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Pituitary Tumors Workup

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

Laboratory Studies

See the list below:

  • Pituitary mass
    • Visual fields and ophthalmologic evaluation are critical in defining the presence of a chiasmal syndrome.
    • Neuroimaging would be appropriate (see Imaging Studies).
  • Prolactinomas
    • Serum prolactin levels should be measured in any patient with a suspected sellar or suprasellar mass. If elevated, investigate the possibility of pharmacologic and other factors prior to ordering extensive neuroimaging studies.
    • Generally, a single elevated prolactin level may confirm the diagnosis. Minor elevations may be somewhat difficult to interpret, since breast manipulation can elevate the serum level. The first level obtained serves as a baseline and guides the course of dopamine-agonist therapy.
    • Serum prolactin level >200 mcg/L in a patient with a macroadenoma greater than 10 mm in size is diagnostic of a prolactinoma. Levels below that range in a macroadenoma suggest hyperprolactinemia secondary to hypothalamic compression.
  • Growth hormone abnormalities
    • Growth hormone (GH) levels are elevated in acromegaly but can fluctuate significantly.
    • Intravenous (IV) GH levels every 5 minutes for 24 hours may show consistent elevation of GH. This is not a practical diagnostic method, but does indicate that a single GH value is not sufficient to make a diagnosis.
    • Serum insulinlike growth factor 1 (IGF-1) level is the best endocrinologic test for acromegaly. IGF-1 reflects GH concentration in the last 24 hours. Technical factors may limit its usefulness in some laboratories.
    • Oral glucose tolerance test is the definitive test for the diagnosis of acromegaly; a positive result is the failure of GH to decrease to < 1 mcg/L after ingesting 50-100 g of glucose.
      • Thyrotrophin-releasing hormone (TRH), 200 mcg, can be given to increase the test's accuracy. A GH level > 5 mcg/L suggests acromegaly.
      • Failure to decrease the GH concentration to < 2 mcg/L after a glucose load and after TRH stimulation is highly suggestive of acromegaly.
  • Cushing disease and Cushing syndrome
    • Twenty-four hour urine is collected for free cortisol. Usually 2 baseline values are obtained.
    • Dexamethasone suppression test: The physiological basis of this test is a decrease in adrenocorticotropic hormone (ACTH) secretion by the pituitary because of exogenous glucocorticoid administration. One mg of dexamethasone is administered. Serum cortisol level is measured the next morning; it should be < 138 nmol/L (ie, < 5 mcg/dL).
    • Standard low-dose dexamethasone: Two-day baseline serum and urine cortisol levels are determined. The patient is then given 4 doses of 0.5 mg of dexamethasone at 6-hour intervals. Normal suppression is a serum cortisol level of < 138 nmol/L or a urine level of less than 55 nmol/L.
    • If cortisol levels are increased abnormally, corticotrophin-releasing factor (CRF) in a dose of 100 mcg can be given to differentiate between Cushing disease and other causes of hypercortisolism (ie, Cushing syndrome). With pituitary adenomas, cortisol secretion is increased over the baseline.
    • High-dose dexamethasone suppression confirms diagnosis of a pituitary adenoma. It suppresses the pituitary gland even in the presence of an adenoma. If cortisol levels remain unchanged, the cause of increased cortisol is not a pituitary adenoma.
    • Metyrapone test: Metyrapone inhibits synthesis of cortisol. Patients with pituitary tumors remain responsive to low levels of cortisol, prompted by metyrapone administration, with increased secretion of cortisol precursors (ie, 11-deoxycortisol).
    • Serum levels of ACTH: The serum concentration of ACTH is higher than normal (>5.5 pmol/L at 9 am and >2.2 pmol/L at midnight).
    • At times, venous sampling of ACTH from the petrosal sinuses by means of cerebral venography may be valuable when making the diagnosis is difficult.
    • Baseline petrosal sinus levels of CRF distinguish patients with Cushing disease from those with ectopic ACTH secretion.
  • Glycoprotein hormones -Thyroid-stimulating hormone, follicle-stimulating hormone, luteinizing hormone
    • Pituitary adenomas that are associated with thyroid-stimulating hormone (TSH) hypersecretion are uncommon. These patients have increased T3 and T4 levels, hyperthyroidism, and goiter with inappropriately high levels of TSH.
    • Increased follicle-stimulating hormone (FSH) levels may be apparent in the histologic examination of a pituitary adenoma in patients without apparent preoperative endocrine abnormalities and in some patients with hypogonadism.
    • Increased luteinizing hormone (LH) levels also may be seen in patients with hypogonadism. The secreted hormone is not intact LH, and serum testosterone levels are not increased.
    • Free alpha and beta subunits of FSH are secreted by pituitary tumors that are thought to be inactive. A high percentage of these tumors have a paradoxical release of FSH subunits in response to TRH stimulation (200 mcg). Rarely, these tumors are associated with precocious puberty or resumption of bleeding in a postmenopausal woman.
    • The initial screening endocrine tests should include levels of prolactin, IGF-1, LH, FSH, TRH and alpha subunit, cortisol, and T4; men should have testosterone level checked.
  • Pituitary apoplexy: CSF may be xanthochromic, with crenated RBCs and high protein level.
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Imaging Studies

MRI of the brain and sellar region with multiplanar thin sections is of critical importance. This provides axial, coronal, and sagittal sections of the sellar contents. Generally, the relationship between the lesion and the optic chiasm and visual pathways is recognized easily. Pregadolinium and postgadolinium images are recommended to ensure that primarily isointense lesions do not escape detection. See the images below.

This contrast-enhanced coronal MRI was obtained inThis contrast-enhanced coronal MRI was obtained in a patient who complained of visual loss.
Coronal T1 precontrast MRI A (left panel), B postcCoronal 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 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.

In a study by Paterno and Fahlbusch of patients who underwent transsphenoidal pituitary adenoma surgery, intraoperative high-field magnetic resonance imaging (iMRI) was used for immediate intraoperative quality control to evaluate extent of tumor removal during the surgical procedure. Use of iMRI allowed resections to be extended in cases in which tumor remnants could be documented as suspicious after total resection. According to the authors, incomplete removal of resectable pituitary adenomas could be avoided in many cases by identifying the location of the tumor remnants. In cases in which it is not possible to achieve complete resection of an adenoma, further treatment can be planned earlier, without having to wait 2-3 months after surgery for conventional postoperative MRI scans to be performed.[10]

CT scan of the brain with sellar images may be sufficiently specific and can detect tumor calcifications. However, the detail is generally inferior to that of MRI.

Cerebral angiography is not performed routinely in the workup of sellar mass lesions. It generally is performed when vascular lesions are suspected.

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Other Tests

See the list below:

  • A final diagnosis generally is not made until the lesion is resected.
  • If a granulomatous or infectious process is the primary concern, other systemic and neurological testing may be required.
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Procedures

See the list below:

  • Visual field testing
  • Petrosal sinus venous sampling for ACTH- or TSH-producing adenomas in selective cases
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Histologic Findings

The role of pathologic examination of pituitary tumors is critical. Routinely perform standard histologic examination, electromicroscopy, and immunohistochemistry for these lesions. Findings then are correlated with clinical and imaging results. The histologic characteristics of these lesions are discussed in Pathophysiology. At times, the differentiation of hyperplasia from adenoma may be difficult. Other nonpituitary mass lesions may be identified easily by pathologic examination.

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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, New York Academy of Sciences

Disclosure: Nothing to disclose.

Coauthor(s)

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.

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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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