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)

The cause of hyperamylasemia associated with chronic liver disease is unclear. In an attempt to identify the tissue of origin of hyperamylasemia in 3 patients with chornic active hepatitis their serum was isoelectrically focused. The isoamylase patterns obtained were compared to those of pancreatic and salivary amylase. The apparent salivary gland origin of the excessive blood amylase in the patients studied was substantiated by radiological demonstration of parotid sialoectasia in one patient and histological evidence of sialoadenitis in another. Further evidence was the coincident isoelectric points of the predominant isoamylase in the sera of the liver disease patients and of patients with parotid inflammatory disease. Hyperamylasemia associated with chronic liver disease may be of salivary gland origin and as such forms part of the spectrum of extrahepatic manifestations of chronic active hepatitis.
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PMID:A cause of hyperamylasemia associated with chronic liver disease. 83 1

Whether and to what extent the pancreas is involved in acute viral hepatitis is still unclear. In order to address this issue we evaluated serum and urinary amylase and isoamylase levels in 92 patients with acute viral hepatitis of different etiology and in 60 healthy volunteers. Furthermore, pancreatic structure and volume were evaluated by ultrasound scanning. Significant increase in serum and urinary pancreatic isoamylases was found in 12 and 35% of patients, respectively, in the early stage of the disease. Increase in serum pancreatic isoamylases was found only in patients suffering from B and non-A, non-B hepatitis. Ultrasonographic evaluation did not show any change in pancreatic structure and volume. In conclusion, this study suggests that mild pancreatic damage may occur during viral hepatitis.
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PMID:Mild pancreatic damage in acute viral hepatitis. 247 80

In a group of 167 patients with acute viral hepatitis (AVH), 11 with type A hepatitis, 125 with type B and 31 type non A, non B, the following enzymes were studied: serum amylase (S-AMY) and its isoenzymes (pancreatic and salivary type), urinary amylase (U-AMY), serum lipase (S-TGL) and serum immunoreactive trypsin (i-TRY). In all groups of patients, in the acute phase of illness, a significant increase in S-AMY was observed, in particular in hepatitis type B and non A, non B (p less than 0.001). An increase in U-AMY excretion was recorded in patients with type A hepatitis. S-TGL levels were significantly higher in all groups, especially in patients with type A hepatitis. i-TRY was only slightly higher in patients with hepatitis A and non A, non B. S-AMY isoenzymes showed a peculiar pattern: the pancreatic type (2) of isoamylase was found to be prevalent in 66% of patients with AVH while in controls the salivary type (1) was prevalent in most cases. Pancreatic enzyme alterations correlated neither with laboratory hepatic function tests nor with the clinical syndrome. These results suggest that a pancreatic injury is not uncommon in AVH, although it is seldom severe.
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PMID:Serum pancreatic enzyme alterations in acute viral hepatitis. 620 14