Background: Autoimmune hypophysitis is a frequent immune-related adverse event (irAE) in cancer patients treated with immunecheckpoint inhibitors. Studies seeking anti-pituitary (APA) and anti-hypothalamus (AHA) antibodies in patients treated with anti-PD-1 and anti-PD-L1 are scarce. The aim of this study is to search for APA and AHA and related pituitary dysfunction in patients treated with these agents. Methods:Cross-sectional and preliminary longitudinal studies were conducted at the Medical Oncology Unit and Endocrinology and Metabolic Diseases Unit of the University of Campania “Luigi Vanvitelli”. Fifty-four cancer patients on treatments with anti-PD-1 or anti-PD-L1 (Group 1) and 50 healthy controls were enrolled for a cross-sectional study; 13 cancer patients (Group 2) were enrolled for our preliminary longitudinal study. APA/AHA titers and changes in biochemical and hormonal profile were evaluated in Group 1; in Group 2, they were evaluated before and after nine weeks from the start of immunotherapy. Results: Patients of Group 1 showed a higher prevalence of APA and AHA than controls: 21 of them had APA, 16 had AHA, and 11 had both autoantibodies. In total, 7 of 13 patients in Group 2 became APA-positive and 3 became AHA-positive after nine weeks of immunotherapy, showing an increase in prolactin and a decrease in ACTH and IGF-1 levels compared with basal values. Conclusions:Anti-pituitary and anti-hypothalamus antibodies seem to play a pivotal role in hypothalamic–pituitary autoimmunity and secondary endocrine-related alterations evoked by anti-PD-1 and PD-L1 antibodies.

Circulating levels of endothelial progenitor cells (EPCs) involved in endothelial homeostasis are often reduced in people with type 1 diabetes (T1D). The Glycemia Risk Index (GRI) quantifies the quality of glucose control by assessing both hypo- and hyperglycemia risk. We aim to investigate the association between the GRI and circulating EPC levels in people with T1D. This cross-sectional study included 132 adults with T1D, on intensive insulin therapy. We calculated GRI from 14 days continuous glucose monitoring-derived metrics and quantified EPCs count by flow cytometry, stratifying results by GRI zones, ranging from A (lowest risk) to E (highest risk). Higher GRI scores were significantly associated with poorer metabolic parameters. Circulating levels of CD34⁺, CD133⁺, KDR⁺, and CD34⁺KDR⁺ cells were lower in participants with a worse GRI compared to adults with a better GRI. Linear regression analyses showed a negative association between GRI and CD34⁺ (β = −1.079, p = 0.006), CD34⁺CD133⁺ (β = −0.581, p = 0.008), and CD34⁺KDR⁺ (β = −0.147, p = 0.010). No significant association was found between HbA_1c and any EPC phenotype. Adults with T1D and a high GRI level had a lower EPCs count. GRI was significantly associated with certain EPC phenotypes, suggesting its potential role as a biomarker for cardiovascular risk assessment.