Endocrine Abstracts

A 35-year-old male was evaluated for a five-year history of erectile dysfunction (ED) and reduced libido. His past medical history included asthma, post-traumatic stress disorder, tinnitus, vitamin D deficiency and mumps infection during adolescence, he was uncertain whether this was complicated by orchitis. Current medications included Fostair inhaler and intermittent salbutamol. He presented with erectile dysfunction and complete absence of morning erections, showing transient improvement with a short course of testosterone gel. There were no additional features suggestive of either primary or secondary hypogonadism. He has three children and no desire for further fertility. Initial workup revealed borderline low testosterone (7.7–10 nmol/l) with inappropriately normal follicle-stimulating hormone (FSH) at 6.1 IU/l and luteinizing hormone (LH) at 4.7 IU/l. Thyroid function test was normal and prolactin was 434 mIU/l. Glucagon test showed inadequate GH and cortisol response. Magnetic resonance imaging (MRI) of the pituitary demonstrated focal nodular enhancement of the pituitary stalk with slight T1 hyperintensity post-contrast. Multidisciplinary team (MDT) review suggested differential diagnoses of pituitary hypophysitis with infiltrative or infective underlying cause, versus pituitary stalk adenoma. Given the radiological and hormonal profile, the patient was initiated on hydrocortisone replacement therapy to address possible secondary adrenal insufficiency. Further work-up excluded systemic infection: serology for hepatitis B, hepatitis C, HIV, and QuantiFERON-TB testing were negative. Autoimmune screening including ANA, ENA, anti-mitochondrial, anti-dsDNA, anti-liver kidney microsomal, and anti-smooth muscle antibodies was negative. Full blood count and ESR were normal. IgG4 levels were within the normal range. Serum ACE was elevated (78 U/l; normal <50), raising the possibility of sarcoidosis, but calcium level was normal and CT thorax-abdomen-pelvis (CT-TAP) showed no lymphadenopathy or systemic involvement. Thus, granulomatous disease was considered unlikely. A subsequent MRI three months later, demonstrated mild reduction in both pituitary height and stalk thickness, suggesting interval improvement. These findings, together with negative systemic investigations, supported the working diagnosis of idiopathic pituitary hypophysitis.

Conclusion: This case highlights the diagnostic challenges of pituitary stalk lesions presenting with endocrine dysfunction. The presence of focal pituitary stalk thickening, together with the exclusion of alternative etiologies, supported a diagnosis of pituitary hypophysitis of unknown origin. Management focused on hormone replacement and close surveillance. This case underscores the need to consider hypophysitis in patients with pituitary stalk abnormalities and unexplained hypopituitarism, while ensuring thorough evaluation for potential underlying causes.