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Updated: Apr 21, 2026

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Is testosterone deficiency a possible risk factor for priapism associated with sickle-cell disease?
Belinda F Morrison1, Uzoma A Anele, Marvin E Reid
1Department of Surgery, University of the West Indies, Mona, Jamaica.
Insights
Testosterone deficiency is common in men with sickle cell disease (SCD). This study found no direct link between testosterone deficiency and priapism in adult men with SCD.
Area of Science:
- Andrology
- Hematology
- Endocrinology
Background:
- Sickle cell disease (SCD) is a genetic blood disorder.
- Priapism and testosterone deficiency are potential complications in men with SCD.
Purpose of the Study:
- To investigate the association between testosterone deficiency and priapism in adult men diagnosed with sickle cell disease.
Main Methods:
- A cross-sectional study involving 50 adult men with SCD (hemoglobin SS).
- Collected blood samples for total and free testosterone, FSH, LH, prolactin, lipids, LDH, and hematological indices.
- Utilized an interviewer-administered questionnaire to assess priapism history; defined testosterone deficiency as total testosterone <12 nmol/L.
Main Results:
- Priapism occurred in 48% of patients, predominantly in those aged 18-25.
- Testosterone deficiency was observed in 22% of patients, with 25% of those with priapism experiencing deficiency.
- No significant difference in mean total testosterone, LH, or FSH levels was found between patients with and without a history of priapism.
Conclusions:
- Testosterone deficiency is prevalent in men with SCD.
- This study did not establish a direct association between testosterone deficiency and priapism in this cohort.
- Further prospective research is required to clarify the relationship between priapism and testosterone deficiency in SCD patients.
Purpose:
The purpose of this study was to determine the association of testosterone deficiency and priapism in adult men with sickle cell disease (SCD).
Methods:
A cross-sectional study of 50 adult men with SCD (hemoglobin SS) was performed. All patients had early morning blood taken for total and free testosterone, FSH, LH, prolactin, lipid levels, LDH and hematological indices. Patients completed an interviewer-administered questionnaire regarding priapism frequency, duration and treatment. Testosterone deficiency was defined as a serum total testosterone<12 nmol/L (346 ng/dL).
Results:
The mean age of the study population was 34.2±8.9 years. Priapism was noted in 24 (48%) patients and was most frequently seen in men between ages 18-25 years. Testosterone deficiency was observed in 11 of the 50 (22%) patients, particularly in 6 of 24 (25%) patients with histories of priapism. There was no difference in mean total testosterone levels in patients with and without a history of priapism (16.7±4.9 nmol/L and 15.4±5.9 nmol/L, respectively) (p=0.43). Similarly, there was no difference in serum LH and FSH levels based on history of priapism.
Conclusion:
Testosterone deficiency is prevalent in patients with SCD; however, we did not identify an association based on a history of priapism. Larger, prospectively gathered data are needed to define the priapism profile of SCD patients with testosterone deficiency.
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