Uterus size and ovarian morphology in women with isolated growth hormone deficiency, hypogonadotrophic hypogonadism and hypopituitarism.

OBJECTIVE AND
SUBJECTS: Current data suggest a permissive role for the somatotrophic axis in the reproductive process, mainly by affecting the onset of puberty and the maintenance of regular menstrual cyclicity. To assess a possible interface between GH and reproductive axes in determining the uterus size, we retrospectively evaluated 58 pelvic ultrasound scans in adult women with either isolated growth hormone deficiency (GHD; n = 12), hypogonadotrophic hypogonadism (HH; n = 24) or hypopituitarism (HP; n = 22) of prepubertal onset. Pelvic ultrasound was performed before oestrogen replacement in patients with HH or HP, and after completion of GH treatment in the majority of patients with HP. Eight women with HH and seven with HP had a second pelvic ultrasound examination after being established on oestrogen replacement therapy. A group of 19 young healthy women with no previous history of pregnancy or miscarriage were included for comparison of ultrasound data.
RESULTS: Uterine measurements, length and uterine cross-sectional area (UXA) were significantly less in the three study groups compared to healthy controls [median UXA: GHD 18.0 cm(2) (range 9.9-28.6 cm(2)), HH 7.0 cm(2) (range 1.3-18.5 cm(2)), HP 11.8 cm(2) (range 1.6-21.8 cm(2)) and controls 23.0 cm(2) (range 16.1-31.7 cm(2)); P < 0.001]. The median age of oestrogen replacement was significantly later in HH [19 years (range 16-26 years)] compared to HP [16.5 years (range 13-20 years)]P = 0.03, while the median age of menarche of GHD patients was 14.5 years (range 11-16 years), which was not statistically different from controls [13.0 years (range 12.5-14.5 years)]. Repeat uterine measurements on oestrogen in the subgroup of 15 patients did not reach the normal values [pretreatment UXA: 4.2 cm(2) (range 1.6-16.1 cm(2)), post-treatment UXA: 12.6 cm(2) (range 4-23 cm(2))]. Ovarian volume was smaller in the two groups of women with gonadotrophin deficiency (HH and HP), while a polycystic ovarian morphology was notably more prevalent in the two groups who had received GH treatment being found in 75 and 58% of women with GHD and HP, respectively, compared with 12.5% in women with HH (P < 0.004).
CONCLUSIONS: Our findings suggest that GHD might have an independent effect in determining uterus size and therefore the consequences of GHD plus oestrogen deficiency on uterus growth might be additive. The fact that uterine measurements between HH and HP patients did not differed significantly in this study may be explained by the fact that oestrogen replacement has been substituted earlier in the latter group. Furthermore, it appears that standard oestrogen replacement therapy did not result in normal uterine growth. A polycystic ovarian morphology may be a consequence of GH treatment.