Journal of Endocrinological Investigation

, Volume 42, Issue 12, pp 1401–1406 | Cite as

A 2019 update on TSH-secreting pituitary adenomas

  • P. Beck-Peccoz
  • C. Giavoli
  • A. LaniaEmail author
Short Review


Thyrotropin-secreting pituitary adenomas (TSH-omas) present with signs and symptoms of hyperthyroidism and they are characterized by elevated serum levels of free thyroid hormones with measurable TSH levels. TSH-omas are very infrequent, accounting for less than 1% of all pituitary adenomas, thus representing a very rare cause of hyperthyroidism. For this reason, data collected on these rare disorders are relatively few, but some new researches shed new light on the etiopathogenesis, the diagnosis and the treatment of such a remarkable disease. Since the same biochemical picture is present in the syndromes of thyroid hormone resistance (RTH), in particular in the form of pituitary RTH, failure in distinguishing these clinical entities may lead to improper patient management. Conversely, early diagnosis and correct treatment of TSH-omas may prevent the occurrence of neurological and endocrinological complications, thus leading to a better rate of cure. In the present short review article, the most relevant recent advances in the pathophysiology of TSH-omas are described.


Thyrotropin-secreting pituitary adenoma TSH-oma Central hyperthyroidism Thyrotropin Free T4 Free T3 Resistance to thyroid hormones Transsphenoidal surgery Somatostatin analogs 


TSH-omas are characterized by an autonomous TSH secretion that is unresponsive to the negative feedback exerted by thyroid hormones. The continuous TSH overstimulation leads to T4 and T3 hypersecretion, this condition being classified as “central hyperthyroidism” [1, 2].

TSH-omas account for 0.5–2% of all pituitary adenomas [2], and the prevalence in the general population is estimated to be 1–2 cases per million. However, recent data obtained from the Swedish Pituitary Registry [13] demonstrated an increase in TSH-omas incidence from 1990 to 2009, the national prevalence in 2010 being 2.8 per 1 million inhabitants. TSH-omas have been documented both as part of multiple endocrine neoplasia type 1 syndrome (MEN 1) [14] and in a single patient with familial isolated pituitary adenoma (FIPA) with AIP mutation [15].

In the past, TSH-omas were diagnosed at the stage of invasive macroadenomas. Nowadays, hyperthyroid patients with unsuppressed TSH are more readily detected, thanks to the ultrasensitive immunometric assays for TSH and the measurement of circulating free thyroid hormones (FT4 and FT3), which are now routinely used. The recent introduction of the so called TSH with Reflex Free T4 strategy (i.e., FT4 measurement only in the presence of abnormal TSH) fails to recognize both central hypo and hyperthyroidism, thus leading to TSH-omas misdiagnosis.

In patients with resistance to thyroid hormones (RTH), thyroid function tests are indistinguishable from those found in TSH-oma patients [3] and signs and symptoms of hyperthyroidism are frequently found in the so called pituitary RTH (PRTH), a condition that is characterized by a more pronounced resistance to TH at the pituitary level.

These rare entities represent a diagnostic and therapeutic challenge, because failure in distinguishing between the two disorders may result in improper treatment, while the correct identification of a TSH-oma may prevent both neurological and endocrinological complications, thus leading to a better cure rate [4, 5, 6, 7, 8, 9, 10, 11, 12].

In this update we will give some new insights in the diagnosis and treatment of this unusual disorder. A number of reviews dealing with the management of TSH-omas have been published in the last few years by many groups [4, 5, 6, 7, 8, 9, 10, 11, 12] and they may help the readers of this update in the clinical assessment of such an unusual disorder.

Pathological aspects

Free or combined with α-subunit of any glycoprotein hormone (α-GSU), TSH beta subunit is found in adenomatous thyrotrope cells [2, 4, 5]. In 70% of the cases, TSH-omas secrete TSH alone, the remaining 30% being mixed adenomas that may co-secrete TSH and other anterior pituitary hormones (GH, PRL and LH/FSH) (Table 1). In this respect, GH and/or PRL co-secretion are the most frequent associations, possibly leading to acromegaly and/or amenorrhea/galactorrhea syndrome. The presence of these mixed adenomas can be explained by the expression of common transcription factors, such as Prop-1 and Pit-1, by thyrotrope, somatotrope, and lactotrope cells [16].
Table 1

Different types of TSH-secreting pituitary adenomas (updated end of November 2018)



% of total

Total TSH-secreting adenomas (TSH-omas)



Pure TSH-omas



Mixed TSH-omas












It is worth noting that a positive immunohistochemistry for one or more pituitary hormones does not necessarily correlate with its or their in vivo hypersecretion, thus leading to silent TSH-omas [5]. Moreover, the coexistence of Hashimoto’s thyroiditis and hypothyroidism with TSH-secreting tumors has been described [2, 17].

Most TSH-omas are macroadenomas invading the surrounding structures (i.e., the dura mater and bone) at the time of diagnosis [2]. Interestingly, patients who underwent previous thyroid ablation by surgery or radioiodine present a significantly higher occurrence of invasive macroadenomas as compared with those with an intact thyroid [1, 2]. To explain this observation, it is conceivable that the reduction of circulating TH levels caused by thyroid ablation alters feedback mechanisms, thus augmenting tumor ability to grow. In the last decade, microadenomas (diameter \(\le\) 1 cm) have been increasingly recorded (up to 30–35%) due to more sensitive an specific assays used to evaluate thyroid function and greater awareness among endocrinologists and general practitioners [6, 18].

The molecular mechanisms leading to the formation of TSH-omas still need to be thoroughly elucidated. According to X-chromosomal inactivation analysis, a number of TSH-omas are monoclonal in origin and molecular analysis failed to identify any mutations affecting either oncogenes (Ras, protein kinase C, G-protein subunits, TRH receptor) or proto oncogenes (Rb, MEN1) [2]. Recently, several candidate somatic mutations and change in copy numbers in 12 sporadic TSH-omas have been identified by whole-exome sequencing [19]. Moreover, somatic mutations of thyroid hormone receptor beta have been reported to be responsible for the defect in negative regulation of TSH secretion in some TSH-omas [20]. Finally, TSH-omas express a variable number of somatostatin receptors, the highest densities being found in mixed GH/TSH adenomas [21], thus explaining the extraordinary efficacy of somatostatin analogs in controlling TSH secretion by neoplastic thyrotropes.

Clinical findings

TSH-omas are usually benign, and only few cases of TSH-secreting pituitary carcinomas have been described [2, 22]. TSH-omas can be diagnosed at any age and there is no major incidence in females as in common thyroid disease. TSH-oma patients generally show signs and symptoms of hyperthyroidism, frequently combined with symptoms of optic chiasm compression (visual field defects or loss of vision) and/or compression of normal pituitary cells (anterior pituitary function deficits). Nonetheless, several untreated patients with TSH-omas are completely asymptomatic.

About one-third of patients with TSH-oma underwent inappropriate thyroidectomy and/or radioiodine treatment as a consequence of an incorrect diagnosis of primary hyperthyroidism (i.e., Graves’ disease or toxic multinodular goiter). Interestingly, atrial fibrillation and/or cardiac failure has been described in sporadic cases and episodes of periodic paralysis have been reported in few patients [2, 23]. Finally, the coexistence of Graves’ disease and TSH-oma has been reported in few cases [24].

In about 65% of cases an enlargement of the thyroid gland is reported and the occurrence of uni- or multinodular goiter is frequently seen in patients with TSH-omas, progression towards functional autonomy having seldom been documented [25]. The coexistence of differentiated thyroid carcinomas was reported in several patients [2, 26]. As a result, Though the prevalence of circulating antithyroid autoantibodies is similar to that found in the general population, some patients develop Graves’ disease after pituitary surgery and others present bilateral exophthalmos due the coexistence of an autoimmune thyroiditis. Finally, it should be taken into account the possibility that a unilateral exophthalmos might be due to orbital invasion by the pituitary tumor [2].

In 30% of female patients, menstrual disorders are reported, mainly in mixed TSH/PRL adenomas. The presence of TSH-omas and/or mixed TSH/FSH adenomas may induce central hypogonadism and decreased libido in a number of males [1, 17].

Biochemical findings

The biochemical hallmarks of hyperthyroidism secondary to TSH-omas are high serum free T3 and T4 concentrations in the presence of inappropriately normal or high serum TSH concentrations. The first step in the differential diagnosis is exclusion of methodological interference in the measurement of either thyroid hormones or TSH. FT4 and/or FT3 overestimation may be related to the presence of anti-T4 and/or anti-T3 antibodies or abnormal albumin/transthyretin forms (e.g., familial dysalbuminemic hyperthyroxinemia [27, 28, 29]. The direct “two-step” method for FT4 and FT3 concentration measurement is now considered the best, since it is able to prevent any interference due to the contact between serum factors and tracers at the time of the assay (e.g., equilibrium dialysis + RIA, adsorption chromatography + RIA, and back-titration) [27]. Considering TSH immunometric assays, the most common factors causing spurious TSH overestimation are circulating heterophilic antibodies, i.e., antibodies directed against mouse gamma-globulins [29].

About 30% of TSH-oma patients with an intact thyroid present normal TSH levels together with high levels of FT4 and FT3 [1], this finding being likely due to an increased biological activity of secreted TSH molecules. A case of TSH-oma with cyclic fluctuations in serum TSH levels has been recently reported [30]. Several patients with macroadenoma are biochemically characterized by elevated circulating free α-GSU levels and α-GSU/TSH molar ratio, these data being in the normal range in the presence of a microadenoma [1, 6, 31]. It has been suggested that the measurements of parameters of peripheral thyroid hormone action in vivo (basal metabolic rate, cardiac systolic time intervals, “Achilles” reflex time) and in vitro (SHBG, cholesterol, angiotensin converting enzyme, soluble interleukin-2 receptor, osteocalcin, carboxyterminal cross-linked telopeptide of type I collagen (ICTP), etc.) could be useful to evaluate the presence of tissue hyperthyroidism [2, 3, 4, 5]. In particular, liver (SHBG) and bone parameters (ICTP) are higher in patients with TSH-oma in comparison to patients with PRTH [1, 2, 3].

Dynamic tests

Dynamic tests have been recommended for the diagnosis of TSH-oma. The T3 suppression test (80–100 μg/day for 8–10 days) is generally used to diagnose patients with TSH-oma whose TSH does not suppress in response to T3 administration. Thus, T3 suppression test is actually considered the most sensitive and specific test, particularly in patients with previous thyroid ablation [2, 10]. However, this test is contraindicated in elderly patients or in those with coronary heart disease. As far as stimulatory tests are considered, TRH administration (200 μg i.v.) does not increase either TSH or α-GSU in up to 85% of TSH-oma patients [2]. Interestingly, TSH is significantly reduced by native somatostatin and somatostatin analogs (i.e., octreotide or lanreotide) in the majority of TSH-omas and this response may predict the efficacy of long-term treatment with SSAs [32].

Imaging studies and localization of the tumor

TSH-omas localization relies on nuclear magnetic resonance imaging (MRI) and high-resolution computed tomography (CT). As previously described, the majority of TSH-omas are macroadenomas and in 60% of cases they present with various degrees of suprasellar extension or sphenoidal sinus invasion. Interestingly, few ectopic localizations of TSH-oma have been reported in both the nasopharyngeal and the suprasellar regions [33, 34]: these tumors have been histologically and immunohistochemically proven to be unequivocally TSH-secreting adenomas and the mass resection has been effective in normalizing TSH levels.

Differential diagnosis

The coexistence of elevated serum FT4/FT3 and measurable TSH levels in a patient with signs and symptoms of hyperthyroidism is sufficient to exclude Graves’ disease or other causes of primary hyperthyroidism. It is worth noting that a measurable TSH associated with high FT4/FT3 levels during a substitutive therapy with LT4 is generally due to poor compliance or to the administration of LT4 before blood sampling.

Once the diagnosis of central hyperthyroidism is confirmed, it is mandatory to differentiate a TSH-oma from RTH [1, 2, 3, 4, 5, 32, 35]. In particular, we should suspect a TSH-oma in the presence of visual defects and/or headache (possible expression of a macroadenoma), and when the synchronous hypersecretion of other pituitary hormones leads to the manifestation of clinical features (i.e., acromegaly, galactorrhea/amenorrhea). Although the presence of a pituitary lesion at neuroradiological imaging strongly favors the diagnosis of TSH-oma, it has been demonstrated that a pituitary lesion is likely to be identified at MRI in about 20% of RTH, thus suggesting the possible coexistence of pituitary incidentaloma and RTH [36].

Though serum TSH levels within the normal range are more frequently found in RTH and elevated α-GSU concentrations and/or high α-GSU/TSH molar ratio are typical of TSH-omas, no differences in terms of age, sex, TSH levels or free thyroid hormone concentrations have been described as significant between patients with TSH-oma and those with RTH [2]. As far as dynamic tests are concerned, typically TSH-omas do not respond to TRH stimulation and/or to T3 suppression tests. Chronic therapy with long-acting somatostatin analogs in patients with central hyperthyroidism is effective in reducing FT3 and FT4 levels in patients with TSH-oma, but not in those with PRTH [32]. Thus, in selected cases, it s possible to administer long-acting somatostatin analogs for at least 2–3 months to make the differential diagnosis. Finally, TRβ gene analysis may be useful in the differential diagnosis, as genomic TRβ mutations have been detected in patients with RTH only [3].

Treatment and outcomes

The European Thyroid Association guidelines [35] recommend surgical resection as first-line therapy for TSH-secreting pituitary tumors, aimed at removing tumor mass and normalizing thyroid function. However, the presence of invasive macroadenomas or the marked fibrosis that characterizes a number of these tumors may affect the radicality of the surgery. According to the largest published series, surgery can effectively restore euthyroidism in up to 80% of patients with TSH-omas [5, 6, 7, 8, 9, 10, 11, 18].

Antithyroid drugs along with propranolol could be administered to restore normal thyroid function before surgery [37]. In this respect, pre-surgical treatment with somatostatin analogs (i.e., Octreotide LAR and Lanreotide autogel) might be effective in reducing TSH-oma size and normalizing circulating thyroid hormones levels in patients with severe hyperthyroidism [38].

A possible consequence of neurosurgical intervention is partial or complete hypopituitarism, thus suggesting the need for a complete anterior pituitary function evaluation to start a replacement therapy if needed. Interestingly, a single case of thyroid storm after pituitary surgery was recently reported [39]. Total thyroidectomy or thyroid ablation with radioiodine are indicated only when pituitary surgery is not curative and the patient suffers from life-threatening hyperthyroidism [40].

Alternative treatments are pituitary radiotherapy and/or medical treatment with somatostatin analogs, they should be considered when the patient is not amenable to surgery or he declines it, and in case of failure [35, 42]. According to published series, somatostatin analogs are effective in restoring normal thyroid function in about 95% and in causing a significant tumor shrinkage in up to 50% of patients [2, 18]. Somatostatin analogs are safe even though untoward side effects, such as cholelithiasis and carbohydrate intolerance, may appear. Interestingly, somatostatin analogs treatment may be safely continued even during pregnancy [43]. If radiotherapy is prescribed, the recommended dose is no less than 45 Gy fractionated at 2 Gy per day or 10–25 Gy in a single dose if a stereotactic Gamma Unit is available and this procedure succeeds in normalizing thyroid function in 37% of patients within 2–4 years [41].

T3 suppression test is the most sensitive and specific test to confirm the complete removal of the adenoma [2, 44] and patients are considered as cured if basal and TRH-stimulated TSH secretion is completely suppressed by T3 administration (Table 2). Although there are no available data regarding TSH-oma recurrence in patients initially considered cured after surgery or radiotherapy, adenoma recurrence seems to be an infrequent event in the first year after successful surgery [44]. In general, postoperatively, patients should be evaluated both clinically and biochemically two or three times during the first year, and once a year thereafter [2]. Pituitary imaging should be performed every 2 or 3 years; however, it should be promptly scheduled whenever an increase in TSH and thyroid hormone levels or the appearance of clinical symptoms occurs [2]. In the case of persistent macroadenoma, a close visual field follow-up is required, as the visual function may be threatened.
Table 2

Criteria evaluating the results of neurosurgical treatment of a TSH-oma



Normalization of circulating TSH levels

Not applicable to patients with normal TSH

Normalization of free thyroid hormone levels

Biochemical remission may be transient

Disappearance of neurological manifestations (adenoma imaging, visual field defects, headache) 

May be transient

Remission from hyperthyroid manifestations (clinical and biochemical) 

Clinical improvement may be transient

Undetectable TSH 1 week after neurosurgery

 Applicable to hyperthyroid patients that stopped treatments at least 10 days before surgery

Normalization of α-GSU levels and α-GSU/TSH m.r.

Not applicable to patients with normal values before neurosurgery

Positive T3-suppression test, i.e., undetectable TSH and no response to TRH (or central hypothyroidism) 

Optimal sensitivity, specificity and predictive value. However, the test is contraindicated in elderly patients or in those with cardiac diseases


Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

Ethical approval

The article does not contain any studies with human participants or animals performed by any of the authors.

Informed consent

There is no identifying patient information present in this manuscript; therefore, informed consent is unnecessary.


  1. 1.
    Beck-Peccoz P, Lania A, Persani L (2015) Chapter 24. TSH-producing adenomas. In: Jameson JL, DeGroot LJ (eds) Endocrinology, 7th edn. W.B. Saunders Pub, Philadelphia, pp 266–274Google Scholar
  2. 2.
    Beck-Peccoz P, Persani L, Lania A (2000) Thyrotropin-secreting pituitary adenomas. In: Feingold KR, Anawalt B, Boyce A, Chrousos G, Dungan K, Grossman A, Hershman JM, Kaltsas G, Koch C, Kopp P, Korbonits M, McLachlan R, Morley JE, New M, Perreault L, Purnell J, Rebar R, Singer F, Trence DL, Vinik A, Wilson DP (eds) Endotext. Inc, South Dartmouth, MAGoogle Scholar
  3. 3.
    Gurnell M, Visser TJ, Beck-Peccoz P, Chatterjee VKK (2015) Resistance to thyroid hormone: in endocrinology, adult and pediatric. In: Jameson LJ, DeGroot LJ (eds), 7th edn, vol II. Elsevier, Philadelphia pp 1648–1665Google Scholar
  4. 4.
    Brucker-Davis F, Oldfield EH, Skarulis MC, Doppman JL, Weintraub BD (1999) Thyrotropin-secreting pituitary tumors: diagnostic criteria, thyroid hormone sensitivity, and treatment outcome in 25 patients followed at the National Institutes of Health. J Clin Endocrinol Metab 84:476–486CrossRefPubMedGoogle Scholar
  5. 5.
    Bertholon-Grégoire M, Trouillas J, Guigard MP, Loras B, Tourniaire J (1999) Mono- and plurihormonal thyrotropic pituitary adenomas: pathological, hormonal and clinical studies in 12 patients. Eur J Endocrinol 140:519–527CrossRefPubMedGoogle Scholar
  6. 6.
    Socin HV, Chanson P, Delemer B et al (2003) The changing spectrum of TSH-secreting pituitary adenomas: diagnosis and management in 43 patients. Eur J Endocrinol 148:433–442CrossRefPubMedGoogle Scholar
  7. 7.
    Yamada S, Fukuhara N, Horiguchi K et al (2014) Clinicopathological characteristics and therapeutic outcomes in thyrotropin-secreting pituitary adenomas: a single-center study of 90 cases. J Neurosurg 121:1462–1473CrossRefPubMedGoogle Scholar
  8. 8.
    van Varsseveld NC, Bisschop PH et al (2014) A long-term follow-up study of eighteen patients with thyrotrophin-secreting pituitary adenomas. Clin Endocrinol (Oxf) 80:395–402CrossRefGoogle Scholar
  9. 9.
    Azzalin A, Appin CL, Schniederjan MJ et al (2016) Comprehensive evaluation of TSHomas: single-center 20-year experience. Pituitary 19:183–193CrossRefPubMedGoogle Scholar
  10. 10.
    Tjörnstrand A, Nyström HF (2017) Diagnostic approach to TSH-producing pituitary adenoma. Eur J Endocrinol 177:R183–R197CrossRefPubMedGoogle Scholar
  11. 11.
    Nazato DM, Abucham J (2018) Diagnosis and treatment of TSH-secreting adenomas: review of a longtime experience in a reference center. J Endocrinol Invest 41:447–454CrossRefPubMedGoogle Scholar
  12. 12.
    Cossu G, Daniel RT, Pierzchala K et al (2019) Thyrotropin-secreting pituitary adenomas: a systematic review and meta-analysis of postoperative outcomes and management. Pituitary 22(1):79–88CrossRefPubMedGoogle Scholar
  13. 13.
    Önnestam L, Berinder K, Burman P et al (2013) National incidence and prevalence of TSH-secreting pituitary adenomas in Sweden. J Clin Endocrinol Metab 98:626–635CrossRefPubMedGoogle Scholar
  14. 14.
    Taylor TJ, Donlon SS, Bale AE et al (2000) Treatment of a thyrotropinoma with octreotide-LAR in a patient with multiple endocrine neoplasia-1. Thyroid 10:1001–1007CrossRefPubMedGoogle Scholar
  15. 15.
    Daly AF, Tichomirowa MA, Petrossians P et al (2010) Clinical characteristics and therapeutic responses in patients with germ-line AIP mutations and pituitary adenomas: an international collaborative study. J Clin Endocrinol Metab 95:E373–E383CrossRefPubMedGoogle Scholar
  16. 16.
    Pereira BD, Raimundo L, Mete O, Oliveira A, Portugal J, Asa SL (2016) Monomorphous plurihormonal pituitary adenoma of pit-1 lineage in a giant adolescent with central hyperthyroidism. Endocr Pathol 27:25–33CrossRefPubMedGoogle Scholar
  17. 17.
    Li J, Li J, Jiang S, Yu R, Yu Y (2018) Case report of a pituitary TSH-secreting macroadenoma with Hashimoto thyroiditis and infertility. Medicine (Baltimore). 97:e9546CrossRefPubMedPubMedCentralGoogle Scholar
  18. 18.
    Malchiodi E, Profka E, Ferrante E et al (2014) Thyrotropin-secreting pituitary adenomas: outcome of pituitary surgery and irradiation. J Clin Endocrinol Metab 99:2069–2076CrossRefPubMedGoogle Scholar
  19. 19.
    Sapkota S, Horiguchi K, Tosaka M, Yamada S, Yamada M (2017) Whole-exome sequencing study of thyrotropin-secreting pituitary adenomas. J Clin Endocrinol Metab 102:566–575PubMedGoogle Scholar
  20. 20.
    Ando S, Sarlis NJ, Oldfield EH, Yen PM (2001) Somatic mutation of TRbeta can cause a defect in negative regulation of TSH in a TSH-secreting pituitary tumor. J Clin Endocrinol Metab 86:5572–5576PubMedGoogle Scholar
  21. 21.
    Gatto F, Barbieri F, Gatti M et al (2012) Balance between somatostatin and D2 receptor expression drives TSH-secreting adenoma response to somatostatin analogues and dopastatins. Clin Endocrinol (Oxf) 76:407–414CrossRefGoogle Scholar
  22. 22.
    Lee W, Cheung AS, Freilich R (2012) TSH-secreting pituitary carcinoma with intrathecal drop metastases. Clin Endocrinol (Oxf) 76:604–606CrossRefGoogle Scholar
  23. 23.
    Pappa T, Papanastasiou L, Markou A et al (2010) Thyrotoxic periodic paralysis as the first manifestation of a thyrotropin-secreting pituitary adenoma. Hormones (Athens) 9:82–86CrossRefGoogle Scholar
  24. 24.
    Lee MT, Wang CY (2010) Concomitant Graves hyperthyroidism with thyrotrophin-secreting pituitary adenoma. South Med J 103:347–349CrossRefPubMedGoogle Scholar
  25. 25.
    Abs R, Stevenaert A, Beckers A (1994) Autonomously functioning thyroid nodules in a patient with a thyrotropin-secreting pituitary adenoma: possible cause-effect relationship. Eur J Endocrinol 131:355–358CrossRefPubMedGoogle Scholar
  26. 26.
    Perticone F, Pigliaru F, Mariotti S et al (2015) Is the incidence of differentiated thyroid cancer increased in patients with thyrotropin-secreting adenomas? Report of three cases from a large consecutive series. Thyroid 25:417–424CrossRefPubMedGoogle Scholar
  27. 27.
    Koulouri O, Moran C, Halsall D, Chatterjee K, Gurnell M (2013) Pitfalls in the measurement and interpretation of thyroid function tests. Best Pract Res Clin Endocrinol Metab 27:745–762CrossRefPubMedPubMedCentralGoogle Scholar
  28. 28.
    Schoenmakers N, Moran C, Campi I et al (2014) A novel albumin gene mutation (R222I) in familial dysalbuminemic hyperthyroxinemia. J Clin Endocrinol Metab 99:E1381–E1386CrossRefPubMedPubMedCentralGoogle Scholar
  29. 29.
    Favresse J, Burlacu MC, Maiter D, Gruson D (2018) Interferences with thyroid function immuno-assays: clinical implications and detection algorithm. Endocr Rev 4339:830–850CrossRefGoogle Scholar
  30. 30.
    Okuma H, Hashimoto K, Ohashi T et al (2018) A case of TSH-secreting pituitary adenoma with cyclic fluctuations in serum TSH levels. Endocr J 65:737–746CrossRefPubMedGoogle Scholar
  31. 31.
    Beck-Peccoz P, Persani L, Faglia G (1992) Glycoprotein hormone α-subunit in pituitary adenomas. Trends Endocrinol Metab 3:41–45CrossRefPubMedGoogle Scholar
  32. 32.
    Mannavola D, Persani L, Vannucchi G et al (2005) Different responses to chronic somatostatin analogues in patients with central hyperthyroidism. Clin Endocrinol (Oxf) 62:176–181CrossRefGoogle Scholar
  33. 33.
    Song M, Wang H, Song L et al (2014) Ectopic TSH-secreting pituitary tumor: a case report and review of prior cases. BMC Cancer 14:544CrossRefPubMedPubMedCentralGoogle Scholar
  34. 34.
    Wang Q, Lu XJ, Sun J, Wang J, Huang CY, Wu ZF (2016) Ectopic suprasellar TSH-secreting pituitary adenoma: case report and literature review. World Neurosurg 95(617):e13Google Scholar
  35. 35.
    Beck-Peccoz P, Lania A, Beckers A, Chatterjee K, Wemeau JL (2013) 2013 European thyroid association guidelines for the diagnosis and treatment of thyrotropin-secreting pituitary tumors. Eur Thyroid J 2:76–82CrossRefPubMedPubMedCentralGoogle Scholar
  36. 36.
    Sriphrapradang C, Srichomkwun P, Refetoff S, Mamanasiri S (2016) A Novel thyroid hormone receptor beta gene mutation (G251V) in a Thai patient with resistance to thyroid hormone coexisting with pituitary incidentaloma. Thyroid 26:1804–1806CrossRefPubMedPubMedCentralGoogle Scholar
  37. 37.
    Dyer MW, Gnagey A, Jones BT et al (2017) Perianesthetic management of patients with TSH-secreting pituitary adenomas. J Neurosurg Anesthesiol 29:341–346CrossRefPubMedGoogle Scholar
  38. 38.
    Fukuhara N, Horiguchi K, Nishioka H et al (2015) Short-term preoperative octreotide treatment for TSH-secreting pituitary adenoma. Endocr J 62:21–27CrossRefPubMedGoogle Scholar
  39. 39.
    Fujio S, Ashari Habu M, Yamahata H et al (2014) Thyroid storm induced by TSH-secreting pituitary adenoma: a case report. Endocr J 61:1131–1136CrossRefPubMedGoogle Scholar
  40. 40.
    Daousi C, Foy PM, MacFarlane IA (2007) Ablative thyroid treatment for thyrotoxicosis due to thyrotropin-producing pituitary tumours. J Neurol Neurosurg Psychiatry 78:93–95CrossRefPubMedPubMedCentralGoogle Scholar
  41. 41.
    Mouslech Z, Somali M, Sakali AK, Savopoulos C, Mastorakos G, Hatzitolios AI (2016) TSH-secreting pituitary adenomas treated by gamma knife radiosurgery: our case experience and a review of the literature. Hormones (Athens) 15:122–128CrossRefGoogle Scholar
  42. 42.
    Kuhn JM, Arlot S, Lefebvre H et al (2000) Evaluation of the treatment of thyrotropin-secreting pituitary adenomas with a slow release formulation of the somatostatin analog lanreotide. J Clin Endocrinol Metab 85:1487–1491CrossRefPubMedGoogle Scholar
  43. 43.
    Blackhurst G, Strachan MW, Collie D et al (2002) The treatment of a TSH-secreting pituitary macroadenoma with octreotide in twin pregnancy. Clin Endocrinol (Oxf) 57:401–404CrossRefGoogle Scholar
  44. 44.
    Losa M, Giovanelli M, Persani L, Faglia G, Beck-Peccoz P (1996) Criteria of cure and follow-up of central hyperthyroidism due to thyrotropin-secreting pituitary adenomas. J Clin Endocrinol Metab 81:3086–3090Google Scholar

Copyright information

© Italian Society of Endocrinology (SIE) 2019

Authors and Affiliations

  1. 1.University of MilanMilanItaly
  2. 2.Endocrinology UnitFondazione IRCCS Ca’ Granda Ospedale Maggiore PoliclinicoMilanItaly
  3. 3.Department of Biomedical SciencesHumanitas UniversityRozzanoItaly
  4. 4.Endocrinology, Diabetology and Andrology UnitHumanitas Research Center IRCSRozzanoItaly

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