[Hepatomegaly. I.-- General aspects of hepatomegaly].
Explore the source record for details and available documents.
Amyloidosis↗
SEARCH · Search PubMed
Results for “HEPATOMEGALY”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[Hepatomegaly. II. Causes of hepatomegaly].
Explore the source record for details and available documents.
Budd-Chiari Syndrome↗
Clinical characteristics and disposition kinetics of the hepatomegaly associated with acute, uncomplicated, Plasmodium falciparum malaria in children.
The clinical characteristics and the kinetics of the disposition of the hepatomegaly associated with acute, uncomplicated Plasmodium falciparum malaria were investigated in 162 children in an endemic area of Nigeria. Hepatomegaly was significantly more common in the younger than in the older children. Complete resolution occurred in 48% following antimalarial chemotherapy. In the children in whom hepatomegaly did not resolve, a reduction in liver size of < 17% by the time parasitaemia was cleared (usually on day 3) was associated with non-resolution of hepatomegaly by days 7 or 14 of follow-up. An increase in liver size to at least 125% of the baseline value by day 4 or 5 was associated with a lack of therapeutic response, providing the child involved was aged < 5 years. In the children who had complete clearance of parasitaemia and resolution of hepatomegaly, there was no significant relationship between the parasitaemia-derived conventional indices of therapeutic response [i.e. time to clearance of 50% (PC50) or 90% (PC90) of the parasitaemia, and the parasite-clearance time (PCT)] and the corresponding parameters derived from measurement of liver size [i.e. time for resolution of 50% (HR50) or 90% (HR90) of the hepatomegaly and the hepatomegaly-resolution time (HRT)] in the same patients. However, as the HR50:PC50, HR90:PC90 and HRT:PCT ratios were similar (range = 1.6-2.1), the liver parameters may have therapeutic application. In the children with drug-sensitive P. falciparum infections and in whom hepatomegaly completely resolved, the area produced by plotting liver size against time (i.e. the area under the curve of hepatomegaly v. time, or AUChp) increased in proportion to the liver size below the costal margin (P = 0.02, from analysis of variance), but there was no significant difference in the half-lives of hepatomegaly (t1/2hp) or in the ratios of liver size to AUChp, indicating that the kinetics of the resolution of hepatomegaly were linear in the range examined. Comparison of the kinetic indices of hepatomegaly and parasitaemia showed that, although the half-lives of parasitaemia and hepatomegaly and the corresponding clearance values were similar, there was no correlation between these parameters among those in whom hepatomegaly completely resolved and parasitaemia completely cleared. These results indicate that routine clinical measurement of the liver size in children with hepatomegaly during acute, uncomplicated, P. falciparum malaria may have some use in evaluating and monitoring the therapeutic responses of infections. The resolution of hepatomegaly, a reflection of pathological changes, lags behind clearance of parasitaemia in children with P. falciparum malaria, and supports the use of the liver 'rate' as a malariometric index for assessing the intensity of transmission in endemic areas.
Adolescent↗
Hepatomegaly in acute falciparum malaria in children.
The characteristics of hepatomegaly in acute falciparum malaria were studied in 114 children presenting consecutively with the disease. Hepatomegaly was more common than splenomegaly and was significantly more frequent in younger than in older children. In children with hepatomegaly at presentation, there was an equal sex distribution, a negative correlation between liver size and age, and a positive correlation between liver enlargement and the reported duration of symptoms at presentation. Symptoms attributable directly to liver involvement were relatively uncommon. There was no correlation between liver and spleen size, presenting core temperature, or peripheral parasite density. Tender hepatomegaly and tender splenomegaly were rare during the acute illness; tenderness resolved within 72 h after commencement of antimalarial therapy. Complete resolution of hepatomegaly occurred in 41% of children after recovery from the acute illness (by days 7 or 14), varying degrees of resolution occurred in 48% and no reduction or an increase in liver size occurred in the remainder. In children with hepatomegaly who failed to clear parasitaemia by days 7 or 14, persistent hepatomegaly was common. These results suggest that hepatomegaly, like splenomegaly, may be assessed as a possible malariometric index of the intensity of transmission in children in an endemic area.
Acute Disease↗
Hepatomegaly and abnormal liver tests due to glycogenosis in adults with diabetes.
In adults with diabetes mellitus, hepatomegaly and abnormalities of liver enzymes occur as a consequence of hepatocellular glycogen accumulation, as has been well described in children. During periods of hyperglycemia glucose freely enters the hepatocytes driving glycogen synthesis, which is augmented further by administration of insulin to supraphysiologic levels. The accumulation of excessive amounts of glycogen in the hepatocytes is a function of intermittent episodes of hyperglycemia and hypoglycemia and the use of excessive insulin. Hepatic glycogenosis occurs in patients with poorly controlled insulin-dependent type I or type II diabetes. The clinical manifestations of this phenomenon may include abdominal pain and obstructive symptoms such as early satiety, nausea, and vomiting. Ascites has rarely been reported. The typical biochemical findings are mildly to moderately elevated aminotransferases, with or without mild elevations of alkaline phosphatase. Liver synthetic function is usually normal. All these abnormalities, including the hepatomegaly, are readily reversible with sustained euglycemic control. The other major cause of hepatomegaly in patients with diabetes is steatosis. This is a function of the body habitus and state of insulin resistance rather than glycemic control. However, the distinction between steatosis and glycogenosis is important: whereas steatosis may progress to fibrosis and cirrhosis, glycogenosis does not, but reflects the need for better diabetic control. Glycogenosis and steatosis cannot be distinguished reliably on ultrasound examination. The histology, however, is definitive. In glycogenosis, as in primary glycogen storage diseases, there is excess glycogen in the cytoplasm, and often also in the nucleus, of hepatocytes. The hepatocytes throughout the lobule appear pale and swollen with clearly defined cell boundaries. Ultrastructural examination reveals cytoplasmic glycogen in clumps displacing organelles to the periphery of the cell, and there is little if any steatosis. We have shown that hepatomegaly due to glycogenosis in adults with diabetes is similar in all respects to the condition seen in children. As in children, liver enzyme abnormalities are unreliable in predicting the presence or the extent of glycogenosis. Hepatic glycogenosis can occur at any age, and therefore should be included in the differential diagnosis of hepatomegaly in all insulin-requiring diabetics.
Adult↗
Undetected hepatomegaly in obese children by primary care physicians: a pitfall in the diagnosis of pediatric nonalcoholic fatty liver disease.
The diagnostic evaluation of nonalcoholic fatty liver disease (NAFLD) relies on the initial detection of hepatomegaly or elevated serum aminotransferases by the primary care provider. In this investigation, the aptitude of the primary care provider to identify children with hepatomegaly and initiate an evaluation for NAFLD is determined. The physical examination findings and requests for diagnostic testing of 18 primary care physicians (and pediatric gastroenterologists) on 11 obese school-aged children, including a subset of children with hepatomegaly and NAFLD, were analyzed. In children with NAFLD, clinicians detected hepatomegaly in 1.4% of encounters and requested serum liver chemistries in 12.5% of encounters. Hepatomegaly is detected poorly in obese children by primary care physicians and thereby increases the likelihood of a delayed or omitted evaluation for NAFLD.
Adolescent↗
Accuracy and reliability of palpation and percussion for detecting hepatomegaly: a rural hospital-based study.
BACKGROUND: Palpation and percussion are standard bedside techniques used to diagnose hepatomegaly. Ultrasonography is a noninvasive and accurate method for measurement of liver size, but many patients in developing countries have limited access to it. We compared the accuracy of palpation and percussion in a rural population in central India, using ultrasonography as a reference standard. METHODS: The study design was a blinded, cross-sectional analysis of a hospital-based case series. Three physicians, blind to clinical data and to each other's results, independently used palpation and percussion to detect hepatomegaly. Diagnostic accuracy was measured by computing sensitivity, specificity, and likelihood ratio values. Inter-physician agreement was assessed using the kappa statistic. RESULTS: Of the 180 study patients, 36 (20%) had enlarged liver on ultrasonography. The likelihood ratios for findings at both palpation (2.2, 3.0, and 2.5 for the three physicians, respectively) and percussion (1.1 for all three physicians) as predictors of true hepatomegaly were low. The kappa values for inter-observer agreement between three physicians for the presence of hepatomegaly at palpation (=0.44-0.53) and percussion (=0.17-0.33) were low, indicating poor reliability of these techniques. CONCLUSION: Clinical assessment of hepatomegaly by palpation and percussion lacks both accuracy and reliability.
Adult↗
Effect of hypolipidaemic drugs on hepatomegaly and micro-bodies in the rat. A new approach to the nature of hepatic peroxisomal proliferation.
Etofylline clofibrate, a new hypolipidaemic drug of low toxicity, was evaluated for effects of induction of peroxisomal proliferation and hepatomegaly in male rats by comparison with standard hypolipidaemic drugs (bezafibrate, clofibrate, fenofibrate). The dose schedule was selected according to standard toxicological methods in an attempt to determine a dose-dependent relationship with particular reference to a possible "nil effect" dose. At high dose levels (250 mg/kg/day), all test drugs induced proliferation and hepatomegaly. At 50 mg/kg/day, all reference compounds induced proliferation and hepatomegaly while etofylline clofibrate indicated only moderate proliferation and no hepatomegaly. At very low dose levels only standards induced proliferation while etofylline clofibrate neither induced proliferation nor hepatomegaly. The latter was still present in bezafibrate and fenofibrate-treated groups. Results indicated a dose-dependent effect of etofylline clofibrate on both parameters with a "nil effect" dose between 11 and 50 mg/kg. Neither a dose-dependent nor a "nil effect" dose was found with any of the standard drugs. For the most potent peroxisomal proliferators (bezafibrate and clofibrate), numerous large and mis-shapen peroxisomes were found at all dose levels. Hepatic changes in terms of pharmacological and toxicological criteria are discussed with special reference to a proposed drug related toxic effect on liver function.
Animals↗
Persistent hepatomegaly: an index of severity in sickle cell anaemia.
Eighty sickle cell anaemia patients, 29 with persistent hepatomegaly and 51 without, were evaluated with respect to clinical severity score. Haemoglobin F (HbF) was also determined in 52 patients, 20 with persistent hepatomegaly and 32 without. The severity scores were computed from the steady state haematocrit, number of transfusions per year, and number of crises per year. The HbF level was determined by the alkali denaturation method. The patients with persistent hepatomegaly had significantly higher clinical severity scores (P < 0.001) and significantly lower levels of HbF (P < 0.0001). The implication of the finding is that patients with persistent hepatomegaly may have a more severe clinical course than those without, and clinicians managing them may have to pay more particular attention to them. In effect, persistent hepatomegaly may be a useful indicator of severity in sickle cell anaemia.
Adolescent↗
Diabetes mellitus-associated glycogen storage hepatomegaly: report of a case and review of the Japanese literature.
A huge hepatomegaly was seen in a 30-yr-old female diabetic who was treated with high dose of insulin for her uncontrollable food ingestion. The liver function at the peak of the hepatic enlargement showed a moderate increase of transaminases, alkaline phosphatase, and gamma-glutamyl transpeptidase. The histology of the enlarged liver revealed PAS-positive granules in enlarged hepatocytes, indicating the presence of massive glycogen storage. On admission, she was maintained under a calorie-restricted diet and received approximately 15 to 20 units per day of insulin supplement. At one month after admission, a marked shrinkage of her enlarged liver and restoration of normal liver function were observed concomitantly with the return of fair control of her blood sugar levels. One year later, she had an episode of diabetic ketoacidosis which subsequently was treated with a continuous low-dose infusion of insulin; however, she showed neither hepatomegaly nor liver dysfunction during this episode. There have been 20 cases reported of Japanese diabetics with marked hepatomegaly, in whom the vigorous treatment of diabetic ketoacidosis with insulin seemed to be a trigger of the enlarged liver. This has occurred mostly in patients with insulin-dependent diabetes mellitus. We present a case of non-insulin-dependent diabetes mellitus with glycogen storage hepatomegaly, presumably due to excessive insulin supplements. This suggests that glycogen storage hepatomegaly in diabetics may not be only due to an acute restoration from diabetic ketoacidosis, but may also be due to an overinsulinization in an attempt to maintain a euglycemic condition in spite of excess food intake.
Adult↗
Results of therapy in stage IV-S neuroblastoma with massive hepatomegaly.
To document the incidence and severity of symptomatic hepatomegaly in patients with Stage IV-S neuroblastoma, we reviewed the charts of children with neuroblastoma seen at Children's Hospital of Pittsburgh between 1951 and 1985. Sixteen met the criteria for IV-S disease, and 11 of these (69%) had massive hepatomegaly. Five children had symptoms referable to their liver size including respiratory distress, gastroesophageal reflux, or decreased urine output. Liver function appeared to be normal or only mildly abnormal in the 9 patients where data were available. Because therapy was so variable, it was not possible to correlate treatment regimen with outcome. However, 3 symptomatic patients who received less than or equal to 600 rad without chemotherapy had prompt subjective responses. Follow-up was available on 10 children 6 months-18 years (median 18 years) from diagnosis. Eight were alive with resolved or resolving hepatomegaly. High dose (greater than or equal to 3,300 rad) radiation-related side effects included multiple rib chondromas, chest- and pelvic-wall hypoplasia in one patient, and radiation nephritis with hepatic fibrosis resulting in death of a second patient. Our results support prior recommendations that for symptomatic hepatomegaly, low doses of radiation be considered.
Adrenal Gland Neoplasms↗
Effect of age on metabolic tolerance and hepatomegaly following chronic ethanol administration.
Chronic consumption of ethanol often results in an increased rate of ethanol metabolism (metabolic tolerance) and in hepatomegaly. However, the extent of these changes is highly variable. We have found that these two phenomena are greatly influenced by age. We studied the effect of age on the development of metabolic tolerance and hepatomegaly and on the increase in hepatic oxygen consumption produced by chronic ethanol administration. The latter has been proposed to contribute to metabolic tolerance to ethanol. Ethanol was administered to female Sprague-Dawley rats with different initial ages (4, 6, 8, 11, and 17 weeks) for a 4-week period in a high-fat liquid diet. Control animals were pair-fed an isocaloric liquid diet in which ethanol was replaced with carbohydrate. Metabolic tolerance and hepatomegaly following chronic ethanol consumption were markedly dependent on the initial age of the animal, with young animals showing the largest increases. Although showing a similar general trend with age, the degree of metabolic tolerance was not linked proportionally with the degree of hepatomegaly. Perfused livers from young rats fed chronically with ethanol showed increases in ethanol metabolism and oxygen consumption, whereas no increase were observed in those from older animals. These findings support the hypothesis that an elevated rate of hepatic oxygen consumption contributes to metabolic tolerance. Total hepatic alcohol dehydrogenase activity was not increased by chronic ethanol consumption in any age group, demonstrating that an increase in the levels of this enzyme is not obligatory for metabolic tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)
Age Factors↗
Assessment of discomfort in rats with hepatomegaly.
An attempt was made to assess discomfort in rats with hepatomegaly induced by feeding a high cholesterol, high cholate diet. After 8 weeks, the rats displayed a more than two-fold increase in liver weight when compared with controls fed a commercial diet. In a small open field test, behaviour of rats with hepatomegaly was similar to the controls. Of 9 parameters scored per rat, only the response to pressure on the right hypochondrium (tension of overlying muscles) scored higher than in control animals. There was considerable between-assessor variation in the assignment of scores. It is suggested, tentatively, that hepatomegaly in rats caused by cholesterol plus cholate feeding, may not cause extreme discomfort. Upon 'blind' palpation of control and test rats, an average of 60% of the rats with hepatomegaly were classified correctly.
Animals↗
Hepatomegaly is an early biomarker for hepatocarcinogenesis induced by peroxisome proliferators.
The relationship between hepatomegaly and the hepatocarcinogenesis associated with by peroxisome proliferators was examined. (1) Male F-344 rats were maintained on diets containing clofibrate, ciprofibrate, nafenopin, gemfibrozil, Wy-14, 643, di(2-ethylhexyl)phthalate (DEHP), or di(2-ethylhexyl)adipate (DEHA) at carcinogenic doses for 1 week. A close correlation between relative liver weights and hepatocarcinogenicity was observed (r = 0.910). (2) Administration of perfluorooctanoic acid (PFOA), perfluorodecanoic acid (PFDA), simfibrate, or DL-040, for which hepatocarcinogenicity is not known, resulted in hepatomegaly in all treated groups, this being especially marked in the PFOA case. Therefore, PFOA may have strong hepatocarcinogenic potential. (3) Administration of the antioxidants butylated hydroxyanisole (BHA) or vitamin E (VE) did not affect the hepatomegaly induced by DEHP. These results suggest that the hepatomegaly may be an early biomarker for prediction of the potential hepatocarcinogenicity of peroxisome proliferators. However, this requires further clarification in terms of its relation to the oxidative stress thought to be involved in peroxisome proliferator-induced hepatocarcinogenesis.
Animals↗
Biochemical and morphological studies of ammonium perfluorooctanoate-induced hepatomegaly and peroxisome proliferation.
Ammonium perfluorooctanoate (APFO) is known to induce a striking hepatomegaly in rats. The purpose of these studies was to determine the causes of the hepatomegaly and compare the effect to other liver-enlarging compounds. Since the total hepatic DNA content was similar in control and APFO-treated rats, the hepatomegaly represented a hypertrophic rather than a hyperplastic response. The cytochrome P-450 content and activity of benzphetamine N-demethylase increased in the livers of APFO-treated rats, indicating the proliferation of the smooth endoplasmic reticulum. In contrast to the membrane-bound enzymes, the soluble enzymes glutathione S-transferase and UDPglucuronyltransferase were unaffected by APFO treatment. The activity of carnitine acetyltransferase was disproportionately increased relative to carnitine palmitoyltransferase in the livers of APFO vs that in control rats, confirming the predominant proliferation of peroxisomes vs that of mitochondria. Morphological studies confirmed the proliferation of the endoplasmic reticulum, mitochondria, and peroxisomes in the livers of APFO-treated rats. In contrast to many other peroxisome proliferating agents, APFO did not possess hypolipidemic activity.
Animals↗
Gemfibrozil-induced peroxisome proliferation and hepatomegaly in male F344 rats.
Gemfibrozil is a widely used hypolipidemic drug in humans that causes peroxisome proliferation and hepatocarcinogenesis in rodents. The induction of hepatomegaly and hepatic peroxisome proliferation (measured as peroxisomal acyl CoA oxidase activity), was determined and compared to another peroxisome proliferator, WY-14,643 (0.1% in the diet) in male F344 rats. In a 21-day study, dietary no-observable-effect and lowest-observable-effect levels of gemfibrozil for both hepatomegaly and peroxisome proliferation were 0.002% and 0.005%, respectively. In a 42-day study, dietary concentrations of 0.9-2.0% gemfibrozil induced a similar magnitude of hepatomegaly to WY-14,643 (2.3-fold) but a higher level of peroxisome proliferation (16-18-fold) than the maximum induction for WY-14,643 (13-fold). The plateau in magnitude of gemfibrozil-induced peroxisome proliferation across the 0.9-2.0% dietary concentrations was associated with a plateau in serum concentration of gemfibrozil (approximately 20 micrograms/ml), similar to concentrations reported in human subjects receiving oral gemfibrozil. These results indicate that maximal induction of peroxisome proliferation by gemfibrozil can exceed that of a more potent compound such as WY-14,643, and further suggest that maximal induction of peroxisome proliferation can be limited by steady-state serum concentrations. Moreover, the reported lack of hepatic responses to gemfibrozil in humans is unlikely to be the result of inefficacy or unavailability of this drug, compared to other peroxisome proliferators, in rodents.
Animals↗
Intermittent and recurrent hepatomegaly due to glycogen storage in a patient with type 1 diabetes: genetic analysis of the liver glycogen phosphorylase gene (PYGL).
We report a 19-year-old woman who had a history of type 1 diabetes with recurrent glycogen accumulation in the liver. During her infantile period she presented with no hepatomegaly nor growth retardation. On admission she was diagnosed with diabetic ketoacidosis (DKA). She also had hepatomegaly and elevated transaminase levels, but these abnormalities had resolved after administration of insulin. However, 4 weeks after DKA marked hepatomegaly and elevated transaminases were reappeared with simultaneous hypoglycemia which suggested an impaired glycogenolysis in the extraordinary conditions. We supposed the partial deficiency of liver glycogen phosphorylase activity in this patient and analyzed the liver glycogen phosphorylase gene (PYGL). Deduced amino acid sequence of the PYGL in this patient was completely identical to that reported by Burwinkel et al. (Y15233), however, the nucleotide sequence of PYGL cDNA was heterozygous for substitutions at positions Asp339 (GAT to GAC) on exon 9 and Ala703 (GCT to GCC on exon 17, respectively. These SNPs were also screened in 51 Japanese normal subjects by PCR-based direct sequencing or PCR-RFLP method. The same genotype observed in this patient was detected in 2 of 51(3.9%) normal subjects. These results suggest that the structure of PYGL coding sequence in this patient is unlikely to account for her excessive liver glycogen accumulation. Further studies including genetic analysis on the promoter region of the gene are necessary to clarify the etiology of susceptibility to excessive liver glycogen storage in patients with type 1 diabetes.
Adult↗
Severe ARDS may cause right heart failure with extreme hepatomegaly but without hepatic failure.
A young trauma patient developed severe adult respiratory distress syndrome (ARDS), right heart failure, hepatic congestion and an extreme hepatomegaly but no hepatic failure. The patient needed 100% oxygen during ventilatory support for 80 days and was weaned from the ventilator after more than 100 days. The hepatomegaly gradually disappeared. Four months after the injury, the anatomical shape of the lungs, heart and liver were normalized. This case illustrates that severe ARDS may cause right heart failure and extreme hepatomegaly due to venous congestion in the liver and spleen, but without hepatic failure.
Heart Failure↗