Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 832 patients with portal hypertension resulting from different etiology was studied by ultrasonograph as a screening test. In 17 of the 832 patients, cavernous transformation of the portal vein was detected by means of ultrasonography. We have prospectively studied these 17 patients, and the diagnosis of cavernous transformation was confirmed by portography in all patients. To evaluate how much biliary tract has been affected from cavernous transformation of the portal vein, and to explain the cause of mildly increased alkaline phosphatase and serum bilirubin levels, endoscopic retrograde cholangiopancreatography (ERCP) was performed in 16 of the 17 patients. There were narrowing, irregularity, undulation and nodular extrinsic defects resulting from compression of thrombosis of the portal vein and the collateral vessels, mimicking cholangiocarcinoma spreading along the common bile duct on the extrahepatic biliary tract in all 16 patients who underwent ERCP. Similar ERCP findings were not found in six patients with portal hypertension due to liver cirrhosis. The ultrasonographic, portographic, and ERCP findings corresponded to surgical findings in six patients who had undergone splenectomy for either hypersplenism or bleeding from esophageal varices. The results indicate that cavernous transformation of the portal vein cause the above-mentioned radiographic findings that we propose to call "pseudo-cholangiocarcinoma sign."
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PMID:Bile duct varices or "pseudo-cholangiocarcinoma sign" in portal hypertension due to cavernous transformation of the portal vein. 144 45

Hepatic tuberculosis was confirmed in 96 patients presenting with the features of liver disease, only 14 of whom had other concomitant hepatic pathology. Although respiratory symptoms occurred in 74 per cent of cases, these were overshadowed by the abdominal manifestations. The latter most frequently included right hypochondrial pain, abdominal distension, firm tender hepatomegaly, splenomegaly and ascites. Icterus was observed in 11 cases (only one of whom had concurrent hepatic pathology) and liver failure was found in 10 patients. A surgical presentation occurred in three patients. Four of 15 patients with pancytopenia were noted to have hypersplenism. Abnormalities in coagulation were noted in 26 patients (24 with low prothrombin index and two with moderately raised fibrinogen degradation products). The characteristic serum profile included hyponatraemia (64 per cent of cases), raised alkaline phosphatase (83 per cent) and gamma glutamyl transferase (77 per cent), hypoalbuminaemia (63 per cent) and hypergammaglobulinaemia (83 per cent). Transaminase levels were moderately elevated in 78 per cent of cases. Hepatic imaging techniques were frequently misleading. Chest radiographs aided the diagnosis but were normal in 25 per cent of cases. Histologically, acid fast bacilli, caseation and granulomas were seen in 9, 83 and 96 per cent of cases respectively. Adverse prognostic features included age (below 20 years), miliary TB, coagulation defects and the presence of predisposing factors; these were of value in selecting appropriate therapy. The overall mortality was 42 per cent. Liver biopsy was the most useful aid to correct diagnosis which was suspected clinically in only 47 per cent of cases.
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PMID:Tuberculosis hepatitis: a clinical review of 96 cases. 651 2

We review the clinical and pathologic features of 39 cases of nodular regenerative hyperplasia of the liver and include two new cases. This is an uncommon but distinct pathological entity characterized by regenerative hepatocytic nodules without fibrosis. Portal hypertension that often leads to hemorrhage from esophageal varices is the most important clinical manifestation. Characteristically, manifestations of hepatic failure are lacking, but a number of patients have elevated alkaline phosphatase of hepatic origin. Felty's syndrome is the entity most often associated with nodular regenerative hyperplasia. Anemia, leukopenia, and thrombocytopenia are frequent hematologic abnormalities secondary to hypersplenism. The etiology and pathogenesis of nodular regenerative hyperplasia of the liver are unknown.
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PMID:Nodular regenerative hyperplasia of the liver: report of two cases and review of the literature. 724 Jun 92

The article deals with differential-diagnostic criteria of inborn liver fibrosis and hepatoportal sclerosis. Congenital liver fibrosis is inherited and manifests at young age. It is characterized by marked hepatomegaly with stony dense liver, moderate splenomegaly with hypersplenism and portal hypertension in high activity of alkaline phosphatase and 5-HT, renal affection. Fibrosis locates around the biliary ducts. Hepatoportal sclerosis manifests more frequently in the adults with moderate hepatomegaly, marked splenomegaly with hypersplenism and predominance of anemia, high portal hypertension. Fibrosis is moderate and locates around portal vein branches in which thrombi are found.
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PMID:[Differential diagnosis of congenital fibrosis of the liver and hepatoportal sclerosis]. 1265 Jan 1