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 consecutive series of 24 cases of primary carcinoma of the liver in Malawi has been investigated. Histologically, all were hepatocellular carcinomas (HCC). All patients were African Bantus, the average age was 42.7, and the sex ratio was men 3.5:women 1. The duration of symptoms attributable to HCC was about 5 months previous to admission to hospital and was in no case preceded by clinically manifest cirrhosis. The clinical picture was rather uniform with pain in the region of the liver, emaciation and nodular hepatomegaly as the most important features. One of the patients had repeated attacks of hypoglycaemic coma. Sera from 11 out of 13 patients contained alpha-feto-protein. Hepatitis-associated antigen and antibody in the serum were found in 7 and 6 out of 16 and 14 cases respectively. Serum B12 and serum unsaturated B12 binding capacity were moderately raised in most patients. The prognosis was poor, the average time of survival was 4.8 weeks after admission. The cause of death was most frequently hepatic coma. HCC in the African Bantu shows some different features from the same disease in the Western Hemisphere: The incidence is much higher; the patients are younger. The neoplasm commonly develops in a clinically latent cirrhosis. The latter is not caused by alcohol, but is presumably a sequel of hepatitis. It is possible that aflatoxin is the carcinogenic factor, acting more readily in a cirrhotic than in a normal liver.
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PMID:Primary carcinoma of the liver in Malawi: a review of 24 cases. 19 21

The clinical and hematological features of 100 patients with sickle cell anemia are reviewed. The heart was enlarged and a murmur was heard in nearly 80 percent of patients. Pneumonia and pulmonary infarction occurred in 43 percent and 12 percent of patients, respectively. Musculoskeletal involvement included the hand-foot syndrome (15 percent), leg ulcers (55 percent), aseptic necrosis ofbone (11 percent), and osteomyelitis (4 percent). Symptoms and signs related to the gastrointestinal system included jaundice (55 percent), hepatomegaly (50 percent), splenomegaly (23 percent), hepatitis (11 percent) and gallstones (9 percent). Three patients underwent cholecystectomy and three patients had their spleens removed. Pyelonephritis occurred in 17 patients, priapism in five and hematuria in seven. Nineteen women had 39 pregnancies, of which 35 resulted in the birth of healthy infants. At least 328 painful crises occurred in 73 patients. There were also 13 hemolytic crises, eight sequestration crises, and five aplastic crises. A trail of alkali therapy in 33 crises in children failed to produce beneficial effects greater than hydration and analgesics alone as used in the control group. Laboratory findings in the 100 patients were comparable to those previously reported in the literature. The renal concentrating defect in most patients was confirmed. There were six deaths: hepatic coma secondary to post-transfusion hepatitis, thrombosis of inferior vena cava, congestive heart failure, exsanguination from erosion of the pancreaticoduodenal artery, extensive bronchopneumonia, and pulmonary infarction.
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PMID:Sickle cell anemia- clinical manifestations in 100 patients and review of the literature. 113 Apr 36

For 2 years a 72-year-old man had suffered from nonspecific upper abdominal discomfort and hepatomegaly. The gamma-glutamate transaminase concentration was increased to 121 U/l, the erythrocyte sedimentation rate was 80 mm in the first hour. Histological examination of tissue from the enlarged liver (22 cm in the midclavicular line) revealed the diagnosis of amyloidosis. The gastric mucosa, duodenum and rectum were not involved. Two years later ascites developed; six months after this he was again hospitalized in hepatic coma. Now, for the first time, a type IgA-lambda paraprotein was demonstrated by serum immunoelectrophoresis. The patient died of slowly progressing anicteric liver failure after having been ill for a total of 4 1/2 years. At autopsy there were extensive amyloid deposits throughout the liver and spleen so that the structure of these organs was hardly recognizable. The amyloid deposits in the liver were restricted to the glomerular region, while there was no amyloid in the heart. Histochemical tests showed that the deposits were strongly positive to the anti-lambda antibody. This was thus a case of primary (AL-lambda) amyloidosis of the liver and spleen which had taken an unusually prolonged course, because the heart was not involved at all and the kidneys only slightly.
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PMID:[Primary amyloidosis of the liver]. 161 10

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

An autopsy case of ATL with acute hepatic failure is reported. A 39-year-old man born in Miyazaki Prefecture was admitted because of jaundice and general malaise of about 10 days' duration. Palpation of the abdomen revealed moderate hepatomegaly: the patient had clear consciousness. The white cell count was 62,500/mm3, with 34% abnormal lymphocytes having lobulated or convoluted nuclei. Marked liver dysfunction (TB 30.5 mg/dl; GOT 2,740 U; GPT 1,031 U; LDH 3,833 U) was noted. He developed hepatic coma and died of acute hepatic failure on the third hospital day. At autopsy, the enlarged liver weighed 2,000 g and was diffusely infiltrated by ATL cells.
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PMID:[An autopsy case of adult T-cell leukemia with acute hepatic failure]. 301 18

A report on 9 cases of infantile hepatopathy and cirrhosis of the liver respectively in cases of hereditary autosome-recessive alpha 1-antitrypsin deficiency (alpha 1-ATM). The genetic variants of the serum-protease-inhibitor (Pi) alpha 1-antitrypsin (alpha 1-AT) were examined by means of iso-electric focusing (Polyacrylamidgelen). The gene incidence was of the allel PiZ 0,0138 in the 868 blood donors from the Tyrol and was therefore within the range of the PiZ-frequencies seen in other Central-European populations. The other alleles PiM1, PiM2, PiM3, and PiS, point to the incidence of 0.7062, 0.1480, 0.1037, and 0.0225. The patients under observation (9) are homozygote PiZZ, the clinically healthy parents heterozygote PiZM. Risk of repetition in siblings of the patients is 25%. Early indicative symptoms are prolonged jaundice, acholic stools and hepatomegaly. Further developments are the fading of the hyperbilirubinaemia, temporary improvement in the pathological liver values, a freedom of symptoms for different lengths of time in each case, in the case of two patients, finally, decompensated cirrhosis of the liver and death in hepatic coma. The histological picture of the liver tissue shows PAS-positive storage granula in hepatozytes, intrahepatic hypoplasia of the bile duct, cholestasis as well as early cell necrobiosis, fibrosis and cirrhotic transformation. Course and severity of the liver complaint differ greatly, and are independent of the quantitative alpha 1-antitrypsin deficiency revealed, treatment is purely symptomatic.
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PMID:[Hereditary alpha 1-antitrypsin deficiency and infantile cirrhosis of the liver]. 676 50