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)

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

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 The drug was withdrawn on presentation to hospital in 11 patients, with rapid clinical improvement in 9.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

A study of liver abnormalities in 36 patients with mixed cryoglobulinemia in the absence of underlying infectious, connective tissue, or lymphoproliferative disorders revealed clinical or biochemical evidence of liver dysfunction in 84%. Hepatomegaly was detected in 77%, splenomegaly in 54%, and abnormalities in bilirubin, alkaline phosphatase, or serum glutamic oxalacetic transaminase in 77%. Only four of the patients had overt liver disease. Of 15 biopsies from 12 patients, there was normal tissue structure in two, minimal nonspecific changes in one, portal fibrosis in three, chronic persistent hepatitis in one, chronic active hepatitis in two, chronic active hepatitis with cirrhosis in four, and postnecrotic cirrhosis in two. These findings, together with the previously reported high incidence of serologic evidence of hepatitis B virus (HBV) infection, support the view that the syndrome of purpura, arthritis, and nephritis is often a consequence of immune-complex vasculitis secondary to HBV infection.
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PMID:Liver involvement in the syndrome of mixed cryoglobulinemia. 90 Jun 72

Hepatomegaly and abnormal liver function can occur in nonmetastatic malignancies. A patient with metastatic prostatic adenocarcinoma that had spared the liver and extrahepatic biliary tree is described. He had puzzling episodes of jaundice for a period of 2 1/2 years. The results of appropriate investigations and an exploratory laparotomy performed dlring the patient's four antemortem hospitalizations were indicative of "recurrent intrahepatic cholestasis," the cause of which remained an enigma even after exploratory laparotomy. At autopsy, no evidence of hepatic metastases or extrahepatic biliary obstruction was found. Alcohol, hepatotoxic drugs, toxins, viral and chronic active hepatitis, hemolysis, and extrahepatic biliary obstruction were eliminated as causes of the jaundice. We believe that the intermittent intrahepatic cholestasis is one of the nonmetastatic manifestations (nonmetastatic hepatopathy of malignancy) of the prostatic adenocarcinoma.
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PMID:Intermittent cholestatic jaundice and nonmetastatic prostatic carcinoma. 92 51

Authors have performed an anatomo-clinico-biological comparison of two groups of hepatitis with lobular inflammation: group I with a simple lobular inflammation, called lobular hepatitis, and group II with a lobular inflammation associated with portal and periportal hepatitis, called chronic active hepatitis (CHA) with lobular hepatitis. Furthermore, a comparative study of these forms with a group of CHA without lobular inflammation was performed. Both forms of lobular inflammation appeared in young patients, the large majority of whom were infected with the hepatitis B virus; in 5 cases of CHA with lobular hepatitis the presence of the delta agent in the liver, possibly responsible of the lobular inflammation, was detected. The two forms of lobular hepatitis are differentiated by: the fivefold increase of ALAT over the normal value, with usually normal gamma-globulins and albumin, in the first group; in the lobular hepatitis, HBsAg was present in 33% of cases in the first group and in none of the patients of the second group, suggesting the integration of HBsAg within the hepatocytic genome; the clinical picture was generally asymptomatic in the first group and noisier, with hepatomegaly, in the second group; the period elapsed since the acute hepatitis was shorter in the first group (4-11 months) in 8 of 15 patients and longer in the second group. The clinical course of these forms of hepatitis if unforeseeable and the diagnosis is established on the basis of the morphological examination.
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PMID:[The significance of lobular inflammation in chronic active hepatitis]. 134 56

Abdominal ultrasonographic examination was performed in 61 hospitalized patients with chronic liver diseases and 253 school children from a village endemic for Schistosoma haematobium and were compared with 142 urban children without exposure to Schistosoma. The prevalence of ultrasound-detectable hepatomegaly and splenomegaly and the degree of periportal fibrosis was compared between those with and without S. haematobium infection. Among 13 patients with biopsy-proven schistosomal hepatic fibrosis, three with coarse changes secondary to S. mansoni infection showed grade III periportal fibrosis, while 10 patients with fine schistosomal hepatic fibrosis due to S. haematobium had borderline (two) or grade I (eight) changes. Ultrasound evidence of periportal fibrosis was not detected in patients with hepatic cirrhosis, chronic active hepatitis, or fatty infiltration. However, three of 14 patients with chronic persistent hepatitis had grade I periportal fibrosis and two had borderline changes. The frequency of ultrasound-detected hepatomegaly and splenomegaly was greater among rural S. haematobium-infected children (35.2% and 22.4%, respectively) than among noninfected rural (21.1% and 13.3%) and urban (16.9% and 4.9%) children. Also, the frequency of grade I periportal fibrosis was significantly greater (P less than 0.01) in S. haematobium-infected children (22.4%) than in noninfected rural (11.7%) and urban (0.7%) children. No patients with S. haematobium infections, either in the hospital or the village, had grade II or III periportal fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ultrasonographic changes of the liver in Schistosoma haematobium infection. 150 89

The case is reported of a 27 year old woman who had mixed connective tissue disease (MCTD) associated with chronic active hepatitis and thyroiditis. Although hepatomegaly is sometimes observed in MCTD, only four cases of MCTD and chronic active hepatitis have been described. It is thought that this is the first report of an association between MCTD, chronic active hepatitis and thyroiditis.
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PMID:Mixed connective tissue disease associated with autoimmune hepatitis and thyroiditis. 158 60

Nine out of 10 patients with primary lymphoma of the liver presented in a manner that did not suggest a tumour. The initial diagnoses were chronic active hepatitis in three cases and "granulomatous cholangitis", inflammatory pseudotumour, and anaplastic carcinoma in one case each. Moreover, extensive haemorrhagic necrosis in three cases initially suggested the Budd-Chiari syndrome. All the tumours were diffuse non-Hodgkin's lymphomas like the 50 cases reported previously, but they differed from most of these in that nine were of T cell phenotype. Five were pleomorphic small T cell, two T zone, and two T lymphoblastic lymphomas: only one was centrocytic and of B cell lineage. This report extends the range of clinical manifestations (diffuse hepatomegaly without a tumour), histological appearances (resemblance to chronic inflammatory or vascular liver diseases) and phenotype (of T cell lineage) of primary lymphoma of the liver: these features seemed to be related in this series. Recognition is important as prognosis remains favourable in appropriately treated cases. Although the appearances of the liver biopsy specimens may be difficult to interpret, the destructiveness of the infiltrate is an important clue to the diagnosis.
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PMID:Primary lymphoma of the liver: clinical and pathological features of 10 patients. 226 72

Clinical, laboratory, and ultrasonographic features of 75 patients of primary hepatocellular carcinoma (PHC) living in the Gizan Area of Saudi Arabia and their follow-up, during a 2-year period, were characterized. Eighty-nine percent of the cases were defined histologically, whereas in the rest, ultrasonographic (US) evidence along with an alphafetoprotein (AFP) level exceeding 480 ng/ml were taken as the positive evidence for PHC. Eighty percent of the cases were male patients, with the peak incidence during the seventh decade. The most common clinical presentations were hepatic enlargement (91%), abdominal pain (76%), splenic enlargement (33%), and acites (33%), followed by bruit, fever, metastases, and varices. Alteration in a liver function test was manifest in 97% of the cases, AFP values greater than 480 ng/ml in 57%, and a hepatitis B virus surface antigen (HBsAg) positivity in 65% of the cases. There was no intersex variation in positivity for HBsAg, antibody to HBsAg (anti-HBs), antibody to hepatitis B virus core antigen (anti-HBc) among the 30 PHC cases studied. Positivity for HBsAg or the overall hepatitis B virus exposure in PHC cases was higher than the normal controls (P less than 0.001). In addition to histologic confirmation of PHC in 67 cases, there was histologic evidence of cirrhosis in 25%, or chronic active hepatitis in 19% of the cases. At the time of diagnosis, the average duration of the presenting illness was less than 2 months, while the mortality in the ensuing 2-month period was 73%. The average span of total illness in the vast majority of cases was 4 to 6 months. Two female patients (one with fibrolamellar carcinoma) however, survived for 2 years. Immunization against hepatitis B virus should be considered for all newborns in such hyperendemic communities. A continuous program should be started in such communities to screen and immunize all those yet unexposed to hepatitis B virus. The established HBsAg carriers should be periodically examined ultrasonographically along with an AFP estimation for initiating the chemotherapeutic and other measures against PHC in fairly early stages of malignancy.
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PMID:A profile of primary hepatocellular carcinoma patients in the Gizan Area of Saudi Arabia. 242 66

Amiodarone has been reported to cause asymptomatic increases in liver function tests in 15-55% of patients. Clinically apparent, symptomatic hepatic disease occurs less frequently, but patients have been reported to have hepatomegaly, jaundice, cirrhosis, or chronic active hepatitis. Less well recognized is the fact that amiodarone has been attributed to six deaths. We cared for a patient with amiodarone hepatotoxicity, which led us to review the literature associated with this serious condition.
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PMID:Hepatotoxicity associated with amiodarone therapy. 264 21


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