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MRI techniques for diagnosing pituitary lesions have witnessed a rapid evolution since it first came to use in the early s. The resolution and sensitivity of these techniques were until the early s comparable to those of CT-scans, but presented a superior soft-tissue resolution and a greater delineation to adjacent structures.

With the introduction of dynamic contrast-enhanced MRI in the early s 69 , the sensitivity for diagnosing pituitary microadenomas increased vastly MRI is usually the only method needed for the morphological investigation of endocrine active pituitary adenomas. Radiologic evaluations differ in regard to the size of the lesion, i. Pituitary macroadenomas are usually located in the center of the sella turcica with extra sellar extension, growing upward toward the third ventricle and sometimes the foramen of Monro 71 , Studies on TSH-producing adenomas using MRI, describe macroadenomas in the majority of cases and usually hypoechoic appearance in respect to normal pituitary tissue after gadolinium administration In comparison to other similar, and more common, pituitary adenomas such as GH- and PRL-producing adenomas , TSH-producing adenomas tend to have a higher degree of microscopic invasion and intra- and peritumoral fibrosis, which correlate with the findings in surgical material In this regard, a protocol with several sequences such as dynamic, contrast enhanced, spin echo T1 and T2 is preferable to not just detect elusive lesions but also to delineate tumor tissue to adjacent structures and normal pituitary tissue.

Such signs of microscopic invasion can contribute with important prognostic information before surgical treatment Microadenomas are more difficult to detect, but have often a hypoechoic signal on contrast-enhanced T1 sequences. Smaller lesions require more complex methods and high-field scanners. Different methods and approaches have been assessed in regard to optimize the detection rate of microadenomas.

Pinker et al. They also showed that the use of a 3. Lee et al. The multiplanar combination of sagittal and coronal projections in gadolinium-enhanced MRI are now the preferred tools for visualization and is considered the modality of choice for pituitary imaging 71 , There are however some disadvantages that comes with the use of MRI at 3.

Prolonged T1 relaxation time, radiofrequency magnetic field inhomogeneity and increased susceptibility artifacts have been proposed Kakite et al. SPGR and fSPGR also demonstrate superior soft-tissue contrast compared with the spin echo technique and can be performed in notably thin-slice sections Masopust et al.

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TSHomas usually manifest as macroadenomas and with a fibrous consistency, and thus the sensitivity of the spin echo sequence is, in most cases, sufficient. A diagnostic imaging with higher specificity would be a better contribution in the current diagnostic workup. In this regard, functional imaging seems to have the potential to provide a better detection rate with higher specificity in pituitary adenomas in general and in TSHomas in particular.

As pituitary gland and pituitary adenomas express somatostatin receptors, SSTR, as oppose to adjacent structures and brain tissue, these receptors provide excellent conditions for functional imaging.


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TSHomas have a high expression density of somatostatin receptors compared to normal pituitary tissue, in particular SSTR 2 and 5, which makes it a good candidate for scintigrahpic evaluation. Scintigraphy with radio-labeled octreotide can successfully localize most hormone-producing adenomas due to high expression rate of somatostatin receptors TSHomas are detectable with this technique 82 ; however, the specificity of this technique is low, as positive scans can occur in the case of a pituitary mass of different types, either secreting or non-secreting, and even in normal pituitary tissue.

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However, the study was unable to predict the response to somatostatin analog treatment. This technique has only been evaluated in a small number of case series with successful results in diagnosing an ectopic TSH-producing adenoma 83 and pituitary carcinoma 84 , thus implying a promising prospect for better functional imaging in future diagnostic workup of TSHomas. The most important differential diagnoses are laboratory interference and mutations resulting in a changed affinity for the thyroid hormone receptor or to carrier molecules.

Also, rarely, thyroxin binding globulin TBG deficiency can result in decreased levels of total thyroid hormone and thereby increased free T4 85 , from lower binding capacity, even if TBG deficiency is most commonly presented as central hypothyroidism. Laboratory interference is not a true increase in thyroid hormone production, but results from interfering substances in the laboratory method used, such as thyroid hormone antibodies 87 , heterophilic antibodies 88 or other method specific interferences 89 , 90 , result in falsely increased thyroid hormone levels In clinical practice, different forms of laboratory interference are rarely diagnosed, as the important issue is to find a TSHoma.

Laboratory interference can be suspected when thyroid hormone levels vary among different laboratory methods: this can be detected through comparing the results from one sample with several analytical platforms. When disturbances due to the laboratory method are excluded, the main differential diagnosis to TSHomas is mutation in the thyroid hormone receptor with the syndrome of RTH 91 Table 2 or mutations in thyroid hormone transport proteins, familiar FDH These conditions have a variety of mutations.

Individuals with genetic variations in thyroid hormone transport proteins are clinically euthyroid, but present with altered thyroid function tests, and do not require treatment. In FDH, laboratory interference may occur as the change of binding affinity to prealbumin interacts differently in different methods. FDH is the most common inherited cause of increased T4 Mutation analyses are costly compared to FT4 and TSH blood samples, thus, a first step may be to analyze thyroid hormones in first-degree relatives, in order to strengthen the suspicion of a heredity cause for the syndrome of inappropriate TSH secretion.

As many patients approach health care with a laboratory constellation of unsuppressed TSH and increased thyroid hormone levels, all differential diagnoses need to be considered in parallel for an effective clinical workup. To support the investigation, clinical presentation can be useful Table 2.

Goiter is common in patients with TSHomas and RTH, but the response to stimulatory tests differs due to the pituitary involvement Table 2. Diagnosing a patient with a syndrome of inappropriate TSH secretion is complicated and requires special competences, especially in situations where patients have received treatment for an assumed primary hyperthyroidism 17 , 19 , 27 or in the rare cases where RTH is coexisting with a TSHoma RTH is considered to predispose to both pituitary hyperplasia and to the development of adenomas and, even in some rare cases, ectopic TSHomas 22 , 23 , 24 , 25 , 26 , 27 , making regular monitoring of these patients a necessity.

In , a case with autonomous functioning thyroid nodules preceded by a TSHoma was first reported Thus, a plausible relationship between TSH stimulation from the pituitary on the thyroid gland was established. A trophic hormone may cause autonomous secretion in the thyroid gland, which resembles what happens in other target glands. Patients exposed to unregulated and inappropriate TSH levels may have an increased risk for well-differentiated thyroid cancer In 62 patients with TSHomas, three cases with this thyroid cancer were found 97 , and it is also reported in other case reports 98 , 99 , , A common disease can inevitably co-exist with a more rare disorder without any causal relationship, but there may be a rationale for excluding neoplastic lesions in the thyroid gland, e.

Exophthalmos is reported in TSHoma because of tumor invasion in the orbit Autoimmune hypothyroidism may co-exist with TSHoma, but any causality is yet unclear , , Pituitary hyperplasia from increased TSH production in hypothyroidism may in some rare cases mimic a macroadenoma In the same way as TSHoma is reported, in RTH, where longstanding stimulation may promote tertiary tumor evolvement 66 , , a secondary hyperplasia may mimic a pituitary tumor However, primary hypothyroidism in parallel may complicate the diagnosis of TSHoma and cause delay Pituitary adenomas rarely turn into pituitary carcinomas.

The majority of pituitary carcinomas secrete ACTH or prolactin and only two known cases of TSH-producing carcinomas are described in the literature , A transforming adenoma should be evaluated for the risk of developing into a carcinoma.


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TSHomas are rare tumors that in most cases demand special competence and involve a complicated routine of investigations. There has been much progress in the ability to separate TSHoma from differential diagnoses with a proper laboratory procedure. As TSHomas are rare and incidentalomas in the pituitary gland are common, an autonomous TSH production needs to be established.

The ideal diagnostic approach would be to simultaneously receive both hormonal and morphologic information, as with functional imaging. The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of this review. This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

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American Journal of Medicine 92 15 — Thyrotropin-secreting pituitary adenomas: report of seven cases.

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Journal of Clinical Endocrinology and Metabolism 72 — Mono- and plurihormonal thyrotropic pituitary adenomas: pathological, hormonal and clinical studies in 12 patients. European Journal of Endocrinology — Thyrotropin-secreting pituitary adenomas: clinical and biochemical heterogeneity.

Case reports and follow-up of nine patients. Annals of Internal Medicine — Mindermann T Wilson CB. Thyrotropin-producing pituitary adenomas. Journal of Neurosurgery 79 — A new strategy for thyroid function testing. Lancet 1 — Measurement of thyrotropin in clinical and subclinical hyperthyroidism using a new chemiluminescent assay.

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Journal of Clinical Endocrinology and Metabolism 69 — Thyrotropin-induced hyperthyroidism caused by selective pituitary resistance to thyroid hormone. Journal of Clinical Investigation 56 — Pituitary adenomas: high-resolution MR imaging at 1. Radiology — Different responses to chronic somatostatin analogues in patients with central hyperthyroidism. Clinical Endocrinology 62 — Pituitary stone: two cases of densely calcified thyrotrophin-secreting pituitary adenomas. Clinical Endocrinology 40 — Clinicopathological characteristics and therapeutic outcomes in thyrotropin-secreting pituitary adenomas: a single-center study of 90 cases.

Journal of Neurosurgery — Journal of Clinical Endocrinology and Metabolism 99 — The changing spectrum of TSH-secreting pituitary adenomas: diagnosis and management in 43 patients. Active and silent thyroid-stimulating hormone-expressing pituitary adenomas: presenting symptoms, treatment, outcomes, and recurrence. World Neurosurgery 82 — National incidence and prevalence of TSH-secreting pituitary adenomas in Sweden.

Journal of Clinical Endocrinology and Metabolism 98 — Thyrotropin-secreting pituitary tumors: diagnostic criteria, thyroid hormone sensitivity, and treatment outcome in 25 patients followed at the National Institutes of Health. Journal of Clinical Endocrinology and Metabolism 84 — European Thyroid Journal 2 76 — Ectopic suprasellar thyrotropin-secreting pituitary adenoma: case report and literature review.

World Neurosurgery 95 Ectopic TSH-secreting pituitary tumor: a case report and review of prior cases. BMC Cancer 14 Thyroid-stimulating hormone-secreting ectopic pituitary adenoma of the nasopharynx. Auris Nasus Larynx 41 — Hyperthyroidism caused by an ectopic thyrotropin-secreting tumor of the nasopharynx: a case report and review of the literature. Thyroid 23 — Ectopic TSH-secreting pituitary adenoma of the vomerosphenoidal junction.

Hyperthyroidism caused by an ectopic TSH-secreting pituitary tumor. Thyroid 6 — Pathohistological classification of pituitary tumors: 10 years of experience with the German Pituitary Tumor Registry. The prevalence of pituitary adenomas: a systematic review. Cancer — High prevalence of pituitary adenomas: a cross-sectional study in the province of Liege, Belgium.

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Journal of Clinical Endocrinology and Metabolism 91 — Prevalence and incidence of pituitary adenomas: a population based study in Malta. Pituitary 16 — Prevalence of pituitary adenomas: a community-based, cross-sectional study in Banbury Oxfordshire, UK. Clinical Endocrinology 72 — The incidence rate of pituitary adenomas in western Sweden for the period — Incidence of pituitary adenomas in Northern Finland in — Journal of Clinical Endocrinology and Metabolism 95 — Melmed S.

Pathogenesis of pituitary tumors. Nature Reviews Endocrinology 7 — Gold EB.

Epidemiology of pituitary adenomas. Epidemiologic reviews 3 — Linking medical needs and performance goals: clinical and laboratory perspectives on thyroid disease. Clinical Chemistry 39 — Thyrotropin-secreting pituitary tumors. Endocrine Reviews 17 — Pituitary tumours: TSH-secreting adenomas. Clinical aspects and therapeutic outcome in thyrotropin-secreting pituitary adenomas: a single center experience.

Journal of Endocrinological Investigation 32 — Kovacs KHE. Tumours of the pituitary gland. Washington, D. Clinicopathological characterization of TSH-producing adenomas: special reference to TSH-immunoreactive but clinically non-functioning adenomas. Endocrine Pathology 20 — Basic fibroblast growth factor expression by two prolactin and thyrotropin-producing pituitary adenomas. Endocrine Pathology 6 — Medical therapy of pituitary adenomas: effects on tumor shrinkage.


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Reviews in Endocrine and Metabolic Disorders 10 — Somatostatin receptor subtypes mRNA in TSH-secreting pituitary adenomas: a case showing a dramatic reduction in tumor size during short octreotide treatment. Endocrine Journal 54 — Cuevas-Ramos D Fleseriu M. Somatostatin receptor ligands and resistance to treatment in pituitary adenomas.