This case describes a young woman with a central hypothyroidism and mild hyperprolactinemia. In this condition, the serum TSH screening alone cannot reveal the dysfunction of the hypothalamic–pituitary–thyroid axis, as TSH levels are most frequently normal [1–3]. Central hypothyroidism is presently known to account for about 1:1,000 hypothyroid patients, but is still probably underestimated and the Endocrinologists should always consider this possibility when hypothyroid manifestations coexist with biochemical alterations or clinical manifestations pointing to a pituitary origin. In this case, the first consultant initially gave little attention to the mild hyperprolactinemia and considered to check more appropriately and extensively thyroid function tests and PRL levels only 2 years after the start of symptoms. Indeed, the correct diagnosis could be suggested by the presence of a pituitary mass or history of pituitary disease, but a more careful recording of the personal history of this woman reporting the head trauma could have helped to anticipate the diagnosis. Indeed traumatic head injury or vascular accidents even of minor entity can account for several cases of central hypothyroidism previously classified as idiopathic. Most frequently, central hypothyroidism is combined with other pituitary hormone deficiencies that may mask the manifestations of a mild hypothyroid state, but their presence would support the central origin of thyroid dysfunction. In this case, the mild hypercholesterolemia was a finding supporting the recent onset of hypothyroidism, while the hyperprolactinemia, the absence of antithyroid autoantibodies and the normal findings at thyroid ultrasound were indeed pointing to the central origin.

LT4 replacement therapy was correctly started. The initial daily dose was mistakenly judged sufficient by the consultant based on normal values of all thyroid function tests. Indeed, TSH determination is not a reliable marker of thyroid hormone action at the hypothalamic–pituitary level in patients with central hypothyroidism but the finding of unsuppressed TSH levels during thyroxine therapy is strongly suggestive of an insufficient regimen [1, 4–6]. Accordingly, LDL-cholesterol was still abnormal despite the dietary restriction. Due to the persistence of hypothyroid manifestations, the patients went to another consultant that correctly interpreted the biochemical results and augmented the daily dose of thyroxine. The regimen of 1.4 μg/kg bw was effective in restoring the wellbeing, normal menstrual activity, and physical performance in this sportswoman. The finding of suppressed TSH accompanied by thyroid hormone levels in the central part of normal range and the normalization of LDL-cholesterol were supporting the correct replacement.