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)

Both carbon tetrachloride and a high-fat, low-protein choline-free diet cause hepatomegaly in rats due to an accumulation of both lipids and proteins with a concomitant increase in deoxyribonucleic acid content. CCl4 causes a decline in hepatic glycogen. Serum albumin level is decreased in CCl4-treated rats and increased in those fed the experimental diet.
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PMID:Changes in serum proteins and in major liver constituents following carbon tetrachloride and a high-fat choline-free diet in rats. 48 88

Alcohol feeding to rats produced hepatomegaly, associated with enlargement of the hepatocytes. The increase in liver dry weight was accounted for not only by fat but also by protein accumulation, primarily in microsomes and cytosol, with a selective increase in export proteins: concentrations of both immunoreactive albumin and transferrin were augmented in liver microsomes and cytosol of ethanol-fed rats. To investigate the mechanism of this protein accumulation, [14C]leucine was injected intravenously and its incorporation into both liver and serum proteins was measured after various time intervals. Rates of synthesis and export were assessed from protein labeling and specific activities of leucyl-tRNA. Synthesis of liver protein and proalbumin were enhanced by chronic ethanol feeding, but this was not associated with a corresponding rise in serum albumin output. Actually, there was a significant retention of the label in liver albumin and transferrin with delayed appearance in the serum of ethanol-fed rats. This indicated that, regardless of the changes in synthesis, the export of protein from the liver into the plasma was impaired. This alteration in export was associated with a decreased amount of polymerized tubulin in the liver of ethanol-treated animals. Thus, both enhanced protein synthesis and defective export contribute to the ethanol-induced accumulation of liver protein, and the decrease in liver microtubules represents a possible site for impairment of protein export.
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PMID:Pathogenesis of alcohol-induced accumulation of protein in the liver. 56 Nov 18

Hepatic fatty infiltration complicating jejunoileal bypass can be massive and may require restoration of gastrointestinal continuity. This fatty infiltration appears to be caused by protein depletion associated with adequate or high carbohydrate intake. The present study has shown that calorie-free amino acid alimentation can reverse these changes. In three of thirteen patients who underwent 12 inch to 6 inch jejunoileal bypass procedures, symptomatic hepatomegaly developed with near total replacement of hepatocytes by massive fatty infiltration. After undergoing liver scan, liver biopsy, and liver function tests, the patients were started on a peripheral infusion of 2L per day of a 4.25 per cent crystalline amino acid solution, allowing for fat mobilization while preserving body protein stores. All oral intake was withheld except for water. At the end of a fourteen to twenty-one day infusion period, serum albumin levels increased by 1 gm in all patients. Decreases in liver volume of 83, 45, and 40 per cent occurred. During the infusion period ketonuria was 4 plus in all patients indicating active lipolysis. Weight loss was impressive (17, 19, and 40 pounds). All patients showed marked symptomatic improvement, and postinfusion liver biopsy specimens showed a return to near normal architecture. Maintenance of normal liver size by a high-protein, low-carbohydrate diet was observed in a five to seven month follow-up period. In contrast to previous studies using standard hyperalimentation solutions, the use of calorie-free amino acid solutions reverses the hepatic fatty infiltration seen after intestinal bypass by mobilization of fat. This fat mobilization does not occur as readily in the presence of large amounts of glucose.
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PMID:Reversal of severe fatty hepatic infiltration after intestinal bypass for morbid obesity by calorie-free amino acid infusion. 80 74

Amiodarone, a commonly used antiarrhythmic agent, has numerous adverse effects. The purpose of this case report is to highlight its hepatotoxicity, an unusual complication of long term amiodarone therapy. Our patient is a 76-year-old man with underlying ischaemic heart disease and recurrent ventricular tachycardia. Eleven months after commencing amiodarone, he developed asymptomatic raised aminotransferases which resolved following drug withdrawal. Amiodarone was then reintroduced and four years later, the patient developed hepatomegaly, worsening liver biochemistry and histopathological changes consistent with early cirrhosis. His symptoms improved following discontinuation of amiodarone. However, hepatomegaly and a low serum albumin still persist four years later.
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PMID:Hepatotoxicity of amiodarone. 129 29

From 1956 through 1989, 38 men and 26 women were seen at the Mayo Clinic with biopsy-proven AA. The underlying disorder was rheumatic disease in 42, infectious disease in 11, inflammatory bowel disease in 6, and other causes in 5. All patients were symptomatic at the time of diagnosis. Fifty-eight of the 64 patients had proteinuria or renal insufficiency. Fourteen also had significant symptoms of gastrointestinal amyloid, and 6 had amyloid goiter. None of the patients had symptomatic cardiac involvement, and only 3 had palpable hepatomegaly. Renal, gastric, rectal, fat, and marrow biopsies were positive for amyloid in 100%, 94%, 82%, 58%, and 46% of tested patients, respectively. The median survival of the entire group was 24.5 months. Thirty-five of the 47 deceased patients died as a direct result of their amyloidosis, primarily from complications of renal failure. Nine were successfully treated and had regression of the disease. Two with bronchiectasis responded to long-term cyclic antibiotic therapy, as did 1 patient with osteomyelitis. One patient with inflammatory bowel disease responded to surgical resection, and 1 with familial Mediterranean fever responded to colchicine. Four patients with rheumatic disease were treated with cyclophosphamide (in 2) and methotrexate (in 2), with complete resolution of their renal disease. All 9 successfully treated patients are alive, with a median follow-up of 58 months. Statistical analysis revealed that creatinine values greater than or equal to 2.0 mg/dl (P less than 0.003) and a serum albumin value less than 2.5 g/dl (P less than 0.02) were associated with a poorer survival. The single strongest variable associated with poor survival was a serum creatinine level greater than 2 mg/dl at presentation, with a median survival of 11.2 months compared to patients with a creatinine level less than 2.0 mg/dl, with a median survival of 56.9 months.
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PMID:Secondary systemic amyloidosis: response and survival in 64 patients. 206 9

Thirty-five patients with primary biliary cirrhosis were seen between 1974 and 1989. The median mean age at presentation was 53 years (range: 30-77) and the female to male ratio was 7.8:1. Thirteen (37%) were asymptomatic and nine (26%) had associated auto-immune disorders. Pruritus and hepatomegaly were present in half of the patients. Advanced histological stages of disease (Stages 3 and 4) were present in 57% of patients. The median period of follow-up was 5 years (range: 0.1-20). Twelve patients died, nine from hepatic causes and three from non-hepatic causes. One has undergone liver transplantation. A Kaplan-Meier curve estimated the median survival to be 11 years. Asymptomatic patients developed progressive disease and survival was similar to that of symptomatic patients. Using Cox's proportional hazards model, age, serum bilirubin and serum albumin were found to be independent prognostic variables correlating with reduced survival.
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PMID:Primary biliary cirrhosis: clinicopathological characteristics and outcome. 212 33

In order to identify non-invasive, biochemical indicators of di(2-ethylhexyl)phthalate (DEHP) exposure, we have compared the effects in blood serum with biochemical effects in liver in rats fed a diet containing 0, 0.25, 0.75 and 2% DEHP for 2 weeks. After 3 days of treatment serum arylesterase activity levels and serum triglycerides were decreased to 60% and 20% of control values, respectively. After a 2-week treatment with DEHP the effects were generally stronger. Compared to a control group, serum arylesterase activity levels, serum triglycerides and serum cholesterol were decreased to 40%, 20% and 50%, respectively. Serum cholinesterase activity levels and serum albumin concentrations were increased by the DEHP treatment to 290% and 135% of control values, respectively. In the livers a hepatomegaly, an induction of cytochrome P-450 IVA1 and induction of the activity of palmitoyl-CoA oxidase and carnitine acetyl-CoA transferase was found to be 180%, 1080%, 1300% and 1700% of control values, respectively. The liver is a more sensitive target for DEHP exposure compared to the biochemical effects in serum, but determination of the serum parameters can be used to determine early biological effects of exposure to DEHP.
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PMID:Effect of di(2-ethylhexyl)phthalate on enzyme activity levels in liver and serum of rats. 227 65

A patient with multiple, pyogenic hepatic abscesses is described, and the pathophysiology, etiologies, clinical and laboratory manifestations, and management of the disease are reviewed. A 55-year-old man with a history of ethanol abuse and pancreatitis developed fever, chills, general malaise, and right upper quadrant abdominal pain two weeks before hospitalization. Baseline laboratory and hematology results included serum albumin concentration, 3.2 g/dL; serum alkaline phosphatase concentration, 239 mIU/mL; total serum bilirubin concentration, 1.3 mg/dL; white blood cell count, 18,400/cu mm; red blood cell count, 4.7 million/cu mm; hemoglobin, 12.5 g/dL; and hematocrit, 38.8%. Abdominal ultrasound showed echo-free cavities throughout the hepatic parenchyma; abdominal computed-tomography (CT) scan showed hepatomegaly and multiple radiolucent spaces. CT-guided needle aspiration of a hepatic mass yielded purulent material that grew Fusobacterium necrophorum under anaerobic conditions. On day 7, the patient was started on i.v. ampicillin sodium-sulbactam sodium. A CT scan two weeks later showed a reduction in the number and sizes of abscesses. The patient continued i.v. therapy for one month, then was discharged on a regimen of p.o. amoxicillin trihydrate-clavulanate potassium. Hepatic abscesses are either amebic or pyogenic; the latter usually has a higher mortality. The etiologies of pyogenic hepatic abscesses include ascending cholangitis, portal vein bacteremia, systemic bacteremia, extension from a contiguous focus of infection, and trauma. Diagnosis is difficult and relies highly on clinical suspicion. Clinical symptoms include hepatomegaly, fever, chills, and malaise. Abnormal laboratory values include leukocytosis, anemia, and hypoalbuminemia. The abscesses are frequently polymicrobial; Escherichia coli is the most commonly isolated species. CT is the best radiological technique for diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ampicillin-sulbactam therapy for multiple pyogenic hepatic abscesses. 229 77

Tow age-matched groups of patients with sickle cell anaemia (SS), one with persistent gross splenomegaly (PGS) and the other without palpable spleens, were studied to determine the clinical and laboratory features associated with PGS. The group with PGS had significantly larger mean liver size, higher serum indirect bilirubin levels, but lower mean haematocrit, blood cell counts and serum albumin: globulin ratio when compared to the control group without splenomegaly. Large palpable livers (greater than 6 cm below the coastal margin) among the PGS group tended to be associated with digital clubbing. A retrospective analysis of their case files showed that patients with PGS had had predominantly anaemic crises while those without splenomegaly had had predominantly vaso-occlusive crises over a 2-year period. No difference was found between the 2 groups, in respect of anthropometric data, prevalence of hepatomegaly or frequency of hospital admissions and blood transfusions.
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PMID:Clinical and laboratory features associated with persistent gross splenomegaly in Nigerian children with sickle cell anaemia. 238 63

During a clinical trial of duration of chemotherapy in small cell lung cancer (SCLC), 71 of 610 patients (11.6%) died in the first 3 weeks. Chemotherapy consisted of cyclophosphamide 1 g m-2 i.v. day 1, etoposide 100 mg t.d.s. orally days 1-3, vincristine 2 mg i.v. day 1. The time of death was found to be nonrandomly distributed within the first chemotherapy cycle, with a peak incidence between days 7 and 12 after chemotherapy. Patients were matched with controls who were the next cases entered into the study who did not die in the first 3 weeks. Patients dying early were more likely to have clinical hepatomegaly (P less than 0.0001), and ECOG score greater than or equal to 1 (P less than 0.00001). As a group these patients also had a higher alkaline phosphatase (P less than 0.0002), an elevated blood urea (P less than 0.00001) and a lower serum albumin (P less than 0.0001) than controls. It is probable that infection contributes to the death of these already ill patients at a time when the blood count is low. Early deaths have been noted in two other large trials using regimens including etoposide. Prophylactic antibiotics or dosage modification may prevent the early death of these high risk patients.
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PMID:Patients at risk of chemotherapy-associated toxicity in small cell lung cancer. 254 22


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