BREAST MILK JAUNDICE REVISITED: NO ROLE FOR B-GLOCORONIDASE OR “UNSTIMULATED LIPASE”

Abstract

To date, the milk factor(s) repsonsible for breast milk jaundice (BMJ) has not been found. The lipases of human milk, lipoprotein lipase (LPL) and bile salt-stimulated lipase (BSSL), require specific activators, apoprotein CII for LPL and primary bile salts for BSSL. It has been suggested that, in BMJ milks, one or both lipases are active in the absence of activator [unstimulated lipase activity (USL) (Pediatr Res 14:1328, 1980)]. More recently, It has been reported that milk β-glucuronldase (β-glu) may be the causative agent (Lancet 1:644, 1986). We have reexamined these questions by analyzing β-glu activity and lipase activity [using highly sensitive techniques (Biochim Biophys Acta 878:209, 1986) for quantitation of stimulated and unstimulated LPL and BSSL activity] in milk samples from 13 mothers of infants with BMJ and 4 mothers of healthy infants. The following results (means and ranges, expressed as umol free fatty acids/min/ml milk for lipases and modified Sigma units/ml for β-glu) were obtained: Within-feed variation in milk collection does not affect the level of β-glu, the activity being 100 (48-189), 115 (48-233), and 132 (54-230) units in fore, mid and hind milk, respectively. These data show that the levels of β-glu, BSSL, LPL and USL activity are not higher in BMJ than in normal milks; therefore, a role for these enzymes in the etiology of BMJ is unlikely. (Supported by NIH grant HO 20833.)