EYES2024 ESE Young Endocrinologists and Scientists (EYES) 2024 Reproductive Endocrinology (10 abstracts)
Testosterone serum levels predict the severity of metabolic dysfunction-associated steatotic liver disease (MASLD) in hypogonadal men
Leonardo Dalla Valentina 1,2 , Giorgia Spaggiari 2,3 , Fabio Nascimbeni 4 , Simonetta Lugari 4 , Cristina Feliciani 4 , Ali Ahmad 1,2 , Antonio R. M. Granata 2,3 , Pietro Andreone 4 , Manuela Simoni 1,2 & Daniele Santi 1,2,3
1Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy; 2Unit of Endocrinology, Department of Medical Specialties, Azienda Ospedaliero-Universitaria of Modena, Modena, Italy; 3Unit of Andrology and Sexual Medicine of the Unit of Endocrinology, Department of Medical Specialties, Azienda Ospedaliero-Universitaria of Modena, Modena, Italy; 4Operating Unit of Internal and Metabolic Medicine, Azienda Ospedaliero-Universitaria of Modena, Civil Hospital of Baggiovara, Modena, Italy
Introduction: Metabolic dysfunction-associated steatotic liver disease (MASLD) is defined by the presence of hepatic steatosis and metabolic risk factors. Both testosterone and estradiol play pivotal roles in hepatic lipid homeostasis, though the underlying mechanisms remain unclear. Low serum testosterone levels are independently associated with MASLD. However, no studies have previously evaluated the prevalence and severity of MASLD in hypogonadal men.
Methods: A prospective, observational, clinical trial was conducted enrolling hypogonadal men. Each patient underwent hepatic ultrasound to evaluate the presence and grade of steatosis, and Fibroscan® and 2-dimensional shear weave elastography (2D-SWE) techniques for the assessment of liver stiffness.
Results: Forty-one hypogonadal men (age 57.7 ± 14.0 years, body mass index 31.9 ± 6.5 kg/m2) were enrolled, of which twenty-three (56.1%) were already under androgen replacement therapy. Hepatic steatosis was detected in 30 patients (75.0%), divided into mild (10.0%), moderate (32.5%) and severe (32.5%) grades. No difference in liver steatosis presence/grade was detected between androgen-replaced patients compared to untreated ones (P = 0.293). Liver fibrosis was detected in six men (14.6%) at Fibroscan® and in 4 (9.8%) at 2D-SWE. The presence of fibrosis was similar between naïve and treated patients (P = 0.565). The presence of liver fibrosis was neither associated, nor predicted by any hormones and biochemical parameter. This lack of significant correlations remained also after subdivision in naïve hypogonadal men and patients under androgen replacement therapy.
Conclusion: Here, we demonstrated a high prevalence of liver steatosis in hypogonadal men, particularly of moderate to severe grades. Moreover, we identified an unexpectedly high prevalence of liver fibrosis, occurring in about 15% of cases. Although our results need further confirmation in larger cohorts, the relatively high prevalence of liver fibrosis in this patient cohort suggests that liver health should be evaluated in the management of male hypogonadism.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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