2021Clinical EndocrinologyRequires access

Compensated hypogonadism in men with sickle cell disease

Anna Paloma Martins Rocha Ribeiro, Caroline Santos Silva, Jean Carlos Zambrano Contreras, Juliana de Oliveira Freitas Miranda, Carlos A. Molina, Cristiano Mendes Gomes, Eduardo Miranda, José de Bessa

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Abstract

OBJECTIVE: To evaluate the prevalence of hypogonadism in a population of men with SCD and characterize its aetiology. Sickle cell disease (SCD) is associated with the development of hypogonadism, but there is still controversy regarding its aetiology and clinical implications. METHODS: We performed a cross-sectional study of 34 men with SCD aged > 18 years. Sociodemographic and clinical data, including anthropometric measurements (weight, height and BMI), were obtained. Early morning, blood samples were collected and total testosterone (TT), free testosterone (FT), luteinizing hormone (LH), follicle stimulating hormone (FSH), a complete blood count and haemoglobin electrophoresis were measured. Eugonadism was defined as T ≥300 ng/dL and LH ≤9.4 mUI/mL; primary hypogonadism as T < 300 ng/dL and LH > 9.4 mUI/mL; secondary hypogonadism as T < 300 ng/dL and LH ≤ 9.4 mUI/mL; and compensated hypogonadism as T ≥ 300 ng/dL and LH > 9.4 mUI/mL. RESULTS: Median age was 33 (26-41) years, and SS genotype was the most frequent (73.5%). The prevalence of eugonadism, compensated hypogonadism and secondary hypogonadism was 67.5%, 26.4% and 5.88%, respectively. No men with primary hypogonadism were identified in our sample. Those with compensated hypogonadism had also higher FSH levels (>7.8 mUI/mL, P < .0001). CONCLUSION: In our study population of men with SCD, a high prevalence of compensated hypogonadism was identified, which is a controversial and distinct clinical entity that warrants monitoring and further research.

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What this paper is about

OBJECTIVE: To evaluate the prevalence of hypogonadism in a population of men with SCD and characterize its aetiology. Sickle cell disease (SCD) is associated with the development of hypogonadism, but there is still controversy regarding its aetiology and clinical implications. METHODS: We performed a cross-sectional study of 34 men with SCD aged > 18 years. Sociodemographic and clinical data, including anthropometric measurements (weight, height and BMI), were obtained. Early morning, blood samples were collected and total testosterone (TT), free testosterone (FT), luteinizing hormone (LH), follicle stimulating hormone (FSH), a complete blood count and haemoglobin electrophoresis were measured. Eugonadism was defined as T ≥300 ng/dL and LH ≤9.4 mUI/mL; primary hypogonadism as T < 300 ng/dL and LH > 9.4 mUI/mL; secondary hypogonadism as T < 300 ng/dL and LH ≤ 9.4 mUI/mL; and compensated hypogonadism as T ≥ 300 ng/dL and LH > 9.4 mUI/mL. RESULTS: Median age was 33 (26-41) years, and SS genotype was the most frequent (73.5%). The prevalence of eugonadism, compensated hypogonadism and secondary hypogonadism was 67.5%, 26.4% and 5.88%, respectively. No men with primary hypogonadism were identified in our sample. Those with compensated hypogonadism had also higher FSH levels (>7.8 mUI/mL, P < .0001). CONCLUSION: In our study population of men with SCD, a high prevalence of compensated hypogonadism was identified, which is a controversial and distinct clinical entity that warrants monitoring and further research.

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Available abstract

OBJECTIVE: To evaluate the prevalence of hypogonadism in a population of men with SCD and characterize its aetiology. Sickle cell disease (SCD) is associated with the development of hypogonadism, but there is still controversy regarding its aetiology and clinical implications. METHODS: We performed a cross-sectional study of 34 men with SCD aged > 18 years. Sociodemographic and clinical data, including anthropometric measurements (weight, height and BMI), were obtained. Early morning, blood samples were collected and total testosterone (TT), free testosterone (FT), luteinizing hormone (LH), follicle stimulating hormone (FSH), a complete blood count and haemoglobin electrophoresis were measured. Eugonadism was defined as T ≥300 ng/dL and LH ≤9.4 mUI/mL; primary hypogonadism as T < 300 ng/dL and LH > 9.4 mUI/mL; secondary hypogonadism as T < 300 ng/dL and LH ≤ 9.4 mUI/mL; and compensated hypogonadism as T ≥ 300 ng/dL and LH > 9.4 mUI/mL. RESULTS: Median age was 33 (26-41) years, and SS genotype was the most frequent (73.5%). The prevalence of eugonadism, compensated hypogonadism and secondary hypogonadism was 67.5%, 26.4% and 5.88%, respectively. No men with primary hypogonadism were identified in our sample. Those with compensated hypogonadism had also higher FSH levels (>7.8 mUI/mL, P < .0001). CONCLUSION: In our study population of men with SCD, a high prevalence of compensated hypogonadism was identified, which is a controversial and distinct clinical entity that warrants monitoring and further research.

Key concepts: Medicine, Testosterone (patch), Internal medicine, Luteinizing hormone, Anthropometry, Endocrinology, Population, Morning

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