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 14-year-old girl was admitted with chief complaints of edema and chest pain. She had hepatomegaly, but did not have heart murmur and accentuation of the pulmonary component of the second heart sound. The electrocardiogram showed right axis deviation, negative T wave in V3,4 and ST depression in III, aVF. But right ventricular hypertrophy was not dominant. Chest radiography showed a cardiothoracic ratio of 54% and a slight prominence of proximal pulmonary arteries. The edema was soon diminished only by the diuretics, but it appeared again without the diuretics. At the cardiac catheterization 3 months after the onset of symptoms, the pulmonary arterial pressure was 150/85 mmHg and the pulmonary resistance was 3,232 dyn/sec/cm5. The right atrial pressure was 9.5 mmHg and oxygen saturation at the pulmonary artery was 31.0%. Prostaglandin E1 reduced the pulmonary artery pressure only a little, but raised the systemic pressure. The patient was treated with several vasodilators, but her condition deteriorated rapidly and she developed severe right ventricular failure. She died only 8 months after the onset of symptoms and 5 months after the catheterization. At autopsy, histological examination demonstrated intimal fibrotic thickening of the small-sized pulmonary arteries and organizing thrombus. But there was not plexiform lesion. Heart failure was easily improved when she was first admitted. But after 3 months the cardiac catheterization revealed that her condition was already severe. Several vasodilators was not effective to such a rapidly progressive primary pulmonary hypertension.
Kokyu To Junkan 1989 Sep
PMID:[A case of rapidly progressive pulmonary pulmonary hypertension in a 14-year-old girl]. 259 31

A 29 year old Chinese female who presented with spontaneous purpura, was found to have gross hepatomegaly and thrombocytopenia. The thrombocytopenia responded to steroid therapy but relapsed when the dose of steroid was tapered down. Subsequent investigations revealed that the hepatomegaly was due to a large haemangioma of her liver. For symptomatic hepatic haemangioma, surgical excision is the treatment of choice; this was refused by the patient.
Med J Malaysia 1989 Sep
PMID:Haemangioma-thrombocytopenia syndrome--a case report. 262 43

In the present study, the effects of chloroquine and ethanol administration during gestation have been investigated on the developing rat fetus. Intragastric administration of chloroquine (700 mg/kg body weight) resulted in several structural abnormalities. The incidence of hepatomegaly was increased by 30%, the liquification of visceral organs was increased by 15% and a 9% higher incidence of cleft palate, wrist drop, clubbed foot and brain liquification was observed in the fetuses from the chloroquine-treated group compared to the corresponding controls. Fetuses from the chloroquine-treated group also showed a decrease of about 40% in the body weight and a 30% reduction in the ossification of the sternum. The teratogenic effects of oral ethanol administration in several respects were similar to those of the chloroquine. Ethanol, when administered as 30% of the total daily calories, resulted in growth retardation, resorption, still births, liquification of the brain, wrist drop and clubbed foot. Additionally, ethanol resulted in the inhibition of several metabolic pathways in the liver and brain of the developing fetuses. This included the inhibition of protein, RNA and DNA metabolism in the fetal livers and brains. The feto-toxic effects of these two xenobiotics and their possible molecular mechanisms have been discussed.
Pharmacol Biochem Behav 1989 Sep
PMID:Toxicological consequences of chloroquine and ethanol on the developing fetus. 262 56

To determine if the carcinogenic potential of peroxisome proliferators is dependent upon their ability to induce cell proliferation, we have investigated the extent of cell proliferation in the livers of rats fed ciprofibrate, a peroxisome proliferator. Male rats were maintained on a diet containing ciprofibrate (0.025% w/w) and killed at selected intervals following 1 week of continuous [3H]thymidine labeling. Evaluation of labeling indices demonstrated a significant increase in cell proliferation during the first week but not in rats killed at the end of 5 and 20 weeks of treatment. Increases in hepatocyte nuclear labeling were found at 40 and 70 weeks of ciprofibrate administration which coincided with the appearance in livers of putative preneoplastic and neoplastic lesions. In a short-term feeding study, ciprofibrate and ethoxyquin were fed to rats at a dietary concentration of 0.025% and 0.5%, respectively, either alone or in combination for 7 days. Ciprofibrate and ethoxyquin either alone or in combination produced marked hepatomegaly and a significant increase in DNA synthesis as demonstrated by [3H]thymidine incorporation and autoradiographic studies. DNA synthesis in the group receiving ciprofibrate and ethoxyquin simultaneously, was slightly more than in animals that received either compound alone, suggesting a synergistic effect, although chronic feeding of these agents together resulted in inhibition of liver carcinogenesis (Rao, M. S. et al. (1984) Cancer Res., 44, 1072-1076). The results of this study further suggest that cell proliferation induced by peroxisome proliferators may be less important in carcinogenesis than peroxisome proliferation induced by these compounds.
Cancer Lett 1989 Sep 15
PMID:Evaluation of liver cell proliferation during ciprofibrate-induced hepatocarcinogenesis. 263 30

Umbilical venous and amniotic fluid pressures were measured in 68 human pregnancies at the time that cordocentesis was performed. Normal umbilical venous pressure was unrelated to gestational age and remained within a tight range (5.3 +/- 2.3 mm Hg, mean +/- SD). Fetuses with an elevated umbilical venous pressure had disorders consistent with either hepatomegaly or congestive heart failure. Umbilical venous pressure was significantly increased before treatment in two fetuses with immune hydrops; it rapidly declined with treatment. Neither gestational age nor umbilical venous pressure was significantly different in the groups that received and did not receive pancuronium. There was a strong relationship between amniotic fluid pressure and gestational age in normal pregnancy (r = 0.54, p less than 0.0001). Women with hydramnios had amniotic fluid pressures greater than control subjects (p = 0.0007). This investigation documents normal human amniotic fluid and fetal umbilical venous pressures. These measurements are altered by disease and may prove to be of diagnostic and therapeutic value in the future.
Am J Obstet Gynecol 1989 Sep
PMID:Normal values for human umbilical venous and amniotic fluid pressures and their alteration by fetal disease. 267 2

An insulin-dependent diabetic was diagnosed at the age of 7 years. After two years of satisfactory control she began to have several bouts of hospitalization with hyperglycaemic ketoacidosis, and developed tender hepatomegaly, which persisted to age 11 years. With restabilisation of her diabetes, the liver regressed and she continued to maintain good health for another 1 1/2 years when she died suddenly while asleep. Post-mortem examination by the coroner revealed ascites in the abdomen, hepatomegaly and fatty metamorphosis of the liver. Her diabetes control required up to 2.3 i.u. insulin per kg body weight per day plus a 1,900 calorie diet. Her growth was well below the tenth percentile, weight for height (Harvard charts). This clinical picture of high insulin dosage, hepatomegaly, unstable diabetes and growth failure approximates to the Mauriac syndrome.
West Indian Med J 1989 Sep
PMID:The Mauriac syndrome. 269 19

In a 7-year period, transatrial membranotomy was performed in 11 patients with membranous obstruction of the inferior vena cava. There were 5 men and 6 women, ranging in age from 23 to 53 years. Clinical symptoms included jaundice in 4 patients, hepatomegaly in 4, leg edema or varicose veins in 10, and venous collaterals over the abdominal and chest wall in all 11 patients. Transatrial membranotomy was performed through a median sternotomy in all patients. When inferior vena cava venography revealed that the obstruction was accompanied by long segmental thrombosis, additional dilation was performed with a Hegar dilator. There was no surgical mortality. Early operative complications included pulmonary embolism in 2 patients and bleeding requiring reoperation in 1. In a mean follow-up period of 30.6 months (range, 2 to 88 months), 9 patients had no symptoms, transient pericardial constriction developed in 1 patient and resolved 1 month later, and restenosis of the inferior vena cava developed in another patient 1 year after the first operation. This latter patient received a second transatrial membranotomy followed by percutaneous balloon angioplasty of the inferior vena cava, with a satisfactory result at 8 months follow-up. We conclude that transatrial membranotomy is an effective and safe procedure for patients with membranous obstruction of the inferior vena cava.
Ann Thorac Surg 1989 Sep
PMID:Transatrial membranotomy for Budd-Chiari syndrome. 240 Feb 84

The effects of various compounds known to be hepatic tumor promoters and toxins in the male B6C3F1 mouse liver, including di(2-ethylhexyl)phthalate (DEHP), acetaminophen (ACT), barbital (BB), and phenobarbital (PB) on hepatic metallothionein (MT) concentrations were assessed after chronic exposure. From 6 weeks of age, male mice were maintained on diets containing DEHP at 12,000 or 6000 ppm, ACT at 10,000 or 5000 ppm, BB at 1,000 ppm, or drinking water with PB at 500 ppm for up to 24 weeks. MT was measured in hepatic cytosol at 0, 2, 8, and 24 weeks of exposure. DEHP proved a very effective inducer, producing elevations of MT as high as 11-fold. The increases in hepatic MT with DEHP were both dose- and time-related. ACT was likewise effective in producing hepatic MT elevations (maximum 6.7-fold) in a dose- and time-related fashion. BB and PB, however, had no effect on hepatic MT levels at any time point. While DEHP, BB, and PB treatments produced hepatomegaly, histopathological analysis at 24 weeks revealed that in both DEHP- and ACT-treated livers hepatocellular proliferation was prominent while livers exposed to BB or PB showed predominantly hepatocellular hypertrophy. Gel-filtration of DEHP-treated liver cytosol revealed that zinc was associated with the MT peak. This peak also bound cadmium in vitro and could be extracted by heat treatment and selective acetone precipitation, both typical characteristics of MT. Further confirmation of the presence of MT after DEHP treatment was obtained by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (10 to 20% acrylamide). Results indicate that some, but not all, tumor promoters can induce target organ MT and that such an induction appears associated with those promoters inducing persistent cellular hyperplasia but not those inducing cellular hypertrophy.
Toxicol Appl Pharmacol 1989 Sep 01
PMID:Induction of hepatic metallothionein in male B6C3F1 mice exposed to hepatic tumor promoters: effects of phenobarbital, acetaminophen, sodium barbital, and di(2-ethylhexyl) phthalate. 278 55

The influence of 1-benzylimidazole on the activities of hepatic monooxygenases cytochromes P-450 dependent, epoxide hydrolases and UDP-glucuronosyltransferases was investigated in male Wistar rats. Several doses (25, 75 and 100 mg/kg/day) were administered gastrically during 5 days in order to evaluate the dose-related induction. The treatment caused a dose-dependent hepatomegaly. 1-Benzylimidazole decreased the plasma level in triglycerides by 60-70%; by contrast the cholesterol content was not changed during the time course of the experiment. Lauric acid hydroxylase, benzphentamine N-demethylase, 7-ethoxyresorufin O-deethylase, 7-ethoxycoumarin O-deethylase activities were increased 3.5-, 4-, 13- and 46-fold, respectively with the highest dose. By immunoblotting, an enhancement in the protein bands corresponding to cytochromes P-450c and P-450b could be simultaneously observed, whatever the dose administered, thus suggesting an induction process. However, 1-benzylimidazole failed to bind with high affinity to the cytosolic Ah receptor. On the other hand, measurement of the activity of the microsomal epoxide hydrolase with benzo(a)pyrene-4,5-oxide as substrate and quantitation of the enzyme protein by immunoassay revealed that the increase in the activity after treatment with the compound was the result of enzyme activation only. By contrast, cytosolic epoxide hydrolase was not affected by 1-benzylimidazole. This compound also stimulated three distinct forms of UDP-glucuronosyltransferase. The activities towards 4-methylumbelliferone, 1-naphthol, morphine or a monoterpenoid alcohol, nopol, supported by two different isozymes were significantly increased only with the highest dose; meanwhile bilirubin glucuronidation was 2-fold enhanced, whatever the dose used. These observations emphasize the variety of the effects of 1-benzylimidazole on drug-metabolizing enzymes.
Biochem Pharmacol 1988 Sep 01
PMID:Effect of 1-benzylimidazole on cytochromes P-450 induction and on the activities of epoxide hydrolases and UDP-glucuronosyltransferases in rat liver. 284 Sep 13

A 68-year-old man was referred to our hospital because of generalized lymphadenopathy. His abnormal findings were hepatomegaly, leukocytosis and elevated serum LDH. Anti-ATLA antibody was positive. As about half of the peripheral lymphocytes reacted to the monoclonal antibody CD25, these cells were considered to be compatible with ATL cells having an interleukin-2 receptor. Initially, recombinant beta-interferon was administered, but it was not effective. A combination of vincristine (VCR) and prednisolone (PDN) was partially effective against the lymphadenopathy, but the hepatomegaly and leukocytosis did not improve. 4'-epi-Adriamycin (Epirubicin), at a doses of 20 mg/body, weekly, was subsequently added to VCR + PDN therapy. The patient achieved complete regression 2 months later, and has been in continuous complete remission for more than 3 months.
Gan To Kagaku Ryoho 1987 Sep
PMID:[A case of adult T-cell leukemia achieving complete remission with epirubicin, vincristine and prednisolone chemotherapy]. 288 35


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