Endocrine Abstracts

Objective: Maternal and female fetal virilization is subject to exaggerating androgen secretion of pregnancy luteomas which is associated with the protective capacity of placenta safeguard against hormone conversion and presents with variable extent of female pesudohermapharotidism as exposure in critical gestational stage.

Patient(s): A nulligravida woman suffering from bilateral hydronephrosis and recurrent acute pyelonephritis caused by bilateral solid ovarian tumors presented virilization during the third trimester. The serum testerosterone levels revealed as high as 200-fold the levels of the normal female. Without prompt surgical intervention, the maternal hyperandrogenemia returned to a normal level and regression of bilateral ovarian tumors spontaneously until a female fetus with clitoral hypertrophy and temporal hyperandrogenemia was delivered. In spite of lacking histology, the clinical course is compared to that of pregnancy luteomas.

Result(s): Regression of androgen-secreting pregnancy luteomas and hyperandrogenism occurred during the puerperium but apparent female fetal clitoral hypertrophy.

Conclusion(s): During pregnancy, exposure to excessive androgen at the critical 9–14 week period leads to variable masculinization in female infant. It has been hypothesized that the placenta is protective in this regard, by virtue of its high capacity to convert androgens to estrogen. Thus, a female fetus is usually not affected. However, the present observations – where the female fetus had exposed to maternal hyperandrogenemia to yield clitoral hypertrophy without affecting the labioscrotal fold due to beyond the critical 9–14th week for external genitalia differentiation. The maternal and female fetal virilization was caused by exaggerating androgen secretion of bilateral ovarian solid tumors. Spontaneous regression of ovarian tumors and hyperandrogenemia during the puerperium is the nature course of pregnancy luteoma, not true neoplasms.