Endocrine Abstracts

Introduction: Several treatments may be proposed against neuroendocrine tumors such as targeted therapies (Tyrosine kinase inhibitors: TKI) and somatostatin agonist. Since the first use of TKI in the oncological field, several studies have shown endocrine side effects type dysthyroidie. Several complex pathophysiological mechanisms and variable from one patient to another have been evoked ranging from a simple thyroiditis to complex autoimmune phenomena (cases of Basedow revealed have been reported as well as hashimoto.

Case: This is a 68-year-old patient cholecystectomized with arterial hypertension and type 2 diabetes who have been on glucophage for 10 years, followed for a pancreatic neuroendocrine tumor of incidental discovery measuring 54×32 mm, with hepatic metastases. Biological check up reveals chromogranin A <100 ng/ml. Puted on tyrosine kinase inhibitor 50 miligramms per day, after 3 therapeutic cycles (4weeks ON 2 weeks OFF), acute renal insufficiency appeared (clearance creatinine: 24 ml/min) and hypothyroidism TSH: 40 Uui/ml (0.46–4.6)/ FT4: 9 pmol/l (9.6–31). Treatment with Sinutinib was discontinued due to digestive side effects (grade 4) in addition to hematotoxic effect (Hemoglobin: 8 g/deciliter). Exploration of the cause of hypothyroidism concluded to a destructive cause. Thyroglobulin < 0.2 ng/ml undetectable. Antibodies (Ab) anti tyroperoxidase and Ab Tyroglobulin are normals. Cervical Ultra sound find a normal overall volume of 10 cm³ with thyroiditis features. The results of histopathological examination of an hepatic metastasis biopsy show proliferation marker Ki67 <3% as well as the digestive intolerance stage 4 have made that Sinutinib is arrested definitively with switch to somatostatin agonists. Hypothyroidism was transient and reversible after 1month stop TKI.

Conclusion: Several studies have appreciated the beneficial effect of hypothyroidism in the survival of renal cancer as well as small-cell lung cancer which is not yet the case To our knowledge for neuroendocrine tumors of the pancreas which will be desirable in the to come up. In the event of confirmation of this latter effect, the treatment of subclinical hypothyroidism (defined by high TSH compared to normal FT4) will depend in this context in the absence of pre-existing cardiovascular pathologies rather than the existence of the symptoms of hypothyroidism. Even somatostatin agonist may have an inhibitory effect on thyroid function which requires regular monitoring of both TSH, FT4 and despite the fact that the mechanism is often central because of the past of destructive thyroiditis in our patient case.