Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet abnormalities associated with hepatobiliary diseases include increased (thrombocytosis) and decreased (thrombocytopenia) numbers of platelets as well as abnormalities in function (thrombocytopathy or thrombasthenia). Hepatic diseases that are accompanied by platelet abnormalities include hepatitis, cirrhosis, portal hypertension, and neoplastic disorders both benign and malignant. The objective of this work is to examine the platelet abnormalities that occur with a variety of hepatobiliary disorders. Thrombocytosis is seen as a reactive entity following splenectomy. Thrombocytopenia is associated with hypersplenism, dysproteinemias and liver disease related disseminated intravascular coagulation (DIC). Qualitative platelet abnormalities are found in hepatic failure, liver diseases associated with high or low levels of lipid, and with medications given for a variety of hepatocellular diseases. Clinically common and significant platelet abnormalities associated with liver disease are thrombocytopenia secondary to portal hypertension and the thrombasthenias following metabolic changes and/or therapeutic interventions of liver disease.
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PMID:Platelet abnormalities in hepatobiliary diseases. 218 3

Methods of CT, echotomography and scintigraphy of the liver were used to investigate 95 patients with diffuse liver diseases (fatty dystrophy, hepatitis, cirrhosis, hemosiderosis and amyloidosis). CT changes in these diseases were described. A high efficacy of CT was established in the detection of diffuse liver lesions and portal hypertension permitting one to give up in some cases invasive puncture biopsy of the organ.
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PMID:[Computed tomography in the diagnosis of diffuse diseases of the liver]. 221 85

A case of idiopathic portal hypertension (IPH) developing after renal transplantation is reported. A 33-year-old Japanese male who had undergone renal transplantation 8 years previously was transferred to our hospital because of hematemesis from ruptured esophageal varices. He had no history of any liver disease before the renal transplantation, but had a history of receiving blood transfusion. Abdominal computed tomography (CT) and ultrasonography revealed marked splenomegaly and collateral channels, but no obliteration which might cause portal hypertension in the hepatic or portal vein. No findings suggestive of hepatitis or liver cirrhosis were found either macroscopically on laparoscopy or by liver biopsy. Light microscopic study of the liver biopsy specimen showed mild periportal fibrosis, inconspicuous portal branches in the most peripheral tracts, but no pseudolobule formation or piecemeal necrosis. However collagen deposition was found in the perisinusoidal space and partly in intercellular space on electron microscopy. We consider that the development of portal hypertension in this case is responsible for the collagen deposition, which may be related to the administration of azathioprine after renal transplantation. There are few reports on IPH after renal transplantation, and it is stressed that a lower amount of azathioprine than previously reported may induce IPH under such conditions.
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PMID:A case of idiopathic portal hypertension after renal transplantation. 222 56

In 36 patients with chronic viral hepatitis and 20 patients with an intact liver we determined the blood flow and blood flow velocities of the portal vein by means of duplexsonography. This was done before and after the intake of a test meal (Biosorbin MCT). According to preexisting data the cases of chronic hepatitis were subdivided into groups consisting of 14 cases having chronic persistent hepatitis, 9 cases having chronic aggressive hepatitis without tendency of cirrhotic transformation and 13 cases of chronic aggressive hepatitis with beginning cirrhotic changes. Patients with known cirrhosis of the liver or signs of portal hypertension were excluded from the study. It was not possible to assign a patient with chronic hepatitis to a definite group merely on the knowledge of his portal blood flow. Only after the intake of the test meal varying increases in blood flow velocity and volume were demonstrated. These increases were found to be smallest in the group of "chronic aggressive hepatitis with developing cirrhosis". In some individual cases this enabled us to conclude from changes of the portal blood flow whether or not a portal hypertension is developing.
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PMID:[Duplex sonography measurement of portal vein blood flow with healthy livers and in patients with chronic hepatitis after a fully absorbable test meal]. 223 57

Sixty patients with kala-azar were studied for liver involvement. Clinically none had any evidence of chronic liver disease. Biochemical evidence of hepatitis was seen in about 25% of cases while radiological and radionuclide studies failed to reveal portal hypertension and/or cirrhosis of liver in any of the patients. Histopathology of the liver in 18 patients failed to reveal any evidence of chronic liver disease or cirrhosis. It is suggested that portal hypertension and cirrhosis of liver probably do not occur as a consequence of kala-azar.
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PMID:Liver in kala-azar. 232 99

Seventy patients, selected from 265 patients with proved variceal bleeding, underwent a distal splenorenal shunt (DSRS) procedure with or without splenopancreatic disconnection (SPD). Alcoholic cirrhosis was the cause of portal hypertension in 57% of the patients. The operative mortality was 13% (Child's classes A and B 2%, class C 66%). Despite fewer varices in all of the patients, variceal rebleeding and death occurred in one patient (2%). Late portal perfusion was observed in 91% of the patients, with worsening in 23%, compared with the preoperative study. Persistent hepatocyte necrosis and incomplete SPD were the most significant prognostic factors for decreased perfusion (presence and absence of necrosis, 38% and 12%, respectively; DSRS and DSRS with SPD, 43% and 12%, respectively). SPD also decreased ongoing hepatocyte damage. Post-shunt encephalopathy was clinically evident in 7% of the patients, but after electroencephalographic evaluation, it increased to 24.6%. Significant factors in its development included decreased portal perfusion (62% versus 14%), active hepatitis (48% versus 17%), and incomplete SPD (43% versus 14%). The higher late liver-related mortality was associated with a lack of or decreased portal perfusion and the absence of SPD.
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PMID:Selective variceal decompression and its role relative to other therapies. 236 77

Based on a rare case of heterotopic hepatic transplantation (HHT) carried out in a 24 year old woman for fulminant hepatitis of viral origin, the authors present the technique used and the principal post-operative events (rejection, resistant large volume ascites and the clinical course for the liver itself). They discuss the rarity of success in this type of graft, where the causes of failure in man have not been entirely elucidated: the venous pre-existing portal hypertension is probably a very unfavorable factor. The place of this particular type of HHT in cases of acute severe hepatic failure is then proposed: this may produce a smaller operative insult than orthotopic transplantation and, in this respect, deserves consideration when advanced hepatic encephalopathy is present, notably due to delay in finding a suitable graft.
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PMID:[Heterotopic hepatic transplantation in fulminating hepatitis]. 250 48

From the standpoint of diagnostic laparoscopy, the frequency and etiological aspect of atrophy of a lobe of the liver was studied. The frequency of hepatic lobe atrophy was 5.3% among 1,208 laparoscopy cases at our department. Lobe atrophy of the liver can be seen not only in congenital anomaly, atrophic cirrhosis and malformation, as described in the OMED database of digestive endoscopy, but also in some other kinds of liver diseases including chronic hepatitis, idiopathic portal hypertension, primary biliary cirrhosis, drug-induced liver injury, scarred liver, autoimmune hepatitis and also in malignancies of other visceral organs. The disorders most frequently associated with hepatic lobe atrophy were idiopathic portal hypertension, and scarred liver, primary biliary cirrhosis, etc.
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PMID:Laparoscopic observation of hepatic lobe atrophy. 255 63

A group of children with autoimmune hepatitis is characterized by the presence in their sera of anti-liver-kidney microsome antibody (LKMA) as defined by immunofluorescence. Immunoblot analysis of the sera of 21 such children using rat-liver microsome total proteins as antigen allowed separation into three groups--group 1, whose sera recognized a 50 kDa protein; group 2, whose sera recognized a 66 kDa protein; and group 3, whose sera recognized both proteins. Patients with the anti-66-kDa reactivity more often displayed an acute onset of the disease, less signs of portal hypertension, better sensitivity to immunosuppressive therapy, and less tendency to relapse. They also displayed a lower titer of anti-rat-liver microsome antibody in enzyme-linked immunosorbent assay (ELISA) and a serum reactivity with a rat-liver cytosolic protein. These results (a) indicate that the LKMA-positive autoimmune hepatitis of children is heterogeneous from both clinical and immunological view points, (b) suggest that children with anti-66-kDa reactivity could have a less severe disease than children with the 50-kDa reactivity, and (c) indicate that immunoblot analysis should be added to ELISA and immunofluorescence studies to achieve better characterization of these patients.
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PMID:Clinical and immunological heterogeneity of anti-liver-kidney microsome antibody-positive autoimmune hepatitis in children. 269 12

Portal circulation in patients with chronic liver diseases was evaluated by [99mTc]pertechnetate per-rectal scintigraphy. Technetium-99m pertechnetate (10 mCi) was instilled into the upper rectum, and serial scintigrams were taken. Radioactivity curves for the liver and heart were then recorded sequentially. Through analysis of these curves, the per-rectal portal shunt index (Sl) was calculated for six healthy subjects and 228 patients, 59 with chronic hepatitis, seven with idiopathic portal hypertension, six with primary biliary cirrhosis, and 156 with cirrhosis. In the healthy subjects, the Sl was 1.9-5.2% (mean 4.1%). In hepatitis, the mean Sl was 7.1%, and in cirrhosis, 52.9%. The Sl was higher in cirrhotic patients with esophageal varices than in those without (p less than 0.001), and in cirrhotic patients with encephalopathy than in those without (p less than 0.01). For some patients with portal hypertension, portal collateral circulation could be depicted, and images of changes in the portal collateral circulation after vascular anastomosis were seen.
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PMID:Portal circulation by technetium-99m pertechnetate per-rectal portal scintigraphy. 283 55


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