Endocrine Abstracts

JOINT2521

Glucocorticoid replacement therapy in secondary adrenal insufficiency is lifesaving, but the currently available literature reveals that overtreatment can result in long-term effects on bone, cardiovascular and metabolic systems. We conducted a retrospective, observational, longitudinal study at our hypothalamic-pituitary pathology unit on 140 patients who had undergone neurosurgery in the hypothalamic-pituitary region before 2020 for PIT-NETs, craniopharyngiomas, Rathke cleft cyst, chordomas and meningiomas, to verify the effects of glucocorticoid replacement therapy. Exclusion criteria encompassed the utilization of corticosteroids for unrelated indications and prior bariatric surgery. The patients were divided into two groups: group A, consisting of 70 patients with pituitary disease and hypoadrenalism who had been treated with glucocorticoid replacement therapy for at least 3 years, and group B, consisting of 70 patients with pituitary disease but without hypoadrenalism. Lipid metabolism, carbohydrate metabolism, body weight and blood pressure were analyzed at baseline (at diagnosis or immediately before neurosurgery) and after 3 years of therapy. Comparing the two groups, there was no difference in age, carbohydrate metabolism, dyslipidemia and hypertension at baseline. At follow-up, a worsening of glucose metabolism was observed in 45/140 patients, and univariate analysis showed a higher incidence in patients receiving glucocorticoid replacement therapy (64.4%) compared to untreated patients (35.6%) (P = 0.019). This result was confirmed by multivariate analysis, which showed an association with glucocorticoid replacement therapy (P = 0.014) and with the presence of impaired glucose tolerance (P = 0.016) and impaired fasting glucose (P = 0.04) at diagnosis. Regarding lipid metabolism, 92/140 patients worsened, of whom 56.5% were on treatment (P = 0.033) and 43.5% were not. However, upon multivariate analysis, the only significant data were treatment for dyslipidemia at baseline (P = 0.001) and central hypothyroidism (P = 0.001). The data on arterial hypertension demonstrated deterioration in 54/140 patients: 30 were undergoing glucocorticoid replacement therapy, while the remaining 24 were not (P = 0.298). Multivariate analysis showed a statistically significant association with older age at diagnosis (P = 0.007) and with hypertension at baseline (P = 0.001). In conclusion, a glucocorticoid replacement therapy that includes a holistic management of the patient, in association with the replacement of other possibly deficient axes, does not have an impact on the risk of developing hypertension and dyslipidemia. Instead, glucocorticoid replacement therapy resulted associated to worsening of glucose metabolism, particularly in patients already predisposed.