Luteinizing hormone supression and snoring as predictors of testosterone therapy-induced erythrocytosis in individuals with differences of sex development

Batatinha Julio Americo Pereira; Mesia Maria Jimena Chafloque; Stefano Alvarenga Galliano; Batgista Rafael Loch; Mendonca Berenice Bilharinho; Sorahia Domenice

doi:10.1530/endoabs.118.PO70

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Endocrine Abstracts (2026) 118 PO70 | DOI: 10.1530/endoabs.118.PO70

IDSD2026 Poster Abstracts Poster Abstracts (93 abstracts)

Luteinizing hormone supression and snoring as predictors of testosterone therapy-induced erythrocytosis in individuals with differences of sex development

Julio Americo Pereira Batatinha ¹ , Maria Jimena Chafloque Mesia ¹ , Stefano Alvarenga Galliano ¹ , Rafael Loch Batgista ^1,2 , Berenice Bilharinho Mendonca ^1,2 & Sorahia Domenice ^1,2

Author affiliations

¹Universidade de São Paulo, São Paulo, Brazil,; ²Disciplina de Endocrinologia e Metabologia, Laboratorio de Hormonios e Genetica Molecular/LIM42, São Paulo, Brazil

Background: Testosterone therapy (TT) is essential for individuals with Differences of Sex Development (DSD) requiring androgen replacement, but carries the risk of erythrocytosis, which increases cardiovascular and thrombotic risk. Risk factors for TT-induced erythrocytosis in this population remain incompletely characterized.

Objective: To evaluate the prevalence of erythrocytosis and identify clinical and laboratory predictors in a cohort of individuals with DSD undergoing TT.

Methods: This retrospective cohort study included 57 adult individuals with DSD receiving testosterone. Erythrocytosis was defined as hematocrit >50%. Clinical, anthropometric, and laboratory variables were compared between erythrocytosis and non-erythrocytosis groups. Univariate logistic regression was performed to identify predictors of erythrocytosis.

Results: Erythrocytosis was identified in 17 of 57 individuals (29.8%). Groups did not statistically differ in karyotype distribution (despite higher erythrocytosis rate on 46,XX individuals), BMI, age at TT onset, or EPO levels. The erythrocytosis group showed significantly higher absolute reticulocyte counts (P =0.015), reticulocyte percentage (P =0.047), and lower LH levels (0.2 vs. 5.6 mIU/mL, P=0.004), with no difference in testosterone levels. Snoring was markedly more prevalent in the erythrocytosis group (66.7% vs. 16.7%, P =0.003). On univariate logistic regression, snoring was the only significant predictor of erythrocytosis (OR=9.46; P =0.007). Testosterone formulation showed a trend toward significance, with cypionate use more frequent than undecanoate in the erythrocytosis group (88.2% vs. 62.5%, P =0.064). Of the 8 patients who underwent polysomnography, 50% were diagnosed with OSAS.

Conclusion: In this cohort of DSD individuals on TT, erythrocytosis prevalence was 29.8%, a rate comparable to that reported in cisgender male cohorts without DSD. Snoring emerged as a strong and independent predictor of erythrocytosis (OR≈9.5), reinforcing OSAS as a key modifiable risk factor in this population. Deeper LH suppression in the erythrocytosis group suggests gonadotropin axis suppression, highlighting the need for individualized dosing, as testosterone levels alone may not be sufficient. Clinicians should actively screen for snoring and OSAS when managing TT in DSD individuals to optimize treatment safety; LH may further serve as a marker of excessive testosterone dosing in this population.