Late presentation of hyperandrogenism in pregnancy: clinical features and differential diagnosis

Abstract

SummaryBackgroundHyperandrogenic states in pregnancy are rare but arise most commonly due to new-onset ovarian pathology in pregnancy. We describe the case of a young woman who presented in the latter half of her pregnancy with features of hyperandrogenism. We review the biochemical and imaging findings and discuss the differential diagnosis.Case presentationA 26-year-old woman presented in the later part of her pregnancy with widespread hirsutism. Biochemical testing confirmed hyperandrogenism (testosterone, 13.7 nmol/l and second-trimester pregnancy range, 0.9–4.9 nmol/l), although she had no history of menstrual disturbance, hirsutism or acne prior to conception. Radiological evaluation (ultrasound and magnetic resonance imaging) revealed multiple cystic lesions in both ovaries, leading to a presumptive diagnosis of hyperreactio luteinalis (HL). The implications of maternal hyperandrogenism on foetal virilisation were considered and the patient was counselled appropriately. She delivered a healthy baby boy uneventfully. Androgen levels, hirsutism and acne normalised within a few weeks of delivery.ConclusionHL can occur at any stage of pregnancy and is an important differential diagnosis in pregnant patients with features of androgen excess. Most cases regress spontaneously after delivery and major interventions are usually not needed.Learning points Hyperandrogenism in pregnancy is rare.Clinical features are similar to the non-pregnant state in the mother but virilisation in the foetus can have profound consequences.HL and pregnancy luteoma are the most common ovarian pathologies leading to hyperandrogenism in pregnancy.Spontaneous regression occurs in the post-partum period in the vast majority of cases and surgery is only required for local complications.

Neonatal Hairy Ear Pinnae and Gestational Diabetes: Just a Coincidence?

“…This is a benign, ethnically related condition that does not need any medical intervention. Other conditions, such as diffuse neonatal hypertrichosis in newborns, may be related to maternal hyperandrogenism, which in turn may be linked to polycystic ovarian syndrome and potentially associated with type 1 maternal diabetes, although ear pinnae hypertrichosis has not been described in this setting.…”

Polymorphism of CAG and GGN repeats of androgen receptor gene in women with polycystic ovary syndrome

“…The 2003 Rotterdam consensus workshop concluded that PCOS was a syndrome with two out of three criteria: (i) oligoor anovulation; (ii) clinical and/or biochemical signs of hyperandrogenism; and (iii) polycystic ovaries (PCO) of ultrasound imaging (with the exclusion of other aetiologies) (Rotterdam, 2004). Hyperandrogenism often presents abnormal biochemical parameters (elevated serum concentrations of testosterone, free testosterone, androstenedione, dehydroepiandrosterone sulphate) (Gluszak et al, 2012), and/or clinical signs (acne, hirsutism, seborrhea, androgenic alopecia, virilization) (Das et al, 2013). The mechanism of hyperandrogenism is still unclear, although the ovarian origin of androgen is well studied (Schweighofer et al, 2012).…”