Advances in Surgery for Pituitary Tumors

Advances in Surgery for Pituitary Tumors

Published: US Neurology - Volume 4 Issue 2
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Although benign in nature, pituitary tumors continue to offer many opportunities for improvement in therapy. Goals of treatment include complete removal or ablation of tumor cells, maintenance of normal pituitary function, normalization of elevated hormone levels in endocrine-active tumors, and minimizing adverse effects from therapy. There have been many recent advances related to the surgical treatment of pituitary tumors and the purpose of this article is to review some of the more significant ones.

Behavior of Pituitary Tumors
One of the most notable features of pituitary adenomas is their ubiquity in population studies compared with the relatively small number of tumors that actually present with clinical problems. Pituitary adenomas have been consistently reported in up to 25% of people in autopsy studies dating back to 1936.1 More recent studies have attempted to clarify the relative prevalence of ‘incidentalomas’ compared with clinically relevant tumors. A meta-analysis performed in 20042 found an incidence of 16.7% with autopsies reporting 14.4% and radiologic studies finding a rate of 22.5%. Prolactinomas represented 25–41% of incidentalomas in studies that included immunohistochemical staining.3,4 A recent population study from Belgium5 found a prevalence of clinically relevant pituitary adenomas of 94 per 100,000. Of this group, 66% were prolactinomas, 14.7% were not endocrine-active, 13.2% had acromegaly, 5.9% had Cushing’s disease, and 20.6% had hypopituitarism. These same authors provided a concise set of recommendations for management of incidentalomas, including initial evaluation and periodic follow-up with magnetic resonance imaging (MRI) and endocrine studies.6

One recent paper reported new findings on the cellular biology of the normal pituitary gland that may ultimately have implications for tumorigenesis of adenomas.7 The investigators used a thoughtfully crafted series of transgenic mice that coupled the gene for nestin (a marker of adult stem cells) to a reporter gene (green fluorescent protein). They found that at birth the anterior pituitary gland is composed of cells that were created by embryonic stem cells. However, throughout post-natal life, adult stem cells contributed new pituitary cells of all major sub-types to the gland. This means that the adult gland represents a mosaic of cells that have similar phenotypes (i.e. lactotrophs, somatotrophs, etc.) but have very different origins (i.e. embryonic or adult progenitor cells). They also provided preliminary evidence that adult stem cells may be involved in tumorigenesis in the pituitary in a mouse model, the retinoblastoma (Rb-1)+/- mouse. This will, no doubt, stimulate considerable interest in the study of the cellular originators of human pituitary tumors.

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