[Recent trends in the pathophysiology and treatment of pituitary adenomas].
Recent molecular pathological investigations have elucidated the cytodifferentiation of pituitary cells and identified several transcriptional factors that regulate this cytodifferentiation of pituitary cells. The patterns of cytodifferentiation are closely related to the pathogenesis of pituitary adenomas. Meanwhile, the role of hypothalamic hormones in the development of pituitary adenomas has recently attracted the attention of investigators. The expression of growth hormone-releasing hormone and corticotrophin releasing hormone in corticotroph adenomas have been demonstrated in somatotroph adenomas and corticotropin adenomas, respectively. This finding indicates that the endogenous expression of hypothalamic hormones and their receptors in human pituitary adenoma cells has ample significance in the autocrine or paracrine regulation of pituitary hormone production and tumor extension induced by hypothalamic hormones produced by adenoma cells. The recent progress in surgical techniques for treatment of pituitary adenomas has provided several alternatives: transsphenoidal surgery vs. transcranial surgery, sublabial approach vs. endonasal approach, and microsurgery vs. endoscopic surgery. There have also been developments in the medical treatment of pituitary adenomas. The frequently used dopamine agonist, cabergoline, is very effective for treating prolactin-producing adenoma. Long-acting octreotide and pegvisomant are now available for the treatment of growth hormone producing adenoma. Cabergoline is also used for growth hormone producing adenoma. Temozolomide has recently been used for atypical adenomas or pituitary carcinomas. Adult growth hormone deficiency sometimes occurs in postoperative patients with pituitary adenomas. Growth hormone replacement is recommended to maintain the quality of life of these patients.
Matsuno
Akira
A
Department of Neurosurgery, Director of Stroke Center, Teikyo University Chiba Medical Center, 3426-3 Anesaki, Ichihara-City, Chiba 299-0111, Japan.
D000236:Adenoma / Q000209:etiology* / Q000235:genetics / Q000628:therapy*; D000970:Antineoplastic Agents / Q000627:therapeutic use; D000077465:Cabergoline; D003346:Corticotropin-Releasing Hormone; D003606:Dacarbazine / Q000031:analogs & derivatives / Q000627:therapeutic use; D004873:Ergolines / Q000627:therapeutic use; D013007:Growth Hormone-Releasing Hormone; D019382:Human Growth Hormone / Q000031:analogs & derivatives / Q000627:therapeutic use; D006801:Humans; D007028:Hypothalamic Hormones; D033162:Incidental Findings; D019635:Neurosurgical Procedures / Q000379:methods / Q000639:trends; D015282:Octreotide / Q000627:therapeutic use; D010911:Pituitary Neoplasms / Q000209:etiology* / Q000235:genetics / Q000628:therapy*; D015175:Prolactinoma; D018013:Receptors, Neuropeptide; D018017:Receptors, Pituitary Hormone-Regulating Hormone; D000077204:Temozolomide
D000970:Antineoplastic Agents; D004873:Ergolines; D007028:Hypothalamic Hormones; D018013:Receptors, Neuropeptide; D018017:Receptors, Pituitary Hormone-Regulating Hormone; D019382:Human Growth Hormone; D003606:Dacarbazine; D003346:Corticotropin-Releasing Hormone; D013007:Growth Hormone-Releasing Hormone; C048250:somatotropin releasing hormone receptor; D000077465:Cabergoline; C406545:pegvisomant; D015282:Octreotide; D000077204:Temozolomide