ISSN 1470-3947 (print)
ISSN 1479-6848 (online)

Searchable abstracts of presentations at key conferences in endocrinology

Published by BioScientifica
Endocrine Abstracts (2010) 22 S20.2 
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Pituitary incidentalomas

Mihail Coculescu

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Current issues relating to pituitary incidentalomas include definitional limits, difficulties in their diagnosis resulting in hidden dangers, unknown pathogeny and management based on expectation. The prevalence of pituitary incidentalomas depends on the method of investigation: 3.2–27% in necroptic studies or 10–23% by imaging (MRI or CT), compared to only 0.1% clinically expressed pituitary adenomas. Diagnosis requires at least imaging and hormonal assays. However, pituitary masses conceal different histopathological features. Besides adenomas there are frequent autoimmune lymphocytic hypophisitis and many other lesions without clinical expression. Non-histological terminology is necessary before the diagnosis of adenomas. PET and SPECT did not significantly improve diagnosis. Non-specific or unexplored symptoms /signs (for example, headaches or sleep disturbances) accompanying the incidentalomas are observed frequently (61/182 in our series). Differential diagnosis is difficult in some cases: incidentaloma with hyperprolactinemia against prolactinomas, incidentaloma with paraneoplasic Cushing syndrome against Cushing`s disease, incidentaloma with premature ovarian failure against gonadotropinoma and pituitary hyperplasia against adenoma. Dynamic tests with aGnRH and gonadotropins can be useful. Hidden dangers include misdiagnosis with subclinical secreting adenomas (including subclinical acromegaly) or growing adenomas. Pathology shows the predominance of small <1 mm-adenomas. Immunohistochemistry may reveal multiple ‘mute’ pituitary hormones, often gonadotropins (25/141 in our series). In foliculostellate cells there are many paracrine products with unknown clinical expression (for example annexin, follistatin, VEGF). Paracrine secretory products are also found in other pituitary cells, as is hypoxia inducible factor-2- alfa in somatotrophs and TRH in gonadotrophs. The pathogeny of pituitary adenomas, especially incidentalomas, is unknown. PTTG seems to be more involved in proliferation of non-functioning cells than of hormone-secreting cells. The role of stem cells is currently in discussion. Therapy is recommended only for growing incidentalomas. The follow-up is not well established: initially every 6 months, thereafter up to 3 years. Screening is neither recommended nor cost-efficient.

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