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 case of the syndrome of sea-blue histiocyte is presented in a 53-year-old Japanese woman, which is the first recorded case in Japan. The patient had hepatosplenomegaly, bleeding manifestations, mild thrombocytopenia, fatty metamorphosis and cirrhosis of the liver, as well as abnormal serum lipid profiles. Her parents were consanguineous and her maternal grandmother with hepatomegaly died of hepatic failure. Histologically, peculiar histiocytes containing numerous, intracytoplasmic sea-blue stained granules on May-Giemsa stain were demonstrated in biopsy materials of the bone marrow, lymph node and liver. The sea-blue granules in these histiocytes proved to have histochemical staining characteristics of lipogenic ceroid-like pigment. Ultrastructurally, these granules showed membrane-bound, pleomorphic inclusions of heterogeneous nature, including electron-dense amorphous or variegatedly osmiophilic, frequently laminated materials. Enzyme cytochemically, localization of acid phosphatase activity was demonstrated in and around the intracytoplasmic inclusions. With regard to the pathogenesis of the sea-blue histiocytes in this case, it may be suggested that the existence of the abnormality in lipid metabolism plays an important role in intralysosomal ceroidogenesis in these histiocytes.
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PMID:Syndrome of the sea-blue histiocyte--the first case report in Japan and review of the literature--. 21 60

A 65 years old, female patient with acquired aplastic anemia secondary to frequent exposure to hair dye. While on treatment with anabolic steroids hormone became jaundiced and developed hepatomegaly eight months later. During laparotomy the liver was enlarged, hard, with multiple whitish nodules on its surgace but was otherwise normal. Liver biopsy showed hepatocellular carcinoma, there were not cirrhosis niether hemochromatosis. A review of the related literature was done and discussed on the experimental and clinical evidences that suggested that androgens may play same role on the etiology of liver cancer.
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PMID:[Androgenic therapy and hepatocellular carcinoma. Report of a case]. 22 17

Occurrence of fever in a patient with liver cirrhosis should suggest the following: 1. Endotoxemia. Endotoxins are normally present in portal blood; in hepatic cirrhosis they are insufficiently cleared by the liver and their presence can be demonstrated in the systemic circulation by the "limulus test". Fever is one of the many consequences ascribed to the presence of endotoxins in the blood. 2. Infections. Cirrhosis and alcoholism (which often accompanies it) impair host defenses against bacteria and other organisms. Thus, infections are actually more frequent in hepatic cirrhosis as is shown by the example of bacterial endocarditis. Spontaneous bacterial peritonitis must be searched for carefully when ascites is present. 3. Alcoholic hepatitis. This diagnosis is established histologically. The usual symptoms, occurring with variable incidence, include anorexia, nausea and vomiting, abdominal pain, fever and jaundice in the presence of hepatomegaly, leukocytosis and an elevated SGOT. Differential diagnosis from obstructive jaundice and a severe prognosis without alcohol abstinence make early diagnosis mandatory. Its evolution in cirrhosis can be astonishingly rapid. In the absence of hepatic encephalopathy, corticosteroids do not appear to be recommended. 4. Hepatoma.
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PMID:[Fever and liver cirrhosis]. 22 38

Sixty-eight patients with plasmacytic neoplasia and osteosclerotic lesions were analyzed. Men predominated in this series. Mean age was 55.3 years and 26 patients were younger than 51 years at diagnosis. Early onset of disease was statistically different from multiple myeloma in general. Thirty patients had peripheral polyneuropathy and often neurological manifestations preceded other symptoms. Skeletal pain was less common, whereas hepatomegaly, splenomegaly, and lymphadenopathy were more common than in myeloma in general. Incidence of azotemia, hypercalcemia, high ESR, and anemia was lower than in myeloma. In one fourth of the patients, the number of skeletal lesions did not exceed three. Mean survival was less than 20 months from first symptom and 12 months from diagnosis. Mortality was related sometimes to polyneuropathy. Thus, in several aspects, plasmacytic neoplasia with osteosclerotic lesions is different from the classical multiple myeloma.
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PMID:Plasma cell neoplasia with osteosclerotic lesions. A study of five cases and a review of the literature. 22 10

Thirty patients with histologically proven hepatocellular carcinoma were examined ultrasonically. All except two of these cases were reported ultrasonically as having a solid mass. Forty-three per cent of these lesions appeared multiple and 90% had irregular walls or boundaries. Stretching or distortion of the inferior margin of the liver is considered significant and 53% of cases demonstrated this feature. Just over two-thirds (67%) of the lesions were echogenic and under one-third (27%) were mixed lesions with echogenic and transonic areas. These transonic areas are considered to be due to the necrosis within the tumour. Most patients presented late and died within three months. Ninety per cent had clinical hepatomegaly or an epigastric mass. So far the main benefits of ultrasonography have been the recognition or exclusion of treatable disease such as liver abscess, cysts and congestive conditions of the liver, which may also present with unexplained hepatomegaly or epigastric masses. The possibility of a recognisable echo pattern for hepatocellular carcinoma emerged from this study. By conducting selective ultrasonic surveys in endemic areas and by employing the ultrasonic criteria described early diagnosis may be possible. Aspects of management and research may be assisted.
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PMID:Grey scale ultrasound appearances in hepatocellular carcinoma. 22 2

The effect of repeated (4 weeks) oral administration of 2,4-, 2,5- or 2,6-xylidine (at dose levels of 400--500 mg/kg/day) on the morphology and microsomal drug metabolising enzyme activity of the liver was studied in rats. All 3 isomers caused hepatomegaly which was considered to be due to proliferation of the smooth endoplasmic reticulum. Decreases in glycogen content and glucose-6-phosphatase activity were demonstrated histochemically. Biochemical investigations showed increases in microsomal protein and cytochrome P-450 content in rats dosed with 2,4- or 2,5-xylidine and in glucuronyltransferase activity in rats given 2,4-, 2,5- or 2,6-xylidine. Aniline hydroxylase activity was increased in all treated rats except males dosed with 2,6-xylidine. The results of the study indicate that all isomes of xylidine can be inducers of microsomal drug-metabolising enzyme activity, that they may be metabolised by oxidation and that the xylidine molecule may be eliminated as a conjugate with glucuronic acid.
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PMID:Hepatic effects of xylidine isomers in rats. 22 31

Six primitive hepatic tumours (two benign and four malignant) collected over a period of seven years, are studied. The symptoms were mild or absent in many of the cases, and all were discovered after investigation of hepatomegaly or abdominal mass. The importance of the co-ordinated use of radiological and gammagraphical findings is pointed out.
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PMID:[Radiological diagnosis of primitive hepatic tumors in infants (author's transl)]. 22 72

The classical features of Type I glycogen storage disease (McKusick 23220) (GSD) are hepatomegaly, hypoglycaemia, and acidosis, enlargement of the kidneys and short stature. Glucose-6-phosphatase (EC 3.1.3.9) activity is defective not only in liver and kidney but also in small intestine (Field et al., 1965). In addition to the classical features, many patients suffer from episodes of diarrhoea (Fine et al., 1969). At the Hospital for Sick Children, Great Ormond Street, patients with the commoner forms of hepatic glycogen storage disease have episodes of diarrhoea or loose stools more commonly than was suspected. We have investigated small intestinal function in three patients with Type I GSD by both in vitro and in vivo techniques.
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PMID:Disordered intestinal function in glycogen storage disease. 22 44

Focal nodular hyperplasia and adenoma of the liver together represent approximately 2% of all primary hepatic tumors and tumor-like lesions in childhood. This study reports the clinical and pathologic features of focal nodular hyperplasia in three children, all females between 27 months and 15 years of age with asymptomatic hepatomegaly. In contrast, massive hemoperitoneum from a ruptured, hemorrhagic mass was the presentation of the hepatic adenoma in a 14-year-old girl. There was no history of administration of steroids in these four children. Angiography in two cases (one case each of focal nodular hyperplasia and hepatic adenoma) revealed hypervascular lesions with abnormal tortuous vessels suggesting a malignant tumor. Pathologically, the adenoma and focal nodular hyperplasia were readily distinguishable and the necessity for this differentiation was reviewed. All four patients are currently doing well.
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PMID:Focal nodular hyperplasia and adenoma of the liver. A pediatric experience. 23 73

A 42 year old woman who had been on oral contraceptives (OCs) for 10 years was admitted to the hospital for pains in the hepatic region. Laparoscopy showed an enlarged liver, and biopsy confirmed the diagnosis of primary carcinoma. The patient died. The literature on the subject has reported on 22 similar cases; common signs of alarm are pain and enlarged liver. The length of contraception and the type of contraceptive do not seem to be of primary importance. It is impossible to state that OCs are carcinogenic although it is highly probable. Hepatic lesions are usually benign, but sometimes they are malignant, and it is possible that genetic predisposition plays a role in such cases. It is also possible that OCs, by diminishing biliar excretion, may augment the hepatic concentration of toxic metabolites. The essential argument against OCs is the regression of benign tumors after use of contraceptives is stopped. Women on OCs should be checked routinely for early recognition of benign or malignant lesions. A national register of cases would be helpful in determining the prevalence of tumors.
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PMID:[Primary malignant tumour of the liver associated with the ingestion of oral contraceptives (author's transl)]. 23 79


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