ECE2019 ePoster Presentations Thyroid (23 abstracts)
Department of diabetology, endocrinology, nutrition and metabolic diseases Hospital Errazi, CHU Mohammed VI, Marrakech, Morocco.
Introduction: Detection of TSH-receptor autoantibodies in the diagnosis of graves disease is well established. however these autoantibodies may not be always present in some forms of correctly observed autoimmune hyperthyroidism. Here, we describe a patient with hyperthyroid Graves disease without detectable thyrotropin receptor antibodies.
Case report: She was A 55-year-old woman, presented with a 2 years history of increased sweating, palpitations, polyphagy and insomnia with weight loss of 10 kg. Clinical examination revealed exophthalmos and lid lag, a fine tremor of her fingers, the pulse was 100/min and a small diffuse goiter without trill. Blood tests demonstrated high FT4=55.3 pmol/L (NR 1222), FT3=29.2 pmol/l (3.16.8), TSH<0.005 mIU/l (0.274.2), Measurement of her thyroid-stimulating hormone was négatif. Thyroid scintigraphy shows an enlarged gland with homogeneous uptake of radiotracer in both lobes.
Discussion: Immunogenic hyperthyroidism (Graves or Basedows disease) is a consequence of pathological stimulation of the thyroid gland by stimulating TSH-receptor autoantibodies (TSAbs). In Differentes studies The results show that it is extremely rare to have negative TSH receptor autoantibody in patients with active hyperthyroid Graves disease. In our case palpation, clinical findings, and the data of thyroid sintigraphy were sufficient to establish the diagnosis of Graves disease despite of TSH receptor autoantibodies were undetectable. Other mechanisms can also activate graves disease than antibody-dependent ones or a local production of antibodies within the thyroid can be suggested.