Increased arterial stiffness and short QTc interval are associated to androgen levels in classical congenital adrenal hyperplasia due to 21 hydroxylase deficiency

Lorenzo Campioni; Carlo Maria Chiara Di; Beatrice Bergoglio; Chiara Sola; Ezio Ghigo; Mirko Parasiliti Caprino; Roberta Giordano

doi:10.1530/endoabs.110.P147

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Endocrine Abstracts (2025) 110 P147 | DOI: 10.1530/endoabs.110.P147

ECEESPE2025 Poster Presentations Adrenal and Cardiovascular Endocrinology (169 abstracts)

Increased arterial stiffness and short QTc interval are associated to androgen levels in classical congenital adrenal hyperplasia due to 21 hydroxylase deficiency

Lorenzo Campioni ¹ , Maria Chiara Di Carlo ¹ , Beatrice Bergoglio ¹ , Chiara Sola ¹ , Ezio Ghigo ¹ , Mirko Parasiliti Caprino ¹ & Roberta Giordano ²

Author affiliations

¹Endocrinology, Diabetes and Metabolism; City of Health and Science University Hospital; Department of Medical Sciences; University of Turin;, Turin, Italy; ²Department of Biological and Clinical Sciences; University of Turin;, Turin, Italy

JOINT1286

Context: Congenital Adrenal Hyperplasia (CAH) is a group of autosomal recessive disorders characterized by impaired cortisol synthesis and hyperandrogenism, current treatment of CAH mainly rely on glucocorticoids (GC) to suppress androgen hypersecretion and to mimic endogenous cortisol secretion. GC therapy, however, often needs to be administered at supra-physiological doses, with an increased risk of long-term complications.

Objective: To evaluate the cardiovascular and metabolic risk in a group of adult patients affected by CAH caused by 21β-hydroxylase deficiency.

Subjects and methods: A cross-sectional study was conducted in a group of 32 adult patients affected from classical CAH due to 21β-hydroxylase deficiency in treatment with different formulations of glucocorticoids (Hydrocortisone HC, Double-release Hydrocortisone DR-HC, Hydrocortisone and dexamethasone HC+DEX), compared with 73 unaffected controls. Anthropometric and metabolic biochemical parameters were collected for each of the subjects, as well as a 24-hour dynamic blood pressure monitoring (ABPM) and an EKG.

Results: The univariate analysis showed a higher weight (P=0.006), systolic blood pressure (P<0.001), glycemia (P=0.031), triglycerides (P=0.025), LDL cholesterol (P<0.001) in the control group when compared to CAH patients; however, the latter being significantly younger than the control group (P=0.035). The CAH group also exhibited a shorter QTc (P=0.006), RR (P=0.045) and QRS (P=0.004) interval. The Ambulatory Arterial Stiffness Index (AASI), derived from the 24-hour ABPM, showed statistically significant higher values in the CAH group (P=0.006), the two groups were matched 1:2 through a propensity score matched analysis, confirming a higher AASI score (P< 0.001) and a shorter QTc interval (P=0.004). Through a multivariate analysis we found the AASI score to be related to CAH diagnosis (coeff. 1.131; P<0.001), Age (coeff. 1.004; P=0.034), BMI (coeff. 1.008; P<0.001) and 17 OHP levels (coeff. 1.001 P=0.049); while a shorter QTc interval seems to be related to CAH diagnosis (coeff. 0.977; P=0.039) and ACTH levels (coeff. 0.999; P=0.021). Patients treated with HC+DEX showed higher AASI (P=0.026) and triglycerides levels (P=0.04) when compared to patients treated with HC only or DR-HC, however no differences in hormonal levels and comorbidities were found between the groups.

Conclusion: The metabolic profile of CAH patients did not differ from unaffected controls, however androgens levels seem to be related to cardiovascular alterations in subjects affected by CAH, especially those in treatment with dexamethasone.