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)

Serum carcinoembryonic antigen (C.E.A.) levels were measured in 381 undiagnosed patients who presented with clinical problems commonly associated with gastrointestinal malignancy. The results were compared with the final diagnosis after follow-up for up to 5 years to see whether C.E.A.-testing added any useful information. Of 307 patients presenting with upper gastrointestinal symptoms, lower gastrointestinal symptoms, or irom deficiency anaemia, C.E.A. levels greater than 20 ng/ml indicated malignancy in 5 but in 3 of these malignancy was also diagnosed after routine investigation. Of 74 patients presenting with obstructive jaundice, hepatomegaly, or abnormal liver function, malignancy was diagnosed in 38. In 9 of these patients the diagnosis of malignancy could otherwise have been reached only by laparotomy. The serum-C.E.A. thus reached only by laparotomy. The serum-C.E.A. thus seems to be of value in the assessment of liver disease but not in patients with gastric or colonic symptoms or iron-deficiency anaemia.
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PMID:Carcinoembryonic antigen concentrations in undiagnosed patients. 8 41

During a 23 year period at Memorial Hospital, the diagnosis of liver cell carcinoma was made in 42 patients who were 11 to 40 years old. Ninety per cent were Caucasian, mostly born in the United states. No occupational hazard was detected. Serum hepatitis antigen was demonstrated in only one patient. Alpha fetoprotein was found in the serum of 55 per cent of nine patients tested. Eight-three per cent were Rh positive, 43 per cent were ABO groups, A or O, respectively. Twenty-three per cent of 13 patients with sufficient material for study had an associated cirrhosis. Of these, active hepatitis with cirrhosis was present in one patient; postnecrotic cirrhosis was present in another. Approximately 7 per cent had a history of previous liver disease. One patient had infectious mononucleosis, and nearly 13 per cent gave a family history of cancer. Weight loss or pain in the right upper abdominal quadrant was present in 65 per cent, and hepatomegaly was found in 88 per cent. Only one patient presented with hemoperitoneum simulating an acute condition within abdomen. The liver profile examinations characteristically revealed an elevation in serum alkaline phosphatase, 5 nucleotidase, and Bromsulphalein retention with normal bilirubin level. The most common finding, upon roentgenographic examination, was an elevated right hemidiaphragm. Selective celiac and superior mesenteric angiography and 99mTc sulfur colloid liver scans were both done in 13 patients. There was a 75 per cent accuracy rate in localization of the tumor. At laparotomy, the tumor was found to be confined to one lobe in seven patients and involved both lobes in ten. Twenty-seven patients were thought to have multicentric tumors and 15 unicentric lesions. Only ten were found to be candidates for hepatic lobectomy. Five and ten years survival rates were 20 per cent; the operative mortality rate was 40 per cent. Twenty per cent died within a year, ten per cent, one patient, is alive with disease at 28 months and another is free of disease at 31-months. Paraneoplastic syndromes were erythrocytosis in two patients, terminal stage of hypoglycemia in one patient, and hypocholesterolemia with associated excess beta globulin in one patient.
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PMID:Liver cell carcinoma during the prime of life. 17 34

This paper gives, in detail, the causes of either liver disease or hepatomegaly in 100 patients, mostly adults, admitted to the medical wards of Angau Memorial Hospital, Lae, during 1968 and 1969. The major findings included liver cell carcinoma, cirrhosis (often with chronic active hepatitis), tropical splenomegaly, pericholangitis and hepatitis. There were 27 with miscellaneous findings including ten with normal, or almost normal, livers despite the definite enlargement. Patients with liver cell carcinoma presented late in the course of their illness and had a poor prognosis. Others, with pericholangitis, had clinical features of portal hypertension indistinguishable from that complicated cirrhosis. There was an unexpected number with chronic active hepatitis and a liver biopsy is essential for such a diagnosis. Hepatic sinusoidal lymphocytosis is almost invariably found in patients with TS but may occasionally be found in those with a non-palpable spleen. Patients with right heart failure of chronic respiratory disease, and jaundice of acute pneumonia were excluded from the study.
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PMID:Liver disease in Papua New Guinea. 19 19

135 children with hepatitis and 179 patients with hepatomegaly of undetermined etiology were investigated for complement fixing antibodies to cytomegalovirus. 69 patients with hepatitis (51%) and 74 patients with hepatomegaly (41%) had a titer of 1:4 or above as compared with a control group of children without hepatic pathology in whom positive response occurred in only 20 resp. 18%. The mean titer found in the sero-positive patients was also significantly higher than that in the control group. In contrast, the incidence of positive sera in newborns with hyperbilirubinemia of unknown etiology did not differ significantly from that in a healthy control collective. Of 57 patients with liver disease, 20 excreted cytomegalovirus which was isolated 55 times from 103 urine specimens. These patients included 9 with hepatitis and 11 with hepatomegaly. Of 129 children without any indication of liver disease, cytomegalovirus could be demonstrated in only 3. Our results point toward a causal connection between the presence of cytomegalovirus and the development of hepatic disease in childhood.
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PMID:[Hepatic disease in childhood and cytomegalovirus infection (author's transl)]. 20 47

Seventy children with hepatomegaly, between the ages of 3 months and 13 years, were investigated including a liver biopsy in 60, to study the general pattern of liver disease in children. Thirty percent had acute viral hapatitis, 20 percent cirrhosis, 17.6 percent pulmonary tuberculosis, 18 percent hereditary diseases and 14 percent miscellaneous diseases involving the liver. None of the cases met the criteria for Indian childhood cirrhosis. It was concluded that in Karachi pulmonary tuberculosis was a common case of hepatosplenomegaly in children and that the aetiology of cirrhosis was probably multifactorial.
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PMID:Aspects of paediatric liver disease in Karachi. 40 63

Male Swiss Webster mice were fed a diet containing 2.5 percent griseofulvin (GF). Serially progressive light and electron microscopic hepatic altertions were present from one day on and grossly visible hepatomegaly from two weeks until termination at 22 weeks. GF induced liver changes included hepatocyte nuclear and cytoplasmic hypertrophy, increased incidence of necrosis and mitosis, Kupffer cell activation, bile duct proliferation and portal fibrosis. Protoporphyrin crystals were present in hepatocyte cytoplasm as early as one day after GF feeding. Hepatocellular hyalin was initially noted at seven weeks. Thereafter, the hyalin increased in prominence and frequency of occurrence. Ultrastructurally, three types of hyalin have been presently demonstrated to correspond to Mallory bodies (MB) reported in human liver disease. Forms intermediate in appearance between various MB types suggested transition from one to another. Areas of organelle free cytosol with abundant, loosely scattered filamentous elements as well as vesicular, smooth surfaced endoplasmic reticulum and ribosomes appeared preceding and closely associated with MB formation. Similarities of hepatocellular MB observed in GF fed mice and reported earlier in human alcoholic liver disease suggest a common pathway in its formation as a response to divergent noxious insults.
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PMID:Light and electron microscopy of hepatocellular changes in griseofulvin fed mice. Particular reference to Mallory bodies. 42 May 10

Twelve patients with liver disease related to methyldopa were seen between 1967 and 1977. Illness occurred within 1--9 weeks of commencement of therapy in 9 patients, the remaining 3 patients having received the drug for 13 months, 15 months and 7 years before experiencing symptoms. Jaundice with tender hepatomegaly, usually preceded by symptoms of malaise, anorexia, nausea and vomiting, and associated with upper abdominal pain, was an invariable finding in all patients. Biochemical liver function tests indicated hepatocellular necrosis and correlated with histopathological evidence of hepatic injury, the spectrum of which ranged from fatty change and focal hepatocellular necrosis to massive hepatic necrosis. Most patients showed moderate to severe acute hepatitis or chronic active hepatitis with associated cholestasis. The drug was withdrawn on presentation to hospital in 11 patients, with rapid clinical improvement in 9. One patient died, having presented in hepatic failure, and another, who had been taking methyldopa for 7 years, showed slower clinical and biochemical resolution over a period of several months. The remaining patient in the series developed fulminant hepatitis when the drug was accidentally recommenced 1 year after a prior episode of methyldopa-induced hepatitis. In this latter patient, and in 2 others, the causal relationship between methyldopa and hepatic dysfunction was proved with the recurrence of hepatitis within 2 weeks of re-exposure to the drug.
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PMID:Patterns of hepatic injury induced by methyldopa. 42 37

Liver size, cytochrome P-450 (P-450) concentration in liver biopsy specimens and antipyrine kinetics were studied in 112 consecutive patients undergoing diagnostic liver biopsy. Compared to subjects with normal parenchyma, those with slight or severe parenchymal alterations had enlarged livers with low P-450 concentration and slow antipyrine elimination. In the normal group, the mean P-450 concentration (+/- 1 SD) was 11.10 +/- 2.14 nmol/g liver tissue and the total amount (estimated liver weight g X P-450 concentration nmol/g) 16.06 +/- 3.29 mumol. Previous therapy with enzyme inducing drugs was associated with enlarged liver in subjects with normal histological findings and with fast antipyrine elimination and high P-450 in all groups. Antipyrine elimination rate correlated with liver weight only in subjects with normal parenchyma. The total amount of P-450 was generally more closely related to its concentration than to the estimated liver weight, although in many individual cases a large liver was able to compensate a low P-450 concentration so that the total P-450 was at the normal level. Despite normal or high total P-450, in vivo drug metabolism was impaired in subjects with altered parenchyma, suggesting that other factors were limiting antipyrine elimination in liver disease.
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PMID:Liver size in evaluating drug metabolizing capacity in man. 46 52

Liver size has been estimated clinically and by a non-invasive ultrasound technique in 16 normal subjects, 16 patients with cirrhosis, 10 patients with chronic biliary obstruction, and three patients with primary hepatoma. Antipyrine disposition was also measured in each subject. Hepatomegaly was not clinically detectable until there was approximately a 20% increase in liver size. Additional increases in size correlated significantly with clinical estimates of hepatomegaly. Antipyrine clearance had a three-fold range in normal subjects. Its mean value was significantly reduced in each subgroup of patients with liver disease. However, 48% of patients with liver disease had values within the normal range. In normal subjects there was a significant correlation between antipyrine clearance and liver volume. Thus, intersubject variation in clearance normalised for liver volume was less than clearance alone. Antipyrine clearance normalised for liver volume in patients with liver disease was significantly lower than in normal subjects and there was no overlap with normal subjects. In conclusion, assessment of drug metabolising efficiency per unit volume of liver increased the discrimination in differentiating subjects with normal from abnormal livers.
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PMID:Antipyrine clearance per unit volume liver: an assessment of hepatic function in chronic liver disease. 48 57

The pathogenesis of jejunoileal bypass-induced liver disease was investigated in the rat model. Male Sprague-Dawley rats were subjected to 90% jejunoileal bypass and compared to rats having undergone 90% jejunoileal resection, to ad libitum and pair-fed controls and to weight-matched (underfed) controls. After 8 weeks the animals were killed and selected analyses performed. Several indications of liver dysfunction were observed in the bypass rats including hepatomegaly, hypotriglyceridemia, hypoproteinemia, elevated SGOT levels, and markedly decreased levels of cytochrome P-450. All of these abnormalities with the exception of elevated SGOT levels and decreased serum proteins were not observed to the same degree in animals in which the defunctionalized bowel was resected. Rats which were underfed (weight matched) did not develop any of the abnormalities of liver injury demonstrated in the bypass rats. Multiple factors appear to be responsible for the production of bypass-induced liver disease, but the defunctionalized bowel plays an important role.
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PMID:Role of defunctionalized bowel in jejunoileal bypass-induced liver disease in rats. 51 91


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