1292 Undiagnosed Acromegaly Presenting as Obstructive Sleep Apnea in a Patient with Craniofacial Abnormalities

Abstract Introduction Obstructive sleep apnea (OSA) is commonly associated with obesity, enlarged neck circumference, central body fat distribution, or craniofacial abnormalities which can result in anatomical narrowing of the upper airway. OSA affects between 20-90% of patients with acromegaly. Acromegaly is characterized by growth hormone (GH) induced soft tissue hypertrophy and coarse facial features, typically due to a pituitary adenoma. OSA in acromegalic patients is due to both hormonal excess and associated craniofacial abnormalities. We present a case of acromegaly diagnosed during evaluation for sleep apnea in a patient undergoing preoperative evaluation for orthognathic surgery. Report of case(s) A 38-year-old male without significant past medical history was referred to Sleep Medicine for evaluation of sleep apnea prior to planned orthognathic surgery for mandibular prognathism and malocclusion. He reported a history of loud snoring, witnessed apneas, excessive daytime sleepiness, and nonrestorative sleep. There was no prior sleep study. On physical examination, the patient had a large mandible, frontal bossing, widely spaced teeth, macroglossia, and enlarged hands and feet. Vital signs were unremarkable. Body mass index (BMI) was 30.1 kg/m². Due to concern for acromegaly, serum IGF-1 level was obtained and found to be markedly elevated at 900 ng/mL (reference range: ~100–300 ng/mL, age-adjusted). Subsequent growth hormone suppression testing was consistent with autonomous GH secretion. Pituitary MRI revealed a 1 cm adenoma within the sella turcica, without compression of the optic chiasm. Polysomnography demonstrated severe OSA with an apnea-hypopnea index (AHI) of 38 events/hour. CPAP titration improved symptoms and oxygenation. The patient was referred to endocrinology and neurosurgery for further management. Transsphenoidal resection of the adenoma was planned, with the orthognathic surgery deferred pending endocrine stabilization. Conclusion Detailed physical examination of patients being evaluated for OSA is crucial. Recognition of features of acromegaly, particularly when caused by a GH-secreting pituitary adenoma, alters the treatment plan and affects outcomes. In such patients, addressing the underlying endocrine dysfunction prior to reconstructive surgery is essential, as ongoing GH excess could lead to recurrence of deformity, and cause worsening OSA. Conversely, treatment of acromegaly is associated with significant improvement in sleep apnea parameters. Support (if any)