I'd like to speak from the standpoint of view in both recently applicable diagnosis of coagulofibrinosis, hepatic fibrosis and hepatitis-related virus markers and the therapy of abnormal coagulofibrinolysis, plasma aminoacids, also as of Interferon.
The coagulofibrinolysis-related tests ought to be more highly appreciated from the pathophysiological standpoint of diagnosis, prediction of severity and prognosis of liver diseases (eg. DIC). Such as thrombomodulin, thrombin-antithrombin complex (TAT), tissue-plasminogen activator (t-PA), plasmin-plasmin inhivitor (PIP) are included.
As to the therapy, methyl gabexate (FOY
®) which has both pharmatheutical effects of antithrombin and anti-plasmin is better to be used to prevent the development to severe liver damage from the earlier stage.
Prolyl hydroxylase, procollagen typeIII peptide (PIIIP), typeIV collagen are excellent parametersto reflect directly the hepatic fibrogenesis and fibrosis, instead of ZTT, γ-globulin
In cases of severe liver diseases, aromatic aminoacid (AAA) is decresed, on the other hand branched amino acid (BCAA) is increased, resulting to decrease in BCAA/AAA ratio. BCAA is synthesized to glutamine in the muscle and metabolized to alanine and ammonia. BCAA administration improves the plasma aminoacid unbalance, albumin, Ch-E, total cholesterol and levels conciousness disturbance in chronic severe liver diseases.
The effects of Interferon on chronic B, C-hepatitis are influenced with the factors of virus copies, genotype, variation (hypervariable region) from virus side, and from host side, hepatic tissue stage, age, immunological responce.
On the administration, above mentioned factors shoud be taken into a consideration comprehensively.
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