<h3>Background</h3> Over the past decade. newer gonadotropin assays have enhanced our understanding of the "GnRH pulse generator" and GnRH analogues have revolutionized the treatment of central precocious puberty. If allowed to progress, precocious puberty can have serious consequences both physically and psychosocially. Premature birth has been recognized as a risk tactor for early sexual maturation in the temale child but to our knowledge there have been no prior reports of this condition manifesting as early as infancy. <h3>Case</h3> T.D. was born at 26 weeks gestation and had suffered many expected complications of premannity including: sepsis, retinopathy and bronchopulmonary dysplasia. At 20 weeks of age. (6 weeks corrected age), while still in hospital, she was referred to paediatric gynaecology because of blood in her diaper. At the time of this initial assessment, she had Tanner II breast buds and a protruding estrogenized hymen with physiologic leukorrhea. The blood was telt to be secondary to local irritation of the prominent and exposed hymen but the features of estrogenization were Surprising. Her only medications were iron and vitamins, but a brief course of Aldactazide had been discontinued one month prior. During the month prior to presentation there was an apparent acceleralion in the rate of growth involving body length and head circwnterence. Investigations revealed a markedly elevated estradiol of 250pmol/L, an FSH of 7U/L, and a normal TSH. Abdominopelvic imaging showed bilaterally enlarged ovaries (2.4cm) with multiple tollicles, but the uterus was not well seen and the adrenal glands were nonnal. Bone age was not advanced. CT and MRI of the head showed diffuse atrophy and bilateral retinal detachment, but no localized lesion otherwise. An LHRH stimulation test demonstrated a positive response yielding an LH level of 16U/L (prepubertal <8). Three months later there had been neither regression nor progression of the tindings on examination. A repeat work up is scheduled for April/98 - stay tuned! <h3>Conclusion</h3> As no focal cause has been identitied for the apparenl central activation of the hypothalamic pituitary ovarian (HPO) axis, we have generated two possible explanations. # 1) This is a rare case of true precocious puberty, whether idiopathic or brain injury related, and it will self-resolve or progress or, #2) the patient is manifesting physiological events that have not yet succumbed to "central restraint" She was old enough that maternal and placental estrogen effects should have regressed but the HPO axis can remain active and pulsatile for several years before undergoing the mid-childhood nadir. In the former scenario, treatment (LHRH analogue) will be withheld unless bone age advancement and/or progression are detected. In other scenario, this case may provide more insight into control mechanisms of the HPO axis, the GnRH pulse generator after birth and the onset of puberty.