Abstract
Factor X a-inhibitor (X a-I) activity was measured in twenty patients with alcoholic liver disease and found to be more than 3 standard deviations below normal in fourteen patients. When trace amounts of heparin were added to these plasmas, the X a-I activity was potentiated to the same level as normal plasma with heparin added. This suggests that X a-I is actually present in alcoholic liver disease, but has less than normal activity. Possible explanations such as the lack of endogenous heparin or the presence of an inhibitor are discussed.
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