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 bleeding syndrome due to severe prothrombin complex deficiency is reported in 93 infants. Most were breast fed (98 per cent), aged 2 weeks to 1 year and there were no serious preceding or associated diseases. Hemorrhagic diathesis, pallor and mild hepatomegaly were the major manifestations. The incidence of intracr anial bleeding was strikingly high (63 per cent) particularly with subdural and subarachnoid hemorrhage. Acute onset, short course and rapid clinical and laboratory improvement after vitamin K therapy were observed. Mortality rate was 35 per cent but has been reduced to 17 per cent since 1969. The location of bleeding, prompt diagnosis and early treatment are the major factors affecting prognosis. Severe prothrombin complex deficiency due to vitamin K deficiency accounted for the pathogenesis of bleeding. Possible causes of vitamin K deficiency were discussed but definite conclusions could not be drawn.
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PMID:A bleeding syndrome in infants due to acquired prothrombin complex deficiency: a survey of 93 affected infants. 30 65

Five children with tuberculosis were treated with isoniazid (20 mg./Kg./day) and rifampin (15 mg./Kg./day). After five to twenty seven days of treatment they presented anorexia, vomiting and jaundice. Hepatomegaly was found in two of them. High indirect bilirubin, S.G.O.T. and S.G.P.T. and low prothrombin levels were present in all of them. Eight to thirty one days after withdrawal of rifampin, all patients were well and their laboratory data was normal.
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PMID:[Toxic hepatitis caused by rifampin and isoniazid in treatment of tuberculosis (author's transl)]. 86 41

A total of 240 cases of a bleeding syndrome in infants due to prothrombin complex deficiency of unknown aetiology were reviewed. The majority of patients were breast fed, aged 1-2 months and the syndrome was more prevalent in males. Clinical manifestations consisted of bleeding, pallor and mild hepatomegaly in the majority of cases. Mild fever, diarrhoea, jaundice, and upper respiratory tract infection were associated in a few patients. Acute onset, short course and a high rate of intracranial bleeding (65%), particularly subdural and subarachnoid, were observed. The haemostatic defects appeared to be a marked reduction in factor II, VII, IX, and X. Complete blood counts remained relatively normal, with the exception of some changes (anaemia, leukocytosis), in response to the acute bleeding. Liver chemistry was normal or slightly impaired. No specific pathological changes were noted at autopsy, there were mild changes of liver cells, such as rare focal necrosis of liver cells, the proliferation of Kupffer cells, extramedullary haemopoeisis and mild cholestasis. Clinical improvement and correction of hemostatic defects were noted after vitamin K therapy alone or with fresh blood transfusion. Mortality rates were high in infants with intracranial bleeding (40-55%), while the overall mortality rate was 25%. The pathogenesis and the possibility of prevention of the syndrome were discussed.
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PMID:A bleeding syndrome in infants: acquired prothrombin complex deficiency of unknown aetiology. 108 22

Forty hospitalized male patients with hepatic functional deficit were treated i.m. for 3 weeks with a total liver extract or placebo. The study was a double-blind. Statistical analysis (Student's t test, analysis of variance. Mann-Whitney test and Fisher's probability test) showed that liver extract therapy was more effective than placebo in improving liver function as indicated by changes in clinical features(digestive disorders, constipation, hepatomegaly) and colloidal and other laboratory tests, e.g. plasma cholesterol, prothrombin time, red cell count and hemoglobin concentration. An overall clinical assessment showed that 60% of patients treated with the liver extract were improved. In addition, no local or general side effects were observed. Present results are in favour of an hepatoprotective activity of a total liver extract.
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PMID:Double-blind study of a total liver extract in patients with hepatic dysfunction. 109 45

This report reviews the manifestations in fifteen children of proved adenoviral pneumonia. Patients' ages ranged from 43 days to 4 years and 1 month. Twelve cases were younger than 2 years old. Adenoviral infections were proved by positive viral cultures or a four-fold increase of the complement fixation titer. Prolonged fever and cough were found in all cases. In 13 patients, respiratory distress occurred; 5 needed mechanical ventilation. Injected throats, conjunctivae and ear drums were common. Other clinical pictures included abdominal discomfort, hepatomegaly, skin rash, convulsion and bleeding tendency. Abnormal laboratory findings were mild anemia, leukopenia, thrombocytopenia, elevated erythrocyte sedimentation rate and C-reactive protein, impaired liver function test, and prolonged prothrombin time and partial thromboplastin time. Anemia (11 cases), leukopenia (7 cases) and elevated transaminases levels (7 cases) were more common than previously reported. All patients had para-hilar peribronchial infiltrates in chest roentgenography. Segmental atelectasis and compensated hyper-expansion were found frequently. Pleural effusion were noted in six of our cases. Air leak syndrome occurred in three patients who had received mechanical ventilation. Three of the 15 patients expired: one had a preceding measles infection, all had disseminated intravascular coagulopathy. For patients with antibiotic-resistant pneumonia, adenoviral studies should be done. Extrapulmonary manifestations, and some abnormal laboratory findings, i.e., mild anemia, leukopenia, impaired liver function are clues to adenoviral infections, while bleeding tendency can be regarded as a poor prognostic sign for children with adenoviral pneumonia.
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PMID:Adenoviral pneumonia in children. 132 94

A fatal case of acute fulminant hepatitis following exposure to dichloropropanols is reported. A 59-year-old male worker in a chemical plant developed general malaise, nausea and vomiting several hours after cleaning a tank that had contained dichloropropanols. He had no previous history of hepatic dysfunction. On admission, hepatomegaly was prominent. Because of highly elevated levels of GOT and GPT in the serum, reduced prothrombin time and a lowered consciousness level, a diagnosis of fulminant hepatitis was made. Significant decreases of leukocytes and platelets were also observed. Serum creatinine and BUN were slightly elevated. Although plasma exchanges were conducted on the third and fourth day, the liver functions continued to deteriorate. The patient died on the fifth day. Because dichloropropanols could be detected in the blood specimens obtained at the time of admission, we considered that fulminant hepatitis in this case was attributed to dichloropropanols exposure. To our knowledge, this is the first case of fulminant hepatitis after dichloropropanols-exposure.
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PMID:[Fulminant hepatitis after the inhalation of dichloropropanols]. 150 13

Liver dysfunction in hyperthyroid patients has not been well characterized. We analyzed the clinical records of 43 patients with hyperthyroidism to define the spectrum of clinical and liver test abnormalities. The patients were divided into three categories: (a) 18 patients with uncomplicated hyperthyroidism (HT) (b) 19 with hyperthyroidism and congestive heart failure (HT/CHF), and (c) 6 with hyperthyroidism and concomitant unrelated liver disease (HT/ULD). Hepatomegaly and/or spenomegaly were noted in 15 of 19 (79%) patients with HT/CHF as compared to 6 of 18 (33%) patients with HT and 3 of 6 (50%) patients with HT/ULD. Four patients with HT/CHF had ascites. Serum aminotransferase levels greater than 250 IU/L were noted in only 1 of 37 (3%) patients without unrelated liver disease. Patients with HT/ULD or HT/CHF had markedly low prothrombin time. Serum bilirubin levels as high as 323 microM were noted in patients with HT. No characteristic liver histology due to hyperthyroidism was noted. Severe liver test abnormalities, including deep jaundice and prolonged prothrombin time, can occur in patients with hyperthyroidism alone or with HT/CHF. This makes the diagnosis of concomitant, unrelated liver disease difficult until the hyperthyroidism has been controlled.
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PMID:Hyperthyroidism and hepatic dysfunction. A case series analysis. 156

We have observed hepatopathy, associated with thrombocytopenia, in children receiving chemotherapy for Wilms' tumor. We have studied this hepatopathy-thrombocytopenia syndrome (HTS) in patients enrolled in the United Kingdom Childrens' Cancer Study Group (UKCCSG) Wilms' tumor trials (UKW1 and UKW2). At the time of this study, 501 patients had completed therapy. Treatment flow sheets were examined for evidence of hepatopathy (hepatomegaly with abnormal liver function tests) and severe thrombocytopenia (platelet count less than 25 x 10(9)/L). No child who developed the syndrome had received irradiation. HTS was seen in five of 355 (1.4%) of patients treated with combination chemotherapy but in none of the 146 patients treated with vincristine alone. In each instance, the onset was less than 10 weeks after diagnosis. In two children, hepatopathy was severe with jaundice, ascites, transaminases greater than 1,000 IU/L, and prolongation of prothrombin time. On average, HTS lasted 12 days, and resolved with supportive treatment. After recovery, the children tolerated chemotherapy, mostly at reduced dosage, without recurrence. There was no evident long-term morbidity. Dactinomycin is the probable cause of this syndrome. We conclude that the HTS is a rare but important complication of dactinomycin-containing combination chemotherapy for Wilms' tumor. Children developing "isolated" thrombocytopenia following dactinomycin are "at risk" of developing the full-blown syndrome and should have their treatment modified accordingly.
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PMID:Hepatopathy-thrombocytopenia syndrome--a complication of dactinomycin therapy for Wilms' tumor: a report from the United Kingdom Childrens Cancer Study Group. 184 5

An attempt was made to estimate noninvasively portal pressure (PP) in patients with chronic liver disease, using the theory of quantification, a kind of multivariate analysis. Forty-one patients with liver cirrhosis and 22 patients with chronic hepatitis in whom hepatic venous catheterization had been performed were studied. Seventeen parameters (age, sex, mean blood pressure, red blood cell count, platelet count, prothrombin time, lactate dehydrogenase, alkaline phosphatase, total bilirubin, albumin, gamma-globulin, indocyanine green retention at 15 min, blood urea nitrogen, hepatomegaly, splenomegaly, ascites and edema) were selected for the estimation of PP. The estimated PP correlated significantly with the data obtained by hepatic venous catheterization with a high correlation coefficient of 0.835 (p less than 0.01). An investigation using the theory of quantification was also undertaken to determine which of the 17 parameters selected above was most useful in estimating PP. Among the 17 parameters indocyanine green retention at 15 min, red blood cell count, prothrombin time, hepatomegaly and splenomegaly seemed to contribute significantly to the estimation of PP. When the formula was applied to 31 successive patients with chronic liver disease (external samples), the correlation between the estimated and measured PP was 0.455 (p less than 0.01). These results indicate that the formula is clinically useful in estimating PP in patients with chronic liver disease.
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PMID:[Estimation of portal pressure using the theory of quantification]. 201 41

Two fatal cases of amiodarone-induced acute, confluent, necrotic hepatitis are described. The patients, aged 28 and 60, had received a high loading dose of amiodarone. After the first and second day respectively following the administration of amiodarone, the patients developed jaundice, hepatomegaly, high serum transaminases, a prolonged prothrombin time and low cholesterol concentration. They died of hepatic coma and acute renal failure on the fourteenth and fourth day respectively. Needle liver biopsy, performed immediately after death, revealed lesions of acute drug-induced hepatitis with confluent and bridging necrosis. It is proposed that rapid administration of a high loading dose of amiodarone can cause acute confluent necrotic hepatitis. The mode of administration and the dosage of the drug should be re-considered.
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PMID:Acute amiodarone-induced hepatitis. 202 92


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