Endocrine Abstracts

TSH-secreting pituitary adenomas (TSH-omas), together with resistance to thyroid hormone (RTH), are defined as syndromes of ‘inappropriate secretion of TSH (IST)’, based on the common hormonal profile characterized by high levels of FT₄ and FT₃ in the presence of measurable TSH concentrations, a finding that contrasted with that observed in primary hyperthyroidism in which TSH is always undetectable. Today, the routine use of ultrasensitive immuno-metric assays for TSH measurement allows a clear distinction between patients with suppressed and those with non-suppressed circulating TSH concentrations, i.e. between patients with primary hyperthyroidism (Graves’ disease or toxic nodular goiter) and those with TSH-oma or RTH. Failure to recognize these different diseases may result in dramatic consequences, such as improper thyroid ablation or unnecessary pituitary surgery in RTH patients. Differential diagnosis mainly rests on dynamic testing, such as TRH and T₃ suppression tests, along with the measurement of glycoprotein hormone α-subunit and some parameters evaluating peripheral thyroid hormone action. In RTH, the finding of the same biochemical profile in relatives is highly consistent with the diagnosis of RTH. Surgical treatment is the first line therapy for TSH-omas, while the majority of patients with RTH does not need any therapy. In RTH patients with tachycardia, treatment with selective beta-blockers is indicated. The medical treatment of TSH-omas mainly rests on the administration of somatostatin analogs (octreotide or lanreotide). Both analogs are effective in reducing TSH and α-subunit secretion in more than 90% of cases with consequent normalization of FT₄ and FT₃ levels and restoration of the euthyroid state in the majority of them. In about one third of patients, a clear shrinkage of tumor mass and vision improvement could be demonstrated. Whether somatostatin analog treatment may be an alternative to surgery and/or irradiation in patients with TSH-oma remains to be established.