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From the evidence presented, it is proposed that 'dysfibrinogenaemia' represents the production of normal fetal fibrinogen by rapidly proliferating liver cells in both regenerating and neoplastic tissue. Prolongation of the reptilase clotting time, which was formerly believed to reflect dysfibrinogenaemia, may be rather the result of hepatocytic death.
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Barr et al. (1978) studied this question.
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