Endocrine Abstracts

JOINT1969

Introduction: Adrenal masses are a common finding during routine radiological procedures. While most are commonly benign, some may be malignant and/or have autonomous hormonal secretion. A rare pathology includes adrenal hemorrhage, leading to the subsequent organization of blood collections into hematomas. The most cases of adrenal hematomas are unilateral and traumatic in origin, though systemic infections and hemostatic disorders may affect both adrenal glands.

Case Presentation: A 57-year-old male patient was admitted to our hospital due to an incidentally discovered adrenal mass. A year before his admittance, he suffered a contusion of the right hemiabdomen, which was followed by persistent chronic chest pain, high blood pressure, headache, excessive sweating, and a rapid heartbeat. The chest CT showed pleural effusion and adrenal mass. Abdominal CT showed an altered morphology of the right adrenal gland, which was enlarged to 46x24x52 mm, suggestive of an adrenal hematoma. Surrounding fat tissue showed a characteristic periadrenal reactive change, typically seen in hematomas. Initial functional tests revealed primary hypocorticism (low morning cortisol: 73.9 nmol/l with compensatory elevated ACTH: 54 pmol/l) and normal electrolytes (Na: 135 mmol/l; K: 4.6 mmol/l). Urinary catecholamine levels were elevated (adrenaline: 18.02, noradrenaline: 803.4, dopamine: 3261.7 nmol/24h). Two months later, follow-up CT has detected a reduction in diameter of hypodense lesion in the right adrenal gland, measuring approximately 28x15 mm, suggesting a hematoma in the resorption phase. During hospitalization in our institution, the abdominal MRI showed a hypoplastic right adrenal gland, FDG PET-CT, performed due to elevated catecholamine levels, showed no evidence of increased metabolic activity suggestive of pheochromocytoma. Control catecholamine and their metabolite levels were normal (adrenaline 76.6; noradrenaline 332.3; dopamine 2492; metanephrine 0.21; normetanephrine 0.56; 3-methoxytyramine 0.92 nmol/24h). Evaluation of the HPA axis indicated the continued presence of hypocorticism (ACTH 15.1 pmol/l; Synacthen test: Cortisol: 152…239…120…38 nmol/l). Regarding the duration of hypocorticism in the presence of normal left adrenal gland additional tests, including immunology and virology, were conducted; the results were negative.

Conclusion: We concluded that hematoma formation resulted from trauma, leading to primary hypocoticism, and the increased catecholamine levels in these circumstances were likely due to adrenal medulla cell lysis. The case illustrates that adrenal hematoma can clinically and biochemically mimic pheochromocytoma. This phenomenon, known as“pseudopheochromocytoma,” is typically characterized by symptoms of sweating, headaches, palpitations, and hypertension, all of which were observed in our patient.

Keywords: adrenal hematoma, primary hypocorticism, pseudopheochromocytoma.