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)

Scrub typhus (tsutsugamushi disease) is an acute infectious disease caused by Rickettsia tsutsugamushi transmitted through the bite of larvae of certain trombiculid mites. Geographical distribution in Asian-Pacific region is much of the roughly triangular area bounded by Japan, Pakistan and Australia. It is an endemic illness in the Pescadores Islands, but has scarcely been reported in central Taiwan. An eleven-year-old boy was admitted to Changhua Christian Hospital with the chief complaints of fever, lethargy and skin rash for seven days. On physical examination, he was found to have painless eschar, conjunctivitis, meningoencephalitis, pneumonitis, ascites, jaundice, hepatomegaly, liver function impairment and thrombocytopenia. His Proteus OX-K agglutinin titer increased from 1:160 in the acute sera to 1:640 in the convalescent sera. A greater than four-fold rise (greater than 1:640) in antibody titers to Karp, Gilliam, Kato strains of R. tsutsugamushi between acute and convalescent sera were demonstrated by immunofluorescent antibody. The patient was treated with minocycline and chloramphenicol and was completely recovered.
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PMID:[Scrub typhus--one case report]. 263 64

Copper poisoning developed in 1 adult and 3 juvenile llamas after excessive dietary intake of copper resulted in an incorrect copper:molybdenum ratio. Total dietary copper was determined to be 36 mg/kg of feed, with a copper:molybdenum ratio of 16.6:1. Clinical signs associated with the toxicosis included acute onset of anorexia and lethargy. Liver enzyme activities (aspartate amino transaminase, lactate dehydrogenase, gamma-glutamyl transferase) and serum copper concentration were high in specimens obtained within 48 hours before death. Gross necropsy findings were limited to mild hepatomegaly. Histologically, hepatic lesions included acute massive necrosis of hepatocytes with and without bile duct proliferation, double hepatic plates with loss of orientation, anisocytosis, anisokaryosis, and an intralobular mosaic pattern of necrosis involving half of the hepatocytes. Analysis of hepatic copper concentrations suggested that juvenile llamas develop signs of poisoning at lower hepatic copper concentrations, compared with adults.
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PMID:Copper poisoning in four llamas. 279 84

Sixty cats with hematologic abnormalities indicative of non-lymphoid hematopoietic neoplasia were classified into two groups, myelodysplastic syndromes (MDS) and acute myelogenous leukemias (AML), using criteria developed for human patients with similar diseases. Cats with myeloblast counts in bone marrow of less than 30% were classed as MDS and cats with myeloblast counts of 30% or greater were classed as AML. The clinical, laboratory, and postmortem findings in each group were described and compared. Clinical signs of disease were similar in both groups, the most common being inappetance, lethargy, and weakness. Non-regenerative anemia, macrocytosis, neutropenia, and thrombocytopenia were frequent hemogram abnormalities in both groups. Diagnostically useful differences in physical and peripheral blood findings were a higher prevalence of splenomegaly and/or hepatomegaly, thrombocytopenia, and severe anemia in the AML group. Circulating myeloblasts were found only in cats in the AML group. Outcome of disease was similar in both groups; 85% of the cats in each group died or were euthanatized within one week of diagnosis. In cats that were necropsied, extramedullary leukemic infiltrates were found in all cats in the AML group and in none of the cats in the MDS group.
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PMID:Non-lymphoid hematopoietic neoplasia in cats: a retrospective study of 60 cases. 282 80

Among 137 members of 30 families, 6% (and 8% of those aged under 15 years) were seropositive for toxocara antibodies. In these seropositive subjects and in 84 patients known to have raised toxocara titres the commonest clinical features were abdominal pain, hepatomegaly, anorexia, nausea, vomiting, lethargy, sleep and behaviour disturbances, pneumonia, cough, wheeze, pharyngitis, cervical adenitis, headache, limb pains, and fever. 61% of patients with raised toxocara titres had recurrent abdominal pain. Eosinophilia was in many cases associated with a raised toxocara titre, but 27% of patients with high titres had normal eosinophil counts. Toxocariasis is common, especially in children, and is associated with clinical features that are generally regarded as non-specific but together form a recognisable symptom complex. Toxocariasis should be considered in the differential diagnosis of such symptoms and especially in recurrent abdominal pain, which might otherwise be labelled as idiopathic. The absence of eosinophilia does not exclude toxocariasis.
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PMID:The expanded spectrum of toxocaral disease. 289 21

3-Hydroxy-3-methylglutaryl-coenzyme A lyase deficiency (HMG-CoA lyase) is an inborn error of leucine catabolism which often leads to life-threatening illness in the neonatal period. The cardinal clinical features include severe infantile hypoglycemia, metabolic acidosis, hepatomegaly, lethargy or coma and apnea. Hyperammonemia is variable. There is a characteristic absence of ketosis. Considerable heterogeneity has been observed in clinical and biochemical presentation. Acute episodes of illness have been mistaken for Reye syndrome. The pattern of organic acids in the urine includes large amounts of 3-hydroxy-3-methylglutaric, 3-methyl-glutaconic, 3-methylglutaric and 3-hydroxyisovaleric acids. Smaller, but appreciable levels of glutaric, adipic and other dicarboxylic acids may also be excreted in the urine. Lactic acid may be present in sizable amounts at times of acute illness. The primary defect is a deficiency of 3-hydroxy-3-methylglutaryl-coenzyme A lyase, a key enzyme in the cycle of ketogenesis.
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PMID:3-Hydroxy-3-methylglutaryl-coenzyme A lyase deficiency: review of 18 reported patients. 306 29

Of 39 captive whooping cranes (Grus americana), 7 died during a 7-week period (Sept 17 through Nov 4, 1984) at the Patuxent Wildlife Research Center, Laurel, Md. Before their deaths, 4 cranes did not develop clinical signs, whereas the other 3 cranes were lethargic and ataxic, with high aspartate transaminase, gamma-glutamyl transferase, and lactic acid dehydrogenase activities, and high uric acid concentrations. Necropsies indicated that the birds had ascites, intestinal mucosal discoloration, fat depletion, hepatomegaly, splenomegaly, and visceral gout. Microscopically, extensive necrosis and inflammation were seen in many visceral organs; the CNS was not affected. Eastern equine encephalitis (EEE) virus was isolated from specimens of the livers, kidneys, lungs, brains, and intestines of 4 of the 7 birds that died, and EEE virus-neutralizing antibody was detected in 14 (44%) of the 32 surviving birds. Other infectious or toxic agents were not found. Morbidity or mortality was not detected in 240 sandhill cranes (Grus canadensis) interspersed among the whooping cranes; however, 13 of the 32 sandhill cranes evaluated had EEE virus-neutralizing antibody. Of the 41 wild birds evaluated in the area, 3 (4%) had EEE virus-neutralizing antibody. Immature Culiseta melanura (the most probable mosquito vector) were found in scattered foci 5 km from the research center.
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PMID:Mortality of captive whooping cranes caused by eastern equine encephalitis virus. 350 15

A 7-year-old adult male ferret had progressive hair loss that was bilaterally symmetric. Also clinically evident were severe dehydration, polydipsia, muffled heart sounds, weak femoral pulses, hepatomegaly, lethargy, weakness, temporal muscular atrophy, dyspnea, and weakness. The blood profile of the ferret indicated profound leukopenia, eosinopenia, and high phosphorus, BUN, creatinine, and potassium concentrations, as well as high aspartate transaminase activity; the albumin concentration was low. The serum cortisol concentration was 8.1 micrograms/dl. Necropsy and histologic findings confirmed a diagnosis of hyperadrenocorticism, complicated by dilatative cardiomyopathy, chronic active hepatitis, and renal disease.
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PMID:Hyperadrenocorticism in a ferret. 365 2

As the results of treatment in Wilson's disease are so dependent on the stage at which penicillamine therapy is started, the antecedent history in 34 patients with Wilson's disease was analysed with particular respect to the earliest manifestations of the disease. Lethargy and anorexia (70%) jaundice (56%) and abdominal pain (48%) were the commonest symptoms and less common were intellectual deterioration (22%) and recurrent epistaxes (22%). The duration of symptoms before diagnosis ranged from five days to three years (mean 10.5 months) and in only five of the patients was the diagnosis established before referral. Analysis of the physical signs at presentation showed hepatomegaly (81%) and splenomegaly (70%) to be common and the only signs which were significantly more common in the 13 fatal cases were jaundice and ascites. In three of these and in one other patient who survived the clinical course was exceptionally severe and was indistinguishable from fulminant hepatic failure. Based on the severity of abnormality of serum aspartate aminotransferase, bilirubin, and prothrombin time on admission a prognostic index was derived which enabled complete separation of fatal and nonfatal cases and when subsequently used in a further nine index cases correctly predicted the outcome. Two further cases found to have indices in the fatal category did well after liver transplantation, which needs to be considered as soon as the diagnosis is established in cases with such severe liver damage.
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PMID:Wilson's disease: clinical presentation and use of prognostic index. 379 21

A 4-year-old cat was examined because of anorexia and lethargy. The cat became icteric within 3 days of admission. Values for aspartate transaminase, alanine transaminase, total bilirubin, alkaline phosphatase, and cholesterol were higher than normal. Radiography revealed hepatomegaly, with loss of detail in the cranioventral portion of the abdomen. Further diagnostic procedures were not permitted, and the cat was euthanatized. At necropsy, cholecystitis, cholangitis, and numerous choleliths were found. Cholelithiasis is a rare cause of obstructive jaundice in the cat.
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PMID:Cholelithiasis in a cat. 397 77

Subacute, nonsuppurative hepatitis was diagnosed in a cynomolgus monkey (Macaca fascicularis) based on histopathologic examination of a liver biopsy specimen. Clinical signs of illness included anorexia, lethargy and hepatomegaly. Abnormal laboratory findings included elevations of serum liver enzymes, bilirubin and a monocytosis. Circulating antibody (anti-HBs) against Hepatitis B surface antigen (HBsAg) was present in serum and antigens reactive with anti-HBsAg antiserum were found in the liver using an immunoperoxidase technique. Of the remaining 18 healthy monkeys in the same room, another cynomolgus monkey was HBsAg seropositive. Both of the seropositive monkeys involved arrived on the same shipment from Indonesia and had been quarantined and housed together continuously during the preceding two years.
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PMID:Subacute nonsuppurative hepatitis associated with hepatitis B virus infection in two cynomolgus monkeys. 404 51


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