Introduction

Hypogonadotropic hypogonadism is characterized by deficient or absent secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus, resulting in reduced luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion and, consequently, low testosterone levels and impaired pubertal development. The condition typically presents during adolescence with delayed or absent puberty, lack of secondary sexual characteristics, small testicular volume, decreased libido, and infertility. Skeletal manifestations include delayed bone age, reduced bone mineral density, and persistent open growth plates beyond the expected age of epiphyseal fusion [1]. Congenital hypogonadotropic hypogonadism is a rare disorder, with estimated incidences ranging from approximately 1 in 8,000 to 1 in 40,000 men and a clear male predominance compared with women [2].

In males, testosterone is essential for the pubertal growth spurt, accrual of bone mineral density, and epiphyseal closure, largely through aromatization to estradiol, which mediates fusion of the growth plates. In addition, testosterone drives the development of secondary sexual characteristics, including enlargement of the testes and penis, growth of facial and body hair, deepening of the voice, and increased muscle mass [3]. The progression of pubertal development and testicular growth is therefore routinely assessed using standardized pubertal staging systems such as Tanner stages for genital and pubic hair development [4] and orchidometric measurement of testicular volume. Standard clinical assessment therefore combines biochemical evaluation with systematic examination of secondary sexual characteristics and pubertal staging, for example, using Tanner stages and testicular volume measurement.

Most patients with congenital hypogonadotropic hypogonadism are diagnosed in adolescence, when failure of normal pubertal progression becomes evident. However, some individuals remain undiagnosed until adulthood and may present incidentally during evaluation for unrelated medical conditions [1,5]. In such cases, persistently open growth plates on radiographs represent a highly unusual and strongly suggestive finding of underlying hypogonadism, although other endocrine and systemic disorders can also delay epiphyseal fusion and must be considered in the differential diagnosis [1,6,7].

This case report describes a 26-year-old male in whom hypogonadotropic hypogonadism was first suspected after incidental detection of unoccluded growth plates during workup of a tibial fracture. The report aims to raise awareness of this atypical presentation in adult trauma patients and to highlight the importance of routine assessment of skeletal maturity and secondary sexual characteristics when interpreting radiographs in young adults.