Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Pituitary Macroadenomas Workup

  • Author: James R Mulinda, MD, FACP; Chief Editor: George T Griffing, MD  more...
 
Updated: Jul 22, 2016
 

Laboratory Studies

Laboratory tests include basal hormone levels and dynamic hormone measurements depending on the tumor studied.

All tumors should have screening basal hormone measurements, which may include prolactin, thyrotropin, thyroxine, adrenocorticotropin, cortisol, LH, FSH, estradiol, testosterone, growth hormone, insulinlike growth factor-1 (IGF-1), and alpha subunit glycoprotein.

Dynamic hormone tests are performed to assess the functionality of a tumor and assist in differential diagnosis. They also can be used to assess anterior pituitary reserve.

Thyrotropin-releasing hormone (TRH) causes elevation of serum prolactin and thyrotropin. Prolactinomas, hyperprolactinemic states, hyperthyroidism, and panhypopituitarism exhibit a blunted response. Gonadotropinomas respond paradoxically to TRH (LH, FSH, LH-beta, and alpha subunit should be measured).

GHRH produces an elevation in growth hormone. This response is blunted in growth hormone deficiency, Cushing disease, and hypothyroidism. Other agents that may be used for this test include insulin, L-dopa, arginine, and clonidine. Acromegaly may produce a paradoxical reduction in growth hormone.

Hyperglycemia suppresses serum growth hormone. This suppression does not occur in pituitary tumors secreting growth hormone, ectopic growth hormone–releasing tumors, Cushing syndrome, and anorexia nervosa. A paradoxical rise in growth hormone may be observed in acromegaly, acute illness, and chronic renal failure. Many people with acromegaly also show paradoxical growth hormone response to TRH and occasionally to GnRH.

CRH causes a rise in corticotropin. This response is exaggerated in Cushing disease but blunted in other causes of Cushing syndrome. When combined with inferior petrosal sinus sampling, this test may assist in differentiating Cushing disease from benign ectopic adrenocorticotropic hormone (ACTH) syndrome.

Insulin-induced hypoglycemia causes a rise in corticotropin, cortisol, and growth hormone. A blunted response is observed in Cushing syndrome, growth hormone deficiency, hypothyroidism, and hyperthyroidism.

Metyrapone causes a rise in morning serum 11-deoxycortisol and urinary 17-hydrocorticosteroids (17-OH steroids). An exaggerated response occurs in Cushing disease, but no response is observed in other causes of Cushing syndrome.

Dexamethasone suppression testing is used in Cushing syndrome evaluation. An overnight 1-mg dexamethasone dose fails to suppress morning serum cortisol in Cushing syndrome but is only a screening test. Low-dose and high-dose dexamethasone suppression tests assist, respectively, in establishing the diagnosis of Cushing syndrome and differentiating between Cushing disease and ectopic production of corticotropin.

Cosyntropin testing and corticotropin infusion testing assist in assessing the hypothalamic-pituitary-adrenal axis for adrenocortical insufficiency.

GnRH causes an increase in LH and FSH levels. This response is blunted in pituitary hypogonadism but exaggerated in primary hypogonadism. Test results, however, are not very dependable.

Next

Imaging Studies

Pituitary imaging is important in confirming the diagnosis of pituitary macroadenoma and also for determining the differential diagnoses of other sellar lesions. Plain skull radiographs are poor at delineating soft tissues and so have been replaced by CT scanning and MRI.

CT scanning is better at depicting bony structures and calcifications within soft tissues than either plain radiography or MRI. Differential diagnoses of tumors with calcification, such as germinomas, craniopharyngiomas, and meningiomas, are better determined with CT scanning. CT scans are valuable when MRI is contraindicated, such as in patients with pacemakers or metallic implants in the brain or eyes. Drawbacks include less optimal soft tissue imaging compared to MRI, use of intravenous contrast media that is needed to enhance images, and exposure to radiation. This makes MRI the modality of choice for pituitary imaging.

MRI is more expensive than CT scans but is the preferred imaging study for the pituitary because it provides better visualization of soft tissues and vascular structures. No exposure to ionizing radiation occurs. Images are generated based upon the magnetic properties of the hydrogen atoms. With spin-echo, T1-weighted images, fat produces high–signal intensity images. Structures such as fatty marrow and orbital fat show up as bright images. T2-weighted images of structures with high water content, such as cerebrospinal fluid and cystic lesions, produce high-intensity signals, while structures with high fat content present with low-intensity signals. At least a 1.5-T magnet should be used for MRI of the pituitary.[2]

Previous
Next

Other Tests

Visual field testing should be performed, especially in tumors involving the optic chiasm. The severity of visual defects may dictate a more aggressive treatment course.

Previous
Next

Histologic Findings

The histology of pituitary macroadenomas shows varying levels of neoplastic activity. Frozen sections are usually not dependable for definitive diagnosis. Hormonal immunohistochemical stains for neuroendocrine markers are useful, especially in the nonfunctioning tumors.

Previous
 
 
Contributor Information and Disclosures
Author

James R Mulinda, MD, FACP Consulting Staff, Department of Endocrinology, Endocrinology Associates, Inc

James R Mulinda, MD, FACP is a member of the following medical societies: American College of Physicians

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.

Yoram Shenker, MD Chief of Endocrinology Section, Veterans Affairs Medical Center of Madison; Interim Chief, Associate Professor, Department of Internal Medicine, Section of Endocrinology, Diabetes and Metabolism, University of Wisconsin at Madison

Yoram Shenker, MD is a member of the following medical societies: American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Additional Contributors

Dimitris A Papanicolaou, MD 

Dimitris A Papanicolaou, MD is a member of the following medical societies: American College of Physicians, Endocrine Society, Royal Society of Medicine

Disclosure: Nothing to disclose.

References
  1. Chahal HS, Stals K, Unterlander 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. Alimohamadi M, Sanjari R, Mortazavi A, Shirani M, Moradi Tabriz H, Hadizadeh Kharazi H, et al. Predictive value of diffusion-weighted MRI for tumor consistency and resection rate of nonfunctional pituitary macroadenomas. Acta Neurochir (Wien). 2014 Dec. 156(12):2245-52. [Medline].

  3. Greenman Y, Stern N. How should a nonfunctioning pituitary macroadenoma be monitored after debulking surgery?. Clin Endocrinol (Oxf). 2009 Jun. 70(6):829-32. [Medline].

  4. Parhar PK, Duckworth T, Shah P, et al. Decreasing Temporal Lobe Dose with Five-Field Intensity-modulated Radiotherapy for Treatment of Pituitary Macroadenomas. Int J Radiat Oncol Biol Phys. 2009 Dec 14. [Medline].

  5. Loeffler JS, Shih HA. Radiation therapy in the management of pituitary adenomas. J Clin Endocrinol Metab. 2011 Jul. 96(7):1992-2003. [Medline].

  6. Marek J, Jezkova J, Hana V, et al. Is it possible to avoid hypopituitarism after irradiation of pituitary adenomas by the Leksell gamma knife?. Eur J Endocrinol. 2011 Feb. 164(2):169-78. [Medline].

  7. Wu JS, Shou XF, Yao CJ, et al. Transsphenoidal pituitary macroadenomas resection guided by PoleStar N20 low-field intraoperative magnetic resonance imaging: comparison with early postoperative high-field magnetic resonance imaging. Neurosurgery. 2009 Jul. 65(1):63-70; discussion 70-1. [Medline].

  8. Fomekong E, Maiter D, Grandin C, et al. Outcome of transsphenoidal surgery for Cushing's disease: a high remission rate in ACTH-secreting macroadenomas. Clin Neurol Neurosurg. 2009 Jun. 111(5):442-9. [Medline].

  9. Theodosopoulos PV, Leach J, Kerr RG, et al. Maximizing the extent of tumor resection during transsphenoidal surgery for pituitary macroadenomas: can endoscopy replace intraoperative magnetic resonance imaging?. J Neurosurg. 2009 Oct 16. [Medline].

  10. Pinar E, Yuceer N, Imre A, Guvenc G, Gundogan O. Endoscopic Endonasal Transsphenoidal Surgery for Pituitary Adenomas. J Craniofac Surg. 2014 Dec 2. [Medline].

  11. Paek SH, Downes MB, Bednarz G, Keane WM, Werner-Wasik M, Curran WJ Jr, et al. Integration of surgery with fractionated stereotactic radiotherapy for treatment of nonfunctioning pituitary macroadenomas. Int J Radiat Oncol Biol Phys. 2005 Mar 1. 61(3):795-808. [Medline].

  12. Han S, Ding X, Tie X, Liu Y, Xia J, Yan A, et al. Endoscopic endonasal trans-sphenoidal approach for pituitary adenomas: Is one nostril enough?. Acta Neurochir (Wien). 2013 Jun 5. [Medline].

  13. Mao ZG, Zhu YH, Tang HL, et al. Preoperative lanreotide treatment in acromegalic patients with macroadenomas increases short-term postoperative cure rates: a prospective, randomized trial. Eur J Endocrinol. 2010 Jan 8. [Medline].

  14. Przybylowski CJ, Dallapiazza RF, Williams BJ, et al. Primary versus revision transsphenoidal resection for nonfunctioning pituitary macroadenomas: matched cohort study. J Neurosurg. 2016 May 20. 1-8. [Medline].

  15. Magro E, Graillon T, Lassave J, et al. Complications Related to the Endoscopic Endonasal Transsphenoidal Approach for Nonfunctioning Pituitary Macroadenomas in 300 Consecutive Patients. World Neurosurg. 2016 May. 89:442-53. [Medline].

  16. Sankhla SK, Jayashankar N, Khan GM. Surgical management of selected pituitary macroadenomas using extended endoscopic endonasal transsphenoidal approach: early experience. Neurol India. 2013 Mar-Apr. 61(2):122-30. [Medline].

  17. Berkmann S, Fandino J, Zosso S, et al. Intraoperative magnetic resonance imaging and early prognosis for vision after transsphenoidal surgery for sellar lesions. J Neurosurg. 2011 Sep. 115(3):518-27. [Medline].

  18. Elhateer H, Muanza T, Roberge D, et al. Fractionated stereotactic radiotherapy in the treatment of pituitary macroadenomas. Curr Oncol. 2008 Dec. 15(6):286-92. [Medline]. [Full Text].

  19. Schalin-Jäntti C, Valanne L, Tenhunen M, et al. Outcome of Fractionated Stereotactic Radiotherapy in Patients with Pituitary Adenomas Resistant to Conventional Treatments: a 5.25- yr Follow-up Study. Clin Endocrinol (Oxf). 2009 Dec 18. [Medline].

  20. Mello PA, Naves LA, Pereira Neto A, Oliveira EH, Ferreira IC, Araújo Júnior AS, et al. Clinical and laboratorial characterization and post-surgical follow-up of 87 patients with non-functioning pituitary macroadenomas. Arq Neuropsiquiatr. 2013 May. 71(5):307-12. [Medline].

  21. Hwang YC, Chung JH, Min YK, et al. Comparisons between macroadenomas and microadenomas in Cushing's disease: characteristics of hormone secretion and clinical outcomes. J Korean Med Sci. 2009 Feb. 24(1):46-51. [Medline]. [Full Text].

  22. Fernandez-Balsells MM, Murad MH, Barwise A, et al. Natural history of nonfunctioning pituitary adenomas and incidentalomas: a systematic review and metaanalysis. J Clin Endocrinol Metab. 2011 Apr. 96(4):905-12. [Medline].

  23. Bardin CW. Anterior pituitary disease. Current Therapy in Endocrinology and Metabolism. 6th ed. St. Louis, Mo: Mosby Year Book; 1997. 33-8.

  24. Becker KL, Bilezikian JP, Bremner WJ. Adenohypophysis. Principles and Practice of Endocrinology and Metabolism. 2nd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 1995. 207-37.

  25. Mulinda JR, Hasinski S, Rose LI. Successful therapy for a mixed thyrotropin-and prolactin-secreting pituitary macroadenoma with cabergoline. Endocr Pract. 1999 Mar-Apr. 5(2):76-9. [Medline].

  26. Takahashi T, Miki Y, Takahashi JA, et al. Ectopic posterior pituitary high signal in preoperative and postoperative macroadenomas: dynamic MR imaging. Eur J Radiol. 2005 Jul. 55(1):84-91. [Medline].

  27. Wilson JD, Foster DW. Pituitary disorders. Williams Textbook of Endocrinology. 8th ed. Philadelphia, Pa: W.B. Saunders, Co; 1992. 260-95.

 
Previous
Next
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.