Background |
The steroid hormone 17-OH-progesterone (17OHP) is produced in the adrenal cortex and in the gonads. Gestagenic effects exerted by 17OHP are small. Nevertheless, this hormone is of clinical significance because it represents the ultimate precursor of 11 beta-desoxycortisol (compounds, CpS). CpS is formed by hydroxylation of the carbon atom C 21. Enzyme activity of 21-hydroxylase in the adrenal cortex may thus be monitored by analyzing the level of 17OHP in the blood. Deficiencies in 21-hydroxylase, most commonly found in congenital adrenal hyperplasia, result in excessive secretion of 17OHP and consequently in enhanced blood levels. Deficiencies in 11-hydroxlase, however, merely lead to moderately increased values of 17OHP. The analysis of this steroid hormone, therefore, plays a significant role in the differential diagnosis of congenital adrenal hyperplasia. In adult non-pregnant women, 17OHP levels in the blood depend on the phase of the menstrual cycle. Like progesterone, 17OHP is secreted by the mature follicle and the corpus luteum. Concentrations are generally higher after ovulation. In addition, levels of 17OHP are influenced by daytime rhythms which correlate with the adrenal secretion of cortisol. Maximal levels are found in samples collected between midnight and 8.00 a.m. In adult men, there are few indications of similar fluctuations of 17OHP levels. During pregnancy, large amounts of 17OHP are produced by the fetus, the placenta and the adrenal cortex. The hormone is secreted into the fetal and the maternal blood circulation. Maternal values of 17OHP strongly increase after the 32nd week of pregnancy reaching 4-fold higher levels than during the luteal phase of the menstrual cycle. 17OHP may also be found in the umbilical cord of newborns. |
