Adrenal gland
Aristidis Diamantopoulos 1 , Marina Koulenti 1 , Eirini Sampanioti 1 , Eirini Evangelatou 1 , Efstathios Dimitropoulos 1 , Panagiota Rapti 1 , Georgia Nikita 1 , Efthimia Botoula 1 , George Kyriakopoulos 2 , Dimitra Argyro Vassiliadi 1 & Stylianos Tsagarakis 1
1Department of Endocrinology, Diabetes and Metabolism, National Expertise Centre for Rare Diseases, Evangelismos General Hospital of Athens, Athens; [email protected]; 2Department of Endocrinology, Diabetes and Metabolism, National Expertise Centre for Rare Diseases, Evangelismos General Hospital of Athens, Athens
Background: ACTH-dependent Cushing’s syndrome (CS) is mostly associated with corticotroph adenomas or, infrequently, ectopic ACTH secretion(EAS). Adrenals may show diffuse bilateral enlargement or even macronodules. Adrenal metastases may occur in various cancers. They are often bilateral, irregular, with attenuation values >20 Hounsfield units(HU) on unenhanced CT scan and elevated SUVmax on FDG-PET scan. They may cause adrenal insufficiency due to the destruction of adrenal cortex, in which case glucocorticoid replacement therapy can improve the patient’s quality of life.
Case Presentation: A 62-year-old male presented with hypokalemia (2.1 meq/l), hyperglycemia (350 mg/dl) and deteriorating muscle weakness. Diagnosis of severe ACTH-dependent CS was confirmed by significantly elevated levels of cortisol (1931 nmol/l), 24-h urinary free cortisol >11×ULN (>2760 nmol/24 hr) and ACTH(60 pg/ml). Adrenal glands were bilaterally enlarged, ~50HU on CT with inhomogeneous contrast enhancement. There were sizable lung and pancreatic tumors and peritoneal implants. On FDG-PET scan, there was uptake on all lesions (adrenals’ SUVmax: 10.5) as well as bones, compatible with multiple metastases. Transbronchial biopsy diagnosed poorly differentiated small cell neuroendocrine lung carcinoma with ACTH production, ki-67:90%. Hypercortisolism responded to metyrapone 2 gr/day (~369 nmol/l) within 4 days. Cortisol levels decreased further after chemotherapy. After 2 cycles of etoposide/cisplatin the patient is eucortisolemic, normokalemic with well-controlled diabetes without metyrapone.
Conclusions: Based on the CT and FDG-PET findings, we consider that the adrenal gland lesions probably represent metastases, rather than ACTH-induced adrenal hyperplasia. Adrenal biopsy that could confirm our hypothesis was not performed since it would not provide patient-relevant benefit. Although adrenal metastases usually cause adrenal insufficiency, in this patient they were associated with severe CS indicating the presence of non-infiltrated adrenal cortex, stimulated by EAS by the primary tumor but also possibly by adjacent metastatic cells.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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