16043
Endocrine Profile at Puberty in Autism Spectrum Conditions
Autism spectrum conditions (ASC) are characterized by a striking male prevalence. Converging evidence suggests that sex hormones may play a role in the link between ASC and maleness. Puberty is a crucial phase of sexual development where the sexual differentiation of the brain, primarily established prenatally, is actively maintained. Puberty and sex hormone profile at puberty have not been yet systematically studied in ASC.
Objectives:
(i) To evaluate the physical and pubertal development in children with ASC, and (ii) To investigate the sex hormone profile of children with ASC during puberty.
Methods:
The study was conducted at the University Hospital ‘G. Rodolico’ in Catania, Italy and approved by the Local Research Ethics Committee. We studied n = 81 male children, n = 43 having a clinical diagnosis of ASC and n = 38 male age- and IQ-matched typically developing children. A physical and growth examination was conducted using the following measures: head circumference (HC), height (H) weight (W), body mass index (BMI), estimation of the target height (TH), Z-scores (standard deviation scores) for HC, H, TH and BMI, Tanner stages (Tanner, 1969) for pubic hair and genitalia. Development of axillary hair, distribution of body hair and presence of acne were determined by visual inspection. Testicular volume was assessed using an orchidometer. The following hormones were analyzed in the serum: androstenedione, dehydroepiandrosterone sulfate (DHEA-S), total-testosterone, sex-hormone binding globulin (SHBG), free-testosterone, progesterone, estradiol, cortisol, luteinizing hormone (LH) follicle-stimulating hormone (FSH), growth hormone (GH), IGF-1.
Results:
Educational level, socioeconomic status, diet preferences, and exercise were investigated and no between-group differences were reported (chi-square tests, all p>0.5). No group differences in H, W, BMI and TH were found. Children with ASC at Tanner stage 2 (n=22, age=9.7 ± 1.16 years) were approximately 8 months younger than controls (n=26, age=10.3 ± 0.7 years) and this difference was significant (p=0.038). The sex-hormone profile showed significantly higher levels of estradiol, progesterone and LH in ASC males. SHBG was significantly lower in ASC compared to controls, leading to significantly higher levels of free-testosterone. Mean levels of androstenedione, total-testosterone, GH and IGF-1 were all increased in the ASC group but between-group differences did not reach significance.
Conclusions:
Male children with ASC started puberty (Tanner stage 2) approximately 8 months earlier than controls and displayed an activation of the sex steroid pathway as demonstrated by higher levels of free-testosterone, estradiol, progesterone and LH. These preliminary results suggest that male children with ASC may have a different hormone profile, and a different start and trajectory of puberty, compared to typically developing children.