Endocrine Abstracts

Introduction: Suppression of TSH usually indicates hyperthyroidism. But the etiology of low TSH is very wide, including pituitary pathology. In this report we describe a case diagnosed and treated for hyperthyroidism. Later on, the persistence of suppressed TSH after therapy of hyperthyroidism was due to a GH-secreting pituitary adenoma.

Case presentation: A 47-year old woman was referred to our clinic for investigations, due to thyroid pathology. The patient was diagnosed in 2016 with hyperthyroidism, due to Toxic adenoma. Therapy was antithyroid drug Methymazole was given for few months and radioiodine treatment was done thereafter. After therapy with radioiodine the patient developed hypothyroidism, TSH increased and Levothyroxine therapy was started. After 1 year, laboratory determinations revealed low TSH and low/normal FT₄. The patient developed exophthalmos. Levothyroxine therapy was stopped, antithyroid therapy was restarted but TSH had continuing to be suppressed. Thyroid ultrasound presented a right nodular goiter, with a solid nodule with increased Doppler vascularization. Thyroid immunological determinations revealed high titers for TSH-Receptors antibodies and anti-Thyroglobulin antibodies, indicating an autoimmune thyroid disease. Laboratory determinations at admittance in our Clinic detected high values for Phosphorus (5.8 mg/dl, NR 2–4.5) and Alkaline Phosphatase (127 U/l). Renal failure and other frequent causes of hyperphosphatemia were excluded. At clinical examination, no signs of hyperthyroidism were detected, but a mild form of mandible prognathism and enlarged hands were notified. IGH-1 determinations revealed high values (891 ng/ml) and increased GH level didn’t suppress after OGTT (GH after OGTT 14.6 ng/dl). Acromegaly was diagnosed and pituitary MRI was performed, that indicated a 13mm pituitary adenoma. The suppression of TSH after treatment with radioactive iodine was due to a pituitary insufficiency.

Conclusion: This case, with an associated thyroid and pituitary pathology, highlights the multiple etiologies for TSH suppression. The presentation illustrates the importance of clinical examination of the patient and the values of all pathological laboratory determinations.