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)

The clinical, radiological and hepatic histological features of 51 patients with hepatobiliary fibropolycystic disease were reviewed. Many of the patients had more than one of the diseases; the combination of both congenital hepatic fibrosis (CHF) and Caroli's disease was most striking. Twelve patients with CHF (50% male) presented at 6 +/- 2 years of age (mean +/- SEM) with hepatosplenomegaly or variceal bleeding. Their main problems were recurrent variceal bleeds and renal disease. Polycystic kidneys and renal stones were present in 79% and chronic renal failure in 30%. Six of the 8 patients with Caroli's disease were male (75%) and presented later (aged 37 +/- 8 years) with hepatomegaly or cholangitis. Recurrent cholangitis developed in most (7/8) and 2 had polycystic kidneys. Twelve patients had a combination of CHF and Caroli's disease presenting with hepatosplenomegaly, bleeding or cholangitis. As in Caroli's disease, most (83%) were male, but the age of presentation (15 +/- 4 years), and the incidence of polycystic kidneys (42%) and renal failure (8%) was intermediate between CHF and Caroli's disease. In these patients, bleeds always predated cholangitis. Histologically, acute cholangitis was superimposed on the changes of CHF. Adult polycystic liver disease (10 patients) presented later (43 +/- 3 years) in females (90%) with pain, a mass or incidentally; polycystic kidneys were present in 33%. Microhamartomas (10 patients), which were usually incidental findings, were diagnosed latest (50 +/- 6 years). Three choledochal cysts were seen. The hazard of cancer in these diseases was reflected by 2 bile duct cancers and 1 pancreatic cancer (incidence 6%). This study has confirmed that hepatobiliary fibropolycystic diseases form part of a family and are often associated together. However, the diseases are of greatly differing severity and the prognosis in an individual patient is determined by the fibropolycystic diseases present.
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PMID:Hepatobiliary fibropolycystic diseases. A clinical and histological review of 51 patients. 395 71

Continuous supraventricular tachycardia was induced in 13 fetal sheep for 72 to 216 hours. The PaO2 decreased from 18.1 +/- 1.2 (SEM) to 15.4 +/- 0.9 mm Hg and the PaCO2 increased from 41.5 +/- 1.2 (SEM) to 46.0 +/- 1.0 (SEM) mm Hg with pacing. The hematocrit, total protein, albumin, serum [Na+] and [K+], and osmolality remained unchanged throughout the study. All study fetuses showed signs of ascites (mean = 88 +/- 67.5 [SD] ml), and one was grossly hydropic. Six fetuses, all of which had greater than or equal to 50 ml of ascites, died as the results of pacing. Gross pathologic findings in 13 fetuses included: cardiomegaly in seven, cyanotic myocardium in two, hepatomegaly in seven, pulmonary congestion in two, generalized edema in three, and massive edema (hydrops) in one. None of these conditions was found in the 14 control animals. There was no correlation of the severity of effects upon the fetus and the induced heart rate, the duration of tachycardia, or the site of implantation of the pacemaker. The conclusion was that organomegaly, generalized edema, and hydrops fetalis were the direct result of supraventricular tachycardia in utero; the exact mechanism of production and the reasons for the variable manifestations of tachycardia remain unclear.
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PMID:Supraventricular tachycardia with edema, ascites, and hydrops in fetal sheep. 706 22

Excessive ingestion of vitamin A during pregnancy causes teratogenic effects on the offspring. However, many of these modifications have not been described at the cellular level. The objective of the present study was to characterize alterations of the smooth muscle cells of the esophagus of rat fetuses. On the tenth day after conception, 42 pregnant rats (5 months of age) subdivided into 6 groups received a single intraperitoneal injection of vitamin A at doses of 30,000, 40,000, 50,000, 70,000, 100,000 or 150,000 IU. Seven pregnant control rats received saline solution. After the twentieth day of pregnancy, the fetuses were delivered by cesarian section and weighed and the length of their umbilical cords was measured. Histologic sections were obtained from the esophagus and characterized with the light microscope under oil immersion. There was a significant increase in the nuclear volume of the cells of esophageal smooth muscle from treated animals compared to the control group. The median for the group treated with 100,000 IU of vitamin A (23.8 microns 3) was significantly greater than that for the control group (12.3 microns 3). The body weight (reported as mean +/- SEM) of fetuses treated with the various doses of vitamin A was lower (1.78 +/- 0.18, 1.77 +/- 0.08, 1.48 +/- 0.20, 1.72 +/- 0.11, 1.70 +/- 0.09 and 1.54 +/- 0.13 g, respectively) than that of the control group (2.14 +/- 0.13 g). The mean length of the umbilical cord of fetuses treated with 30,000 (1.66 +/- 0.15 cm), 40,000 (1.78 +/- 0.18 cm), 50,000 (1.58 +/- 0.15 cm), 70,000 (1.90 +/- 0.19 cm), 100,000 (1.58 +/- 0.24 cm) and 150,000 IU (1.48 +/- 0.11 cm) vitamin A was significantly shorter when compared with the mean length of the umbilical cords of control fetuses (2.1 +/- 0.46 cm). Malformations in treated animals such as agnathia, palpebral aplasia, hepatomegaly, exophthalmos, fochomelia and spina bifida were observed macroscopically.
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PMID:Effects of hypervitaminosis A on rat fetus esophagus smooth muscle cells. 858 Aug 85

Arsenic is an environmental toxicant and a human carcinogen. Epidemiology studies link human arsenic exposure to various diseases and cancers, including liver diseases and hepatocellular carcinoma. However, the molecular mechanisms for arsenic toxicity and carcinogenicity are poorly understood. To better understand these mechanisms, we used the human cancer cDNA expression array to profile aberrant gene expression in arsenic-exposed populations in Guizhou, China. The selected patients had a history of exposure to environmental arsenic for at least 6-10 years, and had arsenic-induced skin lesions and hepatomegaly. Samples were obtained by liver needle biopsy. Histology showed degenerative liver lesions, such as chronic inflammation, vacuolation, and focal necrosis. The University of North Carolina Hospitals provided normal human liver tissues from surgical resection or rejected transplants. Microarray was performed with total RNA from liver samples, and signal intensities were analyzed with AtlasImage software and normalized with 9 housekeeping genes. Means and SEM were calculated for statistical analysis. Approximately 60 genes (10%) were differentially expressed in arsenic-exposed human livers compared to controls. The differentially expressed genes included those involved in cell-cycle regulation, apoptosis, DNA damage response, and intermediate filaments. The observed gene alterations appear to be reflective of hepatic degenerative lesions seen in the arsenic-exposed patients. This array analysis revealed important patterns of aberrant gene expression occurring with arsenic exposure in human livers. Aberrant expressions of several genes were consistent with the results of array analysis of chronic arsenic-exposed mouse livers and chronic arsenic-transformed rat liver cells. Clearly, a variety of gene expression changes may play an integral role in arsenic hepatotoxicity and possibly carcinogenesis.
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PMID:Application of cDNA microarray to the study of arsenic-induced liver diseases in the population of Guizhou, China. 1113 58

Krill oil (KO) is rich in n-3 fatty acids that are present in phospholipids rather than in triglycerides. In the present study, we investigated the effects of dietary KO on cardiometabolic risk factors in male C57BL/6 mice fed a high-fat diet. Mice (n = 6-10 per group) were fed for 8 weeks either: (1) a nonpurified chow diet (N); (2) a high-fat semipurified diet containing 21 wt % buttermilk + 0.15 wt % cholesterol (HF); (3) HF supplemented with 1.25 wt % KO (HFKO1.25); (4) HF with 2.5 wt % KO (HFKO2.5); or (5) HF with 5 wt % KO (HFKO5.0). Dietary KO supplementation caused a significant reduction in liver wt (i.e., hepatomegaly) and total liver fat (i.e., hepatic steatosis), due to a dose-dependent reduction in hepatic triglyceride (mean +/- SEM: 35 +/- 6, 47 +/- 4, and 51 +/- 5% for HFKO1.25, -2.5, and -5.0 vs HF, respectively, P < 0.001) and cholesterol (55 +/- 5, 66 +/- 3, and 71 +/- 3%, P < 0.001). Serum cholesterol levels were reduced by 20 +/- 3, 29 +/- 4, and 29 +/- 5%, and blood glucose was reduced by 36 +/- 5, 34 +/- 6, and 42 +/- 6%, respectively. Serum adiponectin was increased in KO-fed animals (HF vs HFKO5.0: 5.0 +/- 0.2 vs 7.5 +/- 0.6 microg/mL, P < 0.01). These results demonstrate that dietary KO is effective in improving metabolic parameters in mice fed a high-fat diet, suggesting that KO may be of therapeutic value in patients with the metabolic syndrome and/or nonalcoholic fatty liver disease.
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PMID:Dietary krill oil supplementation reduces hepatic steatosis, glycemia, and hypercholesterolemia in high-fat-fed mice. 1976 Dec 11