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Pituitary tumor

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General Information
Stage Information
Treatment Option Overview
Acth-producing Pituitary Tumor
Prolactin-producing Pituitary Tumor
Growth Hormone-producing Pituitary Tumor
Nonfunctioning Pituitary Tumor
Recurrent Pituitary Tumor

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GENERAL INFORMATION

Tumors of the pituitary gland are almost invariably benign and are usually curable. The manifestations of a pituitary tumor depend on the hormone secreted by the tumor as well as the pattern of growth of the tumor within the sella turcica. Tumors that are often hormonally active are the eosinophilic growth hormone-secreting adenomas (GH), basophilic adrenocorticotrophic hormone-secreting adenomas (ACTH), and the prolactin-secreting adenomas (PRL). These tumors may protrude outside of the sella. The hormonally-inactive adenoma, a common pituitary tumor, is often much larger and may exhibit invasive properties. The likelihood for blindness is greater in patients with this tumor because, in the absence of endocrine symptoms, visual loss is the usual initial manifestation. Craniopharyngioma, a type of pituitary tumor, is covered separately. (Refer to the PDQ summary on Adult Brain Tumor Treatment for more information.)

STAGE INFORMATION

The presence of a pituitary tumor is most readily determined by magnetic resonance imaging, although it may also be established by radiographic studies including skull films, tomograms, and computer tomography. Appropriate endocrine studies will help exclude nonpituitary causes of Cushing's syndrome. Pituitary tumors are commonly classified according to cell type. One staging system that is used for pituitary tumors is Leavens.[1]

ACTH-producing tumors (Cushing's Disease)

The major manifestation of the basophilic adenoma is secretion of adrenocorticotrophic hormone, resulting in Cushing's syndrome. These tumors are initially confined to the sella turcica, but may enlarge and become invasive after bilateral adrenalectomy (Nelson's syndrome).

Prolactin-producing tumors

The prolactin-secreting adenoma is typically an intrasellar tumor of the pituitary gland. In women, these adenomas are often small (less than 10 mm). In either sex, however, they can become large enough to enlarge the sella turcica.

Growth hormone-producing tumors

This eosinophilic tumor secretes growth hormone, resulting in gigantism in younger patients and acromegaly in others. Suprasellar extension is not uncommon.

Nonfunctioning tumors

These tumors arise from the adenohypophysis and cause symptoms by extension beyond the sella, resulting in pressure on surrounding structures rather than secretion of a hormonally-active substance.

References:

  1. Leavens ME, McCutcheon IF, Samaan NA: Management of pituitary adenomas. Oncology (Huntington NY) 6(6): 69-79, 1992.

TREATMENT OPTION OVERVIEW

Treatment depends on the type of pituitary tumor and whether it extends into the brain around the pituitary.[1] The hormone-secreting tumors may be treated with surgery or radiation therapy. Drug therapy with bromocriptine has been used with success in patients with prolactin-secreting tumors. Growth hormone- secreting tumors can also be treated by somatostatin analogues, such as Sandostatin, with success.[2] The development of transsphenoidal hypophysectomy represents a major development in the safe surgical treatment of both hormonally-active and nonfunctioning tumors. Transsphenoidal surgery is the usual treatment of choice for lesions confined within the sella turcica. Lesions extending beyond the confines of the pituitary are most frequently the nonfunctioning chromophobe adenomas and require additional radiation therapy. Rapid deterioration of vision is an immediate indication for surgery (to relieve pressure produced by the growing tumor mass). The natural history of GH-secreting and ACTH-secreting pituitary tumors is usually one of slowly progressive enlargement. Prolactin-secreting tumors, however, often stabilize and may improve with time, although some of these tumors may grow beyond the confines of the sella turcica.

The designations in PDQ that treatments are "standard" or "under clinical evaluation" are not to be used as a basis for reimbursement determinations.

References:

  1. Leavens ME, McCutcheon IF, Samaan NA: Management of pituitary adenomas. Oncology (Huntington NY) 6(6): 69-79, 1992.
  2. Gorden P, Comi RL, Maton PN, et al.: Somatostatin and somatostatin analogue (SMS 201-995) in treatment of hormone-secreting tumors of the pituitary and gastrointestinal tract and non-neoplastic diseases of the gut. Annals of Internal Medicine 110(1): 35-50, 1989.

ACTH-PRODUCING PITUITARY TUMOR

Treatment will depend on tumor size and the symptoms which result from excess hormone production.

Standard treatment options:[1-3]
1. Surgery (usually transsphenoidal).

2. Radiation therapy.

3. Surgery plus radiation therapy.

4. Mitotane plus radiation therapy.

Treatment options under clinical evaluation:

Radiation therapy.

References:

  1. Mampalam TJ, Tyrrell JB, Wilson CB: Transsphenoidal microsurgery for Cushing Disease: a report of 216 cases. Annals of Internal Medicine 109(6): 487-493, 1988.
  2. Moore TJ, Dluhy RG, Williams GH, et al.: Nelson's syndrome: frequency, prognosis and effect of prior pituitary irradiation. Annals of Internal Medicine 85(6): 731-734, 1976.
  3. Schteingart DE, Tsao HS, Taylor CI, et al.: Sustained remission of Cushing's disease with mitotane and pituitary irradiation. Annals of Internal Medicine 92(5): 613-619, 1980.

PROLACTIN-PRODUCING PITUITARY TUMOR

When the pituitary tumor secretes prolactin, treatment will depend on tumor size and the symptoms which result from excess hormone production. Bromocriptine has been used with considerable benefit in the treatment of prolactin-secreting tumors, along with surgery and radiation therapy.[1] The drug CV205-502 given once daily has been used successfully with minimal side effects in relapsing or refractory cases after bromocriptine failure.[2]

Standard treatment options:

1. Surgery:

2. Radiation therapy: standard photon radiation therapy.[3]

3. Bromocriptine.[4,5]

4. Combinations of the above.

Treatment options under clinical evaluation:

CV205-502.[2]

References:

  1. Koppelman MCS, Jaffe MJ, Rieth KG, et al.: Hyperprolactinemia, amenorrhea and galactorrhea: a retrospective assessment of twenty-five cases. Annals of Internal Medicine 100(1): 115-121, 1984.
  2. Rasmussen C, Bergh T, Wide L, et al.: Long-term treatment with a new non-ergot long-acting dopamine agonist, CV 205-502, in women with hyperprolactinaemia. Clinical Endocrinology (Oxford) 29(3): 271-279, 1988.
  3. Sheline GE, Grossman A, Jones AE, et al.: Secretory tumors of the pituitary gland: radiation therapy for prolactinomas. In: Black PM, Zervas NT, Ridgway EC, et al., eds.: Progress in Endocrine Research and Therapy. New York: Raven Press, Vol 1, 1984, pp 93-108.
  4. Kleinberg DL, Boyd AE, Wardlaw S, et al.: Pergolide for the treatment of pituitary tumors secreting prolactin or growth hormone. New England Journal of Medicine 309(12): 704-709, 1983.
  5. George SR, Burrow GN, Zinman B, et al.: Regression of pituitary tumors, a possible effect of bromergocryptine. American Journal of Medicine 66(4): 697-702, 1979.

GROWTH HORMONE-PRODUCING PITUITARY TUMOR

Treatment will depend on the size and extent of the tumor, and the need for rapid cessation of hormone function that results in serious clinical sequelae (i.e., hypertension and cardiomyopathy)

Standard treatment options:

1. Surgery:

2. Radiation therapy.[1-3]

3. Bromocriptine.[4]

4. Somatostatin analogue (Sandostatin).[5]

5. Surgery and postoperative radiation therapy.

References:

  1. Kjellberg RN, Shintani A, Frantz AG, et al.: Proton beam therapy in acromegaly. New England Journal of Medicine 278(13): 689-695, 1968.
  2. Lawrence JH, Tobias CA, Linfoot JA, et al.: Successful treatment of acromegaly: metabolic and clinical studies in 145 patients. Journal of Clinical Endocrinology and Metabolism 31(2): 180-190, 1970.
  3. Bloom B, Kramer S: Secretory tumors of the pituitary gland: conventional radiation therapy in the management of acromegaly. In: Black PM, Zervas NT, Ridgway EC, et al., eds.: Progress in Endocrine Research and Therapy. New York: Raven Press, Vol 1, 1984, pp 179-190.
  4. Kleinberg DL, Boyd AE, Wardlaw S, et al.: Pergolide for the treatment of pituitary tumors secreting prolactin or growth hormone. New England Journal of Medicine 309(12): 704-709, 1983.
  5. Gorden P, Comi RL, Maton PN, et al.: Somatostatin and somatostatin analogue (SMS 201-995) in treatment of hormone-secreting tumors of the pituitary and gastrointestinal tract and non-neoplastic diseases of the gut. Annals of Internal Medicine 110(1): 35-50, 1989.

NONFUNCTIONING PITUITARY TUMOR

The selection of treatment will depend on tumor size, the progressive course of the disease, and anatomical structures affected by the tumor extension. The majority of patients present with suprasellar extension and visual field deficits. In addition, many have hormone deficits prior to treatment.

Standard treatment options:

1. Surgery (preferably with a transsphenoidal approach) followed by close
observation with radiation therapy reserved for recurrence.[1,2]

2. Radiation therapy.[3,4]

3. Surgery and postoperative radiation therapy.[5]

References:

  1. Comtois R, Beauregard H, Somma M, et al.: The clinical and endocrine outcome to trans-sphenoidal microsurgery of nonsecreting pituitary adenomas. Cancer 68(4): 860-866, 1991.
  2. Kovalic JJ, Grigsby PW, Fineberg BB: Recurrent pituitary adenomas after surgical resection: the role of radiation therapy. Radiology 177(1): 273-275, 1990.
  3. Flickinger JC, Nelson PB, Martinez AJ, et al.: Radiotherapy of nonfunctional adenomas of the pituitary gland: results with long-term follow-up. Cancer 63(12): 2409-2414, 1989.
  4. McCollough WM, Marcus RB, Rhoton AL, et al.: Long-term follow-up of radiotherapy for pituitary adenoma: the absence of late recurrence after greater than or equal to 4500 cGy. International Journal of Radiation Oncology, Biology, Physics 21(3): 607-614, 1991.
  5. Tsang RW, Brierley JD, Panzarella T, et al.: Radiation therapy for pituitary adenoma: treatment outcome and prognostic factors. International Journal of Radiation Oncology, Biology, Physics 30(3): 557-565, 1994.

RECURRENT PITUITARY TUMOR

The question and selection of further treatment in the patient who relapses is dependent on many factors, including the specific type of pituitary tumor, prior treatment, visual and hormonal complications, and individual patient considerations. Clinical studies of new treatments should be considered. Patients who develop recurrence following surgical resection can be treated with radiation therapy with a high likelihood of local control.[1,2] Re- irradiation of recurrent pituitary adenomas in selected patients is reported to have achieved long-term local control with improvement or stabilization of visual symptoms.[3] The dopamine agonist CV205-502 given once daily, has been used successfully with minimal side effects in relapsing or refractory cases after bromocriptine failure.[4] Octreotide infusion can improve visual defects caused by nonfunctioning and gonadotropin-secreting adenomas in approximately half the patients treated. Patients who respond usually demonstrate improvement within 4 days.[5]

References:

  1. Kovalic JJ, Grigsby PW, Fineberg BB: Recurrent pituitary adenomas after surgical resection: the role of radiation therapy. Radiology 177(1): 273-275, 1990.
  2. Tsang RW, Brierley JD, Panzarella T, et al.: Radiation therapy for pituitary adenoma: treatment outcome and prognostic factors. International Journal of Radiation Oncology, Biology, Physics 30(3): 557-565, 1994.
  3. Schoenthaler R, Albright NW, Wara WM, et al.: Reirradiation of pituitary adenoma. International Journal of Radiation Oncology, Biology, Physics 24(2): 307-314, 1992.
  4. Rasmussen C, Bergh T, Wide L, et al.: Long-term treatment with a new non-ergot long-acting dopamine agonist, CV 205-502, in women with hyperprolactinaemia. Clinical Endocrinology (Oxford) 29(3): 271-279, 1988.
  5. Warnet A, Harris AG, Renard E, et al.: A prospective multicenter trial of octreotide in 24 patients with visual defects caused by nonfunctioning and gonadotropin-secreting pituitary adenomas. Neurosurgery 41(4): 786-797, 1997.
Date Last Modified: 01/2002

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