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 phenytoin-induced hepatitis with mononucleosis is reported, and syndromes associated with phenytoin hypersensitivity reactions are discussed. A 23-year-old black woman with a two-month history of seizure disorder was admitted to a hospital with nausea, vomiting, fever, lymphadenopathy, diffuse maculopapular rash, left-upper-quadrant tenderness, and hepatomegaly. She was receiving phenytoin sodium 300 mg/day; carbamazepine 200 mg four times daily had been discontinued four days before admission because of leukopenia. Phenytoin was discontinued after admission; however, phenytoin 1 g i.v. was given for a tonic-clonic seizure two days after admission, after which swelling of the face and legs and pruritus developed. Over the next few days, signs and symptoms of hepatotoxicity progressed, and she became comatose. Seizures were treated with diazepam. She began to recover after 10 days of supportive therapy and was discharged several weeks later on primidone therapy. Serious phenytoin hypersensitivity reactions may appear as dermatologic, lymphoid, or hepatic syndromes. Fever, rash, and lymphadenopathy often accompany hepatic injury. Encephalopathy and death may occur. Proposed mechanisms for phenytoin hypersensitivity include antigen-antibody reactions, alteration of lymphocyte function, and an enzyme abnormality causing the production of toxic metabolites. Treatment is supportive; phenobarbital and carbamazepine may be used with caution as alternate anticonvulsant therapy. The possibility of phenytoin hypersensitivity reactions should be considered when patients receiving phenytoin have unusual symptoms, particularly fever, rash, and lymphadenopathy.
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PMID:Phenytoin-induced hypersensitivity reactions. 367 71

The case of a 29-year-old man with Niemann-Pick disease and hepatic failure is presented. Massive hepatomegaly with hepatic calcification were noted in association with a course of persistent hepatitis B serum antigenemia with rapid hepatic decompensation, ascites, encephalopathy and renal failure. The possible relationship of the clinical course to the underlying disease process is discussed, and a review of Niemann-Pick disease is presented.
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PMID:Hepatic failure in adult Niemann-Pick disease. 375 63

We have performed a side-to-side portacaval shunt as the treatment of choice in six cases of primary Budd-Chiari syndrome. All the patients (three men and three women, mean age 33 years) had marked hepatomegaly and massive ascites. Four patients had endoscopically proved esophageal varices with no episodes of bleeding. Preoperative angiographic studies, caval pressure measurement, laparoscopy, liver biopsy specimens, liver scanning, and liver function tests confirmed the diagnosis. A possible etiologic factor was evident in only two cases. A plain side-to-side portacaval shunt was performed in four patients, while two required the interposition of a graft. One patient died after surgery of hepatorenal syndrome. Four of the surviving patients are free of ascites and doing well at 29, 27, 25, and 6 months. The remaining patient subsequently developed cirrhosis and died 76 months after surgery. None of the patients who survived developed encephalopathy. Shunt patency was confirmed endoscopically by variceal decompression in the four patients with esophageal varices. We believe the side-to-side portacaval shunt is a reliable and effective procedure for the definitive management of primary budd-Chiari syndrome.
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PMID:Portacaval shunt in the treatment of primary Budd-Chiari syndrome. 402 24

Hornet's venom is known to possess a variety of toxic effects. A 19-mo-old girl who developed a Reye-like syndrome following multiple stings by the Oriental hornet (Vespa orientalis) is described. She presented with encephalopathy associated with hepatomegaly, elevated transaminase levels, low prothrombin time, and hyperammonemia. Liver biopsy demonstrated microvesicular fatty infiltration and diffuse mitochondrial changes. Additional features were acute renal tubular necrosis and massive hemolysis.
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PMID:Multiple hornet stings with features of Reye's syndrome. 405 32

With the advent of effective antiviral treatment for disseminated herpes infection it has become important to be able to make a firm clinical diagnosis of this condition. We undertook a retrospective analysis of 20 patients with disseminated herpes simplex infection diagnosed at necropsy to derive useful clinical pointers to this severe form of the disease. The most useful clinical criteria were malnutrition, post measles state, and local herpes infection in addition to encephalopathy, enlarging hepatomegaly, and deteriorating pneumonia. The liver showed characteristic histological changes in 18 of 19 patients. These clinical criteria combined with liver biopsy were applied in a prospective pilot study of five patients at risk for disseminated herpes infection and the results were encouraging.
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PMID:Usefulness of clinical features and liver biopsy in diagnosis of disseminated herpes simplex infection. 648 59

In order to assess the prevalence of venocclusive disease in autopsied recipients of bone marrow transplantation, we reviewed coded liver histology from 204 consecutive autopsied recipients transplanted for leukemia (142), other malignancies (5), or aplastic anemia (57). Twenty-seven patients with leukemia, 2 with carcinoma, and 3 with aplasia had venocclusive disease and survived 2-86 days post-transplant. Early lesions showed subintimal edema and hemorrhage within small central venules and centrilobular congestion with hepatocyte degeneration. Later lesions showed subtotal to complete fibrous obliteration of the central venule lumina and centrilobular sinusoidal fibrosis. Thirteen patients had a subclinical course, and 19 were symptomatic. Venocclusive disease was life-threatening or lethal in 13. Typical symptoms developed 1-3 wk post-transplant and consisted of sudden weight gain, hepatic enlargement, ascites, high bilirubin, and encephalopathy. Statistical analyses showed a significantly higher prevalence of venocclusive disease associated with transplantation for leukemia (P = 0.014), pretransplant conditioning with more rigorous chemoradiotherapy regimens (P < 0.001) and three- to fourfold increase of venocclusive disease in patients whose conditioning included dimethyl busulfan (P < 0.005). Abnormal liver tests before transplant were also more prevalent among patients with venocclusive disease. No factors predicted the clinical outcome of established venocclusive disease. Venocclusive disease showed no association with hepatic graft-versus-host disease even among prolonged cases with severe periportal hepatitis and cholestasis. Other centrilobular lesions (hepatocyte degeneration, sinusoidal fibrosis, and phlebosclerosis) were identified in 23 patients. These non-specific changes may occur with viral hepatitis, graft-versus-host disease or chemoradiotherapy effects.
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PMID:An analysis of hepatic venocclusive disease and centrilobular hepatic degeneration following bone marrow transplantation. 700 4

The clinical, laboratorial and histological aspects of 50 cases of alcoholic hepatitis were analysed, as well as the follow-up of 24 patients. The mean age of the 50 patients was 42,9 years (range: 25 to 65 years); 44 were males. The beginning of the symptomatology was insidious in great number of cases. The hepatomegaly was most habitual clinical signal (92% of cases). The jaundice was observed in 58% of the cases. Twenty six per cent of the patients had not manifestation of advanced hepatopaty at the moment of diagnosis. The most constant laboratorial alteration (except the increase of gama-glutamil-transpeptidase, dosed in rare cases) was the increase of SGOT (94%). Histological examination showed necrosis and inflammatory exudate in all cases; steatosis in 98%; Mallory bodies in 78%; fibrosis in 84%; cirrhosis in 44%. In the group of patients that came to the obit at the first internation, jaundice, digestive bleeding, encephalopathy, infection, leucocitosis and decreased prothrombin activity. The follow-up of 24 cases (3 months to 5 years) showed aggravation of illness and frequent evolution to cirrhosis in patient that maintained the alcohol ingestion.
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PMID:[Alcoholic hepatitis: clinical, laboratorial and histological study of 50 cases]. 718 21

The clinicopathological features of a previously unrecognised type of acute encephalopathy prevalent among Japanese children is described by reviewing the records of 13 consecutive patients treated and 28 previously reported cases. The hallmark of this encephalopathy, proposed to be a novel entity termed acute necrotising encephalopathy of childhood, is multiple, necrotic brain lesions showing a symmetric distribution. The encephalopathy was noted in previously healthy children after respiratory tract infections, with presenting symptoms of coma, convulsions, vomiting, hyperpyrexia, and hepatomegaly. Laboratory examinations disclosed liver dysfunction, uraemia, and hypoproteinaemia. The histological appearance of the liver was variable and non-specific. Cerebrospinal fluid contained an increased amount of protein. Computed tomography and MRI showed the presence of symmetrically distributed brain lesions of the thalamus, cerebral white matter, brainstem, and cerebellum. Necropsy examination confirmed extensive fresh necrosis of these regions with evidence of local breakdown of the blood-brain barrier. Based on the characteristic combination of clinical and pathological findings, acute necrotising encephalopathy of childhood can be distinguished from previously known encephalopathies, including Reye's syndrome.
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PMID:Acute necrotising encephalopathy of childhood: a new syndrome presenting with multifocal, symmetric brain lesions. 2996 23

Six cases of severe jaundice and encephalopathy due to falciparum hepatitis initially diagnosed as fulminant hepatic failure are reported. This rare presentation of falciparum malaria should be suspected in patients with persistent fever, jaundice, encephalopathy and hepatomegaly. The diagnosis should be further suspected when the liver function tests show a predominantly conjugated hyperbilirubinemia with only modest elevation of liver enzymes and alkaline phosphatase. Liver biopsy is valuable in establishing the diagnosis at all stages of the disease.
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PMID:Falciparum malaria or fulminant hepatic failure? 811 50

100 cases of Kyasanur Forest Disease were studied clinically and autopsy or postmortem biopsies of various organs were done in 8 cases. 1. Our study showed that KFD passes through 4 stages each lasting for about a week. i.e. a prodromal stage with fever, hypotension hepatomegaly, a stage of complication characterized by haemorrhage, neurological manifestation or bronchopneumonia, a stage of recovery followed by a li stage of fever in some cases. 2. The exact of cause of haemorrhage could not be identified though Disseminated Intravascular Coagulation was suspected. 3. Hypotension in KFD could be of Myocardial origin. 4. Encephalopathy in KFD could be due to a metabolic cause probably of hepatic origin. 5. Lung signs could be due to intraalveolar haemorrhage and secondary infection.
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PMID:Clinical study of 100 cases of Kyasanur Forest disease with clinicopathological correlation. 822 55


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