ESPE Abstracts

Delayed puberty is a common condition defined as the lack of sexual maturation by an age ≥ 2 sd above the population mean.

Materials and Methods: to study the structure of the delayed puberty (DP), 96 medical records of patients who were examined in the endocrinology department between 2020 and 2024 were selected: 77 boys (14.8 ± 1.23 years), 19 girls (14.5 ± 2.03 years) by querying the electronic information system of the medical institution for ICD-10 codes (E30.0, E29.1, E23.0). To assess the role of the hereditary factor, 110 case histories were selected: 103 boys and 7 girls. The eligibility criteria for DP were defined in boys ≥14 years old, Tanner P_1-3G₁; girls ≥ 13 years, Tanner P_1-3B₁, absence of menstruation at age ≥ 15 years.

Results: In the structure of DP in children (n = 96), the share of constitutional delay growth and puberty (CDGP) accounted for 56% (54/96), functional hypogonadism (FH) was 18% (17/96), hypogonadotropic hypogonadism (HypoH) -14.5% (14/96) and hypergonadotropic hypogonadism (HyperH) -11.5% (11/96). In the boy’s group, the share of CDGP was 65% (50/77). FH observed in 13% (10/77), was presented by: protein-energy malnutrition-80% (8/10), celiac disease in combination with type 1 diabetes mellitus -10% (1/10), type 1 diabetes mellitus -10% (1/10). HypoH was found in 15.5% (12/77), represented mainly by Kalman syndrome - 50% (4/12). HyperH which was noted in 6.5% (5/77) is due to bilateral testicular atrophy. In the structure of DP in girls, the leader was FH - 37% (7/19), which was represented by: protein-energy malnutrition-43% (3/7), celiac disease - 14.3% (1/7), anorexia nervosa - 14.3% (1/7), non-classic congenital adrenal hyperplasia-14.3% (1/7), hyperprolactinemia - 14.3% (1/7). HyperH (31.5% (6/19)) is represented by Turner syndrome in 66.5% (4/6), DSD 46, XY with complete androgen insensitivity syndrome -16.6% (1/6), with complete gonadal dysgenesis -16.6% (1/6). CDGP accounted for 21% (4/19), HypoH was in 10.5% (2/19). According to the family history, DP is noted significantly more often (P = 0.01) in groups with transient forms of delayed puberty than with permanent ones (44.5% (70/157) vs 8.7% (4/46).

Conclusion: In the structure of DP in children, CDGP prevailed. In the group of boys, CDGP was significantly more common than in girls (65% vs 21%, P = 0.01). In the group of girls, the HyperH (31.5% vs 6.5%, P = 0.01) was significantly higher than among boys (P = 0.01). The hereditary factor associated with the presence of DP in the family was significantly more often observed in adolescents with self-limited DP compared with permanent forms of hypogonadism.