Background: Long QT syndrome (LQTS) is characterized by delayed myocardial repolarization, predisposing to malignant arrhythmias such as torsades de pointes, ventricular fibrillation, and cardiac arrest. Recent reports suggest that acquired LQTS (aLQTS) may represent an early manifestation of hypopituitarism, potentially contributing to its increased cardiovascular mortality, although evidence remains limited to 16 published case reports. Objective: The objective was to investigate the relationship between hypopituitarism and corrected QT (QTc) interval. Methods: We retrospectively analyzed data from 185 patients (121 males) with hypothalamic–pituitary disorders who underwent a 12-lead electrocardiogram between April 2023 and September 2024. Clinical characteristics, hormone replacement therapy, and same-day laboratory parameters (electrolytes, fT3, fT4, IGF-I, testosterone) were recorded. QTc was calculated using Bazett’s formula. Multivariate logistic regression identified predictors of QTc prolongation. Results: Age (OR 1.07–1.09, p = 0.02) was a significant predictor in 5 of 8 models. The presence of expansive lesions other than pituitary adenomas, craniopharyngiomas, and Rathke’s cleft cysts was also associated with QTc prolongation (OR 8.35–17.73, p < 0.05 and p = 0.03). Potassium (OR 0.14–0.17, p = 0.09) and albumin-corrected calcium levels (OR 0.0003, p = 0.06) showed consistent, though borderline, associations. Conclusions: Age and the presence of expansive lesions other than pituitary adenomas, craniopharyngiomas, and Rathke’s cleft cysts are the main predictors of QTc duration in patients with hypothalamic–pituitary disease. Electrolyte imbalances—particularly low potassium and albumin-corrected calcium—may further contribute. The influence of specific pituitary deficiencies remains uncertain, likely due to adequate replacement therapy in most patients.

Background: The diagnosis of adult growth hormone (GH) deficiency (GHD) relies on demonstrating a reduced GH response to stimulation tests. Excess body weight, an increasingly prevalent condition, is associated with a blunted GH response to all types of stimulation tests. Therefore, establishing body mass index (BMI)-dependent cut-offs is essential for accurate interpretation. This study aimed to identify BMI-specific diagnostic thresholds for the insulin tolerance test (ITT), using residual pituitary function as the clinical gold standard. Methods: We retrospectively analyzed 105 patients with hypothalamic-pituitary disorders who underwent ITT. GHD was defined by the presence of at least three pituitary hormone deficiencies, while preserved somatotropic function was defined by the absence of other pituitary deficits and an insulin-like growth factor-I (IGF-I) standard deviation score ≥ 0. Receiver operating characteristic (ROC) curve analysis was used to determine optimal BMI-stratified cut-offs, defined as those maximizing sensitivity (SE) and specificity (SP). Results: The optimal GH cut-off was 2.8 μg/L for patients with normal weight (SE 84.6%, SP 97.4%) and those with overweight (SE 100%, SP 92.3%), and 2.1 μg/L for patients with obesity (SE 88.2%, SP 87.5%). The area under the ROC curve was 0.968, 0.957, and 0.897 for patients with normal weight, overweight, and obesity, respectively. Conclusions: This is the first study to define GH diagnostic thresholds for the ITT according to BMI, using a clinical definition of GHD as reference. More restrictive cut-offs in patients with obesity are needed to avoid GHD overdiagnosis and potential overtreatment. These findings should be considered hypothesis-generating and require prospective external validation before routine clinical implementation.