Abstract
The aim of this study was to determine the frequency of central thyroid dysfunctions in Cushing's syndrome (CS). We also aimed to evaluate the frequency of hyperthyroidism due to the syndrome of the inappropriate secretion of TSH (SITSH), which was recently defined in patients with insufficient hydrocortisone replacement after surgery. We evaluated thyroid functions (TSH and free thyroxine [fT4]) at the time of diagnosis, during the hypothalamo-pituitary-adrenal axis recovery, and after surgery in 35 patients with CS. The patients were separated into two groups: ACTH-dependent CS (group 1, n = 20) and ACTH-independent CS (group 2, n = 15). Patients' clinical and laboratory findings were evaluated in five visits in the outpatient clinic of the endocrinology department. The frequency of baseline suppressed TSH levels and central hypothyroidism were determined to be 37% (n = 13) and 26% (n = 9), respectively. A negative correlation was found between baseline cortisol and TSH levels (r = -0.45, p = 0.006). All patients with central hypothyroidism and suppressed TSH levels showed recovery at the first visit without levothyroxine treatment. SITSH was not detected in any of the patients during the postoperative period. No correlation was found between prednisolone replacement after surgery and TSH or fT4 levels on each visit. Suppressed TSH levels and central hypothyroidism may be detected in CS, independent of etiology. SITSH was not detected in the early postoperative period due to our adequate prednisolone replacement doses.
Highlights
The major regulators of TSH secretion are commonly known as the stimulation effect of TRH and the negative feedback of the fT4 and fT3
We demonstrated the effect of hypercortisolism on thyroid functions in patients with Cushing’s syndrome (CS)
Because it is common knowledge that plasma T3 levels decrease through peripheral type 1 deiodinase enzyme inhibition, we aimed to show the central effects of hypercortisolism on thyroid functions [23]
Summary
The major regulators of TSH secretion are commonly known as the stimulation effect of TRH and the negative feedback of the fT4 and fT3. The presence of hypercortisolemia may decrease TSH secretion by having a direct effect on the pituitary thyrotropin cells through annexin-1, somatostatin, leptin, and dopamine [4,14,15,16,17]. Another possible mechanism in the TSH suppression of glucocorticoids is the type 2 deiodinase enzyme activity that converts T4 to T3 in the hypothalamus and pituitary. Mathioudakis and cols. [7] reported that central hypothyroidism can be seen in patients with ACTH-secreting pituitary microadenomas with a prevalence as high as 18%
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