Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 22 P623

1C.I. Parhon National Institute of Endocrinology, Bucharest, Romania; 2Emergency Hospital, Calarasi, Romania.


Adolescent idiopathic scoliosis (IS) represents an evolutive disease that occurs in puberty and progresses till the skeletal maturation. The neuroendocrine hypothesis involving a melatonin deficiency as the source for IS is one of the proposed causes of this plurifactorial disease.

Objective: To investigate the hormonal changes of both the gonadal and growth axis and circadian rhythmicity in subjects with adolescent idiopathic scoliosis compared to age matched healthy subjects.

Subjects and methods: The study group consisted in 15 patients aged 9–18 years. with (IS) and 8 healthy subjects, age matched, as controls. The study had the Ethical Committee approval. Blood was collected every 4 h during day and 2 h during night of 24 h period (1200, 1600, 2000, 2400, 0200, 0400, 0800 h) for circadian profile. Serum melatonin, cortisole, LH, FSH, E2, T, DHEA, androstendione, GH, GHBP, IGF1, IGFBP3 levels were measured and statistically analyzed. The individual profiles of circadian markers (melatonin and cortisol) and studied hormones were quantified by a fit cosine curve yielding mesor, amplitude and acrophase.

Results: The levels of hormones were measured in blood samples collected at 0800 h showed statistically significant differences in IS group compared to controls: melatonin (24.56±6.39 versus 9.56±3.21 ng/ml, P=0.02), LH (7.26±2.37 versus 2.48±0.63 U/l, P=0.03), E2(107.7±29.61 versus 27.6±10.54 pg/ml), IGF1 (26±53.63 versus 245±44.87 ng/ml P=0.009). Circadian profiles analysis showed a significant increase in 24 h production of IGF1 and a decrease secretion and phase shift in cortisol circadian rhythm. There were no significant differences in melatonin circadian rhythm.

Conclusions: The results showed changes in growth axis. IGF1 significant increase and shifted cortisol rhythm may be components of the plurifactorial etiology of adoloscent idiopathic scoliosis.

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