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Silent (clinically nonfunctioning) pituitary adenomas
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  • 作者:Sarah E. Mayson (1) (2)
    Peter J. Snyder (1)
  • 关键词:Pituitary adenomas ; Silent pituitary adenomas ; Clinically silent pituitary adenomas ; Totally silent pituitary adenomas ; Silent somatotroph adenomas ; Silent corticotroph adenomas
  • 刊名:Journal of Neuro-Oncology
  • 出版年:2014
  • 出版时间:May 2014
  • 年:2014
  • 卷:117
  • 期:3
  • 页码:429-436
  • 全文大小:
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  • 作者单位:Sarah E. Mayson (1) (2)
    Peter J. Snyder (1)

    1. Division of Endocrinology Diabetes and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA
    2. Division of Endocrinology, The Warren Alpert Medical School of Brown University, Providence, RI, 02903, USA
  • ISSN:1573-7373
文摘
Silent, or clinically nonfunctioning, pituitary adenomas can arise from any anterior pituitary cell type. Some are “clinically silent-in that they result in a supranormal serum concentration of the hormonal product of the cell type from which the adenoma arose but do not cause the clinical manifestations typical of excessive levels of that hormone. Others are “totally silent-in that they result in neither hormonal excess nor clinical manifestations. Gonadotroph and null cell adenomas are the most prevalent types and are typically silent. Somatotroph and corticotroph adenomas typically cause clinical syndromes but occasionally are clinically or totally silent. Those that are silent are usually larger and grow more aggressively than those that cause clinical syndromes. Silent adenomas are usually not discovered until they become very large and cause neurologic defects, such as visual impairment, but are also often discovered incidentally when neuroimaging is performed for another reason. Silent adenomas may become, rarely, clinically apparent over time. The diagnosis of a silent pituitary adenoma begins with the detection of a sellar mass by MRI. Biochemical testing can identify the adenoma cell type in those that are clinically silent. Silent adenomas that cause neurologic deficits require transsphenoidal surgery, but those that do not can be followed by MRI. Residual or recurrent disease is treated by radiation therapy, which is usually effective in preventing further growth but results in hormonal deficiencies in about half of patients. Dopamine agonists and somatostatin analogs are usually ineffective, but occasionally have been associated with reduced adenoma size.

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