ECE2021 Audio Eposter Presentations Late Breaking (114 abstracts)
1C.I. Parhon, National Institute of Endocrinology, Bucharest, Romania, Pituitary and neuroendocrine pathology, Bucharest, Romania; 2Carol Davila University of Medicine and Pharmacy, Bucharest, Romania, Endocrinology, Bucharest, Romania; 3Focus medical center, Oncology, Bucharest, Romania
Introduction
Lung Neuroendocrine tumors (NETs) range in aggressiveness from low-grade typical carcinoid (TC) and intermediate-grade atypical carcinoid (AC) to the high-grade large cell neuroendocrine carcinoma (LCNEC) and small cell lung carcinoma (SCLC). TC have excellent prognosis post-surgery and European Neuroendocrine Tumor Society (ENETS) recommands no adjuvant therapy for these well diferentiated tumors.
Case report
A 67-year old, hypertensive woman was referred to our Institute for assessement of thyroid function, accusing exertional dyspnea and chronic hypokalemia. She has a recent history of thyreotoxicosis, treated with antithyroid drugs for a few months. Also, two months before presentation, she underwent a cardiac tamponade with emergency pericardial drainage by left anterolateral thoracotomy. The patient is oncologically monitored for a typical bronchial carcinoid, surgically treated 9 years ago. Her oncologist yearly recommended computer tomography of chest and abdomen, who revealed at the last assessement a left adrenal mass and two hepatic lessions. Soon after that, she performed a FDG-PET CT, which did not show a metabolic active lesion. Her physical examination was normal, except a slightly elevated blood pressure, 140/90 mmHg, and an grade I WHO thyroid goiter. Biochemistry confirmed the hypokalemia (plasma K= 2.9 mmol/l, normal range 3.55). Thyroid function was normal, spontaneously. TSH receptor antibodies and ATPO were negative. Thyroid ecography revealed a hypoechoic, pseudonodular echogenicity. Her plasma metanephrines and normetanephrines, basal cortisol, cortisol after 1mg overnight supression test, ACTH, prolactin and PTH, were also in the normal range values. Plasma Aldosteron level was high (377 pg/ml, normal range 18.8256.7) and plasma renin level supressed (0.68 pg/ml, normal range 2.6427.66), but taken under antihypertensive agents known to interfere with these hormons and under hypokalemia. Her neuroendocrine markers were as follows: Cromogranin A level was 116.9 ng/ml (normal range 20100), serotonin level was 78 ng/ml (normal range 80400), neuron specific enolase level was 15.01 mg/l (normal range 018.3) and urinary 5 hydroxiindolacetic acid level was in the normal range. Octreoscan showed single hepatic and pericardial lesions with somatostatin receptor expression, suggestive for secondary determinations of typical pulmonary carcinoid. She was discharged with the recommendation to increase the dose of antialdosteronic diuretic, potassium supplements, repeat thyroid function after 8 weeks and a recommendation of a hepatic biopsy, followed by resection of the lesion if secondary hepatic determination confirmed. Also, a somatostatin analog therapy was initiated.
Conclusion
For the optimal management of NETs, a detailed anamnesis is necessary and requires decision-making within a multidisciplinary team.