A 32-year-old woman, gravida 2 para 1, at 18 weeks gestation comes to the office for her first prenatal visit. She has noticed new facial hair and acne over the past few weeks. The patient has had no vaginal bleeding or abdominal pain. Some mild nausea earlier in the pregnancy has resolved. The patient has had no vomiting and is eating 5 small meals a day. Her prepregnancy BMI was 24 kg/m2 and she has gained 2.3 kg (5 lb) over the past 2 months. Examination shows acne on her chest and back and coarse hair in the distribution of the upper lip, chin, periareolar area, chest, and lower abdomen. The uterus is nontender and fundal height is 2 cm below the umbilicus. Ultrasonogram shows an intrauterine gestation consistent with dates and bilateral 7-cm solid masses in the ovaries. Which of the following is the best next step in management of this patient?
Causes of hyperandrogenism in pregnancy | |
Diagnosis | Clinical features |
Placental |
|
Luteoma |
|
Theca lutein |
|
Sertoli-Leydig |
|
This patient has new-onset hyperandrogenism during pregnancy (ie, gestational hyperandrogenism) based on the acne and male-pattern terminal hair. Gestational hyperandrogenism arises from either maternal (eg, ovarian masses) or fetal (eg, placental aromatase deficiency) sources that result in maternal and possible fetal virilization. This patient's hyperandrogenism is due to benign ovarian tumors, which typically present as bilateral ovarian masses on ultrasound. The most common benign ovarian tumors resulting in gestational hyperandrogenism are luteomas of pregnancy and theca lutein cysts.
Luteomas of pregnancy, as seen in this patient, often appear as solid, bilateral ovarian masses on ultrasound. Elevated β-hCG levels stimulate the luteoma (composed of large lutein cells) to release androgens, which may cause maternal virilization; some patients are asymptomatic. Women who develop virilization symptoms are at high risk of delivering a female fetus with virilization.
Theca lutein cysts are cystic, bilateral ovarian masses that occur from ovarian hyperstimulation secondary to markedly elevated β-hCG levels (eg, hydatidiform mole, multiple gestation). Theca lutein cysts may cause maternal virilization; however, there is a low risk of female fetal virilization.
Management of bilateral, benign ovarian masses is observation and expectant management, as the masses and symptoms resolve spontaneously after delivery due to falling β-hCG levels.
(Choice A) Polycystic ovary syndrome causes hyperandrogenism, anovulation (eg, oligomenorrhea), and infertility in nonpregnant women. Clomiphene is a first-line infertility treatment in these patients but is not used during pregnancy. However, this diagnosis is unlikely in this patient, as the hirsutism and acne would likely predate the pregnancy and polycystic ovaries would likely be seen on ultrasound.
(Choices B and C) Surgery with either an ovarian biopsy or oophorectomy may be indicated if a malignant ovarian tumor is suspected. Sertoli-Leydig tumors secrete testosterone, which can result in virilization. In contrast to the masses in this patient, these tumors often appear as unilateral, solid, complex masses on ultrasound.
(Choice E) Suction curettage is indicated if a complete hydatidiform mole is seen on ultrasound (eg, "snowstorm" appearance). This patient has a normal intrauterine gestation.
Educational objective:
Hyperandrogenism in pregnancy is commonly due to benign, bilateral ovarian masses such as luteomas and theca lutein cysts. Patients with virilization during pregnancy and bilateral ovarian masses are observed and managed expectantly, as the symptoms and masses spontaneously regress after delivery.