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)

A nine-year-old golden retriever was referred for evaluation of chronic anorexia, vomiting, and diarrhea. Low body weight, mucous membrane pallor, and palpably enlarged liver and spleen were detected by physical examination. Anemia, hyperglobulinemia, and concurrent trichuriasis and coccidiosis were identified upon initial diagnostic evaluation. Punctate vertebral lysis was apparent radiographically. Atypical plasma cell proliferation was found in the bone marrow, liver, and spleen. An immunoglobulin A and immunoglobulin G biclonal gammopathy was demonstrated by serum protein electrophoresis and immunoelectrophoresis. The dog was diagnosed with multiple myeloma and euthanized per owner request. Multiple myeloma should be considered in the differential diagnosis for biclonal gammopathy in the dog.
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PMID:Immunoglobulin A and immunoglobulin G biclonal gammopathy in a dog with multiple myeloma. 897 26

In adults with diabetes mellitus, hepatomegaly and abnormalities of liver enzymes occur as a consequence of hepatocellular glycogen accumulation, as has been well described in children. During periods of hyperglycemia glucose freely enters the hepatocytes driving glycogen synthesis, which is augmented further by administration of insulin to supraphysiologic levels. The accumulation of excessive amounts of glycogen in the hepatocytes is a function of intermittent episodes of hyperglycemia and hypoglycemia and the use of excessive insulin. Hepatic glycogenosis occurs in patients with poorly controlled insulin-dependent type I or type II diabetes. The clinical manifestations of this phenomenon may include abdominal pain and obstructive symptoms such as early satiety, nausea, and vomiting. Ascites has rarely been reported. The typical biochemical findings are mildly to moderately elevated aminotransferases, with or without mild elevations of alkaline phosphatase. Liver synthetic function is usually normal. All these abnormalities, including the hepatomegaly, are readily reversible with sustained euglycemic control. The other major cause of hepatomegaly in patients with diabetes is steatosis. This is a function of the body habitus and state of insulin resistance rather than glycemic control. However, the distinction between steatosis and glycogenosis is important: whereas steatosis may progress to fibrosis and cirrhosis, glycogenosis does not, but reflects the need for better diabetic control. Glycogenosis and steatosis cannot be distinguished reliably on ultrasound examination. The histology, however, is definitive. In glycogenosis, as in primary glycogen storage diseases, there is excess glycogen in the cytoplasm, and often also in the nucleus, of hepatocytes. The hepatocytes throughout the lobule appear pale and swollen with clearly defined cell boundaries. Ultrastructural examination reveals cytoplasmic glycogen in clumps displacing organelles to the periphery of the cell, and there is little if any steatosis. We have shown that hepatomegaly due to glycogenosis in adults with diabetes is similar in all respects to the condition seen in children. As in children, liver enzyme abnormalities are unreliable in predicting the presence or the extent of glycogenosis. Hepatic glycogenosis can occur at any age, and therefore should be included in the differential diagnosis of hepatomegaly in all insulin-requiring diabetics.
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PMID:Hepatomegaly and abnormal liver tests due to glycogenosis in adults with diabetes. 898 49

At least 21 genetic disorders have now been found that are linked to peroxisomal dysfunction. Whatever the genetic defect might be, peroxisomal disorders should be considered in various clinical conditions, dependent on the age of onset. The prototype of peroxisomal disorders is represented by 'classical' Zellweger syndrome (ZS) which is the most severe disorder combining all the characteristic symptoms. ZS is characterized by the association of errors of morphogenesis, severe neurological dysfunction, neurosensory defects, regressive changes, hepatodigestive involvement with failure to thrive, usually early death, and absence of recognizable liver peroxisomes. Other peroxisomal disorders (pseudo-Zellweger syndrome, neonatal adrenoleukodystrophy (NALD), pseudo-neonatal adrenoleukodystrophy, rhizomelic chondrodysplasia punctata (RCDP), and hyperpipecolic acidaemia) share some of these symptoms, but with varying organ involvement, severity of dysfunction, and duration of survival. The diagnosis should not cause difficulty when all the characteristic manifestations are present. Depending on the main presenting sign, peroxisomal disorders in neonates should be suspected in two categories of circumstances: polymalformative syndrome with craniofacial dysmorphism, and severe neurological dysfunction. During the first 6 months of life, the predominant symptoms may be hepatomegaly, prolonged jaundice, liver failure, anorexia, vomiting and diarrhoea leading to failure to thrive resembling a malabsorption syndrome; severe psychomotor retardation, hearing loss and ocular abnormalities become evident. Beyond 4 years of age, behavioural changes, intellectual deterioration, visual impairment and gait abnormalities may be the presenting symptoms. Independently of the clinical symptoms and age of onset, most peroxisomal disorders described so far can be clinically screened by recordings of electroretinogram, visual-evoked responses, and brain auditory-evoked responses, which are almost always abnormal. Nine of the 17 peroxisomal disorders with neurological involvement are associated with an accumulation of very long-chain fatty acids (VLCFA), which suggests that assay of plasma VLCFA should be used as a primary test. However, assays of plasma phytanic acid and plasma/urine bile acid intermediates should also be performed in view of the recent reports of atypical chondrodysplasia variants (without rhizomelic shortening) and isolated trihydroxycholestanoic aciduria. The differential diagnoses in various clinical conditions and age periods are discussed.
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PMID:Clinical approach to inherited peroxisomal disorders. 905 44

During the months of September 1993 through February 1994, an outbreak of hemorrhagic fever occurred in the city of Jayapura, the provincial capital of Irian Jaya, Indonesia. Seventy-two patients (age range = 1-41 years) with suspected dengue hemorrhagic fever (DHF) were enrolled into the outbreak investigation conducted during October-November 1993. The pediatric patient population consisted of 36 individuals ages 1-12 years of age with a similar male to female ratio. From clinical histories obtained from the children diagnosed with DHF (n = 23), the predominant complaints were fever (100%), headache (96.7%), vomiting (47.8%), abdominal pain (39.1%), back/bone pain (39.1%), cough (39.1%), sore throat (21.7%), convulsions (17.4%), and eye pain (13.0%). Clinical findings of the same pediatric patients included a positive tourniquet test result (100%), thrombocytopenia (100%), hemoconcentration (100%), skin petechiae (43.5%), epistaxis (39.1%), and maculopapular rash (26%). All four of the children diagnosed with DHF grade IV had hepatomegaly, pleural effusion, ascites, cold perspiration, and confusion. Serologic data demonstrated that a majority (46 of 70, 68.7%) of the individuals assessed did not have significant levels of IgM specific for dengue viruses at the time of their admission. However, the nine successful dengue virus isolations were only from these serononreactive cases (19.6%). From the other patients assessed, 11.4% had a primary (or first exposure) serologic response to dengue virus antigen (predominantly IgM); 17.1% had a secondary (or subsequent exposure) serologic response to the same dengue antigens (predominantly IgG response) and 5.7% (four adults) had indeterminate serologic data that could not differentiate between reactivity to dengue or Japanese encephalitis virus antigen preparations. Virus culture of blood samples produced nine dengue virus isolates: DEN- 1 (2), DEN-2 (1), and DEN-3 (6). Japanese encephalitis and influenza viruses were not isolated from blood and pharyngeal specimens, respectively, from any of the patients. Thus, this first reported outbreak of DHF in Irian Jaya, Indonesia was found to be attributed to dengue viruses types 1, 2, and 3.
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PMID:The first reported outbreak of dengue hemorrhagic fever in Irian Jaya, Indonesia. 924 17

Four male and three female marmosets in each group were exposed to air only, 1000 ppm of HCFC 225ca or 5000 ppm of HCFC 225cb, for 6 h per day for 28 consecutive days. HCFC 225ca caused a slight reduction in body weight. HCFC 225cb occasionally caused somnolence during exposure and vomiting on the first day of exposure. Clinical chemistry findings included a mild reduction of triglyceride, cholesterol and phospholipid levels and increased GOT level in the HCFC 225ca exposure group. HCFC 225cb also caused a reduction of triglyceride levels in some animals. HCFC 225ca caused a slight increase of hepatic carnitine palmitoyltransferase (CPT) activity while HCFC 225cb slightly increased cyanide-insensitive palmitoyl CoA beta-oxidation (FAOS) activity. In the HCFC 225cb exposure group, an increase in cytochrome P-450 content was also observed. HCFC 225ca caused a fatty change in the hepatic cells. Increased incidence of lipid droplets in the hepatic cells and myelin-like bodies in hepatic cells, Kupffer's cells and hepatic blood vessels were observed electron microscopically in the HCFC 225ca exposure group. A proliferation of smooth endoplasmic reticulum was observed in the HCFC 225cb exposure group. Decreased peroxisome volume density in the HCFC 225ca group, and increased volume density in the HCFC 225cb exposed females were seen. However, organ weight measurement and histopathological examination did not reveal hepatomegaly or hypertrophy with either substance. Although slight changes were noticed in peroxisome volume density and in some of the peroxisomal enzyme activities, the changes related to peroxisome proliferation with HCFC 225ca and 225cb were minimal in marmosets compared to those seen in rats. Histopathological examination and hormonal analysis did not reveal any abnormalities in the pancreas or testes.
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PMID:Four-week repeated inhalation study of HCFC 225ca and HCFC 225cb in the common marmoset. 933 32

Tularemia was diagnosed in 2 cats that were examined because of pyrexia and lethargy; both cats had a history of exposure to wild rabbits. One cat was vomiting, and the other was anorectic. Physical examination revealed dehydration, lymphadenopathy, and hepatomegaly. Hematologic and serum biochemical abnormalities included toxic neutrophils, high band neutrophil count, thrombocytopenia, and hyperbilirubinemia. Diagnosis was confirmed by isolating Francisella tularensis subsp tularensis from bone marrow or lymph node aspirates. Evaluation of samples collected during the acute and convalescent phases of the disease revealed an increase in serum F tularensis antibody titer. Both cats responded to treatment with fluids and antibiotics.
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PMID:Tularemia in two cats. 942 84

Chronic hepatitis associated with hypereosinophilia has been very rarely reported worldwide. A 7-month-old male infant presented with a high fever, cough, non-projectile vomiting and hepatomegaly. The eosinophil count of the peripheral blood increased up to 21,500/mm3 (49% of WBC). The infant had a history of frequent contact with a neighbor keeping a pigsty. The pathologic examinations of the liver showed severe porto-periportal necroinflammation with marked eosinophilic infiltration, giant cell transformation and ballooning degeneration of hepatocytes, and degranulation of the eosinophils. Bone marrow showed increased eosinophils and decreased myeloid series. Pericardial effusion and bilateral pulmonary consolidation were noted. Corticosteroid aggravated the clinical symptoms of the infant. Anthelmintic treatment significantly normalized the eosinophil count and liver function tests, but cardiopulmonary manifestations continued.
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PMID:Eosinophil-induced chronic hepatitis. 961 Jun 27

The differentiation of malaria from other causes of fever in the absence of microscopy is notoriously difficult. Clinical predictors of malaria have been studied in an area of low and unstable transmission on the western border of Thailand. In 1527 children aged 2-15 years who were followed prospectively for 7 months, 82% (1254) had at least one febrile episode. Malaria caused 24% (301) of the first febrile episodes (Plasmodium falciparum 128, P. vivax 151, P. malariae 1, mixed infections with P. falciparum and P. vivax 21). Each malaria case was matched with the next child of similar age presenting to the dispensary with another cause of fever. Clinical symptoms or signs associated with a final diagnosis of malaria were: confirmed fever (> or = 38 degrees C) (odds ratio [OR] 1.6, 95% confidence interval [95% CI] 1.4-1.9), headache (OR 1.5, 95% CI 1.3-1.9), muscle and/or joint pain (OR 2.0, 95% CI 1.6-2.8), nausea (OR 1.7, 95% CI 1.4-2.3), clinical anaemia (OR 1.4, 95% CI 1.3-3.3), palpable spleen (OR 1.3, 95% CI 1.1-1.7), palpable liver (OR 1.4, 95% CI 1.1-2.1), absence of cough (OR 1.6, 95% CI 1.4-2.0), and absence of diarrhoea (OR 1.5, 95% CI 1.2-2.4). None of these signs alone or in combination proved a good predictor of malaria. The best diagnostic algorithms (history of fever and headache without cough, and history of fever with an oral temperature > or = 38 degrees C [sensitivity 51% for both, specificity 72 and 71%, respectively]) would result in prescription of antimalarial drugs in 28-29% of the non-malaria febrile episodes, and only 49% of the true malaria cases. Thus half of the potentially life-threatening P. falciparum infections would not be treated. Although multivariate analysis identified vomiting, confirmed fever, splenomegaly and hepatomegaly as independent risk factors for a diagnosis of falciparum malaria, use of these signs to differentiate falciparum from vivax malaria, and thus to determine antimalarial treatment, was insufficiently sensitive or specific. Malaria diagnosis should be confirmed by microscopical examination of a blood slide or the use of specific dipstick tests in areas of low transmission where highly drug-resistant P. falciparum coexists with P. vivax.
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PMID:Clinical features cannot predict a diagnosis of malaria or differentiate the infecting species in children living in an area of low transmission. 969 50

We report a case of a 2 1/2-year-old girl presenting with abdominal pain, fever, vomiting, and hepatomegaly. In spite of the unusual age at presentation, dynamic gadolinium-enhanced MR findings, which have not been previously illustrated, proved to be highly specific for the diagnosis of infantile hepatic hemangioendothelioma because of the characteristic enhancement pattern.
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PMID:Dynamic gadolinium-enhanced MR findings in infantile hepatic hemangioendothelioma. 975 3

Psittacosis, also referred to as ornithosis, is a disease primarily of birds, which may be transmitted to humans. Psittacosis is caused by Chlamydia psittaci, an obligate intracellular parasite found worldwide. Humans are infected with C. psittaci when the organism enters the blood stream, usually through inhalation of dried excrement from diseased birds or through wound contamination with infected avian secretions. C. psittaci replicates in the liver and spleen and infects the lung and other organs hematogenously.1 The clinical manifestations of human psittacosis range from a mild respiratory infection to a severe systemic illness.1,2 Symptoms are frequently described as flu-like with fever, headache, body aches, and dry or productive cough. Sore throat, chest pain, abdominal pain, vomiting, and diarrhea are variably present. Physical findings may include a pulse-temperature dissociation, localized lung crackles, hepatomegaly, splenomegaly, and a pale macular skin rash. Chest radiographs may demonstrate lesions that are atelectatic, patchy, miliary, nodular, or consolidated in one or both lungs. White cell counts, erythrocyte sedimentation rates, and liver function tests are usually normal. In severe illness, signs and symptoms of liver dysfunction, neurological impairment, and respiratory and renal failure may be present. Since 1879 when psittacosis was recognized as a disease entity, cases have been reported in North and South America, Europe, Asia, and Australia. However, reports of psittacosis in Africa have been rare. An Ethiopian group, studying community-acquired pneumonia, published what they claimed to be the first report of psittacosis in Africa in 1994.3 The report published here is believed to be the first documented case of human psittacosis in Egypt.
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PMID:Psittacosis in Egypt: A Case Study. 981 79


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