الفهرس 
Physiology of pubertyOnly 14 pages are availabe for public view
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Abstract
Delayed puberty is defined as the lack of pubertal development by an age that is 2–2.5 SDs beyond the population mean. It can be the initial presentation of a serious underlying disorder like Hypogonadotropic hypogonadism.
Hypogonadotropic hypogonadism (HH) in males is characterized by impaired testicular function, which can affect spermatogenesis and/or testosterone synthesis as a consequence of congenital or acquired diseases that affect the hypothalamus and/or the pituitary gland leading to absent or in adequate secretion of gonadotropin releasing hormone (GnRH) and/or failure of pituitary gonadotropin secretion (FSH and LH).
At time of puberty, sertoli cells in testis proliferate, produce and secrete inhibin B into the circulation as a response to FSH stimulation. Inhibin B is considered to be an index of Sertoli cell number and integrity. Any changes in inhibin B concentrations reflect mainly the status of germ cell proliferation and development.
In this observational analytical cross sectional study, we measured serum inhibin B level among 21 male patients with hypogonadotropic hypogonadism.
group A included 13 patients with early onset HH due to congenital and idiopathic causes. According to MRI results, this group included 1 patient with congenital HH (8%) due to partial primary empty sella and 12 patients (92%) with normal MRI (idiopathic HH). group B included 8 patients with late onset HH due to acquired causes. According to MRI results, this group included 1 patient (12.5%) with Rathke’s cleft cyst, 5 patients with craniopharyngioma (62.5%), 1 with germinoma (12.5%) and 1 with pituitary microadenoma (12.5%). All of them underwent surgical removal of the tumors with subsequent radiation in 6 patients (75%) and 4 had history of recurrence (50%).
Nearly all of the included patients had to seek medical attention before puberty due to short stature owing to GH deficiency (11 of 13 in group A and 8 of 8 in group B) as a part of combined pituitary hormone deficiency (12 of 13 in group A and 8 of 8 in group B).
Our study results showed wide variations in inhibin B levels ranging from 0.01 to 134.6 pg/ml with median value 0.02 pg/ml (25th- 75th: 0.01 – 9.6). The range of inhibin B level in group A patients (n=13) with congenital/idiopathic HH was (0.01 – 134.6 pg/ml) with median value 6 pg/ml (25th - 75th: 0.01 – 52.59 pg/ml) while in group B, it ranged from 0.01 to 30.5 pg/ml with median value of 0.01pg/mL (25th – 75th: 0.01 – 4.505). Although the difference in inhibin B levels in the two groups was not significant, the median value was higher in group A (6 pg/mL) than in group B (0.01pg/mL). This may be attributed to the small number of patients in each group.
There was no statistical significant difference in Tanner stage or inhibin B level between those who received testosterone replacement (N = 13) or HCG (N = 15) prior to start of study versus those who did not (p >0.05). However the median inhibin B and the 75th percentiles were higher in patients who received either treatment.