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Updated: Nov 19, 2025

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Compensated hypogonadism in men with sickle cell disease
Anna Paloma M R Ribeiro1, Caroline S Silva1, Jean Carlos C Zambrano1
1Division of Public Health, Department of Health, State University of Feira de Santana, Feira de Santana, Bahia, Brazil.
Insights
Compensated hypogonadism is prevalent in men with sickle cell disease (SCD). This condition, characterized by normal testosterone and elevated luteinizing hormone (LH), requires further investigation and monitoring in SCD patients.
Area of Science:
- Endocrinology
- Hematology
- Men's Health
Background:
- Sickle cell disease (SCD) is linked to hypogonadism, but its causes and effects remain debated.
- Hypogonadism in SCD can impact patient health and quality of life.
Purpose of the Study:
- To determine the prevalence of hypogonadism in men with SCD.
- To investigate the underlying causes of hypogonadism in this population.
Main Methods:
- A cross-sectional study involving 34 adult men with SCD.
- Measurement of total testosterone, free testosterone, LH, and FSH levels.
- Classification of hypogonadism based on testosterone and LH levels.
Main Results:
- The study found a high prevalence of compensated hypogonadism (26.4%) and eugonadism (67.5%).
- No cases of primary hypogonadism were observed.
- Compensated hypogonadism was associated with elevated FSH levels.
Conclusions:
- Compensated hypogonadism is a significant finding in men with SCD.
- This distinct clinical entity warrants further research and clinical attention.
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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