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Dorte Glintborg, Guy T'Sjoen, Pernille Ravn, and Marianne Skovsager Andersen

Transgender women are assigned male at birth, but identify as women. The incidence of gender dysphoria is estimated to be around 1% of the population. Gender dysphoria may be associated with depression and low quality of life, which in most cases improves during gender affirming hormonal treatment (GAHT). Feminizing hormonal treatment for transgender women or gender non-binary people typically includes natural estrogen (estradiol). Additional testosterone-blocking treatment is often needed to ensure suppression of the pituitary gonadal axis and may include cyproterone acetate, a gonadotropin releasing hormone agonist (GnRH-a) or spironolactone. The health risks of cyproterone acetate as anti-androgen treatment are debated and randomized protocols with other anti-androgen treatments are requested. Orchiectomy is performed in some transgender women after various duration of GAHT. Currently, natural progesterone is not recommended as part of GAHT due to limited knowledge on the balance between risks and benefits.

In the present article we discuss evidence regarding established and upcoming feminizing treatment for adult transgender women or for gender non-binary people seeking feminization. Data on study populations with transgender women are put into a wider context of literature regarding effects of sex steroid hormones in cisgender study populations. Relevant follow up and monitoring during feminizing treatment is debated. The review has special focus on the pharmacotherapy of feminizing hormonal therapy.

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Maria Othelie Underdal, Øyvind Salvesen, Anne Schmedes, Marianne Skovsager Andersen, and Eszter Vanky


To explore whether gestational prolactin and breast increase are markers of metabolic health in pregnancy and on long-term, in PCOS.


Follow-up study. Women with PCOS, according to the Rotterdam criteria (n = 239), former participants of the randomized controlled trial (RCT) PregMet were invited, 131 participated in the current follow-up study, at mean 8 years after pregnancy.


Metformin 2000 mg/day or placebo from first trimester to delivery in the original RCT. No intervention in the current study.

Prolactin was analyzed in the first trimester and at gestational week 32 and metabolic characteristics which are part of the metabolic syndrome and measures of glucose homeostasis were examined. Metabolic health was also evaluated according to breast increase versus lack of breast increase during pregnancy.


Prolactin increase in pregnancy was negatively correlated to BMI (P = 0.007) and systolic blood pressure (P ≤ 0.001) in gestational week 32. Prolactin at gestational week 32 was negatively correlated to BMI (P = 0.044) and visceral fat area (P = 0.028) at 8-year follow-up in an unadjusted model. Prolactin at gestational week 32 showed no associations to metabolic health at follow-up when baseline BMI was adjusted for. Women who reported lack of breast increase during pregnancy, had higher BMI (P = 0.034), waist-hip ratio (P = 0.004), visceral fat area (P = 0.050), total cholesterol (P = 0.022), systolic (P = 0.027) and diastolic blood pressure (P = 0.011) at 8-year follow-up.


High prolactin levels and breast increase in pregnancy were associated with a more favorable long-term metabolic health in women with PCOS. Both prolactin and breast increase may be mediated by gestational BMI.

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Martin Overgaard, Dorte Glintborg, Henrik Thybo Christesen, Tina Kold Jensen, and Marianne Skovsager Andersen


Low circulating prolactin is a potential marker of metabolic risk during pregnancy. We aimed to investigate associations between prolactin and glucose status in pregnant women with and without gestational diabetes mellitus (GDM) or polycystic ovary syndrome (PCOS).


Prospective observational cohort study. From the Odense Child Cohort, 1497 pregnant women were included.


Blood samples were assessed during first, second (prolactin, hemoglobin A1c (HbA1c)) and third trimester (fasting prolactin, testosterone, HbA1c, insulin, glucose). Oral glucose tolerance test (OGTT) was performed around gestation week 28 in 350 women with risk factors for GDM and in 272 randomly included women. GDM was defined by 2-h plasma glucose ≥9.0 mmol/L.


The median (IQR) prolactin increased from 633 (451–829) mIU/L in first–second trimester to 5223 (4151–6127) mIU/L at third trimester. Prolactin was inversely associated with HbA1c in first (r = −0.19, P < 0.001) and third trimester (r = −0.07, P = 0.014). In third trimester, women with GDM (n = 37; 6.0%) had lower prolactin compared to women without GDM (4269 vs 5072 mIU/L, P = 0.004). Third trimester prolactin multiple of the median (MoM) was inversely associated with risk of GDM in multivariate regression analysis (OR 0.30, P = 0.034). PCOS was diagnosed in 10.0% (n = 146). Early pregnancy prolactin MoM was positively associated to PCOS diagnosis (OR 1.38, P = 0.051).


Low prolactin levels during pregnancy were associated with higher HbA1c and risk of GDM. A diagnosis of PCOS was associated with higher early pregnancy prolactin levels.