Abstract
When operationally defined as an excess of immunoassayable fibrinogen (IAF) over thrombin-clottable fibrinogen (TCF) of ≥ 1 g per L, dysfibrinogenaemia (DF) is demonstrable in more than 1/3 of patients with chronic liver diseases (CLD)1. Some features of this protein suggest a similarity to fetal fibrinogen.2 To further pursue these investigations, it was deemed necessary to identify a population of very young patients who were synthesizing fibrinogen rapidly. Twenty (2C Infected neonates, of gestational ages 24-41 weeks, were selected for study on the basic of TCF levels ≥5 g per L, Using antisera raised in sheep and rabbits, there was no demonstrable excess of IAF in the same plasma samples. Similar data were obtained fron assays in an unselected aeries of umbilical cord plasmas. These findings suggest either thet DF in CLD is not due to the renewed synthesis of fetal fibrinogen, or that fetal fibrinogen, like alpha-fetoprotein and fetal pre-albumin,3 is physiologically I evident only during early embryonic development.1. Barr, R.D. et al. J. Clin. Path. (1978) 31, 89.2. Barr, R.D. Blomedlcine (1979) in press.3. Tatarinov, Y, S. et al. Lancet (1978) 2, 1122.
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