Retention hyperbilirubinemia

Depending on the type of bilirubin present in plasma—ie, unconjugated or conjugated—hyperbihru-binemia may be classified as retention hyperbilirubinemia, due to overproduction, or regurgitation hyperbilirubinemia, due to reflux into the bloodstream because of bihary obstmction. 

One needs to keep in mind that the use of drugs by the mother will sometimes lead to impairment of the activity of bilirubin-UDP-glucuronyltransferase. Phenothiazines are an example of this kind of interaction. The use of drugs in the neonatal intensive care unit also can contribute to hyperbilirubinemia. Usually, the medications that compete for binding sites on albumin are the culprits in this case (see section on Bilburin Transport). An example of this type of interaction is the use of furosimide, which is a diuretic used to decrease fluid retention and improve cardiac function and renal output. 

Norethandrolone, methyltestosterone, and other 17a-alkyl substituted testosterone-like steroids increase the plasma retention of BSP in man (A16, H6, K14, L6) and sometimes cause hyperbilirubinemia (A16, A17) and elevation of alkaline phosphatase (H6). However, the retention of indocyanine green is not affected by norethandrolone (L6). Natural estrogens in very high dosage also increase the plasma retention of BSP in man (M33) and in rats (G2). Steroidal oral contraceptives in therapeutic dosage have a similar effect in a proportion of women (A6, LI). In the child-bearing age, these rarely produce other biochemical signs of liver dysfunction (R7, R8), but in postmenopausal women the effect of oral contraceptives on liver function tends to be more frequent and more severe (E3, P3). 

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