Prevalence and Outcome of Secondary Hypogonadism in Male Patients with Cushing's Syndrome and Mild Autonomous Cortisol Secretion.
Cushing’s syndrome
cortisol
hypogonadism
mild autonomous cortisol secretion
testosterone
Journal
European journal of endocrinology
ISSN: 1479-683X
Titre abrégé: Eur J Endocrinol
Pays: England
ID NLM: 9423848
Informations de publication
Date de publication:
29 Jul 2024
29 Jul 2024
Historique:
received:
29
03
2024
revised:
19
06
2024
accepted:
25
06
2024
medline:
29
7
2024
pubmed:
29
7
2024
entrez:
29
7
2024
Statut:
aheadofprint
Résumé
Secondary hypogonadism (SH) is common in men with Cushing's syndrome (CS), but its impact on comorbidities is largely unknown and longitudinal data are scarce. If SH also affects men with mild autonomous cortisol secretion (MACS) is unknown. We included 30 treatment-naïve adult men with CS and 17 men with MACS diagnosed since 2012. Hypogonadism was diagnosed based on total testosterone (TT) concentrations <10.4 nmol/L and age-specific cut-offs. Outcomes were compared to age- and BMI-matched controls. In 20 men in remission of CS, a longitudinal analysis was conducted at 6, 12, and 24 months. Men with CS had significantly lower concentrations of TT, bioavailable T, and free T compared to controls (p<0.0001) with lowest concentrations in ectopic CS. Likewise, TT was lower in men with MACS compared to controls. At baseline, 93% of men with CS and 59% of men with MACS had SH. Testosterone correlated negatively with late night salivary cortisol and serum cortisol pre- and post 1 mg dexamethasone suppression test. Following successful surgery, TT increased significantly (p=0.001), normalising within six months. Despite normalisation, several RBC parameters remained lower in men with CS even two years after successful surgery. SH is common in men with CS and MACS but usually reversible after successful surgery. The persisting changes observed in RBC parameters need to be further investigated in larger cohorts and longer follow-up durations.
Sections du résumé
BACKGROUND
BACKGROUND
Secondary hypogonadism (SH) is common in men with Cushing's syndrome (CS), but its impact on comorbidities is largely unknown and longitudinal data are scarce. If SH also affects men with mild autonomous cortisol secretion (MACS) is unknown.
METHODS
METHODS
We included 30 treatment-naïve adult men with CS and 17 men with MACS diagnosed since 2012. Hypogonadism was diagnosed based on total testosterone (TT) concentrations <10.4 nmol/L and age-specific cut-offs. Outcomes were compared to age- and BMI-matched controls. In 20 men in remission of CS, a longitudinal analysis was conducted at 6, 12, and 24 months.
RESULTS
RESULTS
Men with CS had significantly lower concentrations of TT, bioavailable T, and free T compared to controls (p<0.0001) with lowest concentrations in ectopic CS. Likewise, TT was lower in men with MACS compared to controls. At baseline, 93% of men with CS and 59% of men with MACS had SH. Testosterone correlated negatively with late night salivary cortisol and serum cortisol pre- and post 1 mg dexamethasone suppression test. Following successful surgery, TT increased significantly (p=0.001), normalising within six months. Despite normalisation, several RBC parameters remained lower in men with CS even two years after successful surgery.
CONCLUSION
CONCLUSIONS
SH is common in men with CS and MACS but usually reversible after successful surgery. The persisting changes observed in RBC parameters need to be further investigated in larger cohorts and longer follow-up durations.
Identifiants
pubmed: 39074212
pii: 7723629
doi: 10.1093/ejendo/lvae097
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© The Author(s) 2024. Published by Oxford University Press on behalf of European Society of Endocrinology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.