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 retrospective analysis was performed for the clinical data of four children with Epstein-Barr virus (EBV)-related acute liver failure. There were two boys and two girls with a median age of 10 months (range 8.5-44 months). Of the four children, three were diagnosed with infectious mononucleosis (IM), among whom two met the diagnostic criteria of hemophagocytic lymphohistiocytosis (HLH), and one was diagnosed with past EBV infection. All the children had positive EBV DNA in blood and all had pyrexia, hepatomegaly, and jaundice on admission. Three children had the symptom of splenomegaly, ascites, or vomiting. Two children had enlargement of cervical lymph nodes, skin rash, or pleural effusion. One child had gastrointestinal bleeding or stage 2 hepatic encephalopathy. All the children had an abnormal lymphocyte count of <10%, and only one child had leukocytosis and thrombocytopenia. Among the four children, alanine aminotransferase level increased by 10-100 times; total bilirubin level increased by 3-5 times; lactate dehydrogenase level increased by many 10 times; prothrombin time prolonged significantly. All the children were given antiviral therapy with intravenously injected acyclovir or ganciclovir, as well as hepatocyte growth factor to promote hepatocyte growth and hormone to alleviate inflammatory response. Two children were given plasma exchange in addition, among whom one was given the combination of continuous venovenous hemodiafiltration. Two children with HLH were given chemotherapy according to the HLH-2004 regimen. Three children survived, and one child with HLH died of multiple organ failure. It is concluded that EBV infection can cause acute liver failure and that early use of multimodality therapy including blood purification may be beneficial for prognosis in these children.
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PMID:[Clinical features of children with Epstein-Barr virus-related acute liver failure: an analysis of four cases]. 3057 93

Aggressive natural killer (NK) cell leukemia (ANKL) is a rare form of leukemia with an aggressive clinical course. It commonly involves the peripheral blood, bone marrow, liver, and spleen but rarely involves the lungs. We report a 36 year-old woman who presented with pulmonary lesions we suspected to be interstitial lung disease on an imaging study. A lung biopsy showed extensive lymphoid infiltrate growing along pre-existing alveolar septa without destroying the alveolar spaces. Further workup revealed hepatomegaly, borderline splenomegaly, and multiple lymphadenopathies. Her laboratory tests showed leukocytosis, anemia, thrombocytopenia, abnormal liver enzymes, and elevated lactate dehydrogenase. A bone marrow (BM) aspirate smear revealed many intermediate to large lymphocytes with dispersed chromatin, basophilic cytoplasm, and some azurophilic granules. A BM biopsy showed hypercellularity with interstitial lymphoid infiltrate in a background of trilineage hematopoiesis and histiocytosis with hemophagocytosis. Immunohistochemical studies performed on both the lung and BM biopsies showed the neoplastic cells to be positive for CD2, CD3, CD7, CD56, granzyme B, phosphor-MAPK (pMAPK), EBER (Epstein-Barr Virus-encoded small RNA) by in situ hybridization; they were negative for CD4, CD5, CD8, CD30, LMP1, and phospho-STAT3 (pSTAT3). A flow cytometry analysis of the BM aspirate identified a population of atypical lymphocytes with the NK cell phenotype. Molecular studies were negative for T-cell receptor gene rearrangements, and the neoplastic cells displayed a complex karyotype. The patient responded initially to chemotherapy but died of multiorgan failure two months after the diagnosis. We present a case of ANKL mimicking interstitial lung disease with the activation of MAPK pathway.
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PMID:Aggressive natural killer cell leukemia mimicking interstitial lung diseases with the activation of the mitogen-activated protein kinase pathway. 3194 37

A 69-year-old man with prostate cancer presented to the hospital with 2 weeks' history of fever, abdominal distension, and fatigue. Laboratory findings showed signs of acute liver failure, and marked elevation of lactate dehydrogenase and tumor marker levels. Abdominal CT showed hepatomegaly with multiple hypodense lesions in both lobes, suggesting metastases. FDG PET/CT scan shows hypermetabolism unusually in the liver with significantly suppressed heart and brain activity, reminiscent of an FDG hepatic superscan. The hypermetabolic lesions confirmed with Tru-Cut needle biopsy of the liver as metastasis of prostate cancer.
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PMID:FDG Hepatic Superscan Due to Metastatic Infiltration of Prostate Cancer. 3236 88

This study aimed at investigating the anti-obesity and anti-dyslipidemic effects of Stachys sieboldii Miq. root (SS) powder in rats following a high-fat and high-cholesterol (HFC) diet for 6 weeks. Thirty-two Sprague-Dawley rats were fed one of the following diets: a regular diet (RD), HFC, HFC supplemented with 3% SS (HFC + 3SS) or HFC supplemented with 5% SS (HFC + 5SS). Following an HFC diet increased body weight (BW) gain (p < 0.001) and the food efficiency ratio (FER; p < 0.001); however, SS consumption gradually prevented the HFC-induced BW gain (p < 0.001) and increase in FER (p < 0.01). The HFC diet resulted in increased liver size (p < 0.001) and total adipose tissue weight (p < 0.001), whereas the SS supplementation decreased hepatomegaly (p < 0.05) and body fat mass (p < 0.001). SS consumption prevented the increased activities of serum alanine aminotransferase (ALT; p < 0.001), aspartate aminotransferase (AST; p < 0.001), alkaline phosphatase (ALP; p < 0.01 in HFC + 5SS) and lactate dehydrogenase (LDH; p < 0.001 in HFC + 5SS) induced by the HFC diet (p < 0.001). The SS supplementation improved lipid profiles in the circulation by lowering triglyceride (TG; p < 0.01), total cholesterol (TC; p < 0.001) and non-HDL cholesterol (non-HDL-C; p < 0.001) levels, as well as the atherogenic index (p < 0.01) and cardiac risk factor (p < 0.01). The lipid distribution in the liver (p < 0.05) and white adipose tissues (WAT; p < 0.001) of the HFC + SS diet-consuming rats was remarkably lower than that of the HFC diet-consuming rats. The average size of the epididymal adipose tissue (p < 0.001) was significantly lower in the HFC + SS diet-fed rats than in the HFC diet-fed rats. The fecal lipid (>3% SS; p < 0.001) and cholesterol (5% SS; p < 0.001) efflux levels were significantly elevated by the SS supplementation compared to those measured in the RD or HFC diet-fed groups. In addition, the hepatic lipid and cholesterol metabolism-related gene expressions were affected by SS consumption, as the hepatic anabolic gene expression (Acc; p < 0.001, Fas; p < 0.001 and G6pdh; p < 0.01) was significantly attenuated. The HFC + 5SS diet-fed rats exhibited elevated hepatic Cyp7a1 (p < 0.001), Hmgcr (p < 0.001) and Ldlr (p < 0.001) mRNA expression levels compared to the HFC diet-fed rats. These results suggest that SS may possess anti-adipogenic and lipid-lowering effects by enhancing lipid and cholesterol efflux in mammals.
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PMID:Stachys sieboldii Miq. Root Attenuates Weight Gain and Dyslipidemia in Rats on a High-Fat and High-Cholesterol Diet. 3266 7


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