Decompensated portal cirrhosis. Effects of large doses of phytonadione

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Abstract
These studies reaffirm the ineffectiveness of vitamin K1 (phytonadione) in the correction of the pro-thrombin time in patients with extensive hepatic parenchymal disease. It is suggested that, whereas there is no justification of the administration of phytonadione in these cases, there appears to be no definite evidence to confirm the claim that prolonged administration of large doses of this vitamin to the adult will increase hepatic damage, produce hemorrhage, or have other untoward effects on the patient. If improvement does take place on long-term vitamin K therapy, it may very well be due to spontaneous improvement in hepatic parenchymal function rather than to the drug. Where significant depression of the prothrom-bin time does occur, available data suggest that it is probably due to continued liver degeneration, with or without added metabolic insult, and is not due to toxic effects of the vitamin. The transient increase in prothrombin time sometimes seen in the early phase of therapy with large doses of vitamin K results from a parallel fall in blood concentration of factors II, V, VII, and X.

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