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 40-year-old man was diagnosed as fatty liver according to our ultrasonographical criteria for fatty liver, i.e., liver-kidney contrast in the ultrasound mass screening of the liver, biliary tract and pancreas. He lacked any signs or symptoms, nor any known causes of fatty liver, i.e., obesity, diabetes, hyperlipidemia, ingestion of alcohol or drugs. Liver biopsy of this patient revealed fatty change of about 50% of the hepatic lobules. It has been difficult to suspect the presence of latent fatty liver which lacked both the abnormality in the liver function test and hepatomegaly, and even impossible when it lacked any risk factors. In the future as the ultrasonography becomes more generally used as a primary screening examination, "idiopathic latent fatty liver", like this patient, will be more frequently found and this, in turn, will contribute to the progress of the epidemiology and etiology of fatty liver.
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PMID:A case of idiopathic fatty liver detectable only by ultrasonography. 662 57

A boy of 6 with diabetic ketoacidosis presented with a disturbance of lipid metabolism characterised by eruptive xanthomata, hepatomegaly, lipaemia retinalis, milky serum and hypertriglyceridemia with type V electrophoretic pattern. All the findings are typical diabetic hyperlipidaemia. The severity of the abnormalities are not solely due to delay in treatment because they are also caused by the unusual sensitivity of lipoprotein lipase to insulin deficiency. A histological and ultrastructural study of the xanthomata was performed.
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PMID:[Diabetic ketoacidosis with severe hypertriglyceridemia and eruptive xanthomata (author's transl)]. 678 45

Changes in a number of morphological and biochemical parameters were observed in genetically obese Zucker rats and in lean controls between 3 and 58 weeks of age. By 3 weeks, the genetically obese rats had higher proportional (wt/100 g body wt) and absolute amounts of adipose tissue, hyperlipemia affecting all the lipid fractions, and hyperproteinemia compared to lean controls. Obesity, hepatomegaly, high concentrations of hepatic lipids and hyperinsulinemia did not appear until the fifth week. In obese animals, liver lipid concentration reached a maximum at 17 weeks of age and then declined. During this time, the triacylglycerol concentration in the serum remained stable, whereas the cholesterol and phospholipid concentrations continued to increase. The glycogen concentration in obese animals increased, both absolutely and compared to lean controls, between the 12th and 43rd weeks of age. From weaning, the Zucker rats, compared to lean controls, exhibited characteristics of obesity (accumulation of adipose tissue, hyperlipemia and hyperproteinemia), which persisted to the age of 58 weeks.
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PMID:Age-related changes in biological parameters in Zucker rats. 703

This article has focused on the appropriate indications for lipid-lowering drugs in adult patients with different lipoprotein disorders, which we have divided into primary hypercholesterolemia, combined hyperlipidemia,and hypertriglyceridemia. The mechanism of action, efficacy, and safety profile of the major drugs have been reviewed, and based on this information, we have presented our views on the appropriate drugs of first choice and appropriate second-choice agents for treatment of adult patients with different dyslipidemias. The rationale for the use of hypolipidemic drugs is strongest in patients with hyperlipidemia who concurrently have evidence for coronary or peripheral vascular disease, in whom the goal of secondary prevention is to retard further progression of atherosclerosis and potentially induce some regression, whereas in selected high-risk patients without evidence of atherosclerosis, the goals of therapy are to prevent the premature development of CAD or, in patients with severe hypertriglyceridemia, prevent the adverse sequelae of hepatomegaly, splenomegaly, and potentially pancreatitis. We have focused on the use of hypolipidemic drugs in adult patients, and the guidelines discussed are not appropriate for use in children with hyperlipidemia, in whom drug therapy should be undertaken selectively and in consultation with a lipid specialist. Many areas of controversy in the use of lipid-lowering drugs remain to be addressed by future studies; these include the use of lipid-lowering drugs in patients with secondary causes of hyperlipidemia (e.g., the nephrotic syndrome), the use of lipid-lowering drugs in women, and recommendations for drug therapy in older patients.
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PMID:Drug treatment of dyslipoproteinemia. 828 33

Hyperlipidemia has been implicated in the pathogenesis of experimental progressive glomerulosclerosis, but its role in human renal injury is controversial. This report describes a 12-yr-old boy presenting with massive proteinuria, hepatomegaly, anemia, severe mixed hyperlipidemia, and progressive renal failure. The initial renal biopsy disclosed large numbers of foam cells that were shown to be monocytes. Evidence is presented suggesting that apoprotein-E2 homozygosity in our patient, together with an 88% reduction in plasma lipoprotein lipase activity associated with severe nephrotic syndrome, is responsible for the atypical clinical features, lipoprotein phenotype III with chylomicronemia, and renal lipidosis. A regimen of dietary lipid restriction, gemfibrozil, and niacin resulted in significant but partial improvement of the dyslipidemia and resolution of the hepatomegaly and ascites. This report stresses the importance of characterizing unique lipid disorders in patients with nephrotic syndrome in order to prescribe effective lipid-lowering strategies. Moreover, the striking resemblance of the clinical and nephrohistologic features of this patient to those occurring in experimental models of coexisting glomerular injury and hyperlipidemia led to the speculation that, in this setting, the hyperlipidemia may contribute to the development of progressive glomerulosclerosis.
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PMID:Atypical hyperlipidemia and nephropathy associated with apolipoprotein E homozygosity. 858 83

Generalized lipodystrophy is a rare condition which can be divided into congenital and acquired types, based on the age at presentation and pattern of inheritance. The congenital type of generalized lipodystrophy or Lawrence-Seip syndrome presents in first two years of life and is inherited in an autosomal recessive pattern. The diagnosis is made on the basis of loss of body fat, muscular hypertrophy, acanthosis nigricans, hirsutism, hepatomegaly with fatty liver, hyperlipidemia and hyperglycemia with insulin resistance. A 2 1/2-year-old Thai girl with the clinical features of Lawrence-Seip syndrome is reported. Abnormal platelet function was detected in this girl.
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PMID:Congenital generalized lipodystrophy, a case report. 862 39

We report a case of Zieve's Syndrome that developed after an important alcohol consumption in a 32-yr-old female patient. She was admitted to the hospital with anorexia, asthenia and jaundice. Physical examination showed liver stigmata and hepatomegaly. Laboratory tests demonstrated increased aminotransferase levels, hyperbilirubinemia, hyperlipidemia and normocytic and normochromic anemia with dianocytes in peripheral blood smear. Ultrasonography showed a hyperechoic liver and a liver biopsy showed acute and chronic alcoholic liver disease. Clinical evolution was satisfactory and the therapy consisted of blood transfusion, parenteral fluids, B-complex vitamin and a fatty free diet. Jaundice, hyperlipidemia and haemolytic anemia define Zieve's Syndrome (Z.S.) There is a pathogenetic relationship among the clinical and biological phenomena in this syndrome, whose starter is an acute alcohol intake. Haemolysis is the distinctive feature with respect to the classical acute alcoholic hepatitis, and it is due to erythrocyte's metabolic and osmotic instability in relation to lipids abnormalities. Its clinical resolution precedes the normalization of serum lipids levels. Therapy is similar to that for acute alcoholic hepatitis although sometimes the anemia requires blood transfusion.
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PMID:[Zieve's syndrome. A case report]. 864 20

The case of a 7-year-old boy with virus-associated hemophagocytic syndrome (VAHS) and serologically proven parvovirus B-19 infection is described. The patient with VAHS presented with fever, hepatosplenomegaly, pancytopenia, and hyperlipidemia type IV. After induction therapy with VP-16 and prednisone, partial remission was achieved. Despite maintenance therapy, reinductions, and the addition of cyclosporine A for 3 months, several relapses occurred. The therapy was stopped because of life-threatening complications (Klebsiella sepsis, neutropenic enterocolitis, and stercoral peritonitis). The complications were treated successfully. The patient status was stabilized after splenectomy. However, hepatomegaly progressed slowly and the hyperlipidemia endured. Ten months after the diagnosis leukocytosis with absolute T lymphocytosis appeared. Reactivation of VAHS was suspected and intravenous immunoglobin and then antilymphocyte immunoglobulin ALG therapy were started. The resultant decrease in leukocytosis was prompt, but lymphopenia did not occur. Virostatic treatment with foscarnet was introduced based on human herpesvirus-6 seroconversion. Twenty-six months after the diagnosis, the patient is well, without any sign of VAHS or lymphoproliferation.
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PMID:Infection-associated hemophagocytic syndrome complicated by infectious lymphoproliferation: a case report. 872 Oct 28

Cardiomyopathy is a consistent feature of diabetic myocardium as well as in prolonged alcohol consumption. Diabetes-induced myocardial dysfunction has been attributed, in part, to calcium overload within individual myocytes. The present study compares the effectiveness of the calcium channel blocker nifedipine (dihydropyridine-type) with verapamil (phenylalkylamine-type) in reversing myocardial dysfunction and diminishing the negative inotropic effect of ethanol on diabetic rat myocardium. Wistar rats were made diabetic with streptozotocin (55 mg/kg, i.v.) and isolated electrically stimulated papillary muscles were studied under isometric conditions in the absence and presence of clinically relevant concentrations of ethanol (80-240 mg/dl, i e., 17.4-52.1 mM). Subgroups of diabetic and normal animals received daily injections of verapamil or nifedipine 2 weeks after induction of diabetes for 8 weeks. Untreated diabetic animals exhibited hyperglycemia, hyperlipidemia, reduced growth, cardiomegaly, and hepatomegaly. Compared to verapamil chronic nifedipine treatment normalized or reversed the effects of diabetes on myocardial mechanical function. The negative inotropic effect of ethanol was attenuated only in muscles from verapamil-treated diabetic animals. Thus, chronic nifedipine treatment may be more effective than verapamil in reducing hyperglycemia, attenuating both cardiac and liver enlargement, and restoring myocardial mechanical function, in experimental diabetes. However, chronic verapamil therapy is more effective in diminishing the negative inotropic effect of ethanol on diabetic myocardium. These findings may have clinical significance among diabetic patients who consume alcoholic beverages while receiving long-term calcium blocker therapy.
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PMID:Differential effects of chronic calcium channel blocker treatment on the inotropic response of diabetic rat myocardium to acute ethanol exposure. 876 17

The objective of this investigation was to determine whether calcium channel blocker (CCB) treatment effectively restores normal baseline mechanical function in diabetic myocardium and to evaluate its effect on the interval-strength relationship. Wistar rats were made diabetic with streptozotocin (55 mg/kg, IV). Left-ventricular papillary muscles from normal and diabetic (10 weeks) rats were superfused with Tyrode's solution at 30 degrees C. A subgroup of diabetic and normal animals received daily injections of verapamil or nifedipine (10 mg/kg, IP; 8 weeks) to compare the effectiveness of a phenylalkylamine to a dihydropyridine in reversing diabetes-induced contractile dysfunction in vitro. Muscles were electrically stimulated at 0.5 Hz with suprathreshold stimuli, and the following parameters were measured: peak tension developed, time to-peak tension, time-to-90% relaxation, and the maximum velocities of tension development and decay. Experimental diabetes was characterized by: severe hyperglycemia, hepatomegaly, reduced body weight gain, cardiomegaly, and increased plasma phospholipid levels. In addition, baseline values of peak tension developed, time to-peak tension, and time-to-90% relaxation were significantly greater in muscles from diabetic animals. Chronic nifedipine treatment reduced hyperglycemia and plasma phospholipid levels, normalized body weight gain, and reduced both heart and liver sizes in diabetic animals. Nifedipine treatment completely reversed diabetes-induced prolongation in both time-to-peak tension and time-to-90% relaxation. In diabetic myocardium, a slightly positive component was present in the interval-strength relationship between 0.01 and 1 Hz, resulting in a rightward shift in the entire curve across a wide range of stimulation frequencies (0.01-5 Hz). This positive component was absent in muscles from diabetic animals treated with both CCBs, and verapamil produced a leftward shift in the frequency response curve. The results of this study suggest that chronic nifedipine treatment may be more effective than verapamil in restoring normal baseline myocardial mechanical function, reducing hyperglycemia and hyperlipidemia, as well as attenuating both cardiac and liver enlargement in experimental diabetes. In contrast, verapamil treatment tended to normalize more effectively the inotropic response to changes in stimulation frequency in diabetic myocardium.
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PMID:Influence of calcium channel blocker treatment on the mechanical properties of diabetic rat myocardium. 877 89


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