ECEESPE2025 ePoster Presentations Pituitary, Neuroendocrinology and Puberty (220 abstracts)
1ULS Santa Maria, Endocrinology, Diabetes and Metabolism Department, Lisbon, Portugal; 2ULS Santa Maria, Rheumatology Department, Lisbon, Portugal
JOINT2482
Introduction: Cushings syndrome (CS) corresponds to a state of glucocorticoid excess. Endogenous CS can be either adrenocorticotropic hormone (ACTH) dependent or independent, with Cushings Disease (CD) being the most common cause of ACTH dependent CS. Along with increased mortality, cardiovascular, metabolic, and musculoskeletal complications, CS also leads to some degree of immunosuppression, mainly by a decrease in lymphoid tissue and lymphopenia. CS cure, on the other hand, stimulates the immune system and may result in the exacerbation of immune mediated diseases.
Case Report: A 49-year-old woman was sent to the endocrinology clinic for a left adrenal incidentaloma. Personal history was notable for severe osteoporosis (spine T-score -2.5 and femur 2.2) and an episode of panuveitis at the age of 18. Further enquiry revealed recent significant weigh gain, buffalo hump, easy bruising, lower limb oedema and hypertension. Abdominal CT scan and MRI described a 1.1cm adenoma in the left adrenal gland. Laboratorial work-up suggested ACTH-dependent hypercortisolism. Desmopressin stimulation was suggestive of CD and pituitary MRI confirmed a right pituitary adenoma with 8 × 11 × 12mm. Transsphenoidal tumorectomy was performed confirming a corticotroph adenoma. Postsurgical serum cortisol was 0.7 mg/dl, and the patient was discharged with hydrocortisone 20+10mg and desmopressin 60mg daily. In the following weeks a cervical/shoulder girdle discomfort appeared with progressive development of arthralgias, persistent coughing and xerostomia. Additional evaluation revealed an erythrocyte sedimentation rate of 120 mm, with a C-reactive protein of 1.84 mg/dl and an angiotensin converting enzyme of 77 IU/L. CT scan confirmed the presence of supraclavicular, mediastinal and hilar lymph nodes, with diffuse areas of consolidation and densification of the pulmonary parenchyma, mainly in the lower lobes. Transbronchial lymph node biopsy was carried out and confirmed the presence of a non-necrotizing granuloma. The bronchoalveolar lavage had lymphocytosis (26%) with a CD4/CD8 ratio of 3. Lung function tests showed a slight decrease in DLCO of 68%. ALL these findings are consistent with sarcoidosis.
Discussion and conclusion: Autoimmune disorders are a possible complication after CS cure. Thyroid disorders and rheumatological diseases are the most common occurrences. Sarcoidosis has been described, usually presenting with skin findings, pulmonary involvement or both. Glucocorticoid-withdrawal syndrome is an important alternative diagnosis with symptoms like myalgia and asthenia being common to CS, adrenal insufficiency and autoimmune disorders. A close follow-up is of utmost importance in the posttreatment period of CS and a high level of suspicion is required when clinical presentation deviates from what is expected.