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)

Hepatomegaly is a common postmortem observation in severely burned children, with the liver often tripling in size when compared with normal livers for age, weight, and sex. Lesions identified at autopsy include deposition of large and small fat droplets in the hepatocyte, congestion, centrilobular necrosis, and cholestasis. The present study was designed to identify the primary causes of hepatomegaly in severely burned children postmortem. For this purpose, 41 autopsies were reviewed and, when available, blood and tissue samples were studied. Histopathologic findings showed that large intrahepatocytic fat droplets within hepatocytes and cholestasis were important contributors to hepatomegaly. Liver density and wet/dry weight ratios significantly decreased with increasing liver size. Hepatocyte volume increased with increasing liver size (P < 0.001) as did total fat content (P < 0.001). The liver enzymes, alanine aminotransferase and aspartate aminotransferase, remained normal except within 5 to 10 days of injury and 5 to 10 days of death. Triglycerides made up 4% to 70% of the total fat, with the percentage of triglycerides increasing with the severity of hepatomegaly. Saturated fatty acids represented about 85% of the total fatty acids in normal-sized livers, whereas in the largest livers (400% of predicted), only 25% of the fatty acids were saturated. This study provides evidence that 85% to 90% of the hepatomegaly observed in severely burned children postmortem is associated with hepatocyte enlargement, which includes up to 19% intracellular fat. Increases in extracellular protein, intracellular glycogen, and fluid accumulation may make a minor contribution to postburn hepatomegaly.
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PMID:Identification of factors contributing to hepatomegaly in severely burned children. 1631 82

In this case report, a young woman with gallbladder sludge and acute pancreatitis due to acute hepatitis A (HAV) is presented. She was admitted to our hospital with abnormal hepatic enzymes. Five days prior to her admission, an initial abdominal ultrasound was performed at another hospital and revealed no abnormality, while her serum aspartate aminotransferase (AST) level was at the upper limit of normal (ULN) x 8. A second ultrasound was performed at our hospital and revealed a gallbladder wall thickness (9.3 mm), gallbladder sludge in the gallbladder lumen, pancreatic edema, ascites, and hepatomegaly while AST was at the ULN x 50. Magnetic resonance imaging and magnetic resonance cholangiopancreatography revealed imaging features of an acute stage of pancreatitis and gallbladder wall thickness with coexisting sludge in the gallbladder lumen. HAV infection was diagnosed by the detection of immunoglobulin M against HAV in the serum. The patient underwent two repeated abdominal ultrasound examinations on the 5th (AST was at the ULN x 3) and the 20th days (AST was at the normal) after her discharge, and both revealed normal findings. In our case, we observed reversible changes in the hepatobiliary and pancreatic system which was related to the severity of hepatic necro-inflammation. HAV-associated pancreatitis may be due to the formation of biliary sludge during the acute phase of the viral illness, but this association needs further investigation.
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PMID:Gallbladder sludge and acute pancreatitis induced by acute hepatitis A. 1790 17

We performed a retrospective study of 25 patients who died of severe falciparum malaria in Thailand and Vietnam using electron microscopy. The aims of the study were: to determine if there was any significant association between parasitized red blood cells (PRBC) sequestered in liver and spleen and particular pre-mortem clinical complications, and to compare the degree of parasite load between the liver and spleen within the same patients. PRBC sequestrations in each organ were compared with the pre-mortem parasitemia, to calculate the sequestration index (S.I.). The S.I. showed that the degree of PRBC sequestration in the spleen was higher than the liver (S.I. median = 3.13, 0.87, respectively) (p < 0.05). The results of quantitative ultrastructural study showed a significantly high parasite load in the liver of patients with jaundice, hepatomegaly and liver enzyme elevation (p < 0.05). We found a significant correlation between PRBC sequestration in the liver and a high serum bilirubin level, a high aspartate aminotransferase (AST) level and an increase in the size of the liver (Spearman's correlation coefficient = 0.688, 0.572, 0.736, respectively). Furthermore, a higher parasite load was found in the liver of patients with acute renal failure (ARF) compared to patients without ARF (p < 0.05). These findings suggest that PRBC sequestration in the liver is quantitatively associated with pre-mortem hepatic dysfunction and renal impairment. There was no significant difference between splenomegaly and PRBC sequestration. The size of a palpable spleen was not correlated with parasite load in the spleen. When ultrastructural features were compared between the two reticuloendothelial organs, we found that the spleen had more PRBC and phagocytes than the liver. The spleen of non-cerebral malaria (NCM) patients had more phagocytes than cerebral malaria (CM) patients. This observation reveals that the spleen plays a major role in malaria parasite clearance, and is associated with host defence mechanisms against malaria.
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PMID:A quantitative ultrastructural study of the liver and the spleen in fatal falciparum malaria. 1661 Jun 35

Neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD) is a kind of inborn errors of metabolism, with the main clinic manifestations of jaundice, hepatomegaly, and abnormal liver function indices. As a mitochondrial solute carrier protein, citrin plays important roles in aerobic glycolysis, gluconeogenesis, urea cycle, and protein and nucleotide syntheses. Therefore citrin deficiency causes various and complicated metabolic disturbances, such as hypoglycemia, hyperlactic acidemia, hyperammonemia, hypoproteinemia, hyperlipidemia, and galactosemia. This paper reported a case of NICCD confirmed by mutation analysis of SLC25A13, the gene encoding citrin. The baby (male, 6 months old) was referred to the First Affiliated Hospital with the complaint of jaundice of the skin and sclera, which it had suffered from for nearly 6 months. Physical examination showed obvious jaundice and a palpable liver 5 cm below the right subcostal margin. Liver function tests revealed elevated enzymatic activities, like GGT, ALP, AST, and ALT, together with increased levels of TBA, bilirubin (especially conjugated bilirubin), and decreased levels of total protein/albumin and fibrinogen. Blood levels of ammonia, lactate, cholesterol, and triglyceride were also increased, and in particular, the serum AFP level reached 319,225.70 microg/L, a extremely elevated value that has rarely been found in practice before. Tandem mass analysis of a dried blood sample revealed increased levels of free fatty acids and tyrosine, methionine, citrulline, and threonine as well. UP-GC-MS analysis of the urine sample showed elevated galactose and galactitol. The baby was thus diagnosed with suspected NICCD based on the findings. It was then treated with oral arginine and multiple vitamins (including fat-soluble vitamins A, D, E, and K), and was fed with lactose-free and medium-chain fatty acids enriched formula instead of breast feeding. After half a month of treatment, the jaundice disappeared, and the laboratory findings, including liver function indices, blood levels of ammonia, lactate and AFP, were returned to normal level. The baby was followed up for 6 months. It developed well, and the abnormal laboratory findings, including MS-MS and UP-GC-MS analysis results, have been corrected, except a slightly elevated lactate level sometimes. SLC25A13 gene mutation analysis for the patient revealed a compound heterozygote of mutation 851del4 and 1638ins23 and therefore NICCD was definitely diagnosed.
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PMID:[A difficult and complicated case study: neonatal intrahepatic cholestasis caused by citrin deficiency]. 1661 6

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

We retrospectively evaluated 73 immunocompetent adult patients assisted at our Infectious Diseases Clinic between March 1999 and March 2004 who presented fever and asthenia, mild to moderate increase of transaminases and serological findings compatible with recent cytomegalovirus infection. We excluded patients with a history of transfusions, drug abuse, immunodeficiencies, preexistent hepatic impairment or serological findings compatible with acute hepatitis A, B and C (HAV, HBV, HCV) and Epstein-Barr virus (EBV). The laboratory diagnosis of recent cytomegalovirus infection was made by especific IgM detection (ELISA) or a significant increase of specific IgG. The most frequent symptoms were fever (85%) and asthenia (83%), followed by cephalea (25%), splenomegaly (20%), adenomegalies (22%), pharyngitis (25%), myalgias (25%) and hepatomegaly (19%). All the patients showed moderate increase of transaminases and lymphomonocytosis (73/73). In average, ALT was increased by 6 fold and AST by 3.5 fold. The clinical characteristics that differentiate CMV infection from Epstein-Barr infection are the lesser frequency of adenomegalies and pharyngitis in the former. The differential diagnosis of CMV infection with hepatic involvement from acute hepatitis A and B, is based on the absence of jaundice, the lower elevation of transaminases, the intense lymphomonocytosis and the presence of specific IgM against CMV that are characteristic of CMV infection. In conclusion, in previously healthy young adults with fever, intense asthenia, lymphomonocytosis and moderate increase in transaminases levels, cytomegalovirus infection should be investigated.
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PMID:[Cytomegalovirus infection with hepatic involvement in immunocompetent adults]. 1687 6

A 3-month-old male Golden Retriever puppy was evaluated for lethargy and fever of 2-days duration. Results of a CBC and biochemical profile revealed marked eosinophilia (6.3 X 10(3)/microL; reference interval 0.1-1.2 X 10(3)/microL), moderate thrombocytopenia, and increased activities of alanine aminotransferase, aspartate aminotransferase, and creatine kinase. Hepatomegaly and peritoneal effusion were found using abdominal ultrasound. Peritoneal fluid analysis revealed eosinophilic inflammation (23,000 nucleated cells/microL with 88% eosinophils). Despite supportive treatment the puppy's condition deteriorated rapidly; euthanasia was requested, and a necropsy performed. Microscopically, there was marked necrosuppurative and eosinophilic hepatitis with vasculitis. Numerous hepatocytes contained protozoal organisms suspected to be Toxoplasma gondii or Neospora caninum. However, serum was negative for both T gondii and N caninum antibodies; polymerase chain reaction assay on hepatic tissue was negative for both organisms; and immunohistochemical evaluation of hepatic tissue using serum raised against T gondii, N caninum, and Sarcocystis neurona also was negative. Schizont morphology suggested that merozoites replicated by endopolygeny, forming rosettes around a central residual body. Transmission electron microscopy revealed that merozoites lacked rhoptries. These findings were consistent with a diagnosis of Sarcocystis canis, an apicomplexan parasite with an unknown life cycle.
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PMID:Fatal hepatic sarcocystosis in a puppy with eosinophilia and eosinophilic peritoneal effusion. 1696 26

In this retrospective study, the epidemiologic and clinical characteristics of 105 adult malaria patients, who had been hospitalized between the period of 1992 and 2006 were evaluated. Nineteen percent of the patients were female, and the mean age was 28 +/- 10 years. Fifty percent of the patients acquired the infection in Southeastern Anatolia, while they were on military duty. The most common complaints were rigor (93%), fever (90%), sweating (90%), headache (76%), nausea (45%), and fatigue (38%). The most common physical examination findings were splenomegaly (86%) and hepatomegaly (62%). Anemia was detected in 23%, leukopenia in 47%, thrombocytopenia in 73%, two fold increase in ALT or AST enzyme levels in 32% of the patients. Plasmodium vivax was detected in 101 (96%) patients, whereas P. falciparum was detected in 4 patients (4%). Although the number of malaria cases in Turkey is declining in recent years, the febrile patients with a history of travel to the endemic regions should raise the suspicion of malaria.
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PMID:[Malaria in Turkey and 14 years of clinical experience]. 1700 53

In this study, dimethyl-4,4'-dimethoxy-5,6,5',6'-dimethylene dioxybiphenyl-2,2'-dicarboxylate (DDB) was examined to justify its role in the hepatoprotection against erythromycin toxicity in male rats. Oral daily administration of toxic dose of erythromycin stearate (EE, 100 mg/kg body weight) was given to male rats for fourteen days to induce hepatotoxicity. It was found at the end of the experiment (14 days) that the total body weight was markedly decreased in rat treated with erythromycin stearate (EE). Hepatomegaly and splenomegaly were recorded in rats treated with erythromycin stearate (EE). The red blood cells (RBCs) count, haemoglobin content (Hb) and haematocrit value (Hct) were significantly reduced in rats treated with EE. The hepatotoxicities were monitored by increased level of plasma enzymes (aspartate aminotransferase; AST and alanine aminotransferase; ALT), total bilirubin, direct bilirubin, cholesterol, total lipids and glucose. The data obtained showed that oral administration of DDB (100 mg/kg body weight) has significantly prevented the occurrence of EE-induced liver damage. The biochemical data were supplemented by histopathological examination of the liver of control and treated rats. DDB showed a better hepatoprotective effect compared with ursodesoxycholic acid or Silymarin (Sil), as a reference drug.
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PMID:Protective role of dimethyl diphenyl bicarboxylate (DDB) against erythromycin induced hepatotoxicity in male rats. 1726 70

Hepatic manifestations are described as unusual complications of dengue and may lead to severe and potentially lethal conditions. Liver abnormalities in 41 patients diagnosed with dengue hemorrhagic fever in Campo Grande, Mato Grosso do Sul, Brazil, between January 1 and March 31, 2002, were evaluated. All were serologically positive for dengue in laboratory tests (IgM ELISA). ALT alterations were observed in 61% (25/41) and AST alterations in 80.5% (33/41), but there were no statistically significant differences between the various clinical forms. The range in ALT levels was 14-547 U/l and in AST levels was 11-298 U/l. Nausea and/or vomiting were reported by 90% (37/41) of the patients; 46.3% (19/41) had abdominal pain and 10% (3/29) presented hepatomegaly at clinical examination. The patients' ages ranged from 18 to 88 years; 23 (56%) were female and 18 (44%) were male.
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PMID:[Liver involvement in patients with dengue hemorrhagic fever: a rare phenomenon?]. 1730 99


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