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Maternal and female fetal virilization caused by pregnancy luteomas

2005; Elsevier BV; Volume: 84; Issue: 2 Linguagem: Inglês

10.1016/j.fertnstert.2005.02.029

1556-5653

Yu-Chi Wang, Her‐Young Su, Jah-Yao Liu, Fung-Wei Chang, Chi‐Huang Chen,

Urologic and reproductive health conditions

ObjectiveTo present the maternal and female fetal virilization caused by excessive androgen secretion of pregnancy luteomas.DesignCase report.SettingUniversity-based teaching hospital.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. Without prompt surgical intervention, the maternal hyperandrogenemia returned to a normal level and regression of bilateral ovarian tumors occurred spontaneously after 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.Intervention(s)Noninvasive imaging assessment.Main Outcome Measure(s)Maternal and female fetal virilization.Result(s)Regression of androgen-secreting pregnancy luteomas and hyperandrogenism during the puerperium but apparent female fetal clitoral hypertrophy.Conclusion(s)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 natural course of pregnancy luteomas, not true neoplasms. To present the maternal and female fetal virilization caused by excessive androgen secretion of pregnancy luteomas. Case report. University-based teaching hospital. A nulligravida woman suffering from bilateral hydronephrosis and recurrent acute pyelonephritis caused by bilateral solid ovarian tumors presented virilization during the third trimester. Without prompt surgical intervention, the maternal hyperandrogenemia returned to a normal level and regression of bilateral ovarian tumors occurred spontaneously after 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. Noninvasive imaging assessment. Maternal and female fetal virilization. Regression of androgen-secreting pregnancy luteomas and hyperandrogenism during the puerperium but apparent female fetal clitoral hypertrophy. 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 natural course of pregnancy luteomas, not true neoplasms.