ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2019) 63 P1110 | DOI: 10.1530/endoabs.63.P1110

Isolated central hypothyroidism as a clue for empty sella syndrome

Sofia Gouveia

Amato Lusitano Hospital, Castelo Branco, Portugal.

Introduction: Isolated central hypothyroidism is a rare disease. Acquired causes for central hypothyroidism include iatrogenic, traumatic, immunologic, infiltrative, infectious, vascular or space-occupying lesions. Empty sella may present with endocrine dysfunction, mainly hyperprolactinemia and growth hormone or gonadotropin deficiency. Few cases of empty sella associated with isolated TSH deficiency were published.

Case report: A 66-years-old female with a diagnosis of hypothyroidism established five years before was referred to Department of Endocrinology due to challenges on levothyroxine dose management. She had a previous history of acute coronary syndrome, heart failure, bronchitis, obesity, hypertension, type 2 diabetes and depression. She had three uneventful pregnancies and entered menopause at 55. She denied previous cranial surgery, trauma or irradiation. At first Endocrinology’s appointment, her pharmacologic habits included 137 μg levothyroxine, pantoprazole, clopidogrel, telmisartan, lercanidipine, ivabradine, sitagliptin/metformin, tiotropium, fluoxetine, bupropion, sertraline, quetiapine, alprazolam and vinpocetine. Cervical ultrasound showed a normal sized homogeneous thyroid. Her blood results were the following: TSH-2.73 μUI/mL[0.40–4.40], FT4-0.73ng/dL[0.80–1.80], TT4-3.60 μg/dL[4.50–10.90], FT3-2.43pg/mL[2.0–4.2], TT3-0.99ng/dL[0.60–1.81], TPOAb-42.7U/mL[0–60], TGAb-15.5U/mL[0–60]. She also presented analysis performed 8 years earlier (without levothyroxine replacement) with a TSH of 2.21 μUI/mL[0.40–4.40] and a FT4 of 0.67ng/dL[0.89–1.76]. Levothyroxine dose was increased to 150 μg and the patient was advised to take it 30 minutes before pantoprazole and breakfast. Considering the low FT4/TT4 levels and normal TSH, a pituitary MRI and hormonal evaluation were requested. MRI showed an empty sella without evidence of adenoma on the flattened pituitary tissue. No further pituitary hormone deficiencies were detected: FSH-43.69UI/L[23.0–116.3], LH-21.19UI/L [15.9–54.0], estradiol-13.35pg/mL[0–32.2], progesterone<0.21ng/mL [<0.73], prolactin-4.25ng/mL [1.8–20.3], TSH-0.18 μUI/mL[0.40–4.40], FT4-0.83ng/dL [0.80–1.80], IGF1-95ng/mL[81–225], ACTH-10pg/mL[9–52]; cortisol post-tetracosactide at 0/30/60 minutes-5.21/23.35/27.32 μg/dL[4.3–22.40] and urine specific gravity 1.017. Anti-pituitary antibodies were negative.

Discussion: It needs to be emphasized that low FT4 levels with inappropriate low/normal TSH (without a background of non-thyroidal illness syndrome or pharmacologic interference) should trigger investigation for central hypothyroidism. It is crucial to determine the underlying cause and exclude multiple pituitary hormone deficiencies, which may alter the therapeutic approach. Central hypothyroidism is sometimes overlooked. In the current case, the type of hypothyroidism was misdiagnosed for a long period of time, which could have had a deleterious impact in case of an underlying sellar/suprasellar tumour or concomitant adrenal insufficiency. The only identified cause for central hypothyroidism in this patient was empty sella. This disorder remains as an uncommon cause for isolated TSH deficiency.

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