Endocrine Abstracts

Introduction: In acromegaly GH excess leads to impaired insulin sensitivity with an alteration of beta-cell function. The consequent hyperglycemia leads to a further increased cardiovascular risk and mortality.

Case report: A 16 years old patient was first referred to the Department of Pediatrics in 2014 with accentuated growth since the age of 10. The reason of the first referral was a sport injury (head trauma during playing basketball). Sella MRI depicted hypophysis macroadenoma and a concomitant severe hyperglycemia was found therefore human conservative intensified insulin therapy (ICT) was initiated. The diabetes could be insufficiently controlled and ceased only after hypophysis surgery. Residual tumor was diagnosed and consequent recurrent GH and IGF-1 elevation occurred followed by gamma-knife radiosurgery and repeated transsphenoidal hypophysis operation. After the second operation first generation somatostatin analogue (SSA) lanreotide treatment was initiated. After the second surgery hyperglycemia was treated with metformin initiated at the age of 18. After two years the patient was referred to adult endocrinology department with severe hyperglycemia (HgA1c: 12%), high GH and IGF-1 levels and a 5 mm microadenoma remnant. As during the earlier ICT recurring episodes of hypoglycemia were present leading to a decline in quality of life our patient rejected introduction of ICT regime. Trying to control hyperglycemia first a triple combination of metformin, sitagliptin and dapagliflozin was tested, which failed to control the symptoms, as he was admitted with severe recurrent hyperglycemia. Within a month thoroughful reeducation and administration of fixed injectable combination of degludec insulin and GLP1 analogue liraglutide led to a better control of hyperglycemia accompanied by a significant improvement in quality of life. Meanwhile Glutamic Acid Decarboxylase Autoantibodies (GADA) were found to be elevated with high level of C peptide, suggesting that the patient has a mixed type of diabetes mellitus.

Conclusion: hyperglycemia is a consequence of insulin resistance and a relative insulin deficit in acromegaly. Pharmacological therapy of acromegaly can alter glucose homeostasis. First generation SSAs reduce pancreatic insulin and glucagon secretion. In a rare case of mixed diabetes an ultra-long acting insulin analogue combined with a long acting GLP-1 analogue and metformin can result in sufficient glucose control with an improved quality of life.