Pituitary Tumors Treatment & Management

  • Author: Jorge C Kattah, MD; Chief Editor: Robert A Egan, MD   more...
 
Updated: Aug 15, 2011
 

Medical Care

  • Prolactinomas: The majority of these lesions respond to dopamine receptor agonists. Improvement in visual field abnormalities, resolution of symptoms associated with hyperprolactinemia, and visible diminution of the actual mass can result with treatment.
  • Acromegaly: Somatostatin analogues (octreotide) can be helpful in the treatment of increased postoperative levels of GH. In some cases, the tumor may shrink modestly. Gallstones are a frequent complication of somatostatin-analogue therapy. Dopamine agonists also have been used.
  • Replacement therapy for decreased or absent hormones should be instituted as needed.
  • All hormone-based treatment should be directed by a consulting endocrinologist.
Next

Surgical Care

  • Transsphenoidal surgery
    • Transsphenoidal microscopic surgery is the most frequent surgical approach for the resection of pituitary tumors. With larger lesions, a transfrontal approach may become necessary to decompress the visual pathways.
    • Minimally invasive endoscopic surgery using a 4-mm endoscope through a nostril is a possibility in selective cases.
    • Open low-field intraoperative MRI monitoring for transsphenoidal surgical resection is gaining acceptance to monitor the precise extent of tumor resection.
    • Null cell tumors and gonadotrophinomas are best treated with transsphenoidal surgery.
    • The main complication after transsphenoidal surgery (from the endocrine standpoint) is hypopituitarism.
    • Low- and high-field intraoperative monitoring is used to minimize resectable tumor.[7]
  • Prolactinomas
    • Microprolactinomas: Transsphenoidal resection of the tumor offers a chance for a cure without the need for long-standing dopamine agonist therapy; however, many patients choose dopaminergic therapy.
    • Macroadenomas that secrete prolactin are best treated with dopamine agonists.
  • Acromegaly
    • Transsphenoidal surgery decreases GH levels to less than 5 mcg/L in 60% of cases.
    • Normal pulsatile secretion of GH is not always regained, and 20% of patients continue to have increased GH levels in response to TRH.
    • Radiotherapy is an alternative, although GH levels may not decrease for 2-4 years.
    • Elevated GH levels may be treated with somatostatin analogues and dopamine agonists, if tolerated.
  • Cushing disease
    • Transsphenoidal tumor resection is the first line of treatment in patients with basophilic adenomas of the pituitary gland. It is curative in 80% of cases.
    • Pituitary irradiation is required in the remaining cases to prevent the development of Nelson syndrome.
    • In children, pituitary irradiation and adrenalectomy are highly effective.
Previous
Next

Consultations

  • The treatment team should consist of any or all of the following specialists: ophthalmologist or neuro-ophthalmologist, neuroradiologist, endocrinologist, gynecologist, neurosurgeon, neuropathologist, and radiation medicine specialist.
  • Different specialists may be involved as indicated by the patient's specific symptoms.
Previous
Next

Diet

  • Dietary factors are important in patients with acromegaly or Cushing disease.
  • Patients with hypothyroidism, hypoadrenalism, or hypopituitarism have specific dietary needs.
Previous
Next

Activity

  • Activities of daily living (ADLs) generally are not restricted in these patients.
  • Exercise tolerance may be limited in some cases.
Previous
Proceed to Medication
 
 
Contributor Information and Disclosures
Author

Jorge C Kattah, MD  Head, Associate Program Director, Professor, Department of Neurology, University of Illinois College of Medicine at Peoria

Jorge C Kattah, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, and New York Academy of Sciences

Disclosure: Biogen Honoraria Consulting; Bayer Corporation Honoraria Consulting

Specialty Editor Board

Frederick M Vincent Sr, MD  Clinical Professor, Department of Neurology and Ophthalmology, Michigan State University Colleges of Human and Osteopathic Medicine

Frederick M Vincent Sr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners, American College of Legal Medicine, American College of Physicians, and Michigan State Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Robert A Egan, MD  Director of Neuro-Ophthalmology, St Helena Hospital

Robert A Egan, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, North American Neuro-Ophthalmology Society, and Oregon Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Robert A Egan, MD  Director of Neuro-Ophthalmology, St Helena Hospital

Robert A Egan, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, North American Neuro-Ophthalmology Society, and Oregon Medical Association

Disclosure: Nothing to disclose.

References
  1. Chahal HS, Stals K, Unterländer M, et al. AIP mutation in pituitary adenomas in the 18th century and today. N Engl J Med. Jan 6 2011;364(1):43-50. [Medline].

  2. Vlotides G, Eigler T, Melmed S. Pituitary tumor-transforming gene: physiology and implications for tumorigenesis. Endocr Rev. Apr 2007;28(2):165-86. [Medline].

  3. Riss D, Jin L, Qian X, et al. Differential expression of galectin-3 in pituitary tumors. Cancer Res. May 1 2003;63(9):2251-5. [Medline].

  4. Zhang X, Horwitz GA, Heaney AP, Nakashima M, Prezant TR, Bronstein MD, et al. Pituitary tumor transforming gene (PTTG) expression in pituitary adenomas. J Clin Endocrinol Metab. Feb 1999;84(2):761-7. [Medline].

  5. Ambrosi B, Dall'Asta C, Cannavo S, et al. Effects of chronic administration of PPAR-gamma ligand rosiglitazone in Cushing's disease. Eur J Endocrinol. Aug 2004;151(2):173-8. [Medline].

  6. Talkad AV, Kattah JC, Xu MY, et al. Prolactinoma presenting as painful postganglionic Horner syndrome. Neurology. Apr 27 2004;62(8):1440-1. [Medline].

  7. Kreutzer J, Fahlbusch R. Diagnosis and treatment of pituitary tumors. Curr Opin Neurol. Dec 2004;17(6):693-703. [Medline].

  8. Giustina A, Barkan A, Casanueva FF, et al. Criteria for cure of acromegaly: a consensus statement. J Clin Endocrinol Metab. Feb 2000;85(2):526-9. [Medline].

  9. Semple PL, Webb MK, de Villiers JC, Laws ER Jr. Pituitary apoplexy. Neurosurgery. 2005;56(1):65-72; discussion 72-3. [Medline].

  10. Biousse V, Newman NJ, Oyesiku NM. Precipitating factors in pituitary apoplexy. J Neurol Neurosurg Psychiatry. Oct 2001;71(4):542-5. [Medline].

  11. Rotenberg BW, Saunders S, Duggal N. Olfactory outcomes after endoscopic transsphenoidal pituitary surgery. Laryngoscope. Aug 2011;121(8):1611-3. [Medline].

  12. Gnanalingham KK, Bhattacharjee S, Pennington R, et al. The time course of visual field recovery following transphenoidal surgery for pituitary adenomas: predictive factors for a good outcome. J Neurol Neurosurg Psychiatry. Mar 2005;76(3):415-9. [Medline].

  13. Alameda C, Lucas T, Pineda E, et al. Experience in management of 51 non-functioning pituitary adenomas: indications for post-operative radiotherapy. J Endocrinol Invest. Jan 2005;28(1):18-22. [Medline].

  14. Colin P, Jovenin N, Delemer B, et al. Treatment of pituitary adenomas by fractionated stereotactic radiotherapy: a prospective study of 110 patients. Int J Radiat Oncol Biol Phys. Jun 1 2005;62(2):333-41. [Medline].

  15. Conomy JP, Ferguson JH, Brodkey JS, Mitsumoto H. Spontaneous infarction in pituitary tumors: neurologic and therapeutic aspects. Neurology. Jun 1975;25(6):580-7. [Medline].

  16. David, NJ, Gargano FP, Glaser JS. Pituitary apoplexy in clinical perspective. In: Neurophthalmology Symposium. Vol 8. St Louis: CV Mosby; 1975:140-165.

  17. Dawson BH, Kothandaram P. Acute massive infarction of pituitary adenomas. A study of five patients. J Neurosurg. Sep 1972;37(3):275-9. [Medline].

  18. Gharib H, Frey HM, Laws ER, et al. Coexistent primary empty sella syndrome and hyperprolactinemia. Report of 11 cases. Arch Intern Med. Jul 1983;143(7):1383-6. [Medline].

  19. Greenberg HS, Chandler WF, Ensminger WD. Radiosensitization with carotid intra-arterial bromodeoxyuridine +/- 5-fluorouracil biomodulation for malignant gliomas. Neurology. Sep 1994;44(9):1715-20. [Medline].

  20. Jho HD. Endoscopic endonasal pituitary surgery: Technical aspects. Contemporary Neurosurgery. 1997;19:1-8.

  21. Jho HD, Carrau RL, Ko Y, Daly MA. Endoscopic pituitary surgery: an early experience. Surg Neurol. Mar 1997;47(3):213-22; discussion 222-3. [Medline].

  22. Levy A, Lightman SL. Diagnosis and management of pituitary tumours. BMJ. Apr 23 1994;308(6936):1087-91. [Medline].

  23. Melmed S. Acromegaly. N Engl J Med. Apr 5 1990;322(14):966-77. [Medline].

  24. Molitch ME. Pregnancy and the hyperprolactinemic woman. N Engl J Med. May 23 1985;312(21):1364-70. [Medline].

  25. Oldfield EH, Doppman JL, Nieman LK, Chrousos GP, Miller DL, Katz DA, et al. Petrosal sinus sampling with and without corticotropin-releasing hormone for the differential diagnosis of Cushing's syndrome. N Engl J Med. Sep 26 1991;325(13):897-905. [Medline].

  26. Orth DN. Cushing's syndrome. N Engl J Med. Mar 23 1995;332(12):791-803. [Medline].

  27. [Best Evidence] Rotenberg BW, Saunders S, Duggal N. Olfactory outcomes after Endoscopic Transphenoidal Pituitary surgery. The Laryngoscope. 2011;121:1611-1613.

  28. Thorner MO, Vance ML, Laws ER. The anterior pituitary. In: Williams, ed. Textbook of Endocrinology. Philadelphia: WB Saunders; 1998:249-340.

  29. Zhang X, Horwitz GA, Heaney AP, Nakashima M, Prezant TR, Bronstein MD, et al. Pituitary tumor transforming gene (PTTG) expression in pituitary adenomas. J Clin Endocrinol Metab. Feb 1999;84(2):761-7. [Medline].

Previous
Next
 
This is a characteristic bitemporal hemianopic visual field defect.
This contrast-enhanced coronal MRI was obtained in a patient who complained of visual loss.
This visual field was plotted using a Goldman perimeter (ie, kinetic perimetry). It was obtained from a patient who reported visual loss and had a normal endocrine workup. The dark areas correspond to the impaired peripheral visual field. This visual field defect is consistent with an intrasellar lesion.
Coronal T1 precontrast MRI A (left panel), B postcontrast (middle panel) and T2 (right panel) showing a sellar mass causing obvious left and upward displacement of the optic chiasm. The mass is a histologically proven pituitary macroadenoma, which presented initially with a large cystic subfrontal extension that was successfully resected in April of 2006. This patient has been observed closely for 2.5 years and despite obvious mass effect, he has no visual complaints and the neuro-ophthalmologic evaluation is normal. Although infrequent, clinicians should be aware of this possibility. Close follow-up is required.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.