Summary The distribution of bilirubin in the body has been described in terms of diffusion equilibria and competitive binding of tissue elements for the circulating bilirubin which is chemically dissociated from albumin. The supposition was made that only dissociated bilirubin can gain access to intracellular fluid by permeation of cell membranes. The amount of bilirubin diffusing into cell fluid is then dependent upon the concentration gradient of dissociated bilirubin across cell membranes rather than total bilirubin concentration. It was shown that the dissociated bilirubin concentration can be increased in extracellular fluids independently of total bilirubin concentration by reducing the binding capacity of plasma proteins for bilirubin. This situation occurs clinically (1) in premature babies who have a relative hypoalbuminemia, and (2) in some newborn infants whose plasma contains substances which reduce the bilirubin binding capacity of albumin. Such substances are hematin, sulfonamides, salicylate, caffeine sodium benzoate, and increased hydrogen ion concentration. By increasing the circulating albumin concentration, it was shown that the administered albumin will increase the total plasma bilirubin concentration by causing a shift of bilirubin from the extravascular tissues into the plasma. The potential therapeutic value of such a procedure was discussed but requires further study before it can be recommended.

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bilirubin binding capacity concentration gradient cell membranes total plasma bilirubin proteins tissue elements diffusion equilibria

Gerard B. Odell,.The dissociation of bilirubin from albumin and its clinical implications. 55 (3),268-279.

Gerard B. Odell,"The dissociation of bilirubin from albumin and its clinical implications" 55

Gerard B. Odell,"The dissociation of bilirubin from albumin and its clinical implications"