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Fibrinogen in Liver Disease
JACOB FINE, MD
Stanford, Calif
Arch Surg. 1975;110(7):848.
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To the Editor.—In the December 1974 issue of the ARCHIVES (109:741), E. N. Wardle presents data that confirm previous reports showing a high correlation between the development of endotoxemia and the hemorrhagic complications of major injury to the liver. One can account for this effect of endotoxin by its capacity to aggregate platelets and, thus, release vasoactive agents that can cause the endotoxemia and become self-sustaining. Dr. Wardle refers to the report by Das et al that states that endotoxin binds to platelets by virtue of the fact that the larger fraction, if not all, of the circulating endotoxin is found in platelet-rich and not in platelet-poor plasma. Since we could not, in a joint study with Deykin (unpublished data), confirm the alleged binding of endotoxin to the platelets, it appears that the data of Das et al reflect the variation in particle size of circulating endotoxin. Thus, the
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