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)

A 76 year old female with atypical leukemia complicated by vitamin B12 deficiency demonstrated marked fluctuation in blast percentage and hemopoiesis over 8 month period. She underwent surgical removal of pancreas head cancer 5.5 years ago. In January 1989 severe pancytopenia and mild increase of bone marrow blast were found. Blood transfusions and inadvertent administration of Vitamin B12 resulted in alleviation of pancytopenia and decrease in blast percentage. Several months later her bone marrow blast exceeded 30%, when serum B12 concentration was below 90 pg/ml. B12 injection and blood transfusion resulted in significant improvement in her hematological condition, but shortly thereafter she died of fulminant hepatitis. Her bone marrow cells showed a polyclonal constitution, as assessed by the RFLP-methylation technique using the PGK gene as a probe. The coexistence of leukemic- and normal clones under Vitamin B12 deficiency conditions and the differing behavior of such clones to B12 supplementation may explain the unusual clinical course observed in this patient.
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PMID:[Atypical leukemia accompanied by vitamin B12 deficiency]. 160 9

During the therapy of fatty liver (resp. fatty liver hepatitis) the additional application of Hepavis besides the prohibition of alcohol does not have any advantages in comparison to an additional application of a placebo. So the significant decrease of the fat content of the liver under those circumstances seems to be only the consequence of lacking alcohol consume, but not a specific effect of Hepavis. Consequently the treatment of alcoholtoxic fatty liver can be no other than to avoid alcohol, one of the most important causes of illness nowadays.
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PMID:[Does Hepavis have value in the therapy of fatty liver caused by alcohol poisoning?]. 265 94

In vitamin K deficiency or treatment with vitamin K antagonists, a precoagulant of prothrombin (Factor II) called preprothrombin has been established. We measured preprothrombin with Clarke-Freeman electrophoresis in 26 patients with acute viral hepatitis (21 HBS-AG positive) who did not suffer from vitamin K deficiency. Prothrombin and the vitamin-K dependent Factors VII, IX, and X were determined by standard coagulometric methods. Prothrombin was additionally estimated by immunoelectrophoresis according to Laurell. Three patients with acute HBS-AG positive hepatitis showed preprothrombin in their plasma. The activity of Factors II, VII, IX, and X was slightly below normal with normal concentration of Factor II in the immunoelectrophoresis. Liver parenchymal damage and cholestasis were slight; the pseudocholinesterase showed subnormal levels in all three patients. Possible causes for the appearance of preprothrombin in the peripheral blood in acute viral hepatitis and the possible connections with liver cell damage are discussed.
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PMID:[Preprothrombin in acute viral hepatitis B]. 717 63