Introduction: Functioning gonadotroph adenomas (FGPAs) in males are rare and typically present with macroorchidism. In elderly patients, the presentation can be confounding. This case illustrates a unique scenario where a pituitary tumor masked the physiological decline of testosterone, maintaining the patient’s stamina despite Introduction testicular involution. Case: A 65-year-old male was referred for a pituitary macroadenoma (10.7 × 10.6 × 11.4 mm) following progressive headaches. Remarkably, the patient denied symptoms of andropause; his stamina, mood, and libido were wellpreserved. Investigations revealed elevated folliclestimulating hormone (15.42 mIU/mL) and luteinizing hormone (12.1 mIU/mL) with normal testosterone levels. Scrotal ultrasound showed bilateral testicular involution (right: 8.66 mL, left: 7.21 mL), contradicting the expected macroorchidism of FGPA. Although the patient felt his vision was normal, a confrontation test revealed temporal visual field defects, indicating chiasmatic compression. This case presents a striking clinical discordance where tumorinduced gonadotropin hypersecretion provided a supraphysiological drive to the involuting testes, maintaining testosterone levels and masking andropause. The primary indication for transsphenoidal surgery is the Introduction evidence of visual field defects. However, removing the adenoma will abruptly eliminate this “hormonal drive.” Postoperative management will focus on rigorous hormonal monitoring. Testosterone replacement therapy is not immediately indicated; rather, it will be carefully planned only if postoperative evaluations demonstrate a significant hormonal decline accompanied by symptomatic hypogonadism. This tailored approach ensures that the benefits of intervention outweigh the potential risks in an elderly patient. Conclusion In elderly patients, FGPAs can mask age-related hormonal decline. In this case, clinicians must treat the patient, not just the tumor. Anticipating a potential decline in postoperative stamina is as crucial as the surgery itself. Comprehensive hormonal evaluation and a personalized approach to therapy are essential to preserve quality of life after the “masking” effect is removed.
Male ; Andropause ; Gonadotrophs

Introduction: Autoimmune thyroid disease can follow a triphasic course: thyrotoxicosis, a transient euthyroid period, and eventual hypothyroidism, and may coexist with myelodysplastic syndrome (MDS) in the context of immune dysregulation. Case: We describe a 35-year-old male with MDS (multilineage dysplasia) receiving cyclosporine who initially presented with painless thyrotoxicosis, with suppressed thyroidstimulating hormone (TSH) and elevated free thyroxine (FT4). During this hyperthyroid phase, thyrotropin receptor antibody (TRAb) was positive. Over time, his thyroid status fluctuated, progressing to overt hypothyroidism, and he had poor adherence to thyroid medications. On admission, he had prominent hypothyroid features (fatigue, cold intolerance, slowed movement, periorbital puffiness) with severe biochemical hypothyroidism (TSH 49.5 µIU/mL; FT4 0.419 ng/dL). Anti-thyroid peroxidase (anti-TPO) antibodies 12.62 IU/mL (negative <5.61 IU/mL; positive ≥5.61 IU/mL) showed an autoimmune response to the thyroid. Thyroid ultrasound showed heterogeneous, hyperechoic with some hypoechoic parts, and no significant increase in thyroid vascularity was observed, supporting autoimmune thyroiditis representation. His hematologic profile remained consistent with MDS, with chronic macrocytic anemia and thrombocytopenia. Conclusion This case highlights a dynamic autoimmune thyroiditis phenotype progressing from a hyperthyroid phase with TRAb positivity to higher anti-TPO overt hypothyroidism in a patient with MDS. In individuals with MDS and changing thyroid function tests, clinicians should keep autoimmune thyroiditis variants in mind and use thyroid antibodies together with ultrasound to secure the diagnosis when the clinical pattern is typical.
Myelodysplastic Syndromes ; Thyroiditis, Autoimmune ; Hypothyroidism ; Thyrotoxicosis