Pineal gland metabolism in patients with adolescent idiopathic scoliosis

[email protected] INTRODUCTION: The observation that an experimental pinealectomy in newborn chickens leads to a spinal deformity similar to idiopathic scoliosis in humans initiated a new neuroendocrine hypothesis for the cause of idiopathic scoliosis. A deficiency of melatonin, which is the principal product of the pineal gland, was believed to be responsible for this deformity, because both autografting of the pineal gland and substitution of melatonin prevented the development of scoliosis in the pinealectomised chickens. Machida et al (1) also reported significantly lower levels of serum melatonin in adolescents with progressive scoliosis compared with patients with stable scoliosis or healthy control subjects. However, no alteration in the serum or urinary melatonin level in patients with adolescent idiopathic scoliosis was found by others. Therefore, the role of the pineal gland function in the pathogenesis of human adolescent idiopathic scoliosis requires further investigation. We examined the urinary excretion of 6-sufatoxyl-melatonin and the pineal gland glucose metabolism using F-18 fluorodeoxyglucose (FDG) brain positron emission tomography (PET) in patients with adolescent idiopathic scoliosis and in gender-matched healthy control subjects.