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)

Serum carcinoembryonic antigen (C.E.A.) levels were measured in 381 undiagnosed patients who presented with clinical problems commonly associated with gastrointestinal malignancy. The results were compared with the final diagnosis after follow-up for up to 5 years to see whether C.E.A.-testing added any useful information. Of 307 patients presenting with upper gastrointestinal symptoms, lower gastrointestinal symptoms, or irom deficiency anaemia, C.E.A. levels greater than 20 ng/ml indicated malignancy in 5 but in 3 of these malignancy was also diagnosed after routine investigation. Of 74 patients presenting with obstructive jaundice, hepatomegaly, or abnormal liver function, malignancy was diagnosed in 38. In 9 of these patients the diagnosis of malignancy could otherwise have been reached only by laparotomy. The serum-C.E.A. thus reached only by laparotomy. The serum-C.E.A. thus seems to be of value in the assessment of liver disease but not in patients with gastric or colonic symptoms or iron-deficiency anaemia.
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PMID:Carcinoembryonic antigen concentrations in undiagnosed patients. 8 41

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

A 6-week-old breast-fed infant had obstructive jaundice and hepatomegaly. When a dry-cleaning solvent, tetrachloroethylene, was detected in the mother's milk and blood, breast-feeding was discontinued. Rapid clinical and biochemical improvement followed. The child grew normally and had normal liver function during 2 years of follow-up.
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PMID:Obstructive jaundice due to a chlorinated hydrocarbon in breast milk. 91 29

Extrahepatic biliary obstruction due to mechanical obstruction of the common bile duct is a relatively rare complication of pancreatic pseudocyst. When jaundice does occur, clinical or laboratory evidence of associated primary hepatobiliary disease or acute pancreatitis has invariably been present. The patient described had a 3-month history of painless juandice, 40-lb weight loss, pruritus, and hepatomegaly, but no clinical or biochemical evidence of acute or chronic pancreatitis. After initial evaluation, including an abdominal echogram and a transhepatic cholangiogram, carcinoma of the head of the pancreas was diagnosed preoperatively. At laparotomy, a small pancreatic pseudocyst obstructed the terminal portion of the common bile duct. This case illustrates that a pancreatic pseudocyst should be considered in the differential diagnosis of obstructive jaundice, even in the absence of clinical evidence of pancreatitis or pseudocyst formation.
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PMID:Silent pancreatic pseudocyst. An unusual cause of extrahepatic biliary obstruction. 113 Mar 80

A series of 137 patients with amoebic liver abscess has been studied. Recognition of clearly defined but diverse clinical syndromes was found to be necessary not only in diagnosis but also in planned surgical management. The majority of patients had the classic syndrome of fever, right abdominal or chest pain, hepatomegaly, hepatic tenderness and radiological abnormalities. Other syndromes of presentation included the silent abscess, acute amoebic colitis, the acute abdomen, the intraabdominal lump, the external sinus, pyrexia of obscure origin, obstructive jaundice and renal, pleuro-pulmonary and cardiac symptoms. The syndromes due to an abscess in different parts of the right lobe and in the left lobe of the liver are to some extent distinct. In spite of the varied modes of presentation of amoebic liver abscess, the key to diagnosis is an understanding of the chronological sequence of the disease and its progression from one syndrome to another. Diagnostic methods of value and the mortality are discussed.
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PMID:Syndromes in amoebic liver abscess. 126 Feb 53

Fifty infants with obstructive jaundice were reviewed. Other than jaundice, hepatomegaly and splenomegaly were the other common presentations. The mean age of referral was 9.4 weeks. This was unsatisfactory as the prognosis depends on the age of corrective surgery. Majority of the non surgical cholestasis were due to idiopathic hepatitis. These patients did well as all of them were asymptomic and had no evidence of liver disease at 2 years of age.
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PMID:A clinical study of obstructive jaundice among Singapore infants. 130 62

Major biliary tract obstruction caused by tumour invasion is a rare manifestation of hepatocellular carcinoma. The authors had the opportunity to diagnose and treat five such cases, three of whom had features of acute cholangitis. The prevalence of both hepatocellular carcinoma and recurrent pyogenic cholangitis is high in patients from the Far East. The former may first present under the guise of the latter. Gastroenterologists and surgeons should be aware of hepatocellular carcinoma when managing these patients who present with obstructive jaundice, gross hepatomegaly and cholangitis.
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PMID:Biliary tract invasion and obstruction by hepatocellular carcinoma: report of five cases. 133 82

Echinococcosis is an infectious disease of humans caused by the larval (metacestode) stage of the cestode species Echinococcus granulosus (cystic echinococcosis or hydatid disease) or Echinococcus multilocularis (alveolar echinococcosis or alveolar hydatid disease). Clinical manifestations depend primarily on localization and size of hepatic lesions and may include hepatomegaly, obstructive jaundice, or cholangitis. Prognostically, alveolar echinococcosis is considered similar to liver malignancies, including a lethality rate of 90% for untreated cases. Diagnosis is based on imaging techniques coupled with immunodiagnostic procedures. Antibody detection tests for E. multilocularis have markedly improved with the use of affinity-purified Em2 antigen and recombinant antigen II/3-10 in enzyme immunoassays. Antigens of corresponding quality for E. granulosus are still unavailable. The detection of circulating antigens and immune complexes in the sera of patients with cystic echinococcosis, the demonstration of in vitro lymphocyte proliferation in response to stimulation with Echinococcus antigens, and the discrimination of serum immunoglobulin isotype activity to various Echinococcus antigens in both cystic and alveolar echinococcosis have been suggested for diagnostic purposes as well as for monitoring patients after treatment. New diagnostic molecular tools include DNA probes for Southern hybridization tests and polymerase chain reaction for the amplification of E. multilocularis and E. granulosus species-specific DNA fragments.
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PMID:Molecular and immunological diagnosis of echinococcosis. 149 67

Some clinical clues should alert paediatricians to the possibility of metabolic liver diseases. They can be classified into three categories: (i) Manifestations due to hepatocellular necrosis, acute or subacute, which can reveal galactosaemia, hereditary fructose intolerance, tyrosinaemia type I, Wilson disease and alpha 1-antitrypsin deficiency. Symptoms and signs suggestive of Reye syndrome should lead to a study of fatty acid oxidation and urea cycle enzymes. All these manifestations may necessitate a rapid diagnosis and treatment when liver dysfunction is severe. (ii) Cholestatic jaundice can reveal alpha 1-antitrypsin deficiency, Byler's disease, cystic fibrosis, Niemann-Pick disease and some disorders of peroxisome biogenesis. (iii) Hepatomegaly can reveal disorders with liver damage but also storage diseases such as glycogen storage diseases, cholesteryl ester storage disease and, when associated with splenomegaly, lysosomal storage diseases. Appropriate investigations for recognizing all these entities are proposed.
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PMID:Clinical presentation of metabolic liver disease. 174 17

Three cases of pancreatic tuberculosis are described. The first patient presented with abdominal pain, weight loss, anorexia, vomiting, hepatomegaly, and mass in the head of the pancreas, on computerized tomographic (CT) scan. The second patient presented with low grade fever, anorexia, and weight loss, and was investigated for gallbladder disease. The third patient presented with obstructive jaundice and mass lesion in the head of the pancreas. Two patients underwent laparotomy for suspected pancreatic tumors. The findings of pancreatic disease was incidental during laparotomy in the second patient. The histopathology revealed caseating granuloma in all of them. The first patient responded well to treatment, and the second patient stopped treatment after 2 months and is well. The third patient is being followed. If malignancy can be ruled out, tuberculosis should be considered in relevant geographic areas, and a tissue diagnosis should be made.
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PMID:Tuberculosis of the pancreas: report of three cases. 203 2


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