Background: Adult growth hormone deficiency (AGHD) is caused by structural pituitary disease, pituitary surgery or cranial irradiation.1, 2 Gonadotroph adenomas, the most commonly resected pituitary tumours,3 are an important cause of AGHD.4 AGHD is characterised by insulin resistance, osteoporosis, fatigue, depression, and increased premature cardiovascular mortality.5 We aimed to evaluate current detection and management of AGHD in patients with gonadotroph adenomas.
Methods: In a retrospective cohort study, patients with histologically proven gonadotroph adenomas were identified from the hospital pituitary database (2009-2025). Those without available insulin-like growth factor 1 (IGF1) levels were excluded. Clinical data, including comorbidities, hypopituitarism, malignancy history, growth hormone (GH) replacement, and biochemical and radiological data, were evaluated. Patients with newly identified low IGF1 levels without two other existing hypopituitary axis deficiencies were referred for a glucagon stimulation test.
Results: A total of 128 patients were included; 15.6% had a prior AGHD diagnosis, and low IGF1 was detected in 7.8% (n=10/128) of the remainder. Of these, two resolved spontaneously post-operatively, one normalised on repeat testing, two were lost to follow-up, one was referred for glucagon stimulation testing, and four are followed elsewhere. Among 13 patients on GH therapy, 61.5% reported symptom improvement, adenoma recurrence/progression occurred in two, and no new or recurrent extracranial malignancy was identified. No significant differences in the presence of metabolic, cardiovascular, or bone comorbidities were found between GH-deficient and GH-replete patients, or between GH-deficient patients receiving therapy and those not, in our small cohort.
Conclusion: Systematic IGF1 screening improves detection of AGHD in gonadotroph adenoma patients, and GH replacement appears clinically beneficial and safe, with no new or recurrent extracranial malignancy observed. Adenoma recurrence/progression occurred in a minority, within the ranges reported in the literature for gonadotroph adenomas regardless of GH therapy.6, 7 Nonetheless, experts recommend individualised discussion with patients before commencing GH therapy.8