Pathology of GH-producing pituitary adenomas and GH cell hyperplasia of the pituitary

Syro, Luis V.; Rotondo, Fabio; Serna, Carlos; Ortíz, León Darío; Kovács, Kálmán

doi:10.1007/s11102-016-0748-8

Cited by 36 publications

(30 citation statements)

References 71 publications

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“…Yet, compared with somatotroph adenomas that do not harbor GNAS mutations, GNAS mutation-positive adenomas secrete more GH (70,71) and are less responsive to GHRH (70) but are highly responsive to octreotide (71)(72)(73). These same features are common to densely granulated somatotroph adenomas (74), which tend to be smaller in size, produce more GH per unit volume, and respond better to octreotide compared with sparsely granulated adenomas (75). We also observed higher expression of somatotroph adenoma p53 and p21 Wif1/Cip1 , which are known to induce cell-cycle arrest upon DNA damage (76).…”

Section: Discussionmentioning

confidence: 99%

DNA damage and growth hormone hypersecretion in pituitary somatotroph adenomas

Ben-Shlomo¹,

Deng²,

Ding³

et al. 2020

Journal of Clinical Investigation

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Section: Discussionmentioning

confidence: 99%

DNA damage and growth hormone hypersecretion in pituitary somatotroph adenomas

Ben-Shlomo¹,

Deng²,

Ding³

et al. 2020

Journal of Clinical Investigation

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“…Mixed GH and PRL adenomas or mammosomatotroph adenomas account for up to 30% of cases of acromegaly in humans [34, 35]. PRL-positive cells accounted for <10% of positive cells in 87% of the acromegalic pituitaries, with the remaining samples containing 10.5%, 10.5%, 16%, and 20.5% of PRL-positive cells.…”

Section: Discussionmentioning

confidence: 99%

Pituitary Pathology and Gene Expression in Acromegalic Cats

Scudder

Mirczuk

Richardson

et al. 2018

Journal of the Endocrine Society

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The prevalence of GH-secreting pituitary tumors in domestic cats (Felis catus) is 10-fold greater than in humans. The predominant inhibitory receptors of GH-secreting pituitary tumors are somatostatin receptors (SSTRs) and D2 dopamine receptor (DRD2). The expression of these receptors is associated with the response to somatostatin analog and dopamine agonist treatment in human patients with acromegaly. The aim of this study was to describe pathological features of pituitaries from domestic cats with acromegaly, pituitary receptor expression, and investigate correlates with clinical data, including pituitary volume, time since diagnosis of diabetes, insulin requirement, and serum IGF1 concentration. Loss of reticulin structure was identified in 15 of 21 pituitaries, of which 10 of 15 exhibited acinar hyperplasia. SSTR1, SSTR2, SSTR5, and DRD2 mRNA were identified in the feline pituitary whereas SSTR3 and SSTR4 were not. Expression of SSTR1, SSTR2, and SSTR5 was greater in acromegalic cats compared with controls. A negative correlation was identified between DRD2 mRNA expression and pituitary volume. The loss of DRD2 expression should be investigated as a mechanism allowing the development of larger pituitary tumors.

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“…Sparsely-granulated somatotroph tumors are more common in patients who are younger than 50 years of age; they often present with a more rapidly growing tumor and are larger at diagnosis, compared to densely-granulated tumors [16,17,19,29,31,32]. The clinical manifestations of acromegaly may be more subtle in these patients where the hormonal syndrome may be missed and the tumor misclassified as clinically “silent” [33]. Levels of GH and IGF-1 might not be as high as in patients with densely-granulated somatotroph tumors [16,17,19].…”

Section: Primary Pituitary Causesmentioning

confidence: 99%

“…These are distinct from mammosomatotroph tumors, which are composed of a single monomorphous cell population that expresses both hormones. These tumors express Pit1 in all tumor cells, but only the cells that express prolactin also express ERα [33].…”

Section: Primary Pituitary Causesmentioning

confidence: 99%

The Clinicopathological Spectrum of Acromegaly

Akirov

Sylvia

Amer

et al. 2019

JCM

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Background: Acromegaly results from a persistent excess in growth hormone with clinical features that may be subtle or severe. The most common cause of acromegaly is a pituitary tumor that causes excessive production of growth hormone (GH), and rare cases are due to an excess of the GH-releasing hormone (GHRH) or the ectopic production of GH. Objective: Discuss the different diseases that present with manifestations of GH excess and clinical acromegaly, emphasizing the distinct clinical and radiological characteristics of the different pathological entities. Methods: We performed a narrative review of the published clinicopathological information about acromegaly. An English-language search for relevant studies was conducted on PubMed from inception to 1 August 2019. The reference lists of relevant studies were also reviewed. Results: Pituitary tumors that cause GH excess have several variants, including pure somatotroph tumors that can be densely or sparsely granulated, or plurihormonal tumors that include mammosomatotroph, mixed somatotroph-lactotroph tumors and mature plurihomonal Pit1-lineage tumors, acidophil stem cell tumors and poorly-differentiated Pit1-lineage tumors. Each tumor type has a distinct pathophysiology, resulting in variations in clinical manifestations, imaging and responses to therapies. Conclusion: Detailed clinicopathological information will be useful in the era of precision medicine, in which physicians tailor the correct treatment modality to each patient.

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Pathology of GH-producing pituitary adenomas and GH cell hyperplasia of the pituitary

Abstract: The importance of morphologic classification and identification of different subgroups of patients with GH-producing adenomas and their impact on clinical management is discussed.

Cited by 36 publications

References 71 publications

DNA damage and growth hormone hypersecretion in pituitary somatotroph adenomas

DNA damage and growth hormone hypersecretion in pituitary somatotroph adenomas

Pituitary Pathology and Gene Expression in Acromegalic Cats

The Clinicopathological Spectrum of Acromegaly

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