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It also controls the function of certain organs, such as the kidneys, breasts, and uterus. The pituitary has three parts or lobes, each with its own job in the body. Its job is to make and release many "signaling" hormones into the bloodstream.

Anatomy of the pituitary and sella

These hormones move through the blood to other glands and organs, where they signal the organs and glands to start or stop working. The back part of the gland, the posterior pituitary, does not make any hormones itself. Instead, it contains nerve endings of brain cells that come from the hypothalamus. These brain cells make the hormones, which then move down to and are stored in the posterior pituitary for later use. The hypothalamus and the pituitary work hand-in-hand.

The hypothalamus makes hormones that, in turn, signal the pituitary to release its hormones. A pituitary adenoma is a growth or tumor on the pituitary. Most pituitary adenomas are slow-growing and benign, which means they are not cancer and do not spread to other parts of the body. However, as they grow big they can put pressure on nearby structures, such as the nerves that connect the eyes to the brain, and cause symptoms.

A large adenoma can also crush normal pituitary cells and keep them from working properly, leading to a condition called hypopituitarism. This condition can cause low blood pressure, tiredness, and changes in your sex drive and function. It can also make you feel less able to manage stress. Pituitary adenomas are labeled based on their size. Tumors smaller than 1 cm are called microadenomas. Hormone-inactive adenomas are larger tumors that, due to their size, may damage the pituitary gland or exert pressure on surrounding brain tissues. The most common hormone-producing adenomas are named in conjunction with the hormone they stimulate:.

In both cases, individuals continue to grow and reach an unusually large size. Excess production of the hormone prolactin shuts down menstrual periods, causes breast enlargement, and production of breast milk. The symptoms hormone-producing adenomas cause are related to the hormone that is affected by the tumor as already noted. Hormone-inactive adenomas exert pressure on surrounding brain structures and can produce a variety of symptoms depending upon the area of the brain affected by the tumor.

Compression of the pituitary gland by a hormone-inactive tumor can result some form of pituitary failure with one or more of the following pituitary tumor symptoms :. Compression of the pituitary stalk which connects the pituitary gland to the hypothalamus can result in mildly elevated levels of prolactin, causing irregular menstrual periods in females.

Multiple Pituitary Adenomas: A Systematic Review

This condition is different from a prolactin-secreting pituitary adenoma. A macroadenoma that grows upward from the pituitary gland can impact the optic chiasm, part of the pathway in the brain between the eye and the visual cortex. The visual cortex is the portion of the brain that ultimately controls eyesight.

This type of pituitary adenoma results in:. Pituitary apoplexy can be a severe result of any type of pituitary adenoma. With pituitary apoplexy the adenoma bleeds into itself and causes a sudden headache accompanied by a loss in vision. Pituitary apoplexy is a medical emergency. A pituitary adenoma diagnosis is typically accomplished by an endocrinologist through sophisticated blood tests that measure applicable hormone levels along with MRI magnetic resonance imaging of the brain and pituitary gland. Medical management with drugs through an endocrinologist is the first-line treatment for pituitary adenomas secreting prolactin.

Pituitary tumors rarely require any other treatment. Otherwise, surgery to remove the adenoma is the treatment of choice. Some patients with incidentally discovered non-secretory adenomas may be best treated with observation alone. Transsphenoidal tumor resection is the name of the surgical technique used to remove a pituitary adenoma. The surgeon enters the body through the nostrils and the sphenoid sinus cavity. The surgeon then creates a small hole in the bone at the back of the sinus cavity. This hole allows the surgeon to view the pituitary gland and the adenoma and ultimately remove the tumor.

The surgeon utilizes specially designed tools during a transsphenoidal tumor resection. Fluoroscopy, an imaging system that transfers a stream of images to a screen, assists the surgeon in inserting a tube through the nostril and into the sinuses. Inside the tube a high-powered surgical microscope magnifies the internal structures, giving the surgeon an enhanced image of the pituitary gland, the adenoma and the surrounding tissues.

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Depending on the size of the adenoma, it is removed intact or larger tumors are removed in small pieces. Regarding the immunoreactivity, it resulted that The most frequent combination immunoprofile was represented by mixt GH and PRL secretion, in fact, resembling the high incidence of composite GH-PRL secretion encountered in single pituitary adenomas. In a review of double pituitary adenomas, including tumors with pathological report albeit incomplete endocrine evaluation, Iacovazzo et al. In most of the cases, tumors staining for PRL were silent 7.

Specifically, each of the tumors can secrete one or several hormones; hence, making different combinations of pituitary adenomas possible. A number of genetic e.

General Information About Pituitary Tumors

However, limited information is available with regard to oncogenesis of multiple adenomas of the pituitary gland. Coincidental monoclonal expansion of two distinct genetically mutated pituitary cell types could result in the development of synchronous tumors. Evidence of distinct tumor capsules at microdissection of surgical specimens, recognized even in the contiguous tumor phenotype 29 , favors the concept of a multicentric origin of MPA. Alternatively, cells of one already constituted pituitary adenoma could transdifferentiate into another cell type, with different morphologic and phenotypic characteristics including secretory features and local behavior.

Insight to the pathogenesis of MPA was gained by immunohistochemical localization of transcription factors, which allows classification of pituitary tumors according to the lineage of cell differentiation irrespective of the tumor hormone substance.

Pituitary Tumors Treatment (PDQ®)–Patient Version

Occasionally, genetic analysis for clonality has practical value as the demonstration of true lineage infidelity in the pathology specimen readily suggests multiple adenomas 40 , although single plurihormonal adenomas exhibiting heterogeneous cell populations of different clonal origin were also recognized As such, combination patterns in that tumors releasing secretory products consistent with multiple clonal proliferations were certified by genetic analysis in few cases of composite pituitary adenomas 43 , Transcription factors immunoprofiling revealed in two of three cases of double pituitary adenomas lineages of distinct origin, with Pit-1 expression in PRL-secreting cells and the hormone-negative cell component expressing SF-1 Double tumors with different clonality rather support the true multiple adenomas theory 45 , whereas transdifferentiation might be more plausible in cases of MPA sharing immunoreactivity to any of the hormones secreted by one of the three different lineages into which pluripotent progenitor cells from the normal pituitary gland differentiate Pituitary tumor-expressed growth factors and hormone receptors may participate in tumor development through auto- or paracrine mechanisms 46 , and this hypothesis could apply for MPA as well.

The particular condition of GH-secreting adenomas, which release mitogenic GH and IGF-1 to stimulate development of a second tumor, is prototypical 5. In addition to that, MEN-1 gene mutation was also confirmed in one of the patients with hyperprolactinemia harboring two distinct lesions on pituitary MRI 11 , not included in our analysis.

Notwithstanding, specific testing for genetic causes related to pituitary tumors was not offered to all patients, which in addition to the small study population may impair data accuracy, thus requiring further studies.

Furthermore, Kim et al. Additionally, somatic mutations e. Transcriptional studies may reveal whether coexisting tumors originate from one cell type A somatic mutation in the ubiquitin-specific protease 8 USP8 gene 51 was reported in about one-thirds to two-thirds of ACTH-secreting adenomas, which is the most prevalent functional tumor found in MPA.

Nevertheless, none of the cases with USP8 mutations exhibited double or multiple adenomas. However, particularly incipient disease clinical features in acromegaly might be mild; according to Endocrine Society guidelines, IGF-1 screening in each patient with confirmed pituitary mass is recommended Hyperprolactinemia in acromegaly patients points out to either mixt GH and PRL tumor release or pituitary stalk compression in the setting of suprasellar macroadenoma but raises also the possibility of two independent GH- and PRL-secreting adenomas. In agreement to this, Tolis et al.

Apparently, about 1. Three cases of double pituitary lesions were reported by Meij et al. Additionally, two out of three patients with double pituitary tumors reported by McKelvie et al. Up to the moment, only two clinical cases featuring clearly separated pituitary adenomas, both ACTH-secreting, were reported 30 , The source of ACTH hypersecretion in ACTH-immunoreactive forms of MPA is mainly eutopic due to hyperfunctional pituitary corticotroph adenoma cells; however, ACTH may also derive from ectopic corticotroph tumor cells located in the parasellar area, the neurohypohysis, or the pituitary stalk 30 , Nevertheless, clear distinction between persistent disease after unsuccessful surgery and disease recurrence should be made 69 , as the latter is also increasingly reported in cured pituitary ACTH-secreting adenoma However, variability between studies is relatively high and the small numbers of cases significantly impairs accuracy.

Older studies reported low accuracy for MRI diagnosis of MPA, such as in the case series of Ratliff, where none of the seven cases harboring clearly separated double pituitary tumors identified by surgery had been previously detected by MRI as such Most challenging situations remain contiguous MPA, resulting in single tumor appearance, even on high-resolution MRI exam 34 or macroadenomas masking small coexisting tumors 36 , As true MPA are rare, false-positive findings of double or multiple tumors on pituitary MRI might be detected; thus, diagnosis is confirmed following pathological exam.

High-resolution MRI techniques need to be employed in hormonally active tumors with non-diagnostic imaging tests Thin-sliced and dynamic MRI represents a readily accessible option to improve resolution and increasingly detect multiple lesions. Alternatively, 3. Exploratory pituitary surgery should be reserved only to cases with high suspicion or during second-look surgery as well as for ACTH-secreting tumors with normal MRI and non-diagnostic inferior petrosal sinus sampling IPSS. Immunohistochemistry allows the exclusion of false double pituitary lesions by detecting distinct immunochemical signatures in surgical specimens.

Even if both tumors are correctly removed, unequivocal diagnosis of MPA is difficult when adenomas show identical immunoreactivity; in these cases, variability in cells size, conventional staining, and cytoplasm appearance 36 , 55 or presence of a thin lamellae of compressed normal pituitary tissue separating the tumors might be of help. Electron microscopy scanning may provide additional information e. Furthermore, quantitation of O -methylguanine-DNA methyltransferase MGMT immunoexpression, the Ki nuclear labeling index, or supplemental transcription factors 82 may show significant differences among tumors in patients suspected for multiple adenomas.

However, definitive diagnosis should be concluded based upon pathological examinations. Persistence of endocrine disturbances after pituitary surgery leads to a high index of suspicion for MPA. Up to this moment, the etiopathogeny of MPA remains elusive, in spite of various theoretical concepts and higher prevalence of MEN-1 mutation among genotyped cases. Further, molecular analysis will provide new insights into the pathogenesis of pituitary adenomas and the mechanisms of multidirectional phenotypic differentiation.

RMB collected data and drafted the manuscript.

Pituitary adenoma

CEG is responsible for the design of the work, contributed to data analysis, and wrote the review. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. National Center for Biotechnology Information , U. Journal List Front Endocrinol Lausanne v. Front Endocrinol Lausanne.

Published online Feb 1. Renata M. Budan 1 and Carmen E. Carmen E. Author information Article notes Copyright and License information Disclaimer. Georgescu, moc. Specialty section: This article was submitted to Pituitary Endocrinology, a section of the journal Frontiers in Endocrinology. Received Nov 15; Accepted Jan 8. The use, distribution or reproduction in other forums is permitted, provided the original author s or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.

No use, distribution or reproduction is permitted which does not comply with these terms. This article has been cited by other articles in PMC. Abstract PubMed, Scopus, and Web of Science Core Collection databases were systematically searched for studies reporting synchronous double or multiple pituitary adenomas MPA , a rare clinical condition, with a vague pathogenesis.

Prevalence of MPA: The Size of the Problem Autopsy Reports Since the first report on multiple pituitary tumors by Kraus in 15 , estimates provided by autopsy studies on the prevalence of incidentally detected MPA varied widely, ranging from 0.

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Table 1 MPA incidence from five large surgical series, with specifications regarding most frequent clinical presentation. Open in a separate window. Table 2 Clinical presentation of MPA. The Multiple-Hit Multicentricity Theory Coincidental monoclonal expansion of two distinct genetically mutated pituitary cell types could result in the development of synchronous tumors. The Transdifferentiation Theory Alternatively, cells of one already constituted pituitary adenoma could transdifferentiate into another cell type, with different morphologic and phenotypic characteristics including secretory features and local behavior.

Author Contributions RMB collected data and drafted the manuscript. Conflict of Interest Statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. References 1. Characterization of aryl hydrocarbon receptor interacting protein AIP mutations in familial isolated pituitary adenoma families.

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Medicine 78 — Pituitary adenomas in mice transgenic for growth hormone-releasing hormone. Endocrinology —9. Double adenomas of the pituitary: a clinicopathological study of 11 tumors. Neurosurgery 31 —9. Asynchronous pituitary adenomas with differing morphology. Arch Pathol Lab Med 8 — Double pituitary adenomas. Endocrine 43 2 —7.

Collision sellar lesions: experience with eight cases and review of the literature. Pituitary 13 :8— Double pituitary adenoma — two case reports. Neurol Med Chir 36 — Multiple adenomas of the human pituitary. A retrospective autopsy study with clinical implications. J Neurosurg 74 2 —7. Sahdev A, Jager R. Bilateral pituitary adenomas occurring with multiple neoplasia type one.