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Background: The fetus lacks 3ß-hydroxysteroiddehydrogenase (3ß-HSD) activity until the last trimenon (requiring placental progesterone) and active cortisol concentration is regulated by synthesis through 11ß-hydroxylase and inactivation by 11ß-hydroxysteroiddehydrogenase (11ß-HSD). In this study we estimate enzyme activity of 3ß-HSD and 11ß-HSD in preterm infants. Method: A 24-hour profile of glucocorticoid metabolites was obtained in the urine of 61 preterm infants of < 28 wks GA and 81 preterm infants >= 32 wks GA using gaschromatography-masspectrometry (GC-MS). Enzyme activity was calculated using substrate/product ratios. Results: There was no influence of severity of disease on enzyme activity on day 3 and week 3 of life, but significant influence of postnatal age and gestational age (p = 0.019; p < 0.001). Patients < 28 wks GA in contrast to the patients >= 32 wks displayed a significant increase in 3ß-HSD activity from day 3 (median 11.73; IQR 6.20 18.53) to week 3(7.69; 4.70 9.75). 11ß-HSD activity decreased postnatally until the third week of life to the level of more mature patients. Conclusion: Severity of illness had no significant influence on 3ß-HSD and 11ß-HSD activity in preterms. Instead there is significant increase in 3ß-HSD activity in preterms < 28 wks during the first three weeks postnatal and reduced inactivation of active cortisol. Introduction Immaturity of steroid biosynthesis is assumed to cause relative adrenal insufficiency in preterm infants [1]. Even if the rate-limiting step is still unclear the current knowledge allows identifying several candidate enzymes [2]. The most interesting enzyme is the 3ß-hydroxysteroiddehydrogenase (3ß-HSD), which is necessary to produce cortisol from cholesterol or pregnenolone. None of the zones of the adrenal cortex expresses 3ß-HSD before 23 wks of gestation and it is generally assumed that the fetus does not produce cortisol de novo until about 30 wks [2]. Excluding a recently described short period in the first trimester [3] fetal cortisol production depends on supply of progesterone by the placenta to bypass 3ß-hydroxysteroiddehydrogenase [2].

Enzyme Activity of 3ß-HSD and 11ß-HSD as Important Indicators of Steroid Bio-Synthesis and Inactivation in Preterm Infants