic changes included an increased occurrence of vacuolated cells in thymus. Phosphate trapping and its metabolic consequences are common phenomena in the experimental injury induced b 2-deoxy-D-galactose and in some hereditary diseases such as uridylyltransferase deficiency galactosaemia, fructose intolerance and glucose-6-phosphatase deficiency.
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PMID:Consequences of recurrent phosphate trapping induced by repeated injections of 2-deoxy-D-galactose. Biochemical and morphological studies in rats. 4 10

A retrospective study was designed to analyse the mode of presentation, clinical signs, haematological, biochemical and histological features in 46 Indian patients admitted with cirrhosis to R. K. Khan and King Edward VIII Hospitals, Durban, between 1977-1981. The commonest presenting feature was swelling of the body followed by pain in the right upper quadrant, most patients had hepatomegaly, jaundice and ascites, and splenomegaly was detected in one-third of cases. Biochemical investigations indicated that most patients had a high globulin and low albumin concentration. Liver function tests revealed raised bilirubin and gamma-glutamyltransferase values in most cases. On histological examination, micronodular cirrhosis predominated (95%) with a high incidence of fat and iron deposition. Changes consistent with alcoholic hepatitis were superimposed in one-third of cases while immunological and viral markers were absent. This study suggests that alcohol is the predominant cause of cirrhosis in Natal Indians.
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PMID:Patterns of cirrhosis in Natal Indians. 320 19

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

Clinical, haematological and pathological studies were undertaken in Jordan in a stud of 103 racing horses clinically suffering from babesiosis and apparently healthy animals. Out of 47 horses which participated in strenuous exercise, three mares showed sudden onset of immobility and reluctance to move and two mares died. Clinical examination revealed that these five horses (group 1) had fever, anorexia, weakness and severe icterus and, in two mares, haemoglobinuria. Haematological examination revealed that all five horses were heavily parasitized with Babesia equi. This was also found in four horses (group 2) with no evidence of clinical babesiosis. In group 3 (94 horses), neither clinical signs nor B. equi were observed in the blood. The horses in group 1 and 2 recovered after treatment with imidocarb. When the mean values of white blood cell count, red blood cell count, haemoglobin and packed cell volume in group 1 were compared with those for groups 2 and 3, a significant difference was found (P < 0.05). A significant difference was also found when the mean values were compared before and after treatment. Examination of serum total protein, bilirubin and serum enzymes revealed a significant decrease in the mean value of total serum protein (P < 0.05), and a significant increase in the mean values of bilirubin (P < 0.05) in group 1 compared to groups 2 and 3. A significant elevation in the mean value of aspartate aminotransaminase, gamma-glutamyltransferase and creatine phosphokinase and a substantial elevation in the mean value of alkaline phosphatase was also observed in group 1 compared to groups 2 and 3. Postmortem examination of the dead horses showed that the animals had icterus, hepatomegaly and full urinary bladder with deep-red urine. Histopathological examination of the liver showed massive centrilobular degeneration and necrosis. The bile canaliculi and bile ducts were prominent and plugged with dark-brown to canary-coloured bile pigments. The lungs had congestion, oedema, and thrombosis of pulmonary veins. Our results suggest that the horses suffered from B. equal with clinical manifestation following exercise. The clinical, haematological and pathological findings indicate that the animals suffered from haemolytic anaemia which responded to imidocarb therapy.
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PMID:Equine babesiosis associated with strenuous exercise: clinical and pathological studies in Jordan. 918 24

To study prevalence of cytomegalovirus (CMV) infection in patients with viral hepatitis and its clinical characteristics, serum anti-CMV-IgM was detected in 6411 hospitalized hepatitis cases, and clinical symptoms, signs and liver function in 115 cases with CMV infection were compared with 192 cases of non-CMV infection. Results showed a CMV infection rate of 1.79% in them with an average age of 33.6 years, a sex ratio of 2.13, and dual superinfection with CMV and hepatitis accounting for 44.74%, and triple and quadruple superinfection for 47.37% and 7.89%, respectively. Proportion of those with fever, digestive symptoms, hepatomegaly, changes of gallbladder in ultra sound scan, rising activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyltransferase (gamma-GT) were more, and duration of hospitalization longer in the cases with CMV infection. It suggests that CMV can be found in the cases with viral hepatitis, most in a form of dual or multiple infection, and it can aggravate hepatitis.
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PMID:[An analysis of CMV infection in 115 cases with viral hepatitis]. 920 27

Socioeconomic development has led to a progressive increase of alcohol consumption in Taiwan, with an accompanying increase in alcohol-related psychiatric problems, traffic accidents, and liver disease. The prevalent rates of alcohol dependence for Han Chinese and Fomosan aborigines were 0.1% and 1%, respectively in 1950. The rate of alcohol dependence increased to 23% for aborigines in 1995. The number of cases of death and serious injuries due to alcohol-related traffic accident has decreased, and the number of fatalities resulting from these accidents has decreased from third to eighth since the inception of a program of random traffic stops with alcohol breath test in 1997. Alcohol liver disease (ALD) was defined as daily alcohol consumption of 60 g, for a duration of longer than 5 years. We classified ALD patients into two groups: (1) those whose average daily consumption of alcohol exceeded 120 g for a duration longer than 15 years (group A); and (2) all other patients (group B). The case records of 33 cases of biopsy-confirmed ALD were obtained for study. The average of daily alcohol consumption in these cases was 160 g. All but one of these patients were male, age ranged from 26 to 69 years, with an average of 43.1. Clinically, ill-defined gastrointestinal symptoms were the most common presentation (61%), and hepatomegaly was the main physical sign (73%). The average mean corpuscular volume values of ALD and non-ALD patients were 102.3 +/- 10.94 and 94.5 +/- 8.1, respectively (p < 0.01). The mean corpuscular volume values of group A and group B were 102.9 +/- 9.7 vs. 96.5 +/- 9.11 (p < 0.05). Result from serum SGOT/SGPT and gamma-glutamyltransferase/alkaline phosphatase for ALD and non-ALD revealed statistically significant differences between these groups. Using the avidin-biotin complex technique, tissue IgA deposition for ALD patients was found to be different from that of non-ALD patients. Ten of 13 ALD patients vs. 2 of 13 non-ALD patients had continuous-form IgA deposition. Histologically, 45.5% of ALD patients had alcoholic cirrhosis, whereas alcoholic hepatitis was present in only 9.1% of patients. Overall, 88% of cases showed various severity of fatty metamorphosis.
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PMID:Alcohol-related problems in Taiwan with particular emphasis on alcoholic liver diseases. 962 97

Myotonic dystrophy (DM) is an autosomal dominant multisystem disorder. Little evidence suggests the existence of liver damage in a small number of patients. We have prospectively evaluated liver and gallbladder function in 53 patients with DM in relation to clinical and genetic parameters. None of the patients had an enlarged liver, signs of cirrhosis, or portal hypertension. All were free of medication, and none were pregnant or had a history of alcohol abuse. In 35 (66%) patients, serum activity of at least one of six liver enzymes assayed was abnormal. An elevated level of alkaline phosphatase was found in 50.9%, of gamma-glutamyltransferase in 52.8%, of 5' nucleotidase in 43.4%, of serum aspartate aminotransferase in 35.8%, of serum alanine aminotransferase in 33.9%, and of lactate dehydrogenase in 37.7%. Liver function test results did not correlate with severity of muscle weakness, disease duration, or serum levels of creatine kinase, glucose, or lipids. Motility of gallbladder and abdominal ultrasonography were normal. Cytosine-thymidine-guanine repeat expansion by southern blot did not correlate with liver enzyme abnormalities. We conclude that elevation of liver enzymes is frequent in DM and should be included as an additional laboratory finding of the disease.
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PMID:Abnormal liver test results in myotonic dystrophy. 964 14

Spontaneous amyloidosis was diagnosed in 11 male and 1 female chimpanzees and confirmed histologically and immunohistochemically. The chimpanzees were > or = 15 years of age when first diagnosed and averaged 22.4 years of age. The average survival time after diagnosis of systemic amyloidosis was 1.86 years with a standard deviation of 4.06 years (n = 7). The chimpanzees with amyloidosis were asymptomatic except for hepatomegaly, which became more detectable with age. Significant increases in clinical chemistry values, as compared with referenced normals and established normals, of blood urea nitrogen (BUN), asparate aminotransferase (AST), gamma-glutamyltransferase (GGT), globulin, total protein, creatinine phosphokinase (CPK), sedimentation rate, and triglycerides were found in animals 7 years of age or older with amyloidosis. These serum chemistry values, while increased in chimpanzees with amyloidosis, were generally within normal limits. Immunohistochemistry for both amyloid A protein and amyloid P component-labeled extracellular amyloid in all chimpanzees with amyloidosis was determined. Amyloid was deposited primarily in the liver. Amyloidosis in the chimpanzee is a chronic, intractable, progressive, fatal disease, and appears to be similar to secondary amy loidosis in other species.
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PMID:Spontaneous amyloidosis in twelve chimpanzees, Pan troglodytes. 1199 Feb 41

Secondary amyloidosis is a progressive systemic disease for which there is no reliable diagnostic assay, preventive measure, or treatment. In an attempt to elucidate an antemortem diagnosis, 30 female pig-tailed macaques (Macaca nemestrina) at the Washington National Primate Research Center were surveyed for amyloidosis. Amyloid was demonstrated histologically in 47% (14 of 30) of the animals. The distribution and severity of amyloid deposition was variable. Affected animals had a mean age (+/-1 standard deviation) of 13.2 +/- 4.9 y, which was significantly greater than the mean age of unaffected animals (9.3 +/- 4.1) y. Twelve tests were evaluated for detection of amyloidosis; the diagnostic value of each was determined through comparison of histologically positive and histologically negative animals. Diagnostic tests evaluated were endoscopic examination and biopsy of the stomach and colon, abdominal ultrasonography, hepatic radiology, serum amyloid A (SAA), endothelin 1, alpha-fetal protein, aspartate aminotransferase (AST), alanine aminotransferase, gamma-glutamyltransferase (GGT), alkaline phosphatase, cholesterol, blood urea nitrogen, total bilirubin, C-reactive proteins, and erythrocyte sedimentation rate. Amyloidotic animals demonstrated a distinctive serologic profile: elevated SAA, GGT, and AST in combination with decreased total protein and albumin. Radiology demonstrated hepatomegaly in animals with hepatic amyloid deposition. In the absence of known infection or trauma, an amyloidotic serologic profile and radiologic hepatomegaly are consistent with systemic amyloidosis in M. nemestrina.
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PMID:Detection of systemic amyloidosis in the pig-tailed macaque (Macaca nemestrina). 1663 79

A 1-year-old Thoroughbred filly was presented to the Cornell University Hospital for Animals with a 10-day history of fever, diarrhea, inappetance, and hypodipsia. Clinical pathology abnormalities found by the referring veterinarian included erythrocytosis, hyperproteinemia, and increased serum gamma-glutamyltransferase and lactate dehydrogenase activities. At Cornell University, the laboratory abnormalities were confirmed and also included thrombocytosis and hypoglycemia. Erythrocytosis persisted despite vigorous fluid therapy. Ultrasound examination revealed an extremely enlarged liver with abnormal echogenicity and a 21 x 25-cm hepatic mass with varied echogenicity. Imprints of an ultrasound-guided biopsy of the mass revealed a neoplastic epithelial population of uncertain origin, although the cells did not resemble hepatocytes. Together with the presenting signs, signalment, ultrasonographic findings, and persistent erythrocytosis, the cytologic findings were considered to be most consistent with hepatoblastoma. Histopathologic examination of the mass at necropsy confirmed the diagnosis and findings also included bone marrow erythroid hyperplasia. Serum erythropoietin concentration was 28.0 mU/mL (reference interval 1.0-11.8 mU/mL), supporting erythropoietin production by the tumor and secondary inappropriate erythrocytosis. To our knowledge, this report is the first to document secondary erythrocytosis with increased erythropoietin concentration in a horse with hepatoblastoma, and also the first to describe the cytopathologic features of this rare tumor.
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PMID:What is your diagnosis? Biopsy impression smear of a hepatic mass in a yearling Thoroughbred filly. 1876 30


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