SUPRASELLAR AND HYPOTHALAMIC REGION LESIONS AND PITUITARY DISORDERS IN JUVENILES/ADOLESCENTS AND THEIR INFLUENCE ON THE DEVELOPMENT OF IDIOPATHIC SCOLIOSIS: LITERATURE REVIEW OF HORMONAL INFLUENCES ON GROWTH PLATE CHONDROCYTES

2005 
Introduction Delayed puberty and delayed skeletal maturation have been implicated as risk factors for the progression of idiopathic scoliosis. Genetic defects (Turner syndrome) and hypothalamic- pituitary disorders are known causes of delayed puberty. Although it is recognized that the incidence of idiopathic scoliosis is elevated in Turner syndrome, human studies regarding the incidence/severity of scoliosis in children with suprasellar, hypothalamic region and pituitary tumours/ disorders is deficient. Methods A medical records search in five Australian states for suprasellar, hypothalamic region and pituitary tumours/disorders was performed. Identified patients underwent clinical or radiological evaluation for scoliosis. Pathology varied from suprasellar-hypothalamic region tumours, pan-hypopituitarism, pituitary tumours and growth hormone deficiency as well as a craniopharyngioma, arachnoid cyst, retinoblastoma and encephalocele. Results Of 23 identified patients, ten are female. Mean age at presentation was 8.4 years. Three have right thoracic scoliosis with a Cobb angle less than 20 degrees. Two are males; one with pituitary hormone deficiency and the other with Cushing’s disease treated with radiotherapy. The only female is on a growth hormone treatment program for idiopathic growth hormone deficiency. Discussion The only female with scoliosis was 12 years old. Delayed puberty could not be linked to either male with scoliosis. Although the incidence of idiopathic scoliosis in this cohort is greater than expected from Caucasian population studies (2–3%), the male preponderance is unusual. No relationship between delayed skeletal maturation and idiopathic scoliosis could be established.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    0
    References
    0
    Citations
    NaN
    KQI
    []