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Pituitary Tumors Medication

  • Author: Jorge C Kattah, MD; Chief Editor: Robert A Egan, MD  more...
Updated: Oct 26, 2015

Medication Summary

All hormone-related therapy should be initiated and directed by a consulting endocrinologist. The specific disorders are treated as follows:

Pituitary disorders associated with hormonal excess

Prolactinomas - Dopamine agonists (eg, bromocriptine, cabergoline)

Acromegaly - Octreotide (somatostatin analogue), dopamine agonists

Syndromes associated with hormonal deficiency and hypopituitarism

Hypothyroidism - Synthroid

Adrenocorticosteroid deficiency - Cortisol

Male hypogonadism - Testosterone

Female hypogonadism - Estrogen/progesterone

Growth hormone deficiency - GH replacement may be needed, more often in children than in adults

Many patients who have undergone surgery may experience posterior pituitary hypofunction with resultant diabetes insipidus and may require transnasal arginine vasopressin (DDAVP).


Somatostatin analogues

Class Summary

These agents are used to treat disorders associated with acromegaly. Recent work suggests the use of pegvisomant; however, no definite guideline indication has been determined.[12]

Octreotide (Sandostatin)


Hypothalamic polypeptide that inhibits production of GH. Acts primarily on somatostatin receptor subtypes II and V. Has multitude of other endocrine and nonendocrine effects, including inhibition of glucagon, VIP, and GI peptides.

More effective than dopamine agonists in acromegaly.


Dopamine agonists

Class Summary

Dopamine receptors in the hypothalamus exert an inhibitory action on some pituitary cells, particularly those producing prolactin and, to a lesser extent, GH.

Bromocriptine (Parlodel)


Ergot alkaloid derivative with dopaminergic properties. Inhibits prolactin secretion.

Cabergoline (Quinazoline, Dostinex)


Formerly CV205-502. Long-acting dopamine receptor agonist with high affinity for D2 receptors. Prolactin secretion by anterior pituitary predominates under hypothalamic inhibitory control exerted through dopamine.

Pergolide (Permax)


Pergolide was withdrawn from the US market March 29, 2007, because of heart valve damage resulting in cardiac valve regurgitation. It is important not to abruptly stop pergolide. Health care professionals should assess patients' need for dopamine agonist (DA) therapy and consider alternative treatment. If continued treatment with a DA is needed, another DA should be substituted for pergolide. For more information, see FDA MedWatch Product Safety Alert and Medscape Alerts: Pergolide Withdrawn From US Market.

Potent dopamine receptor agonist at both D1 and D2 receptor sites. Approximately 10-1000 times more potent than bromocriptine on mg per mg basis. Inhibits secretion of prolactin; causes transient rise in serum concentrations of GH and decrease in serum concentrations of LH.



Class Summary

These agents are used in the management of adrenocortical insufficiency.

Hydrocortisone (Cortef, Solu-Cortef, Hydrocort)


DOC because of mineralocorticoid activity and glucocorticoid effects.


Thyroid products

Class Summary

These agents are used as supplemental therapy in hypothyroidism.

Levothyroxine (Synthroid, Levoxyl, Levothroid)


DOC. Rapidly inhibits the release of thyroid hormones via a direct effect on the thyroid gland and inhibits the synthesis of thyroid hormones. Iodide also appears to attenuate cAMP-mediated effects of thyrotropin. In active form, influences growth and maturation of tissues. Involved in normal growth, metabolism, and development.


Estrogen derivatives

Class Summary

These agents are used in the treatment of hypoestrogenism.

Estrogens (Premarin)


Contains a mixture of estrogens obtained exclusively from natural sources, occurring as the sodium salts of water-soluble estrogen sulfates blended to represent the average composition of material derived from pregnant mares' urine. Mixture of sodium estrone sulfate and sodium equilin sulfate. Contains as concomitant components, sodium sulfate conjugates, 17-alpha-dihydroequilenin, 17-alpha-estradiol, and 17-beta-dihydroequilenin.

Restores estrogen levels to concentrations that induce negative feedback at gonadotrophic regulatory centers, which, in turn, reduces release of gonadotropins from pituitary. Increases synthesis of DNA, RNA, and many proteins in target tissues.

Important in developing and maintaining female reproductive system and secondary sex characteristics; promotes growth and development of vagina, uterus, fallopian tubes, and breasts. Affects release of pituitary gonadotropins; causes capillary dilatation, fluid retention, and protein anabolism; increases water content of cervical mucus; and inhibits ovulation. Predominantly produced by the ovaries.



Class Summary

These agents are used in the treatment of male hypogonadism.

Testosterone (Depo-Testosterone, Andro-LA, Delatest)


Promotes and maintains secondary sex characteristics in androgen-deficient males.


Growth Hormone

Class Summary

These agents are used in the replacement of endogenous growth hormone in patients with adult growth hormone deficiency.

Human growth hormone (Genotropin, Humatrope, Nutropin)


Stimulates growth of linear bone, skeletal muscle, and organs. Stimulates erythropoietin, which increases red blood cell mass.

Currently widely available in SC injection form. Adjust dose gradually based on clinical and biochemical responses assessed at monthly intervals, including body weight, waist circumference, serum IGF-1, IGFBP-3, serum glucose, lipids, thyroid function, and whole body dual-energy x-ray absorptiometry. In children, assess response based on height and growth velocity. Continue treatment until final height or epiphysial closure or both have been recorded.


Vasopressin analogs

Class Summary

These agents are used in the treatment of diabetes insipidus.

Desmopressin (DDAVP, Stimate)


Synthetic analogue of hypothalamic/posterior pituitary hormone 8-arginine vasopressin (antidiuretic hormone [ADH]). Has no effect on V1 receptors, which are responsible for vasopressin-induced vasoconstriction. Instead, acts on V2 receptors at renal tubuli, increasing cellular permeability of collecting ducts, which are responsible for antidiuretic effect. Effect is prevention of nocturnal diuresis and elevated BP in the mornings, resulting in reabsorption of water by kidneys. Formulated as a tab and a nasal spray. Tab is more convenient to administer.

Contributor Information and Disclosures

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, New York Academy of Sciences

Disclosure: Nothing to disclose.


Andrew J Tsung, MD Assistant Professor of Neurosurgery, University of Illinois College of Medicine at Peoria; Director, INI Brain Tumor Center, Director of Neurosurgery Research, Department of Neurosurgery, Illinois Neurological Institute; Physician Director, Intermediate Neuroscience Care Unit, OSF St Francis Medical Center; Attending Physician, Illinois Neurological Institute Physicians, LLC

Andrew J Tsung, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, Illinois State Medical Society, Society for Neuro-Oncology, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

Joseph V Hanovnikian University of Illinois College of Medicine

Joseph V Hanovnikian is a member of the following medical societies: Illinois State Medical Society, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Robert A Egan, MD Director of Neuro-Ophthalmology and Stroke Service, 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, Oregon Medical Association

Disclosure: Received honoraria from Biogen Idec for speaking and teaching; Received honoraria from Teva for speaking and teaching.

Chief Editor

Robert A Egan, MD Director of Neuro-Ophthalmology and Stroke Service, 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, Oregon Medical Association

Disclosure: Received honoraria from Biogen Idec for speaking and teaching; Received honoraria from Teva for speaking and teaching.

Additional Contributors

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 Institute, American College of Legal Medicine, American College of Physicians

Disclosure: Nothing to disclose.

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

  2. Villwock JA, Villwock M, Deshaies E, Goyal P. Significant increases of pituitary tumors and resections from 1993 to 2011. Int Forum Allergy Rhinol. 2014 Sep. 4(9):767-70. [Medline].

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

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

  5. 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. 1999 Feb. 84(2):761-7. [Medline].

  6. Kosmorsky GS, Dupps WJ Jr, Drake RL. Nonuniform pressure generation in the optic chiasm may explain bitemporal hemianopsia. Ophthalmology. 2008 Mar. 115(3):560-5. [Medline].

  7. Thomas ST. Finite Element Modleing of Chiasmal Compression. J of Undergraduate Engineering Res. 2009. 12:1-30.

  8. 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. 2004 Aug. 151(2):173-8. [Medline].

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

  10. Paterno' V, Fahlbusch R. High-Field iMRI in transsphenoidal pituitary adenoma surgery with special respect to typical localization of residual tumor. Acta Neurochir (Wien). 2014 Mar. 156(3):463-74; discussion 474. [Medline].

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

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

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

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

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

  16. 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. 2005 Mar. 76(3):415-9. [Medline].

  17. 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. 2005 Jan. 28(1):18-22. [Medline].

  18. Castinetti F, Régis J, Dufour H, Brue T. Role of stereotactic radiosurgery in the management of pituitary adenomas. Nat Rev Endocrinol. 2010 Apr. 6(4):214-23. [Medline].

  19. Ciric I, Zhao JC, Du H, Findling JW, Molitch ME, Weiss RE, et al. Transsphenoidal surgery for Cushing disease: experience with 136 patients. Neurosurgery. 2012 Jan. 70(1):70-80; discussion 80-1. [Medline].

  20. 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. 2005 Jun 1. 62(2):333-41. [Medline].

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

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

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

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

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

  26. Jagannathan J, Yen CP, Pouratian N, Laws ER, Sheehan JP. Stereotactic radiosurgery for pituitary adenomas: a comprehensive review of indications, techniques and long-term results using the Gamma Knife. J Neurooncol. 2009 May. 92(3):345-56. [Medline].

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

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

  29. Koutourousiou M, Gardner PA, Fernandez-Miranda JC, Paluzzi A, Wang EW, Snyderman CH. Endoscopic endonasal surgery for Giant Pituitary adenomas: Advantages and Limitations. J of Neursurg. January/2013. E Pubahead of print:

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

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

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

  33. 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. 1991 Sep 26. 325(13):897-905. [Medline].

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

  35. Rotenberg BW, Saunders S, Duggal N. Olfactory outcomes after Endoscopic Transphenoidal Pituitary surgery. The Laryngoscope. 2011. 121:1611-1613.

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

  37. 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. 1999 Feb. 84(2):761-7. [Medline].

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.
Axial, sagittal, and coronal MRI of the sellae in a patient with a severe headache, normal neuro-ophthalmologic examination, and no evidence of endocrine failure. A hyperintense mass is observed in the sella with suprasellar extension. This case illustrates the clinical spectrum of pituitary apoplexy. Transsphenoidal resection confirmed the diagnosis of pituitary apoplexy.
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