Endocrine Abstracts

Acromegaly is a rare disorder caused by growth hormone (GH) and insulin-like growth factor I (IGF-I) overproduction, associated with increased morbidity and mortality. It has different complications, among which insulin resistance, prediabetes and diabetes mellitus are substantial. GH affects glucose metabolism through different mechanisms. The therapy of GH overproduction (for example surgical or radiotherapy) improves glucose metabolism, while different types of medical therapy may worsen it. We present the medical history of an acromegalic patient, diagnosed at the age of 30 years. Although his GH-producing giant adenoma had been operated twice, only partial resection was achieved with intra- and suprasellar tumour remnant. He was initially treated with dopamine agonist, followed by a high dose of first-generation somatostatin receptor ligand (SRL) octreotide LAR. In the meantime, he developed type 2 diabetes mellitus. Since the acromegaly was still active, the therapy was changed to the GH receptor antagonist pegvisomant. Despite its high dose, we couldn’t achieve biochemical control. Once the second generation SRL pasireotid LAR was available, ha was given 60 mg monthly, which improved his IGF-I levels, but worsened the glycaemic control. Because of tumour concern and impaired glucose metabolism, the acromegaly is now controlled by a pasireotide LAR and pegvisomant combination therapy. His diabetes is treated with insulin, metformin, SGLT2 inhibitor and a GLP-1 receptor agonist. An overproduction of the contra-insulin GH worsens glucose metabolism. Therefore, lowering pathologically high GH levels by surgery, medical or radiotherapy improves glucose homeostasis. On the other hand, first generation SRLs might worsen glucose metabolism, while second generation SRL pasireotide causes hyperglycaemia in the majority of cases. The optimal therapy for acromegalic patients should be individually taking into account different aspects of the disease.