SUN-081 Transient Supression of Pituitary Function Induced by Treatment with TNF-alfa inhibitor- Hypophysitis or Impairment in Regulation of Calcium as Intracellular Mediator?

Abstract Disclosure: I.N. Rosa: None. L.A. Naves: None. Background. A variety of immune-related adverse events (irAE) have been described in patients under biologic treatment, specially immune checkpoints inhibitors (ICI). Although the impairment of pituitary function related to biological disease-modifying antirheumatic drugs (bDMARDs), as TNF-α inhibitors, is uncommon. We present a clinical case and discuss the potential mechanisms associated to immune and intracellular mediators as calcium regulation in pituitary during TNF-α inhibitor treatment. Clinical Case: A 27-year women presented at the Endocrinology Service, complaining of recurrent holocranial headache, fatigue, drowsiness and amenorrhea in the last six months. The patient had previous diagnosis of Psoriatic Arthritis and Hydroadenitis, under treatment with Adalimumab for 12 months. She presented a significant improvement of the inflammatory indexes (DAPSA, HAQ-DI, VAS, IHS4) on the first months of treatment, that remained stable during therapy. Hormonal evaluation suggested suppression of lactotrophic (PRL:4,3 ng/mL), somatotropic (IGF-1-1 SD) and gonadotropic axes FSH 0.5 mUI/mL; LH 0.07 mUI/mL; Oestradiol< 11 pg/mL, Testosterone 7ng/dL), since the third month of treatment; with integrity of corticotropic and thyrotrophic axes. MRI suggested a reduction on pituitary volume. Genetic predisposition was evaluated by investigation of HLA DQ2 e DQ8. Adalimumab was carried out and replaced by Secuquimumab. Hormonal evaluation was performed after 3 and 6 months, and a recovery of Lactotropic and Somatotropic axes was observed. Gonadotropic axes were still suppressed. Discussion and Conclusion: The hypothesis of TNF-α involvement in adenohypophysis hormone secretion was previously related to intracellular calcium mobilization, in experimental studies on prolactin and GH releases. Adalimumab is a recombinant monoclonal antibody involved in the inhibition of the binding of TNF-α to its receptors, p55 (TNFR1) and p75 (TNFR2), disrupting cytokine-driven inflammatory processes. In this case, central hypogonadism, and GH and prolactin secretion were transiently impaired during treatment with TNF-α inhibitors, reversible after Adalimumab replacement. The reduction in pituitary volume and gonadotropic, somatotropic and lactotropic axis may suggest hypophysitis, but TNF-α inhibitors can reduce intracellular Ca2+ and could interfere along the secretory pathway. Presentation: Sunday, July 13, 2025