Warning: fopen(/home/virtual/enm-kes/journal/upload/ip_log/ip_log_2026-02.txt): failed to open stream: Permission denied in /home/virtual/lib/view_data.php on line 100 Warning: fwrite() expects parameter 1 to be resource, boolean given in /home/virtual/lib/view_data.php on line 101 Epidemiology of Functioning Pituitary Adenomas
Skip Navigation
Skip to contents

Endocrinol Metab : Endocrinology and Metabolism

clarivate
OPEN ACCESS
SEARCH
Search
Advanced Search
mobile menu button

Articles

Page Path
HOME > Endocrinol Metab > Volume 35(2); 2020 > Article
Review Article
Epidemiology of Functioning Pituitary Adenomas
Sang Ouk Chinorcid
Endocrinology and Metabolism 2020;35(2):237-242.
DOI: https://doi.org/10.3803/EnM.2020.35.2.237
Published online: June 30, 2020

Department of Endocrinology and Metabolism, Kyung Hee University College of Medicine, Seoul, Korea

Corresponding author: Sang Ouk Chin. Department of Endocrinology and Metabolism, Kyung Hee University College of Medicine, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea, Tel: +82-2-958-8200, Fax: +82-2-968-1848, E-mail: jan27th@khu.ac.kr
• Received: April 21, 2020   • Revised: May 11, 2020   • Accepted: May 12, 2020

Copyright © 2020 Korean Endocrine Society

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

  • 15,599 Views
  • 350 Download
  • 21 Web of Science
  • 21 Crossref
  • 27 Scopus
prev next
Full Article

Download PDF Download PDF

  • Pituitary adenomas (PAs) are defined as benign monoclonal tumors in the pituitary gland that cause symptoms due to either hormonal hypersecretion or a space-occupying effect, and are classified as functioning or non-functioning. Because of their rarity and slow-growing with symptomless nature in most cases, it has been challenging to investigate the epidemiology of PAs. Considering their public health impact and association with increased morbidity and mortality, however, it is essential to understand the prevalence and incidence of PAs in order to improve patient outcomes and to minimize the resultant burden on the health care system. Fortunately, developments in imaging modalities and easier access to large-scale population data have enabled investigators to analyze the epidemiology of PAs more accurately. This review summarizes previously reported epidemiologic data on functioning PAs in Korea and other countries.
  • Keywords: Pituitary neoplasms; Epidemiology; Korea
Pituitary adenomas (PA) are defined as benign monoclonal tumors in the pituitary gland that cause symptoms due to either hormonal hypersecretion or a space-occupying effect [1]. These generally slowly-growing tumors are known to be the most common cause of hormonal hypersecretion or hyposecretion in adults. Following gliomas and meningiomas, PAs are the third most common type of brain tumor, accounting for 10% to 15% of all brain tumors [2], and they are the most common type of neuroendocrine tumor found in the central nervous system [3]. Pituitary carcinomas—defined as pituitary tumors with distant metastasis—are very rare, accounting for fewer than 0.2% of all cases of pituitary tumors [4].
PAs are divided into macroadenomas (>10 mm in diameter) or microadenomas (≤10 mm in diameter), and those with a diameter >40 mm are also called giant adenomas [4,5]. In addition, PAs are classified as either functioning or non-functioning depending on whether they have a hormonal hypersecretory capacity [6]. Depending on the type of hormone secreted, functioning PAs are sub-classified as prolactin-, growth hormone (GH)-, adrenocorticotropic hormone (ACTH)-, or thyrotropin-producing adenomas. A third of PAs are non-functioning, mostly including macroadenomas that frequently secrete gonadotropin or prolactin but have no symptoms resulting from hormonal hypersecretion [3,7–9]. Also, the pathologic classifications based on the immunohistochemical analyses, electron microscopy findings, and the demonstration of various transcription factors have been also introduced (Table 1) [10].
PAs were previously considered to be very rare, but recent data have revealed that their prevalence is higher than previously reported, potentially due to developments in imaging techniques and the increased detection of incidentalomas found during radiological work-ups for other diseases [11]. Traditionally, epidemiologic data on PAs were collected from anatomical studies using data obtained from the autopsy studies or the magnetic resonance imaging. However, these methods often have the limitations of representing a relatively old population or not reflecting the actual epidemiology of clinically relevant PAs [1]. Epidemiologic data on PAs based on a national-level cancer registry have been reported, but it has also limitation of underestimating the actual prevalence of PAs due to the lack of mandatory reporting [12]. Recently, population studies on the basis of big data analysis using national insurance claims data in Korea have been published [13,14]. Despite the issue on the accuracy of their operational definitions, used in these studies, they have the advantage of enabling investigators to obtain epidemiologic data from the general population, and this method has therefore been applied in various studies for other diseases [15–17]. This review summarizes the previously reported epidemiologic data on functioning PAs in Korea and other countries.
Acromegaly is a chronic disease caused by the hypersecretion of GH, and GH-producing PAs are found in 95% of acromegaly patients [18]. Although acromegaly has also been reported to be caused by ectopic hypersecretion of GH [19,20] or excess production of GH-releasing hormone [21], these etiologies are very rare. Since GH-producing PAs account for most cases of acromegaly, it is reasonable to assume that the prevalence and incidence of acromegaly are identical to those of GH-producing PAs. According to large population-based studies published as of 2000, the prevalence of GH-producing PAs was 3.3 to 13.7 cases per 100,000, and the annual incidence was 0.2 to 1.1 cases per 100,100 [22–33]. These figures are relatively higher than those reported before 2000 (prevalence: 3.8 to 6.9/100,000; annual incidence: 0.28 to 0.4/100,000) [34–37]. As described above, this difference may be due to the disparities in the study population (general population vs. limited cases from tertiary centers or smaller numbers of included cases), developments in imaging techniques, and the increased frequency of performing imaging work-ups.
Not many studies have investigated the epidemiology of acromegaly in Korea. The first case of acromegaly in Korea was reported in 1965 [38], and the Survey Committee for Endocrine Diseases in the Korean Endocrine Society performed a nationwide survey regarding PAs in Korea in 1994. Based on the clinical information of 279 cases of acromegaly collected from 26 university hospitals in Korea, the annual incidence rate was estimated to be 1.4 cases per million [39]. This was lower than the rates previously reported in other countries, and the discrepancy was speculated to be due to limitations in the survey methodology. In the early 2000s, the Rare Disease Study Group in the Science and Research Committee of the Korean Endocrine Society conducted an updated version of nationwide survey of acromegaly in Korea. Clinical information of 1,350 patients with acromegaly diagnosed and treated between 2003 and 2007 at 74 hospitals in Korea was collected and analyzed. The annual incidence was calculated as 3.9 cases per million and the prevalence was 27.9 cases per million [40]. A limitation of survey methods is their high likelihood of representing patients treated at tertiary hospitals. In order to compensate for this limitation, Park et al. [13] analyzed the Korean Health Insurance Review and Assessment (HIRA) claims database between 2010 and 2014 and reported an annual incidence rate of 3.57 per million.
With mostly benign, prolactin-producing PAs (prolactinomas) are known to be one of the most common causes of hyperprolactinemia. Although hyperprolactinemia can be caused by various etiologies, including pregnancy, breastfeeding, exercise, stress, renal or thyroid insufficiency, drugs, and pituitary stalk compression by a non-prolactin-producing tumor or other parasellar masses [41], prolactin-producing PAs are considered to be the most clinically important etiological factor underlying hyperprolactinemia [42].
Ezzat et al. [43] performed a meta-analysis demonstrating that prolactinomas were the most common PAs, accounting for 25% to 41% according to radiologic or autopsy studies. According to the community-based cohort studies conducted in Liège, Belgium and Banbury, the United Kingdom (UK), prolactinomas were found to be the most common PAs (66.2% in Liège, Belgium and 57% in Banbury, UK), with a prevalence of 6 to 44.4 cases per 100,000 [22,23]. Both studies demonstrated a female predominance of prolactinomas with being most common in those under the age of 60. Consistent results were reported in a retrospective analysis of patients who received surgical therapy for PAs; prolactinomas were 10-fold more common in female patients aged between 18 to 50 years, but the male-to-female ratio equalized in older patients [44].
As with acromegaly, there are not many studies which have investigated the epidemiology of prolactinomas in Korea. Cho et al. [3] retrospectively reviewed the clinical data of 506 patients who underwent surgical therapy for PAs between 2006 and 2011 at a single center, and reported that prolactinomas accounted for 16.6% of PAs, making them the most common type. According to the analysis by Park et al. [14] of the HIRA claims database between 2009 and 2013, the prevalence of prolactinomas in Korea increased from 38.5 to 68.6 cases per million, while the annual incidence showed a sex disparity, at 1.0 to 1.6 cases per million in males and 27 to 29 cases per million in females [14].
Cushing syndrome (CS) was first reported by Dr. Harvey Cushing in 1912 [45]. It is divided into exogenous CS, which is caused by glucocorticoid use, and endogenous CS, which is classified as (1) ACTH-producing PAs (Cushing disease [CD]); (2) cortisol overproduction by adrenal adenomas or carcinomas via ACTH-independent mechanisms; and (3) ectopic production of ACTH or corticotropin-releasing hormone by neuroendocrine tumors [46]. ACTH-producing PAs are the most common cause of endogenous CS, accounting for approximately 60% of cases [46].
CD is a very uncommon disease. Most publications presenting epidemiologic data on CD focused on the entire spectrum of endogenous CS, while few studies have investigated the epidemiology of CD only. A population-based study from Vizcaya in a region of Basque Country (Spain) between 1975 and 1992 reported that there were 49 patients diagnosed with CD, corresponding to an annual incidence of 2.4 cases per million and a prevalence of 39.1 cases per million [47]. A similar study conducted using the National Patient Register of the Danish National Board of Health between 1985 and 1995 found that approximately 60% of patients with endogenous CS were diagnosed with CD, with 73 (1985 to 1990) and 99 cases (1991 to 1995) of CD among a total of 166 cases of endogenous CS [48]. The annual incidence was 1.2 (1985 to 1990) and 1.7 cases (1991 to 1995) per million [48].
In Korea, the Survey Committee for Endocrine Diseases in the Korean Endocrine Society performed a nationwide survey to collect clinical data from patients diagnosed with endogenous CS between 1992 and 1998. In total, 180 cases of endogenous CS from 51 university hospitals in Korea were collected and analyzed, yielding an annual incidence of 0.84 cases per million [49]. The proportion of CD was 48.3%, similar to that of adrenal CS (48.9%) [49]. Since then, no additional studies have investigated the epidemiology of CD in Korea. A report by Park et al. [14] only demonstrated the prevalence of endogenous CS because of the small number of CD cases collected during the analysis. The annual incidence of endogenous CS was 4.5 cases (male) and 17.2 cases (female) per million, and the prevalence was 51.7 cases per million in 2013 [14].
Thyrotropin-producing PAs are extremely rare, accounting for the smallest proportion of functional PAs. This disorder may be suspected when thyroid-stimulating hormone (TSH) is inappropriately normal or elevated in patients with hyperthyroidism. Defined as central hyperthyroidism, this condition requires a careful differential diagnosis between thyrotropin-producing PAs and thyroid hormone resistance syndrome. Thyrotropin-producing PAs were first reported by Jailer and Holub [50] in 1960, and more than 450 cases have been reported worldwide [50,51].
In the United States, a single-center study that investigated a total of 1,628 patients who underwent surgical treatment for PAs between 1993 and 2013 demonstrated that 1.2% of the cases (n=20) were found to be thyrotropin -producing PAs, and their proportion increased in recent years [52]. In Japan, a single-center study reported that 2.7% of patients (n=90 of 3,276) who underwent surgical treatment for PAs had a diagnosis of a thyrotropin-producing PA [53]. Yoon et al. [54] reported the first patient with a thyrotropin-producing PA in Korea, and since that time 11 cases have been reported in Korea [55]. According to the result of a single-center study in Korea that analyzed the clinical information of 484 patients who received surgical treatment for PAs, 1.65% (n=8) of the patients had a diagnosis of a TSH-producing PA [55].
A study in Sweden using the Swedish Pituitary Registry reported that the annual incidence of thyrotropin-producing PAs recently increased from 0.05 (1990 to 1994) to 0.26 cases per million (2005 to 2009) [56]. The annual incidence was reported to be 0.32 per million in Finland [27]. This trend is likely due to physicians’ increased awareness regarding the concept of inappropriate secretion of TSH, the introduction of ultrasensitive immunometric TSH assays that reliably differentiate between suppressed and normal TSH levels, and advances in pituitary imaging techniques that detect pituitary microadenomas more accurately [57].
Because of their rarity and slow-growing, symptomless nature in most cases, it is very difficult to collect clinically reliable information on patients with PAs, which presents a solid barrier to investigations of the epidemiology of this disorder. As population studies based on big-data analyses have become more common and provided easier access to more dependable data; however, the prevalence and incidence of PAs have been found to increase over the past years. Considering their impacts upon public health and their associations with increased morbidity and mortality, as well as the economic burden that they place on the health care system, it is essential to understand the epidemiology of PAs. As mentioned repeatedly, not many studies have investigated the epidemiology of PAs in Korea, and updated and larger studies regarding the epidemiology of PAs are necessary.
Acknowledgements
I would like to express my most sincere gratitude to professor Sung-Woon Kim in Kyung Hee University for giving me wonderful opportunities and teaching to take part in and enjoy the field of neuroendocrinology.

CONFLICTS OF INTEREST

No potential conflict of interest relevant to this article was reported.

Table 1
Classification of Pituitary Adenomas
Size Function Hormone Pathology (WHO)a Morphofunctional subclassificationa
Microadenoma
Macroadenoma
Giant adenoma		 Functioning
Non-functioning		 Prolactin Lactotroph adenoma (LA) Sparsely granulated LA
Densely granulated LA
Acidophilic stem cell adenoma
Growth hormone Somatotroph adenoma (SA) Densely granulated SA
Sparsely granulated SA
Mammosomatotroph adenoma
Mixed somatotroph and lactotroph adenoma
Adrenocorticotropic hormone Corticotroph adenoma (CA) Sparsely granulated CA
Densely granulated CA
Acidophilic stem cell adenoma
Thyroid-stimulating hormone Thyrotroph adenoma
Luteinizing hormone/follicular-stimulating hormone Gonadotroph adenoma (GA) null cell adenoma Sparsely granulated GA
Plurihormonal Plurihormonal adenoma Plurihormonal PIT1-positive adenoma
Adenomas with unusual IHC combinations
Double adenoma Distinct adenomas

WHO, World Health Organization; PIT1, pituitary-specific positive transcription factor 1; IHC, immunohistochemical.

a Adapted from Laws et al. [10], with permission from Springer Nature.

  • 1. Aflorei ED, Korbonits M. Epidemiology and etiopathogenesis of pituitary adenomas. J Neurooncol 2014;117:379–94.ArticlePubMedPDF
  • 2. Sivakumar W, Chamoun R, Nguyen V, Couldwell WT. Incidental pituitary adenomas. Neurosurg Focus 2011;31:E18.Article
  • 3. Cho HJ, Kim H, Kwak YJ, Seo JW, Paek SH, Sohn CH, et al. Clinicopathologic analysis of pituitary adenoma: a single institute experience. J Korean Med Sci 2014;29:405–10.ArticlePubMedPMC
  • 4. Raverot G, Jouanneau E, Trouillas J. Management of endocrine disease: clinicopathological classification and molecular markers of pituitary tumours for personalized therapeutic strategies. Eur J Endocrinol 2014;170:R121–32.ArticlePubMed
  • 5. Buchfelder M, Schlaffer S. Imaging of pituitary pathology. Handb Clin Neurol 2014;124:151–66.ArticlePubMed
  • 6. Arafah BM, Nasrallah MP. Pituitary tumors: pathophysiology, clinical manifestations and management. Endocr Relat Cancer 2001;8:287–305.ArticlePubMed
  • 7. Krysiak R, Okopien B, Korzekwa M. Atypical pituitary tumors. Pol Merkur Lekarski 2012;32:323–8.PubMed
  • 8. Chanson P, Brochier S. Non-functioning pituitary adenomas. J Endocrinol Invest 2005;28:93–9.PubMed
  • 9. Fleseriu M, Bodach ME, Tumialan LM, Bonert V, Oyesiku NM, Patil CG, et al. Congress of neurological surgeons systematic review and evidence-based guideline for pretreatment endocrine evaluation of patients with nonfunctioning pituitary adenomas. Neurosurgery 2016;79:E527–9.ArticlePubMed
  • 10. Laws ER Jr, Penn DL, Repetti CS. Advances and controversies in the classification and grading of pituitary tumors. J Endocrinol Invest 2019;42:129–35.ArticlePubMedPDF
  • 11. Hemminki K, Forsti A, Ji J. Incidence and familial risks in pituitary adenoma and associated tumors. Endocr Relat Cancer 2007;14:103–9.ArticlePubMed
  • 12. Davis FG, Kupelian V, Freels S, McCarthy B, Surawicz T. Prevalence estimates for primary brain tumors in the United States by behavior and major histology groups. Neuro Oncol 2001;3:152–8.ArticlePubMedPMC
  • 13. Park KH, Lee EJ, Seo GH, Ku CR. Risk for acromegaly-related comorbidities by sex in Korean acromegaly. J Clin Endocrinol Metab 2020;105:dgz317.ArticlePubMedPDF
  • 14. Park KH, Choi JG, Tae ES, Song SO, Nam JY, Song YD. Rare intractable pituitary diseases: analysis on their epidemiology and use of benefit extension policy (No. 2015-20-025); Goyang: National Health Insurance Service Ilsan Hospital; 2015.
  • 15. Seo GH, Choe EK, Park KJ, Chai YJ. Incidence of adhesive bowel obstruction after colon cancer surgery and its risk factors: a nationwide claim study. Ann Surg 2018;268:114–9.ArticlePubMed
  • 16. Yun JM, Shin DW, Hwang SS, Cho J, Nam YS, Kim JH, et al. Effect of public disclosure on antibiotic prescription rate for upper respiratory tract infections. JAMA Intern Med 2015;175:445–7.ArticlePubMed
  • 17. Seong SC, Kim YY, Khang YH, Heon Park J, Kang HJ, Lee H, et al. Data resource profile: the national health information database of the national health insurance service in South Korea. Int J Epidemiol 2017;46:799–800.PubMed
  • 18. Melmed S. Acromegaly pathogenesis and treatment. J Clin Invest 2009;119:3189–202.ArticlePubMedPMC
  • 19. Melmed S, Ezrin C, Kovacs K, Goodman RS, Frohman LA. Acromegaly due to secretion of growth hormone by an ectopic pancreatic islet-cell tumor. N Engl J Med 1985;312:9–17.ArticlePubMed
  • 20. Beuschlein F, Strasburger CJ, Siegerstetter V, Moradpour D, Lichter P, Bidlingmaier M, et al. Acromegaly caused by secretion of growth hormone by a non-Hodgkin’s lymphoma. N Engl J Med 2000;342:1871–6.ArticlePubMed
  • 21. Thorner MO, Perryman RL, Cronin MJ, Rogol AD, Draznin M, Johanson A, et al. Somatotroph hyperplasia. Successful treatment of acromegaly by removal of a pancreatic islet tumor secreting a growth hormone-releasing factor. J Clin Invest 1982;70:965–77.ArticlePubMedPMC
  • 22. Fernandez A, Karavitaki N, Wass JA. Prevalence of pituitary adenomas: a community-based, cross-sectional study in Banbury (Oxfordshire, UK). Clin Endocrinol (Oxf) 2010;72:377–82.ArticlePubMed
  • 23. Daly AF, Rixhon M, Adam C, Dempegioti A, Tichomirowa MA, Beckers A. High prevalence of pituitary adenomas: a cross-sectional study in the province of Liege, Belgium. J Clin Endocrinol Metab 2006;91:4769–75.ArticlePubMedPDF
  • 24. Tjornstrand A, Gunnarsson K, Evert M, Holmberg E, Ragnarsson O, Rosen T, et al. The incidence rate of pituitary adenomas in western Sweden for the period 2001–2011. Eur J Endocrinol 2014;171:519–26.ArticlePubMed
  • 25. Agustsson TT, Baldvinsdottir T, Jonasson JG, Olafsdottir E, Steinthorsdottir V, Sigurdsson G, et al. The epidemiology of pituitary adenomas in Iceland, 1955–2012: a nationwide population-based study. Eur J Endocrinol 2015;173:655–64.ArticlePubMed
  • 26. Hoskuldsdottir GT, Fjalldal SB, Sigurjonsdottir HA. The incidence and prevalence of acromegaly, a nationwide study from 1955 through 2013. Pituitary 2015;18:803–7.ArticlePubMedPDF
  • 27. Raappana A, Koivukangas J, Ebeling T, Pirila T. Incidence of pituitary adenomas in Northern Finland in 1992–2007. J Clin Endocrinol Metab 2010;95:4268–75.ArticlePubMed
  • 28. Dal J, Feldt-Rasmussen U, Andersen M, Kristensen LO, Laurberg P, Pedersen L, et al. Acromegaly incidence, prevalence, complications and long-term prognosis: a nationwide cohort study. Eur J Endocrinol 2016;175:181–90.ArticlePubMed
  • 29. Bex M, Abs R, T’Sjoen G, Mockel J, Velkeniers B, Muermans K, et al. AcroBel–the Belgian registry on acromegaly: a survey of the ‘real-life’ outcome in 418 acromegalic subjects. Eur J Endocrinol 2007;157:399–409.ArticlePubMed
  • 30. Mestron A, Webb SM, Astorga R, Benito P, Catala M, Gaztambide S, et al. Epidemiology, clinical characteristics, outcome, morbidity and mortality in acromegaly based on the Spanish Acromegaly Registry (Registro Espanol de Acromegalia, REA). Eur J Endocrinol 2004;151:439–46.ArticlePubMed
  • 31. Gruppetta M, Mercieca C, Vassallo J. Prevalence and incidence of pituitary adenomas: a population based study in Malta. Pituitary 2013;16:545–53.ArticlePubMedPDF
  • 32. Burton T, Le Nestour E, Neary M, Ludlam WH. Incidence and prevalence of acromegaly in a large US health plan database. Pituitary 2016;19:262–7.ArticlePubMedPMCPDF
  • 33. Caputo M, Ucciero A, Mele C, De Marchi L, Magnani C, Cena T, et al. Use of administrative health databases to estimate incidence and prevalence of acromegaly in Piedmont Region, Italy. J Endocrinol Invest 2019;42:397–402.ArticlePubMedPDF
  • 34. Sader MA, McGrath KC, Hill MD, Bradstock KF, Jimenez M, Handelsman DJ, et al. Androgen receptor gene expression in leucocytes is hormonally regulated: implications for gender differences in disease pathogenesis. Clin Endocrinol (Oxf) 2005;62:56–63.ArticlePubMed
  • 35. Bengtsson BA, Eden S, Ernest I, Oden A, Sjogren B. Epidemiology and long-term survival in acromegaly. A study of 166 cases diagnosed between 1955 and 1984. Acta Med Scand 1988;223:327–35.ArticlePubMed
  • 36. Ritchie CM, Atkinson AB, Kennedy AL, Lyons AR, Gordon DS, Fannin T, et al. Ascertainment and natural history of treated acromegaly in Northern Ireland. Ulster Med J 1990;59:55–62.PubMedPMC
  • 37. Etxabe J, Gaztambide S, Latorre P, Vazquez JA. Acromegaly: an epidemiological study. J Endocrinol Invest 1993;16:181–7.ArticlePubMedPDF
  • 38. Lee SJ, Chai ES, Chough CB, Kim CH, Choi HJ. Case report: two cases of active acromegaly. Korean J Med 1965;8:241–7.
  • 39. Yang IM. Clinical characteristics of acromegalic patients in Korea. J Korean Soc Endocrinol 1994;9:290–306.
  • 40. Kwon O, Song YD, Kim SY, Lee EJ, et al. Rare Disease Study Group; Science and Research Committee. Nationwide survey of acromegaly in South Korea. Clin Endocrinol (Oxf) 2013;78:577–85.ArticlePubMed
  • 41. Melmed S, Casanueva FF, Hoffman AR, Kleinberg DL, Montori VM, Schlechte JA, et al. Diagnosis and treatment of hyperprolactinemia: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2011;96:273–88.ArticlePubMedPDF
  • 42. Vroonen L, Daly AF, Beckers A. Epidemiology and management challenges in prolactinomas. Neuroendocrinology 2019;109:20–7.ArticlePubMed
  • 43. Ezzat S, Asa SL, Couldwell WT, Barr CE, Dodge WE, Vance ML, et al. The prevalence of pituitary adenomas: a systematic review. Cancer 2004;101:613–9.ArticlePubMed
  • 44. Colao A, Sarno AD, Cappabianca P, Briganti F, Pivonello R, Somma CD, et al. Gender differences in the prevalence, clinical features and response to cabergoline in hyperprolactinemia. Eur J Endocrinol 2003;148:325–31.ArticlePubMed
  • 45. Cushing H. The pituitary body and its disorders: clinical states produced by disorders of the hypophysis cerebri; Philadelphia: JB Lippincott; 1912.
  • 46. Pivonello R, Isidori AM, De Martino MC, Newell-Price J, Biller BM, Colao A. Complications of Cushing’s syndrome: state of the art. Lancet Diabetes Endocrinol 2016;4:611–29.ArticlePubMed
  • 47. Etxabe J, Vazquez JA. Morbidity and mortality in Cushing’s disease: an epidemiological approach. Clin Endocrinol (Oxf) 1994;40:479–84.ArticlePubMed
  • 48. Lindholm J, Juul S, Jorgensen JO, Astrup J, Bjerre P, Feldt-Rasmussen U, et al. Incidence and late prognosis of cushing’s syndrome: a population-based study. J Clin Endocrinol Metab 2001;86:117–23.ArticlePubMed
  • 49. The Korean Society of Endocrinology; The Survey Committee for Endocrine Disease in Korea. The incidence and clinical characteristics of Cushing’s syndrome in Korea. J Korean Soc Endocrinol 2000;15:31–45.
  • 50. Jailer JW, Holub DA. Remission of Graves’ disease following radiotherapy of a pituitary neoplasm. Am J Med 1960;28:497–500.ArticlePubMed
  • 51. Amlashi FG, Tritos NA. Thyrotropin-secreting pituitary adenomas: epidemiology, diagnosis, and management. Endocrine 2016;52:427–40.ArticlePubMedPDF
  • 52. Azzalin A, Appin CL, Schniederjan MJ, Constantin T, Ritchie JC, Veledar E, et al. Comprehensive evaluation of thyrotropinomas: single-center 20-year experience. Pituitary 2016;19:183–93.ArticlePubMedPDF
  • 53. Yamada S, Fukuhara N, Horiguchi K, Yamaguchi-Okada M, Nishioka H, Takeshita A, et al. Clinicopathological characteristics and therapeutic outcomes in thyrotropin-secreting pituitary adenomas: a single-center study of 90 cases. J Neurosurg 2014;121:1462–73.ArticlePubMed
  • 54. Yoon HJ, Hong DS, Hong KS, Cha BY, Kim YW, Son HY. A case of TSH secreting pituitary tumor. J Korean Soc Endocrinol 1986;1:55–62.
  • 55. Lee WK, Hwang S, Lim JS, Kim HM, Lee EY, Lee SK, et al. Clinical and biochemical characteristics and treatment of patients with thyrotropin-secreting pituitary adenomas. Korean J Med 2011;80:47–55.
  • 56. Onnestam L, Berinder K, Burman P, Dahlqvist P, Engstrom BE, Wahlberg J, et al. National incidence and prevalence of TSH-secreting pituitary adenomas in Sweden. J Clin Endocrinol Metab 2013;98:626–35.ArticlePubMed
  • 57. Beck-Peccoz P, Lania A, Beckers A, Chatterjee K, Wemeau JL. 2013 European Thyroid Association guidelines for the diagnosis and treatment of thyrotropin-secreting pituitary tumors. Eur Thyroid J 2013;2:76–82.ArticlePubMedPMC

Figure & Data

References

    Citations

    Citations to this article as recorded by  
    • The Diagnostic Value of Conventional MRI Combined With Diffusion‐Weighted Imaging in Microprolactinomas
      Min‐Yang Wang, Ying Yu, Yu Han, Yang Yang, Wan Jiang, Jin Liu, Lin‐Feng Yan, Guang‐Bin Cui
      Journal of Magnetic Resonance Imaging.2025; 61(3): 1155.     CrossRef
    • Non-recurrent mutations and copy number changes predominate pituitary adenoma genomes
      Dipika R Mohan, Ticiana Paes, Jacobo Buelvas Mebarak, David M Meredith, Beatriz Soares, Victor Vaz, Rona S Carroll, Ursula B Kaiser, Timothy R Smith, Wenya L Bi, Antonio M Lerario, Ana Paula Abreu
      European Journal of Endocrinology.2025; 192(5): 590.     CrossRef
    • Spherical type of amyloidogenic pituitary prolactinoma in a 50 year old male
      Madhala Divya, Balasubramanian Archana, Lawrence D Cruze, D. Balasubramanian
      Interdisciplinary Neurosurgery.2024; 36: 101957.     CrossRef
    • Clinical aspects of the plurihormonal pituitary adenoma formation
      I. A. Khripun, S. V. Vorobyev, N. A. Kuzmenko, E. S. Engibaryan, V. O. Perevalova
      South Russian Journal of Therapeutic Practice.2024; 5(2): 98.     CrossRef
    • Anaesthesia for pituitary surgery
      K. Raveendran, S. Kwok, L. Glancz
      BJA Education.2024; 24(12): 433.     CrossRef
    • Manifestations of Endocrine Disease in the Lower Extremities: Beyond the Diabetic Foot
      Kleoniki I. Athanasiadou, Christothea A. Tsiridis, Ioanna A. Paschou, Stavroula A. Paschou, Nikolaos Papanas
      The International Journal of Lower Extremity Wounds.2024;[Epub]     CrossRef
    • Predicting Tumor Type and Residual Status of Suprasellar Lesions Using Indian Discharge Summaries
      Priyanka C. Nair, Deepa Gupta, Bhagavatula Indira Devi, Vani Kanjirangat, P. Deepak
      IEEE Access.2024; 12: 134379.     CrossRef
    • Spontaneous Cerebrospinal Fluid Rhinorrhea in Pre-operative Pituitary Adenoma: A Report of Two Cases
      Jessica E Eisold, Dace Dimante, Jonathan Pollock, Alireza Shoakazemi, Nemanja Stojanovic
      Cureus.2024;[Epub]     CrossRef
    • Surgical effect of the medial wall resection of the cavernous sinus for functional pituitary adenomas
      Xiao Liang, Zhuoqun Li, Mengyang Xing, Wenbo Gao, Pengfei Liu
      Frontiers in Surgery.2024;[Epub]     CrossRef
    • Transcriptome of GH-producing pituitary neuroendocrine tumours and models are significantly affected by somatostatin analogues
      Rihards Saksis, Olesja Rogoza, Helvijs Niedra, Kaspars Megnis, Ilona Mandrika, Inga Balcere, Liva Steina, Janis Stukens, Austra Breiksa, Jurijs Nazarovs, Jelizaveta Sokolovska, Ilze Konrade, Raitis Peculis, Vita Rovite
      Cancer Cell International.2023;[Epub]     CrossRef
    • Prognostic Models in Growth-Hormone- and Prolactin-Secreting Pituitary Neuroendocrine Tumors: A Systematic Review
      Roxana-Ioana Dumitriu-Stan, Iulia-Florentina Burcea, Teodor Salmen, Catalina Poiana
      Diagnostics.2023; 13(12): 2118.     CrossRef
    • Salivary microbiome profiles for different clinical phenotypes of pituitary adenomas by single-molecular long-read sequencing
      Xuefei Ji, Pingping Li, Qinglong Guo, Liao Guan, Peng Gao, Bingshan Wu, Hongwei Cheng, Jin Xiao, Lei Ye, Justin R. Kaspar
      Microbiology Spectrum.2023;[Epub]     CrossRef
    • Endoscopic endonasal surgical management of giant pituitary adenomas with extension into ventricle system
      Mykola O. Guk, Oleksii V. Ukrainets
      Ukrainian Neurosurgical Journal.2023; 29(4): 13.     CrossRef
    • Uso de resonancia magnética nuclear intraoperatoria en la resección transesfenoidal de adenomas hipofisiarios: ¿qué resultados se han obtenido?
      María Laura Boschetti Saer, Levino Roberto Boschetti, Jose Pastor Linarez Veloz, Michael Ortega-Sierra
      Archivos de Neurociencias.2023;[Epub]     CrossRef
    • Single Cell Metabolic Landscape of Pituitary Neuroendocrine Tumor Subgroups and Lineages
      Sai Batchu, Michael Joseph Diaz, Keldon Lin, Namrata Arya, Karan Patel, Brandon Lucke-Wold
      OBM Neurobiology.2023; 07(01): 1.     CrossRef
    • Epidemiology of common and uncommon adult pituitary tumors in the U.S. according to the 2017 World Health Organization classification
      Luz E. Castellanos, Catherine Gutierrez, Timothy Smith, Edward R. Laws, J. Bryan Iorgulescu
      Pituitary.2022; 25(1): 201.     CrossRef
    • The kinome, cyclins and cyclin-dependent kinases of pituitary adenomas, a look into the gene expression profile among tumors from different lineages
      Keiko Taniguchi-Ponciano, Lesly A. Portocarrero-Ortiz, Gerardo Guinto, Sergio Moreno-Jimenez, Erick Gomez-Apo, Laura Chavez-Macias, Eduardo Peña-Martínez, Gloria Silva-Román, Sandra Vela-Patiño, Jesús Ordoñez-García, Sergio Andonegui-Elguera, Aldo Ferreir
      BMC Medical Genomics.2022;[Epub]     CrossRef
    • IL-10 Gene Rs1800871, Rs1800872, and Rs1800896 Polymorphisms and IL-10 Serum Levels Association with Pituitary Adenoma
      Migle Palivonaite, Greta Gedvilaite, Brigita Glebauskiene, Loresa Kriauciuniene, Vita Rovite, Rasa Liutkeviciene
      Biomedicines.2022; 10(8): 1921.     CrossRef
    • Genome wide analysis of circulating miRNAs in growth hormone secreting pituitary neuroendocrine tumor patients’ plasma
      Helvijs Niedra, Raitis Peculis, Helena Daiga Litvina, Kaspars Megnis, Ilona Mandrika, Inga Balcere, Mihails Romanovs, Liva Steina, Janis Stukens, Austra Breiksa, Jurijs Nazarovs, Jelizaveta Sokolovska, Rasa Liutkeviciene, Alvita Vilkevicute, Ilze Konrade,
      Frontiers in Oncology.2022;[Epub]     CrossRef
    • Identification of mutant K-RAS in pituitary macroadenoma
      Veronica Aran, Manoela Heringer, Paulo Jose da Mata, Leandro Kasuki, Renan Lyra Miranda, Felipe Andreiuolo, Leila Chimelli, Paulo Niemeyer Filho, Monica Roberto Gadelha, Vivaldo Moura Neto
      Pituitary.2021; 24(5): 746.     CrossRef
    • Surgery is a safe, effective first-line treatment modality for noninvasive prolactinomas
      Ji Yong Park, Wonsuk Choi, A Ram Hong, Jee Hee Yoon, Hee Kyung Kim, Woo-Youl Jang, Shin Jung, Ho-Cheol Kang
      Pituitary.2021; 24(6): 955.     CrossRef

    • PubReader PubReader
    • ePub LinkePub Link
    • Cite
      Cite
      export Copy Download
      Close
      Download Citation
      Download a citation file in RIS format that can be imported by all major citation management software, including EndNote, ProCite, RefWorks, and Reference Manager.
      Format:
      • RIS — For EndNote, ProCite, RefWorks, and most other reference management software
      • BibTeX — For JabRef, BibDesk, and other BibTeX-specific software
      Include:
      • Citation for the content below
      Epidemiology of Functioning Pituitary Adenomas
      Endocrinol Metab. 2020;35(2):237-242.   Published online June 24, 2020
      DOI: https://doi.org/10.3803/EnM.2020.35.2.237
      Close
    • XML DownloadXML Download
    Epidemiology of Functioning Pituitary Adenomas
    Epidemiology of Functioning Pituitary Adenomas
    Size Function Hormone Pathology (WHO)a Morphofunctional subclassificationa
    Microadenoma
    Macroadenoma
    Giant adenoma    		 Functioning
    Non-functioning    		 Prolactin Lactotroph adenoma (LA) Sparsely granulated LA
    Densely granulated LA
    Acidophilic stem cell adenoma
    Growth hormone Somatotroph adenoma (SA) Densely granulated SA
    Sparsely granulated SA
    Mammosomatotroph adenoma
    Mixed somatotroph and lactotroph adenoma
    Adrenocorticotropic hormone Corticotroph adenoma (CA) Sparsely granulated CA
    Densely granulated CA
    Acidophilic stem cell adenoma
    Thyroid-stimulating hormone Thyrotroph adenoma
    Luteinizing hormone/follicular-stimulating hormone Gonadotroph adenoma (GA) null cell adenoma Sparsely granulated GA
    Plurihormonal Plurihormonal adenoma Plurihormonal PIT1-positive adenoma
    Adenomas with unusual IHC combinations
    Double adenoma Distinct adenomas
    Table 1 Classification of Pituitary Adenomas

    WHO, World Health Organization; PIT1, pituitary-specific positive transcription factor 1; IHC, immunohistochemical.

    Adapted from Laws et al. [10], with permission from Springer Nature.

    Table 1

    Endocrinol Metab : Endocrinology and Metabolism
    © Korean Endocrine Society.
    TOP