Endocrine Abstracts

Background: Acromegaly is an acquired disorder related to excessive production of growth hormone (GH) and insulin-like growth factor-1 (IGF-1). Empty sella (ES) is an anatomical condition of sella turcica that is partially or completely filled with cerebrospinal fluid mainly due to intrasellar herniation of subarachnoid space. Here, we describe a rare case of a patient who presented with clinical and biochemical features of acromegaly who had an ES on pituitary magnetic resonance imaging (MRI).

Case report: A 51 year old female patient, with a recent prediabetes history, Hypertension well controlled under monotherapy. The patient has no history of pituitary apoplexy and has never noticed morphotype changes. Acromegaly was suspected by an endocrinologist during a consultation for goitre. Serum IGF1=481.4 ng/ml (N: 55-234), An oral glucose tolerance test showed no suppression of GH values. Serum levels of prolactin, cortisol, prolactin, TSH and FT4 were normal. Sella contrast-enhanced MRI was performed for tumor localization: T1 and T2 - weighted images revealed ES with no adenoma. Visual field examination was normal. Due to lack of availability, PET/CT couldn’t be performed To rule out an ectopic GH secretion. We have decided to start medical treatment with long-acting Lanreotid 120 mg per 28 days, and reeavaluate clinical, Biological and radiological features in 6 months.

Discussion: Acromegaly stems from GH-secreting pituitary tumors in approximately 95% of all cases, and most tumors are visible on MRI of the sella. In 5% of cases, it is caused by the ectopic secretion of growth hormone-releasing hormone (GHRH), which is responsible for pituitary hyperplasia. Primary ES may occur due to the inherent weakness of the diaphragm sella and/or the increase in intracranial pressure promoting herniation of the arachnoid membrane into the pituitary pit. When ES is seen after surgery, irradiation, or medical treatment of pituitary adenoma, it is defined as secondary. Pituitary hyperfunction is rarely seen in ES and acromegaly is the least common finding. The mechanism underlying the association of acromegaly and ES remains unclear. Apoplexy on existing pituitary adenoma and then formation of necrosis can proceed to ES. Since our patient did not have a history of pituitary apoplexy and we could not find any reason for secondary ES, we considered primary ES.