A 19-year-old male presented with complaints of failure to develop secondary sexual characteristics. He was born at term through normal vaginal delivery, and his developmental milestones were normal. He was average in scholastic performance and studied up to tenth standard. He had history of learning disabilities but no behavioral abnormalities. He was tallest among his peers during late teenage. He noticed appearance of pubic and axillary hair by 15 years of age, but failed to develop facial or body hair or increase in penile length or size of the testes. There was no history of head trauma, surgery for midline defects, chronic systemic illness, testicular trauma, mumps, or drug abuse. He had no history of abnormality in smell, visual deficits, headache, seizure disorder, or other neurological deficits. There was no family history of delayed puberty, infertility, or gynecomastia. He did not receive any medical treatment prior to visit to this hospital. On examination, his height was 170 cm (height -1 SDS, height age 15 years, target height 173 cm), weight was 55 kg (weight age 15 years), and blood pressure was 110/70 mmHg. Anthropometry showed eunuchoidal proportions with upper segment/lower segment ratio (US: LS, 80:90 cm) 0.88 and arm span exceeding height by 10 cm. There was no gynecomastia. Tanner stage of pubertal development was A+, P2, and both testes were present within poorly developed scrotal sac and soft in consistency and measured 1 ml each. The stretched penile length was 8 cm. His sense of smell was normal. He had genu valgum but no midline defects, synkinesia, nystagmus, ataxia, and visual deficits. On investigations, complete blood count and liver and renal function tests were normal. Hormonal profile revealed serum LH 0.29 mIU/ml (N 1.7–8.6), FSH 0.69 mIU/ml (N 1.5–12.4), testosterone 0.44 nmol/L (N 9.9–27.8), estradiol 12.3 pg/ml (N 7.6–42.6), prolactin 9.6 ng/ml (N 4–15.2), T4 7.32 μg/dl (N 4.8–12.7), TSH 1.9 μIU/ml (N 0.27–4.2), and 0800 h cortisol 447 nmol/L (N 171–536). His bone age was 15 years. CEMRI sella and olfactory region did not display any abnormality. LH response to triptorelin at 4 h was 2.8 mIU/ml. Serum testosterone at baseline was 0.45 nmol/L, and in response to hCG, it increased to 1.2 nmol/L (after 24 h of last injection of hCG). Based on available clinical and biochemical profile, a diagnosis of congenital idiopathic hypogonadotropic hypogonadism (IHH) was considered, and he was initiated with testosterone enanthate 100 mg intramuscularly every fortnightly. The doses of testosterone were increased gradually to 200 mg every fortnightly over a period of 2 years. On testosterone therapy, he developed gynecomastia. He is planned for gonadotropin therapy for induction of spermatogenesis after the attainment of virilization (Fig. 7.1).