Pituitary Adenoma

  • Dana-Farber/Brigham and Women's Cancer Care

    Pituitary adenomas are typically non-cancerous, slow-growing tumors that arise from cells in the pituitary gland (the master gland that regulates the body’s hormones). Learn about pituitary tumors and find information on how we support and care for people with pituitary adenoma before, during, and after treatment.

Treatment 

The Center for Neuro-Oncology offers state-of the-art treatments for patients with brain tumors, spinal cord tumors, and neurologic complications from cancer.

We specialize in services for patients with benign or malignant tumors, including:

  • Brain tumors: high-grade glioma, astrocytoma, oligodendroglioma, anaplastic glioma, glioblastoma, medulloblastoma, and meningioma
  • Pituitary, acoustic and skull base tumors: chordoma, meningioma, acoustic neuroma, hemangioblastoma, and pituitary adenoma

Our clinicians are experts in precise neurosurgical techniques, radiation therapy that targets tumors while sparing surrounding tissues, and a variety of chemotherapy and molecular drugs targeting your type of cancer.

Our approach to compassionate care centers on the needs of our patients and their families. Our specialists work as a team to ensure that you receive carefully coordinated treatment and support. We focus on helping you cope with your illness and maintain the quality of your life.

Our research program is a leader in clinical trials for brain tumors. Our goal is to bring laboratory discoveries directly to patients, allowing us to offer new treatment options. We offer our patients access to a range of clinical trials for various types and stages of brain and spinal cord cancers.

We believe that you and your family are key members of the care team. While we understand your illness, you understand your own body. We welcome your questions and value your participation as we make decisions together.

Learn more about treatment for brain tumors in the Center for Neuro-oncology 

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General Information About Pituitary Tumors

A pituitary tumor is a growth of abnormal cells in the tissues of the pituitary gland.

Pituitary tumors form in the pituitary gland, a pea-sized organ in the center of the brain, just above the back of the nose. The pituitary gland is sometimes called the "master endocrinegland" because it makes hormones that affect the way many parts of the body work. It also controls hormones made by many other glands in the body.

Drawing of the inside of the brain showing ventricles (fluid-filled spaces), choroid plexus, hypothalamus, pineal gland, pituitary gland, optic nerve, brain stem, cerebellum, cerebrum, medulla, pons, and spinal cord. 
Anatomy of the inside of the brain, showing the pineal and pituitary glands, optic nerve, ventricles (with cerebrospinal fluid shown in blue), and other parts of the brain.

 

Pituitary tumors are divided into three groups:

  • Benign pituitary adenomas: Tumors that are not cancer. These tumors grow very slowly and do not spread from the pituitary gland to other parts of the body.
  • Invasive pituitary adenomas: Benign tumors that may spread to bones of the skull or the sinuscavity below the pituitary gland.
  • Pituitary carcinomas: Tumors that are malignant (cancer). These pituitary tumors spread into other areas of the central nervous system (brain and spinal cord) or outside of the central nervous system. Very few pituitary tumors are malignant.

Pituitary tumors may be either non-functioning or functioning.

  • Non-functioning pituitary tumors do not make hormones.
  • Functioning pituitary tumors make more than the normal amount of one or more hormones. Most pituitary tumors are functioning tumors. The extra hormones made by pituitary tumors may cause certain signs or symptoms of disease.

The pituitary gland hormones control many other glands in the body.

Hormones made by the pituitary gland include:

  • Prolactin: A hormone that causes a woman’s breasts to make milk during and after pregnancy.
  • Adrenocorticotropic hormone (ACTH): A hormone that causes the adrenal glands to make a hormone called cortisol. Cortisol helps control the use of sugar, protein, and fats in the body and helps the body deal with stress.
  • Growth hormone: A hormone that helps control body growth and the use of sugar and fat in the body. Growth hormone is also called somatotropin.
  • Thyroid-stimulating hormone: A hormone that causes the thyroid gland to make other hormones that control growth, body temperature, and heart rate. Thyroid-stimulating hormone is also called thyrotropin.
  • Luteinizing hormone (LH) and follicle-stimulating hormone (FSH): Hormones that control the menstrual cycle in women and the making of sperm in men.

Having certain genetic conditions increases the risk of developing a pituitary tumor.

Anything that increases your risk of getting a disease is called a risk factor. Having a risk factor does not mean that you will get cancer; not having risk factors doesn’t mean that you will not get cancer. Talk with your doctor if you think you may be at risk. Risk factors for pituitary tumors include having the following hereditary diseases:

  • Multiple endocrine neoplasia type 1 (MEN1) syndrome.
  • Carney complex.
  • Isolated familial acromegaly.

Possible signs of a pituitary tumor include problems with vision and certain physical changes.

Symptoms can be caused by the growth of the tumor and/or by hormones the tumor makes. Some tumors may not cause symptoms. Conditions other than pituitary tumors can cause the symptoms listed below. Check with your doctor if you have any of these problems.

Signs and symptoms of a non-functioning pituitary tumor  

Sometimes, a pituitary tumor may press on or damage parts of the pituitary gland, causing it to stop making one or more hormones. Too little of a certain hormone will affect the work of the gland or organ that the hormone controls. The following symptoms may occur:

  • Headache.
  • Some loss of vision.
  • Loss of body hair.
  • In women, less frequent or no menstrual periods or no milk from the breasts.
  • In men, loss of facial hair, growth of breast tissue, and impotence.
  • In women and men, lower sex drive.
  • In children, slowed growth and sexual development.

Most of the tumors that make LH and FSH do not make enough extra hormone to cause symptoms. These tumors are considered to be non-functioning tumors.

Signs and symptoms of a functioning pituitary tumor  

When a functioning pituitary tumor makes extra hormones, the symptoms will depend on the type of hormone being made.

Too much prolactin may cause:  

  • Headache.
  • Some loss of vision.
  • Less frequent or no menstrual periods or menstrual periods with a very light flow.
  • Trouble becoming pregnant or an inability to become pregnant.
  • Impotence in men.
  • Lower sex drive.
  • Flow of breast milk in a woman who is not pregnant or breast-feeding.

Too much ACTH may cause:  

  • Headache.
  • Some loss of vision.
  • Weight gain in the face, neck, and trunk of the body, and thin arms and legs.
  • A lump of fat on the back of the neck.
  • Thin skin that may have purple or pink stretch marks on the chest or abdomen.
  • Easy bruising.
  • Growth of fine hair on the face, upper back, or arms.
  • Bones that break easily.
  • Anxiety, irritability, and depression.

Too much growth hormone may cause:  

  • Headache.
  • Some loss of vision.
  • In adults, acromegaly (growth of the bones in the face, hands, and feet). In children, the whole body may grow much taller and larger than normal.
  • Tingling or numbness in the hands and fingers.
  • Snoring or pauses in breathing during sleep.
  • Joint pain.
  • Sweating more than usual.
  • Dysmorphophobia (extreme dislike of or concern about one or more parts of the body).

Too much thyroid-stimulating hormone may cause:  

  • Irregular heartbeat.
  • Shakiness.
  • Weight loss.
  • Trouble sleeping.
  • Frequent bowel movements.
  • Sweating.

Other general signs and symptoms of pituitary tumors:  

  • Nausea and vomiting.
  • Confusion.
  • Dizziness.
  • Seizures.
  • Runny or "drippy" nose (cerebrospinal fluid that surrounds the brain and spinal cord leaks into the nose).

Imaging studies and tests that examine the blood and urine are used to detect (find) and diagnose a pituitary tumor.

The following tests and procedures may be used:

  • Physical exam and history: An exam of the body to check general signs of health, including checking for signs of disease, such as lumps or anything else that seems unusual. A history of the patient’s health habits and past illnesses and treatments will also be taken.
  • Eye exam: An exam to check vision and the general health of the eyes.
  • Visual field exam: An exam to check a person’s field of vision (the total area in which objects can be seen). This test measures both central vision (how much a person can see when looking straight ahead) and peripheral vision (how much a person can see in all other directions while staring straight ahead). The eyes are tested one at a time. The eye not being tested is covered.
  • Neurological exam: A series of questions and tests to check the brain, spinal cord, and nerve function. The exam checks a person’s mental status, coordination, and ability to walk normally, and how well the muscles, senses, and reflexes work. This may also be called a neuro exam or a neurologic exam.
  • MRI (magnetic resonance imaging) with gadolinium: A procedure that uses a magnet, radio waves, and a computer to make a series of detailed pictures of areas inside the brain and spinal cord. A substance called gadolinium is injected into a vein. The gadolinium collects around the cancer cells so they show up brighter in the picture. This procedure is also called nuclear magnetic resonance imaging (NMRI).
  • Blood chemistry study: A procedure in which a blood sample is checked to measure the amounts of certain substances, such as glucose (sugar), released into the blood by organs and tissues in the body. An unusual (higher or lower than normal) amount of a substance can be a sign of disease in the organ or tissue that makes it.
  • Blood tests: Tests to measure the levels of testosterone or estrogen in the blood. A higher or lower than normal amount of these hormones may be a sign of pituitary tumor.
  • Twenty-four-hour urine test: A test in which urine is collected for 24 hours to measure the amounts of certain substances. An unusual (higher or lower than normal) amount of a substance can be a sign of disease in the organ or tissue that makes it. A higher than normal amount of the hormone cortisol may be a sign of a pituitary tumor and Cushing syndrome.
  • High-dosedexamethasone suppression test: A test in which one or more high doses of dexamethasone are given. The level of cortisol is checked from a sample of blood or from urine that is collected for three days.
  • Low-dose dexamethasone suppression test: A test in which one or more small doses of dexamethasone are given. The level of cortisol is checked from a sample of blood or from urine that is collected for three days.
  • Venous sampling for pituitary tumors: A procedure in which a sample of blood is taken from veins coming from the pituitary gland. The sample is checked to measure the amount of ACTH released into the blood by the gland. Venous sampling may be done if blood tests show there is a tumor making ACTH, but the pituitary gland looks normal in the imaging tests.
  • Biopsy: The removal of cells or tissues so they can be viewed under a microscope by a pathologist to check for signs of cancer.

    The following tests may be done on the sample of tissue that is removed:

    • Immunohistochemistry study: A laboratory test in which a substance such as an antibody, dye, or radioisotope is added to a sample of cancer tissue to test for certain antigens. This type of study is used to tell the difference between different types of cancer.
    • Immunocytochemistry study: A laboratory test in which a substance such as an antibody, dye, or radioisotope is added to a sample of cancer cells to test for certain antigens. This type of study is used to tell the difference between different types of cancer.
    • Light and electron microscopy: A laboratory test in which cells in a sample of tissue are viewed under regular and high-powered microscopes to look for certain changes in the cells.
     

Certain factors affect prognosis (chance of recovery) and treatment options.

The prognosis (chance of recovery) depends on the type of tumor and whether the tumor has spread into other areas of the central nervous system (brain and spinal cord) or outside of the central nervous system to other parts of the body.

Treatment options depend on the following:

  • The type and size of the tumor.
  • Whether the tumor is making hormones.
  • Whether the tumor is causing problems with vision or other symptoms.
  • Whether the tumor has spread into the brain around the pituitary gland or to other parts of the body.
  • Whether the tumor has just been diagnosed or has recurred (come back).

Stages of Pituitary Tumors

Once a pituitary tumor has been diagnosed, tests are done to find out if it has spread within the central nervous system (brain and spinal cord) or to other parts of the body.

The extent or spread of cancer is usually described as stages. There is no standard staging system for pituitary tumors. Once a pituitary tumor is found, tests are done to find out if the tumor has spread into the brain or to other parts of the body. The following test may be used:

  • MRI (magnetic resonance imaging): A procedure that uses a magnet, radio waves, and a computer to make a series of detailed pictures of areas inside the body. This procedure is also called nuclear magnetic resonance imaging (NMRI).

Pituitary tumors are described in several ways.

Tumor size compared to everyday objects; shows various measurements of a tumor compared to a pea, peanut, walnut, and lime 
Pea, peanut, walnut, and lime show tumor sizes.

Pituitary tumors are described by their size and grade, whether or not they make extra hormones, and whether the tumor has spread to other parts of the body.

The following sizes are used:

  • Microadenoma: The tumor is smaller than 1 centimeter.
  • Macroadenoma: The tumor is 1 centimeter or larger.

Most pituitary adenomas are microadenomas.

The grade of a pituitary tumor is based on how far it has grown into the surrounding area of the brain, including the sella (the bone at the base of the skull, where the pituitary gland sits).

Recurrent Pituitary Tumors

A recurrentpituitary tumor is cancer that has recurred (come back) after it has been treated. The cancer may come back in the pituitary gland or in other parts of the body.

Treatment Option Overview

There are different types of treatment for patients with pituitary tumors.

Different types of treatments are available for patients with pituitary tumors. Some treatments are standard (the currently used treatment), and some are being tested in clinical trials. A treatment clinical trial is a research study meant to help improve current treatments or obtain information on new treatments for patients with cancer. When clinical trials show that a new treatment is better than the standard treatment, the new treatment may become the standard treatment. Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.

Four types of standard treatment are used:

Surgery

Many pituitary tumors can be removed by surgery using one of the following operations:

  • Transsphenoidal surgery: A type of surgery in which the instruments are inserted into part of the brain by going through an incision (cut) made under the upper lip or at the bottom of the nose between the nostrils and then through the sphenoid bone (a butterfly-shaped bone at the base of the skull) to reach the pituitary gland. The pituitary gland lies just above the sphenoid bone.
    Transsphenoidal surgery; drawing shows an endoscope and a curette inserted through the nose and sphenoid sinus to remove cancer from the pituitary gland. The sphenoid bone is also shown. 
    Transsphenoidal surgery. An endoscope and a curette are inserted through the nose and sphenoid sinus to remove cancer from the pituitary gland.
  • Endoscopic transsphenoidal surgery: A type of surgery in which an endoscope is inserted through an incision (cut) made at the back of the inside of the nose and then through the sphenoid bone to reach the pituitary gland. An endoscope is a thin, tube-like instrument with a light, a lens for viewing, and a tool for removing tumortissue.
  • Craniotomy: Surgery to remove the tumor through an opening made in the skull.
    Drawing of a craniotomy showing a section of the scalp that has been pulled back to remove a piece of the skull; the dura covering the brain has been opened to expose the brain. The layer of muscle under the scalp is also shown. 
    Craniotomy: An opening is made in the skull and a piece of the skull is removed to show part of the brain.

Even if the doctor removes all the cancer that can be seen at the time of the surgery, some patients may be given chemotherapy or radiation therapy after surgery to kill any cancer cells that are left. Treatment given after the surgery, to lower the risk that the cancer will come back, is called adjuvant therapy.

Radiation therapy

Radiation therapy is a cancer treatment that uses high-energy x-rays or other types of radiation to kill cancer cells or keep them from growing. There are two types of radiation therapy. External radiation therapy uses a machine outside the body to send radiation toward the cancer. Internal radiation therapy uses a radioactive substance sealed in needles, seeds, wires, or catheters that are placed directly into or near the cancer.

Stereotactic radiation surgery uses a rigid head frame attached to the skull to aim a single large dose of radiation directly to a tumor, causing less damage to nearby healthy tissue. It is also called stereotaxic radiosurgery, radiosurgery, and radiation surgery. This procedure does not involve surgery.

The way the radiation therapy is given depends on the type of the cancer being treated.

Drug therapy

Drugs may be given to stop a functioning pituitary tumor from making too many hormones.

Chemotherapy

Chemotherapy may be used as palliative treatment for pituitary carcinomas, to relieve symptoms and improve the patient's quality of life. Chemotherapy uses drugs to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. When chemotherapy is taken by mouth or injected into a vein or muscle, the drugs enter the bloodstream and can reach cancer cells throughout the body (systemic chemotherapy). When chemotherapy is placed directly into the cerebrospinal fluid, an organ, or a body cavity such as the abdomen, the drugs mainly affect cancer cells in those areas (regional chemotherapy). The way the chemotherapy is given depends on the type of the cancer being treated.

New types of treatment are being tested in clinical trials.

Information about clinical trials is available from the NCI Web site.

Patients may want to think about taking part in a clinical trial.

For some patients, taking part in a clinical trial may be the best treatment choice. Clinical trials are part of the cancer research process. Clinical trials are done to find out if new cancer treatments are safe and effective or better than the standard treatment.

Many of today's standard treatments for cancer are based on earlier clinical trials. Patients who take part in a clinical trial may receive the standard treatment or be among the first to receive a new treatment.

Patients who take part in clinical trials also help improve the way cancer will be treated in the future. Even when clinical trials do not lead to effective new treatments, they often answer important questions and help move research forward.

Patients can enter clinical trials before, during, or after starting their cancer treatment.

Some clinical trials only include patients who have not yet received treatment. Other trials test treatments for patients whose cancer has not gotten better. There are also clinical trials that test new ways to stop cancer from recurring (coming back) or reduce the side effects of cancer treatment.

Clinical trials are taking place in many parts of the country. See the Treatment Options section that follows for links to current treatment clinical trials. These have been retrieved from NCI's listing of clinical trials.

Follow-up tests may be needed.

Some of the tests that were done to diagnose the cancer or to find out the stage of the cancer may be repeated. Some tests will be repeated in order to see how well the treatment is working. Decisions about whether to continue, change, or stop treatment may be based on the results of these tests. This is sometimes called re-staging.

Some of the tests will continue to be done from time to time after treatment has ended. The results of these tests can show if your condition has changed or if the cancer has recurred (come back). These tests are sometimes called follow-up tests or check-ups.

Treatment Options for Pituitary Tumors

A link to a list of current clinical trials is included for each treatment section. For some types or stages of cancer, there may not be any trials listed. Check with your doctor for clinical trials that are not listed here but may be right for you.

Non-functioning Pituitary Tumors

Treatment may include the following:

  • Surgery (transsphenoidal surgery, if possible) to remove the tumor, followed by watchful waiting (closely monitoring a patient’s condition without giving any treatment until symptoms appear or change). Radiation therapy is given if the tumor comes back.
  • Radiation therapy alone.

Treatment for luteinizing hormone-producing and follicle-stimulating hormone-producing tumors is usually transsphenoidal surgery to remove the tumor.

Prolactin-Producing Pituitary Tumors

Treatment may include the following:

  • Drug therapy to stop the tumor from making prolactin and to stop the tumor from growing.
  • Surgery to remove the tumor (transsphenoidal surgery or craniotomy) when the tumor does not respond to drug therapy or when the patient cannot take the drug.
  • Radiation therapy.
  • Surgery followed by radiation therapy.

ACTH-Producing Pituitary Tumors

Treatment may include the following:

  • Surgery (usually transsphenoidal surgery) to remove the tumor, with or without radiation therapy.
  • Radiation therapy alone.
  • Drug therapy to stop the tumor from making ACTH.
  • A clinical trial of stereotactic radiation surgery.

Growth Hormone–Producing Pituitary Tumors

Treatment may include the following:

  • Surgery (usually transsphenoidal or endoscopic transsphenoidal surgery) to remove the tumor, with or without radiation therapy.
  • Drug therapy to stop the tumor from making growth hormone.

Thyroid-Stimulating Hormone–Producing Tumors

Treatment may include the following:

  • Surgery (usually transsphenoidal surgery) to remove the tumor, with or without radiation therapy.
  • Drug therapy to stop the tumor from making hormones.

Pituitary Carcinomas

Treatment of pituitarycarcinomas is palliative, to relieve symptoms and improve the quality of life. Treatment may include the following:

  • Surgery (transsphenoidal surgery or craniotomy) to remove the cancer, with or without radiation therapy.
  • Drug therapy to stop the tumor from making hormones.
  • Chemotherapy.

Recurrent Pituitary Tumors

Treatment may include the following:

  • Radiation therapy.
  • A clinical trial of stereotactic radiation surgery.

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with pituitary tumor. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. General information about clinical trials is available from the NCI Web site.

To Learn More About Pituitary Tumors

For more information from the National Cancer Institute about pituitary tumors, see the Pituitary Tumors Home Page.

For general cancer information and other resources from the National Cancer Institute, see the following:

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A clinical trial is a study to answer a scientific question, such as whether one treatment is better than another. Trials are based on past studies and what has been learned in the laboratory. Each trial answers certain scientific questions in order to find new and better ways to help cancer patients. During treatment clinical trials, information is collected about the effects of a new treatment and how well it works. If a clinical trial shows that a new treatment is better than one currently being used, the new treatment may become "standard." Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.

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This information is provided by the National Cancer Institute.

This information was last updated on January 18, 2013.


General Information About Pituitary Tumors

Pituitary tumors represent from 10% to 25% of all intracranial neoplasms. Depending on the study cited, pituitary tumors can be classified into three groups according to their biological behavior:[1][2]

  • Benign adenoma.
  • Invasive adenoma.
  • Carcinoma.

Adenomas comprise the largest portion of pituitary neoplasms with an overall estimated prevalence of approximately 17%. Only a minority of adenomas are symptomatic.[3] In addition, pituitary adenomas may be distinguished anatomically as intrapituitary, intrasellar, diffuse, and invasive.[4] Invasive adenomas, which account for approximately 35% of all pituitary neoplasms, may invade the dura mater, cranial bone, or sphenoid sinus.[5] Carcinomas account for 0.1% to 0.2% of all pituitary tumors.[6][7]

Clinical Presentation

The most characteristic-presenting features of pituitary adenomas include inappropriate pituitary hormone secretion and visual field deficits.[8]

Rare signs and symptoms of pituitary disease include:[8]

  • Cranial nerve palsies.
  • Temporal lobe epilepsy.
  • Hydrocephalus.
  • Cerebrospinal fluid rhinorrhea.

The signs and symptoms commonly associated with pituitary tumors derived from each specific cell type (i.e., prolactinomas, corticotroph adenomas, somatotroph adenomas, thyrotroph adenomas, and nonfunctioning adenomas) are as follows:

Prolactin-producing pituitary tumors

Signs and symptoms of prolactin (PRL)-producing pituitary tumors, also known as prolactinomas and lactotroph adenomas, may include:[8]

  • Headache. (Refer to the PDQ summary on Pain for more information.)
  • Visual field deficits.
  • Oligomenorrhea or amenorrhea.
  • Reduced fertility. (Refer to the Fertility Issues section in the PDQ summary on Sexuality and Reproductive Issues for more information.)
  • Loss of libido. (Refer to the Treatment-related Factors Secondary to Radiation section in the Factors Affecting Sexual Function in People With Cancer section and the Selective Serotonin Reuptake Inhibitors section in the Pharmacological Effects of Supportive Care Medications on Sexual Function section of the PDQ summary on Sexuality and Reproductive Issues for more information.)
  • Erectile dysfunction.
  • Galactorrhea in the estrogen-primed female breast.

Adrenocorticotrophic hormone-producing pituitary tumors

Signs and symptoms of adrenocorticotrophic hormone (ACTH)-producing pituitary tumors, also known as corticotroph adenomas, may include:[8]

  • Headache. (Refer to the PDQ summary on Pain for more information.)
  • Visual field deficits.
  • Proximal myopathy.
  • Centripetal fat distribution.
  • Neuropsychiatric symptoms. (Refer to the PDQ summary on Adjustment to Cancer: Anxiety and Distress and the Symptoms and Risk Factors section in the Assessment and Diagnosis section of the PDQ summary on Depression for more information.)
  • Striae.
  • Ability to easily bruise.
  • Skin thinning.
  • Hirsutism.
  • Osteopenia.

Growth hormone-producing pituitary tumors

Signs and symptoms of growth hormone (GH)-producing pituitary tumors, also known as somatotroph adenomas, may include:[8]

  • Headache. (Refer to the PDQ summary on Pain for more information.)
  • Visual field deficits.
  • Growth of hands and feet.
  • Coarsening of facial features.
  • Carpal tunnel syndrome.
  • Snoring and obstructive sleep apnea. (Refer to the Assessment section and the Special Considerations section in the PDQ summary on Sleep Disorders for more information.)
  • Jaw growth and prognathism.
  • Osteoarthritis and arthralgia. (Refer to the PDQ summary on Pain for more information.)
  • Excessive sweating. (Refer to the PDQ summary on Fever, Sweats, and Hot Flashes for more information.)
  • Dysmorphophobia.

Thyrotropin-producing pituitary tumors

Signs and symptoms of thyrotropin (thyroid-stimulating hormone [TSH])-producing tumors, also known as thyrotroph adenomas, may include:[9]

Nonfunctioning adenomas

Signs and symptoms of nonfunctioning adenomas (most commonly gonadotroph adenomas) may include:[10]

  • Headache. (Refer to the PDQ summary on Pain for more information.)
  • Visual field deficits.
  • Pituitary insufficiency, which is due to compression of the pituitary stalk or destruction of normal pituitary tissue by the tumor, and predominantly manifests as secondary hypogonadism.
  • Rarely, ovarian overstimulation, testicular enlargement, or increased testosterone levels.

In addition to cell-type specific presentations, pituitary apoplexy (i.e., pituitary adenoma apoplexy) represents another important clinical presentation of pituitary adenomas. Pituitary apoplexy can result from an acute hemorrhagic or ischemic infarction of the pituitary in patients harboring often unrecognized secreting or nonfunctioning pituitary adenomas. In a series analyzing 40 cases of pituitary apoplexy, the presenting signs and symptoms included headache (63%), vomiting (50%), visual field defects (61%), ocular paresis (40%), mental deterioration (13%), hyponatremia (13%), and syncope (5%); in only four cases pituitary tumor was diagnosed prior to presentation.[11]

The development of pituitary adenomas may also occur as a component of three familial cancer syndromes:[8]

  • Multiple endocrine neoplasia 1 (MEN 1).
  • Carney complex (e.g., cardiac myxomas, spotty skin pigmentation, and tumors of the adrenal gland and anterior pituitary).
  • Isolated familial acromegaly.

A number of other lesions should be considered in the differential diagnosis of sellar masses. Although rare, lymphocytic (i.e., autoimmune) hypophysitis should be considered in the differential diagnosis of any nonsecreting pituitary mass, especially when occurring during pregnancy or postpartum.[12] In addition, the clinician should consider craniopharyngioma and Rathke cleft cyst in the differential diagnosis of pituitary tumors. Sellar masses may also result from tumors that are metastatic to the pituitary. This typically occurs as a part of a generalized metastatic spread and is usually associated with five or more additional metastatic sites, especially osseous; breast and lung cancer are the most common primary neoplasms metastasizing to the pituitary.[13]

References:

  1. Asa SL, Ezzat S: The cytogenesis and pathogenesis of pituitary adenomas. Endocr Rev 19 (6): 798-827, 1998.

  2. Landman RE, Horwith M, Peterson RE, et al.: Long-term survival with ACTH-secreting carcinoma of the pituitary: a case report and review of the literature. J Clin Endocrinol Metab 87 (7): 3084-9, 2002.

  3. Ezzat S, Asa SL, Couldwell WT, et al.: The prevalence of pituitary adenomas: a systematic review. Cancer 101 (3): 613-9, 2004.

  4. Kovacs K, Horvath E, Vidal S: Classification of pituitary adenomas. J Neurooncol 54 (2): 121-7, 2001.

  5. Scheithauer BW, Kovacs KT, Laws ER Jr, et al.: Pathology of invasive pituitary tumors with special reference to functional classification. J Neurosurg 65 (6): 733-44, 1986.

  6. Pernicone PJ, Scheithauer BW, Sebo TJ, et al.: Pituitary carcinoma: a clinicopathologic study of 15 cases. Cancer 79 (4): 804-12, 1997.

  7. Ragel BT, Couldwell WT: Pituitary carcinoma: a review of the literature. Neurosurg Focus 16 (4): E7, 2004.

  8. Levy A: Pituitary disease: presentation, diagnosis, and management. J Neurol Neurosurg Psychiatry 75 (Suppl 3): iii47-52, 2004.

  9. Vance ML: Treatment of patients with a pituitary adenoma: one clinician's experience. Neurosurg Focus 16 (4): E1, 2004.

  10. Losa M, Mortini P, Barzaghi R, et al.: Endocrine inactive and gonadotroph adenomas: diagnosis and management. J Neurooncol 54 (2): 167-77, 2001.

  11. Lubina A, Olchovsky D, Berezin M, et al.: Management of pituitary apoplexy: clinical experience with 40 patients. Acta Neurochir (Wien) 147 (2): 151-7; discussion 157, 2005.

  12. Caturegli P, Newschaffer C, Olivi A, et al.: Autoimmune hypophysitis. Endocr Rev 26 (5): 599-614, 2005.

  13. Komninos J, Vlassopoulou V, Protopapa D, et al.: Tumors metastatic to the pituitary gland: case report and literature review. J Clin Endocrinol Metab 89 (2): 574-80, 2004.

Cellular Classification of Pituitary Tumors

Pituitary adenomas can be classified according to staining affinities of the cell cytoplasm, size, endocrine activity, histologic characteristics, hormone production and contents, ultrastructural features, granularity of the cell cytoplasm, cellular composition, cytogenesis, and growth pattern.[1] Recent classifications, however, omit criteria based on tinctorial stains (i.e., acidophilic, basophilic, and chromophobic) because of the poor correlation between staining affinities of the cell cytoplasm and other pathological features of pituitary tumors, such as the type of hormone produced and cellular derivation.[1][2]

A unifying pituitary adenoma classification incorporates the histological, immunocytochemical, and electron microscopic studies of the tumor cells, and stresses the importance of hormone production, cellular composition, and cytogenesis. This classification emphasizes the structure-function relationship and attempts to correlate morphologic features with secretory activity.[1]

Pituitary adenomas may be classified based on:[2]

  1. An anatomical approach, which classifies pituitary tumors by size based on radiological findings. Tumors are divided into microadenomas (i.e., the greatest diameter is <10 mm) and macroadenomas (i.e., the greatest diameter is ≥I0 mm).[3] Most pituitary adenomas are microadenomas. Historically, the most widely used radioanatomical classification was based primarily on a neuroradiological examination including skull x-rays, pneumoencephalography, polytomography, and carotid angiography [4] and subsequently validated by the application of more accurate computed tomography (CT) and magnetic resonance imaging (MRI).

    An MRI scan is now considered the imaging modality of choice for the diagnosis of pituitary disorders because of its multiplanar capability and good soft tissue contrast enhancement.[3] Sagittal T1-weighted images, clearly displaying the anterior and posterior lobes and the stalk on the same plane, and coronal images, displaying the relation between the pituitary and cavernous sinuses, are optimal for identifying a pituitary adenoma. A 3-mm thin slice typically is used to obtain optimal resolution.[5] A computed tomography (CT) scan may also be a useful diagnostic tool with coronal scans providing the optimal view;[6] however, CT scans appear to be less sensitive than MRI scans in this application.[7] For each imaging technique, a focal hypointensity within the pituitary gland is considered abnormal and suggestive of an adenoma. An MRI scan is also the best diagnostic imaging choice for pituitary carcinomas; metastases may be found in the cerebral lobes, cerebellum, spinal cord, leptomeninges, and subarachnoid space.[8]

    This radioanatomical classification places adenomas into 1 of 4 grades (I–IV).[9] (Refer to the Stage Information For Pituitary Tumors section of this summary for more information.) The grades are as follows:

    • Stage I are microadenomas (<1 cm) without sella expansion.
    • Stage II are macroadenomas (≥1 cm) and may extend above the sella.
    • Stage III are macroadenomas with enlargement and invasion of the floor or suprasellar extension.
    • Stage IV is destruction of the sella.
  2. Histological criteria, which use:
    • Immunohistological characterization of the tumors in terms of hormone production. Immunocytochemical staining for pituitary hormones generally correlates with hormone serum levels. Twenty percent of pituitary adenomas have no readily identifiable hormone production.
    • Ultrastructural criteria, which can confirm that nonfunctional lesions are of pituitary origin and characterize the cytological differentiation of tumor cells in terms of anterior pituitary cell types.
  3. Functional criteria, which are used to define tumors in terms of their endocrine activity. Clinical endocrinologists often use the functional classification of pituitary adenomas and define these tumors based on their hormonal activity in vivo. A retrospective review of the pituitary adenoma literature indicates that prolactinomas are by far the most common form of pituitary adenoma as determined by immunohistochemical criteria; tumors secreting adrenocorticotropic hormone (ACTH), growth hormone (GH), luteinizing hormone (LH), and thyroid-stimulating hormone (TSH) follow in decreasing frequency.[3][10] Functionally inactive pituitary adenomas, however, comprise approximately 30% to 35% of the pituitary tumors in most series and are the most common type of macroadenoma.[11]

    Using functional criteria, pituitary adenomas can be characterized as:[9]

    • Prolactin (PRL)-producing, also known as lactotroph, adenomas causing hyperprolactinemia and its clinical sequelae.
    • ACTH-producing, also known as corticotroph, adenomas associated with Cushing or Nelson syndromes.
    • GH-producing, also known as somatotroph, adenomas associated with acromegaly and/or gigantism.
    • Rare thyrotropin TSH-producing, also known as thyrotroph, tumors.
    • The large group of clinically nonfunctioning (i.e., the endocrine-inactive) adenomas. This group is comprised predominantly of gonadotroph adenomas. Gonadotroph adenomas synthesize follicle-stimulating hormone-(FSH) and/or LH, or the alpha or beta subunits of these heterodimers. They are usually detected incidentally or because of the presence of neurologic symptoms. Gonadotroph adenomas are inefficient secretors of the hormones they produce, so they rarely result in a clinically recognizable hormonal hypersecretion syndrome.
    • Because of the relative abundance of adenomas that secrete both GH and PRL, the category of mixed adenomas has also become a designation.

    Hormone-secreting pituitary carcinomas may elicit similar signs and symptoms according to the particular hormone that is secreted; they may also produce signs and symptoms related to malignant spread.[8] Because no unequivocal histopathologic features of carcinoma exist, the diagnosis of malignancy is reserved for pituitary neoplasms that have metastasized to remote areas of the central nervous system (CNS) or outside of the CNS.[12][13][14] In a review of 95 cases of pituitary carcinoma, 68% of the cases were found to be hormone-producing and PRL (26%) and ACTH (25%) were the most common hormonal subtypes.[15] Pituitary carcinomas producing GH were the second most common of the hormonal subtypes, and FSH/LH-producing and TSH-producing carcinomas were even more rarely reported. Other reports indicate that as many as 88% of pituitary carcinomas are endocrinologically active, and ACTH-secreting tumors are the most common.[8] Although only 2% to 10% of pituitary adenomas are ACTH-secreting, the percentage of pituitary carcinomas that secrete ACTH is estimated to be much higher at 25% to 34%.[15][16][17][18][19] In a series of 15 cases, carcinomas showed a greater tendency toward systemic metastasis than craniospinal metastasis; the rate of systemic metastasis was 71% for PRL-producing cell tumors and 57% for ACTH-producing tumors.[16]

Prolactin (PRL)-Producing Pituitary Tumors

PRL-producing pituitary tumors, also known as prolactinomas and lactotroph adenomas, secrete PRL and are typically an intrasellar tumor. In women, these adenomas are often small (<10 mm). In either sex, however, they can become large enough to enlarge the sella turcica. These adenomas represent the most common hormone-producing pituitary tumors and account for 25% to 41% of tumor specimens.[3]

Adrenocorticotrophic Hormone (ACTH)-Producing Pituitary Tumors

The major manifestation of ACTH-producing pituitary tumors, also know as corticotroph adenomas, is secretion of adrenocorticotropic hormone (ACTH), which results in Cushing syndrome. These tumors are initially confined to the sella turcica, but they may enlarge and become invasive after bilateral adrenalectomy (i.e., Nelson syndrome). These adenomas represent the second or third most common hormone-producing pituitary tumors, depending on the series; in one series, these tumors accounted for 10% of all tumor specimens.[1][3]

Growth Hormone (GH)-Producing Pituitary Tumors

GH-producing pituitary tumors, also known as somatotroph adenomas, produce GH, resulting in gigantism in younger patients and acromegaly in others. Suprasellar extension is not uncommon. These adenomas represent the second or third most common hormone-producing pituitary tumors, depending on the series; in one series these adenomas accounted for 13% of tumor specimens.[1][3]

Thyrotropin-Producing Pituitary Tumors

Thyrotroph-producing pituitary tumors, also known as thyrotroph adenomas, secrete thyroid-stimulating hormone (TSH), also known as thyrotropin, which results in hyperthyroidism without TSH suppression. Many are large and invasive, may be plurihormonal, and secrete both GH and/or PRL.[20] These tumors are rare and account for no more than 2% of tumor specimens.[1][3][20]

Gonadotroph (FSH-Producing and/or LH-Producing) Adenomas

Gonadotroph adenomas may secrete FSH and/or LH, or the alpha or beta subunits that comprise these heterodimers, which, depending on gender, may result in ovarian overstimulation, increased testosterone levels, testicular enlargement, and pituitary insufficiency caused by compression of the pituitary stalk or destruction of normal pituitary tissue by tumor. Many gonadotroph tumors, however, are unassociated with clinical or biochemical evidence of hormone excess and may be considered to be nonfunctioning or endocrine-inactive tumors.[21] Functional, clinically detectable gonadotroph adenomas are rare.[9]

Plurihormonal Adenomas

Plurihormonal tumors produce more than one hormone. Morphologically, they can be either monomorphous or plurimorphous. Monomorphous plurihormonal adenomas consist of one cell population that produces two or more hormones. The adenoma cells often differ from nontumorous adenohypophysial cells, and their cellular derivation may remain obscure despite extensive morphological studies. Plurimorphous plurihormonal adenomas consist of two or more distinct cell types, and each produces one hormone.[1] Thyrotroph adenomas are often plurihormonal.[20]

Nonfunctioning (Endocrine-Inactive) Adenomas

These tumors arise from the adenohypophysis and cause symptoms when they extend beyond the sella, which results in pressure on the surrounding structures rather than secretion of a hormonally active substance. Endocrine-inactive adenomas show positive immunostaining for one or more pituitary hormones;[1] however, they are not associated with clinical and biochemical evidence of hormone excess. Gonadotrophic hormones, as detected by antisera to beta-FSH and beta-LH, are present in many clinically nonfunctioning adenomas. Some of these adenomas are recognized by electron microscopy to have gonadotrophic differentiation, but some have characteristics of less well-differentiated cells and resemble the null cells that were initially thought to be undifferentiated precursors of adenohypophysial cells.[9] Endocrine-inactive pituitary adenomas comprise approximately 30% to 35% of the pituitary tumors in most series and are the most common type of macroadenoma.[11]

Oncocytic Tumors

Oncocytic tumors of the pituitary, also known as pituitary oncocytomas, are characterized by an abundance of mitochondria, which may fill up to 50% of the cytoplasmic area, which is normally around 8%, and obscure other organelles. These tumors are usually unassociated with clinical and biochemical evidence of hormone excess; in some cases, they may be accompanied by various degrees of hypopituitarism and/or mild hyperprolactinemia. Oncocytic change may occur in several other pituitary tumor types.[1]

Carcinomas

Pituitary carcinomas are usually endocrinologically functional, and ACTH-producing and PRL-producing tumors are the most frequent.[2][8] The histological and cytological characteristics of pituitary carcinomas vary from bland and monotonous to frankly malignant.[22] Carcinomas show a variable degree of nuclear atypia and cellular pleomorphism, but they also show significantly higher mitotic rates and cell proliferation indices than adenomas.[2] Carcinomas account for 0.1% to 0.2% of all pituitary tumors.[8][16]

Metastatic Tumors

Breast and lung cancer are the most common primary neoplasms metastasizing to the pituitary. Although tumors that are metastatic to the pituitary have been reported to be as high as 28% in autopsy series, the majority of metastatic tumors are clinically silent.[23]

Other Tumors

Other tumors that arise in the pituitary include craniopharyngiomas, meningiomas, and germ cell tumors; the rare granular cell tumors, pituicytomas, and gangliogliomas; and the even rarer gangliocytomas, lymphomas, astrocytomas, and ependymomas.[2]

References:

  1. Kovacs K, Horvath E, Vidal S: Classification of pituitary adenomas. J Neurooncol 54 (2): 121-7, 2001.

  2. Ironside JW: Best Practice No 172: pituitary gland pathology. J Clin Pathol 56 (8): 561-8, 2003.

  3. Ezzat S, Asa SL, Couldwell WT, et al.: The prevalence of pituitary adenomas: a systematic review. Cancer 101 (3): 613-9, 2004.

  4. Hardy J: Transsphenoidal surgery of hypersecreting pituitary tumors. In: Kohler PO, Ross GT, eds.: Diagnosis and treatment of pituitary tumors: proceedings of a conference sponsored jointly by the National Institute of Child Health and Human Development and the National Cancer Institute, January 15-17, 1973, Bethesda, Md. Amsterdam, The Netherlands: Excerpta medica, 1973, pp 179-98.

  5. Elster AD: Modern imaging of the pituitary. Radiology 187 (1): 1-14, 1993.

  6. Chambers EF, Turski PA, LaMasters D, et al.: Regions of low density in the contrast-enhanced pituitary gland: normal and pathologic processes. Radiology 144 (1): 109-13, 1982.

  7. Hall WA, Luciano MG, Doppman JL, et al.: Pituitary magnetic resonance imaging in normal human volunteers: occult adenomas in the general population. Ann Intern Med 120 (10): 817-20, 1994.

  8. Ragel BT, Couldwell WT: Pituitary carcinoma: a review of the literature. Neurosurg Focus 16 (4): E7, 2004.

  9. Asa SL, Ezzat S: The cytogenesis and pathogenesis of pituitary adenomas. Endocr Rev 19 (6): 798-827, 1998.

  10. McComb DJ, Ryan N, Horvath E, et al.: Subclinical adenomas of the human pituitary. New light on old problems. Arch Pathol Lab Med 107 (9): 488-91, 1983.

  11. Yeh PJ, Chen JW: Pituitary tumors: surgical and medical management. Surg Oncol 6 (2): 67-92, 1997.

  12. Scheithauer BW, Kovacs KT, Laws ER Jr, et al.: Pathology of invasive pituitary tumors with special reference to functional classification. J Neurosurg 65 (6): 733-44, 1986.

  13. Della Casa S, Corsello SM, Satta MA, et al.: Intracranial and spinal dissemination of an ACTH secreting pituitary neoplasia. Case report and review of the literature. Ann Endocrinol (Paris) 58 (6): 503-9, 1997.

  14. Kemink SA, Wesseling P, Pieters GF, et al.: Progression of a Nelson's adenoma to pituitary carcinoma; a case report and review of the literature. J Endocrinol Invest 22 (1): 70-5, 1999.

  15. Kaltsas GA, Grossman AB: Malignant pituitary tumours. Pituitary 1 (1): 69-81, 1998.

  16. Pernicone PJ, Scheithauer BW, Sebo TJ, et al.: Pituitary carcinoma: a clinicopathologic study of 15 cases. Cancer 79 (4): 804-12, 1997.

  17. Kovacs K, Horvath E: Pathology of pituitary tumors. Endocrinol Metab Clin North Am 16 (3): 529-51, 1987.

  18. Thapar K, Scheithauer BW, Kovacs K, et al.: p53 expression in pituitary adenomas and carcinomas: correlation with invasiveness and tumor growth fractions. Neurosurgery 38 (4): 765-70; discussion 770-1, 1996.

  19. Garrão AF, Sobrinho LG, Pedro-Oliveira, et al.: ACTH-producing carcinoma of the pituitary with haematogenic metastases. Eur J Endocrinol 137 (2): 176-80, 1997.

  20. Teramoto A, Sanno N, Tahara S, et al.: Pathological study of thyrotropin-secreting pituitary adenoma: plurihormonality and medical treatment. Acta Neuropathol (Berl) 108 (2): 147-53, 2004.

  21. Snyder PJ: Extensive personal experience: gonadotroph adenomas. J Clin Endocrinol Metab 80 (4): 1059-61, 1995.

  22. Pernicone PJ, Scheithauer BW: Invasive pituitary adenoma and pituitary carcinoma. In: Thapar K, Kovacs K, Scheithauer BW, et al., eds.: Diagnosis and Management of Pituitary Tumors. Totowa, NJ: Humana Press, 2001, pp 369-86.

  23. Komninos J, Vlassopoulou V, Protopapa D, et al.: Tumors metastatic to the pituitary gland: case report and literature review. J Clin Endocrinol Metab 89 (2): 574-80, 2004.

Stage Information for Pituitary Tumors

As with other tumors of the central nervous system (CNS), no tumor, nodes, metastases-based American Joint Committee on Cancer classification and staging system for pituitary tumors exists.[1] Pituitary tumors are classified according to size and divided into microadenomas (i.e., the greatest diameter is <10 mm) and macroadenomas (i.e., the greatest diameter is ≥I0 mm).[2] Most pituitary adenomas are microadenomas.

The most widely used radioanatomical classification was based primarily on a neuroradiological examination including skull x-rays, pneumoencephalography, polytomography, and carotid angiography.[3] Subsequently validated by the application of more accurate magnetic resonance imaging (MRI) and computed tomography, this radioanatomical classification places adenomas into 1 of 4 grades (I–IV) and has been augmented by additional studies including immunohistochemistry and electron microscopy.[4]

Currently, MRI is considered the imaging modality of choice for the diagnosis of pituitary disorders because of its multiplanar capability and good soft tissue contrast enhancement.[2] Because no unequivocal histopathologic features of pituitary carcinoma exist, the diagnosis of malignancy is reserved for pituitary neoplasms that have metastasized to remote areas of the CNS or to outside of the CNS.[5][6][7]

The radiographical classification for pituitary adenomas is as follows:[3][8]

  • 0: Normal pituitary appearance.
  • I: Enclosed within the sella turcica, microadenoma, smaller than 10 mm.
  • II: Enclosed within the sella turcica, macroadenoma, 10 mm or larger.
  • III: Invasive, locally, into the sella.
  • IV: Invasive, diffusely, into the sella.

The grading schema for suprasellar extensions is as follows:[3][8]

  • A: 0 to 10 mm suprasellar extension occupying the suprasellar cistern.
  • B: 10 mm to 20 mm extension and elevation of the third ventricle.
  • C: 20 mm to 30 mm extension occupying the anterior of the third ventricle.
  • D: A larger than 30 mm extension, beyond the foramen of Monro, or Grade C with lateral extensions.

References:

  1. Brain and spinal cord. In: Edge SB, Byrd DR, Compton CC, et al., eds.: AJCC Cancer Staging Manual. 7th ed. New York, NY: Springer, 2010, pp 593-7.

  2. Ezzat S, Asa SL, Couldwell WT, et al.: The prevalence of pituitary adenomas: a systematic review. Cancer 101 (3): 613-9, 2004.

  3. Hardy J: Transsphenoidal surgery of hypersecreting pituitary tumors. In: Kohler PO, Ross GT, eds.: Diagnosis and treatment of pituitary tumors: proceedings of a conference sponsored jointly by the National Institute of Child Health and Human Development and the National Cancer Institute, January 15-17, 1973, Bethesda, Md. Amsterdam, The Netherlands: Excerpta medica, 1973, pp 179-98.

  4. Asa SL, Ezzat S: The cytogenesis and pathogenesis of pituitary adenomas. Endocr Rev 19 (6): 798-827, 1998.

  5. Scheithauer BW, Kovacs KT, Laws ER Jr, et al.: Pathology of invasive pituitary tumors with special reference to functional classification. J Neurosurg 65 (6): 733-44, 1986.

  6. Della Casa S, Corsello SM, Satta MA, et al.: Intracranial and spinal dissemination of an ACTH secreting pituitary neoplasia. Case report and review of the literature. Ann Endocrinol (Paris) 58 (6): 503-9, 1997.

  7. Kemink SA, Wesseling P, Pieters GF, et al.: Progression of a Nelson's adenoma to pituitary carcinoma; a case report and review of the literature. J Endocrinol Invest 22 (1): 70-5, 1999.

  8. Yeh PJ, Chen JW: Pituitary tumors: surgical and medical management. Surg Oncol 6 (2): 67-92, 1997.

Treatment Option Overview

The goals of treatment of pituitary adenomas include normalization of hormonal secretion (i.e., normalization of hypersecretion and improvement in hypofunction) and resolution or cessation of the progression of neurological defects.

Standard treatments for patients with pituitary tumors include:

  • Surgery.
  • Radiation therapy.
  • Medical therapy.
  • A combination of surgery, radiation therapy, and medical therapy.

The treatment of choice must be individualized and is dictated by the type of tumor, the nature of the excessive hormonal expression, and whether or not the tumor extends into the brain around the pituitary.[1][2]

The transsphenoidal microsurgical approach to a pituitary lesion is the most widely employed surgical approach to pituitary lesions and represents a major development in the safe surgical treatment of both hormonally active and nonfunctioning tumors.[3][4][5] This approach is often successful in debulking tumors, even those that have a significant suprasellar extension.

A contraindication to this approach includes tumors with a significant suprasellar extension with an hourglass-shaped narrowing between the intrasellar and suprasellar component because blind attempts to reach the suprasellar tumor may lead to cerebral damage. In addition, an infection in the sphenoid sinus is potentially a contraindication to the transsphenoidal approach. In such cases, craniotomies via a pterional or subfrontal approach may be performed. Rapid deterioration of vision is an immediate indication for surgery to relieve pressure produced by an expanding tumor mass, except in the case of macroprolactinomas (where intensive observation with a patient on dopaminergic agonists may be an acceptable alternative). Progressive deterioration of visual fields is often the primary neurological criterion on which surgical management decisions are based.[6]

Conventional radiation therapy is an effective adjunct to the treatment of pituitary tumors.[3] The advantages of radiation therapy are that it is noninvasive and suitable for surgically high-risk patients. The clinical and biochemical response, however, is slow and may require from 2 years to 10 years for complete and sustained remission. In addition, radiation therapy carries a substantial risk of hypopituitarism (i.e., approximately 30% at 10 years).

Hormone-secreting tumors may be treated with surgery or radiation therapy. Surgical therapy is the treatment of choice for growth hormone-(GH) producing, adrenocorticotropic hormone-(ACTH) producing, and endocrine-inactive adenomas. GH-secreting tumors can be treated with somatostatin analogues, dopamine analogues, and the newer GH-receptor antagonists, such as pegvisomant.[6] Ketoconazole, an inhibitor of steroidogenesis, is considered the first drug of choice as adjunctive medical therapy for ACTH-producing tumors.[3] Somatostatin analogues are the drugs of choice for treatment of thyroid-stimulating, hormone-producing adenomas; however, the efficacy of treatment may wane with time.[6]

The natural history of growth hormone-secreting and ACTH-secreting pituitary tumors is usually one of slowly progressive enlargement.[3] Microprolactinomas, however, often remain unchanged, or decrease in size over time, and have been observed to undergo complete, spontaneous resolution on occasion.[6]

Treatments under clinical evaluation for patients with pituitary tumors include:

  • Stereotactic radiation surgery.[7]

References:

  1. Asa SL, Ezzat S: The cytogenesis and pathogenesis of pituitary adenomas. Endocr Rev 19 (6): 798-827, 1998.

  2. Landman RE, Horwith M, Peterson RE, et al.: Long-term survival with ACTH-secreting carcinoma of the pituitary: a case report and review of the literature. J Clin Endocrinol Metab 87 (7): 3084-9, 2002.

  3. Yeh PJ, Chen JW: Pituitary tumors: surgical and medical management. Surg Oncol 6 (2): 67-92, 1997.

  4. Hardy J: Transsphenoidal microsurgery of the normal and pathological pituitary. Clin Neurosurg 16: 185-217, 1969.

  5. Hardy J: Transsphenoidal hypophysectomy. J Neurosurg 34 (4): 582-94, 1971.

  6. Levy A: Pituitary disease: presentation, diagnosis, and management. J Neurol Neurosurg Psychiatry 75 (Suppl 3): iii47-52, 2004.

  7. Laws ER, Sheehan JP, Sheehan JM, et al.: Stereotactic radiosurgery for pituitary adenomas: a review of the literature. J Neurooncol 69 (1-3): 257-72, 2004 Aug-Sep.

Prolactin-Producing Pituitary Tumors Treatment

Standard Treatment Options for Prolactin (PRL)-Producing Pituitary Tumors

Standard treatment options for PRL-producing pituitary tumors include the following:

  1. Dopamine agonists, such as cabergoline and bromocriptine.[1][2][3][4][5]
  2. Surgery (second-line).[1][2]
  3. Radiation therapy (occasionally).[1][2]

When the pituitary tumor secretes PRL, treatment will depend on tumor size and the symptoms that result from excessive hormone production. Patients with PRL-secreting tumors are treated with surgery and radiation therapy.[1]

Most microprolactinomas and macroprolactinomas respond well to medical therapy with ergot-derived dopamine agonists, including bromocriptine and cabergoline.[2] For many patients, cabergoline has a more satisfactory side effect profile than bromocriptine. Cabergoline therapy may be successful in treating patients whose prolactinomas are resistant to bromocriptine or who cannot tolerate bromocriptine, and this treatment has a success rate of more than 90% in patients with newly diagnosed prolactinomas.[3][4][5] In a prospective study, cabergoline was safely withdrawn in patients with normalized prolactin levels and no evidence of tumor, which may effect a cure rate of approximately 70%.[6] On the basis of its safety record in pregnancy, however, bromocriptine is the treatment of choice when restoration of fertility is the patient’s goal.[7]

Microprolactinomas change little in size with treatment, but macroprolactinomas can be expected to shrink, sometimes quite dramatically. Microprolactinomas may decrease in size over time and have been observed to undergo complete, spontaneous resolution on occasion.[8] Surgery is typically reserved for those patients who cannot tolerate dopamine agonists, who suffer pituitary apoplexy during treatment, or whose macroprolactinomas are not responsive to medical therapy.[2] Occasionally, these tumors may ultimately require radiation therapy.[9]

Current Clinical Trials

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with pituitary tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.

References:

  1. Yeh PJ, Chen JW: Pituitary tumors: surgical and medical management. Surg Oncol 6 (2): 67-92, 1997.

  2. Levy A: Pituitary disease: presentation, diagnosis, and management. J Neurol Neurosurg Psychiatry 75 (Suppl 3): iii47-52, 2004.

  3. Colao A, Di Sarno A, Landi ML, et al.: Macroprolactinoma shrinkage during cabergoline treatment is greater in naive patients than in patients pretreated with other dopamine agonists: a prospective study in 110 patients. J Clin Endocrinol Metab 85 (6): 2247-52, 2000.

  4. Cannavò S, Curtò L, Squadrito S, et al.: Cabergoline: a first-choice treatment in patients with previously untreated prolactin-secreting pituitary adenoma. J Endocrinol Invest 22 (5): 354-9, 1999.

  5. Colao A, Di Sarno A, Landi ML, et al.: Long-term and low-dose treatment with cabergoline induces macroprolactinoma shrinkage. J Clin Endocrinol Metab 82 (11): 3574-9, 1997.

  6. Colao A, Di Sarno A, Cappabianca P, et al.: Withdrawal of long-term cabergoline therapy for tumoral and nontumoral hyperprolactinemia. N Engl J Med 349 (21): 2023-33, 2003.

  7. Schlechte JA: Clinical practice. Prolactinoma. N Engl J Med 349 (21): 2035-41, 2003.

  8. Ezzat S, Asa SL, Couldwell WT, et al.: The prevalence of pituitary adenomas: a systematic review. Cancer 101 (3): 613-9, 2004.

  9. Nomikos P, Buchfelder M, Fahlbusch R: Current management of prolactinomas. J Neurooncol 54 (2): 139-50, 2001.

Adrenocorticotropic Hormone-Producing Pituitary Tumors Treatment

Standard Treatment Options for Adrenocorticotropic Hormone (ACTH)-Producing Pituitary Tumors

Standard treatment options for ACTH-producing pituitary tumors include the following:

  1. Surgery (usually a transsphenoidal approach).[1][2][3]
  2. Surgery plus radiation therapy.[1][2][4]
  3. Radiation therapy.[1][2][4]
  4. Steroidogenesis inhibitors, including mitotane, metyrapone, ketoconazole, and aminoglutethimide.[1][2][5]

For patients with corticotroph adenomas, transsphenoidal microsurgery is the treatment of choice.[1][2] Remission rates reported in most series are approximately 70% to 90%.[1] In a series of 216 patients, who were operated on using a transsphenoidal approach, 75% experienced long-term remission, 21% experienced persistence of Cushing disease, and 9% had recurrence after the initial correction of the hypercortisolism.[3] The average time interval for reoperation was 3.8 years. Seventy-nine percent of the tumors were microadenomas, and 18% were macroadenomas; 86% of the cases with microadenoma had long-term remission, whereas, only 46% of those with macroadenoma had remission. In cases in which hypercortisolemia persists, early repeat exploration and/or radiation therapy or laparoscopic bilateral adrenalectomy may be required.[2]

Radiation therapy has been used in patients who are deemed to be poor surgical candidates and has also been used as adjunctive therapy in patients with residual or recurrent active tumor.[1][4]

Drug therapy is considered to be an adjunct to transsphenoidal microsurgery in cases in which there is a residual tumor and in cases in which one is awaiting the effects of the radiation therapy.[1] Steroidogenesis inhibitors, including mitotane, metyrapone, ketoconazole, and aminoglutethimide are used. Ketoconazole is the best tolerated of these agents and is effective as monotherapy in about 70% of patients.[5]

If untreated, patients frequently succumb to cardiovascular disease or infection.

Treatment Options Under Clinical Evaluation for ACTH-Producing Pituitary Tumors

Treatment options under clinical evaluation for ACTH-producing pituitary tumors include the following:

  • Stereotactic radiation surgery.[4][6][7]

Current Clinical Trials

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with pituitary tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.

References:

  1. Yeh PJ, Chen JW: Pituitary tumors: surgical and medical management. Surg Oncol 6 (2): 67-92, 1997.

  2. Levy A: Pituitary disease: presentation, diagnosis, and management. J Neurol Neurosurg Psychiatry 75 (Suppl 3): iii47-52, 2004.

  3. Mampalam TJ, Tyrrell JB, Wilson CB: Transsphenoidal microsurgery for Cushing disease. A report of 216 cases. Ann Intern Med 109 (6): 487-93, 1988.

  4. Mahmoud-Ahmed AS, Suh JH: Radiation therapy for Cushing's disease: a review. Pituitary 5 (3): 175-80, 2002.

  5. Nieman LK: Medical therapy of Cushing's disease. Pituitary 5 (2): 77-82, 2002.

  6. Devin JK, Allen GS, Cmelak AJ, et al.: The efficacy of linear accelerator radiosurgery in the management of patients with Cushing's disease. Stereotact Funct Neurosurg 82 (5-6): 254-62, 2004.

  7. Wong GK, Leung CH, Chiu KW, et al.: LINAC radiosurgery in recurrent Cushing's disease after transsphenoidal surgery: a series of 5 cases. Minim Invasive Neurosurg 46 (6): 327-30, 2003.

Growth Hormone-Producing Pituitary Tumors Treatment

Standard Treatment Options for Growth Hormone (GH)-Producing Pituitary Tumors

Standard treatment options for GH-producing pituitary tumors include the following:

  1. Surgery (usually a transsphenoidal approach).
  2. Dopamine analogues, such as bromocriptine.
  3. Somatostatin analogues, such as octreotide.
  4. The GH-receptor antagonist, pegvisomant.[1][2]
  5. Surgery and postoperative radiation therapy.

Treatment for patients with acromegaly includes surgical, radiation, and medical therapies.[3] 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).

Microadenomectomy or macroadenoma decompression is approached transsphenoidally in most patients. Increasingly, endoscopic surgery is used to allow the entire surgical field to be viewed and to allow tumor tissue that would otherwise be inaccessible with rigid instruments to be safely resected. Complete return of GH concentrations to normal, however, is not often achieved. Increasingly, adjunctive radiation therapy is reserved for tumors that extend beyond the safe operative area and appear to pose an ongoing threat.

Drug treatment, whether used as an adjuvant or primary therapy in appropriately selected patients, which is advocated by some,[4] includes the use of somatostatin analogues, such as octreotide; dopamine analogues, such as bromocriptine; and, the GH-receptor antagonist, pegvisomant. As the first of a new class of GH-receptor antagonists, pegvisomant works by inhibiting functional dimerization of GH receptors and thereby inhibits GH action. Preliminary results indicate that it may be the most effective medical treatment for acromegaly reported to date.[1][2]

In acromegalic patients, impaired glucose tolerance, hypertension, and hyperlipidemia should be vigorously treated concurrently with definitive therapy. A multidisciplinary clinical approach may be required for the treatment of arthritis, carpal tunnel syndrome, obstructive sleep apnea, and prognathism.[5] Mortality is related primarily to cardiovascular and respiratory diseases.[5]

Current Clinical Trials

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with pituitary tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.

References:

  1. Stewart PM: Pegvisomant: an advance in clinical efficacy in acromegaly. Eur J Endocrinol 148 (Suppl 2): S27-32, 2003.

  2. Muller AF, Kopchick JJ, Flyvbjerg A, et al.: Clinical review 166: Growth hormone receptor antagonists. J Clin Endocrinol Metab 89 (4): 1503-11, 2004.

  3. Levy A: Pituitary disease: presentation, diagnosis, and management. J Neurol Neurosurg Psychiatry 75 (Suppl 3): iii47-52, 2004.

  4. Kleinberg DL: Primary therapy for acromegaly with somatostatin analogs and a discussion of novel peptide analogs. Rev Endocr Metab Disord 6 (1): 29-37, 2005.

  5. Colao A, Ferone D, Marzullo P, et al.: Systemic complications of acromegaly: epidemiology, pathogenesis, and management. Endocr Rev 25 (1): 102-52, 2004.

Thyrotropin-Producing Tumors Treatment

Standard Treatment Options for Thyrotropin-Producing Tumors

Standard treatment options for thyrotropin-producing tumors include the following:

  1. Surgery (usually a transsphenoidal approach), with or without adjuvant radiation therapy.[1][2]
  2. Somatostatin analogues, such as octreotide.[3][4]

Transsphenoidal surgery is the treatment of choice for patients with thyrotropic adenomas.[1] Adjuvant radiation therapy may be employed when surgery is known to be noncurative even if the patient is still euthyroid because relapse is inevitable, and the full effect of radiation therapy requires months or years.

Medical therapy may be required for patients who still have hyperthyroid symptoms despite surgery and external radiation. Somatostatin analogues are the drugs of choice for treatment; however, the efficacy of treatment may wane with time.[1][2][3][4]

Current Clinical Trials

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with pituitary tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.

References:

  1. Brucker-Davis F, Oldfield EH, Skarulis MC, et al.: Thyrotropin-secreting pituitary tumors: diagnostic criteria, thyroid hormone sensitivity, and treatment outcome in 25 patients followed at the National Institutes of Health. J Clin Endocrinol Metab 84 (2): 476-86, 1999.

  2. Levy A: Pituitary disease: presentation, diagnosis, and management. J Neurol Neurosurg Psychiatry 75 (Suppl 3): iii47-52, 2004.

  3. Caron P, Arlot S, Bauters C, et al.: Efficacy of the long-acting octreotide formulation (octreotide-LAR) in patients with thyrotropin-secreting pituitary adenomas. J Clin Endocrinol Metab 86 (6): 2849-53, 2001.

  4. Teramoto A, Sanno N, Tahara S, et al.: Pathological study of thyrotropin-secreting pituitary adenoma: plurihormonality and medical treatment. Acta Neuropathol (Berl) 108 (2): 147-53, 2004.

Nonfunctioning Pituitary Tumors Treatment

Standard Treatment Options for Nonfunctioning Pituitary Tumors

Standard treatment options for nonfunctioning pituitary tumors include the following:

  1. Surgery (preferably with a transsphenoidal approach) followed by close observation with radiation therapy reserved for recurrence.[1][2]
  2. Radiation therapy.[1][2][3]
  3. Surgery and postoperative radiation therapy.[1][2]

The selection of treatment for patients with nonfunctioning (endocrine-inactive) tumors 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. The initial treatment of patients with gonadotroph adenomas is usually by transsphenoidal surgery, particularly if the adenoma presents with neurological symptoms, because the effect of radiation therapy occurs too slowly, and no reliable medical therapy exists.[4]

Surgical management is typically considered the first choice of treatment for patients with endocrine inactive pituitary adenomas because of its effectiveness in ameliorating symptoms of chiasmal compression and headache.[1] Radical removal of the tumor, however, is difficult to obtain because of the frequent invasiveness into the cavernous sinus. Seventy percent to 80% of patients experience normalization or improvement of visual field defects, and almost 100% of patients with headache as a presenting symptom experience relief. Regrowth of the tumor after radiologically confirmed gross total removal appears to be uncommon. In a series of 32 patients, only 2 (6.2%) with gross total tumor removal and no postoperative radiation therapy showed radiological recurrence of the tumor at a mean follow-up of 5.5 years.[5]

Radiation therapy has been administered routinely in the postoperative period and after clear radiological evidence of residual or recurrent tumor has been demonstrated.[1][2][3] Drug therapy appears to be of limited value.[1][2][3]

Current Clinical Trials

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with pituitary tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.

References:

  1. Losa M, Mortini P, Barzaghi R, et al.: Endocrine inactive and gonadotroph adenomas: diagnosis and management. J Neurooncol 54 (2): 167-77, 2001.

  2. Yeh PJ, Chen JW: Pituitary tumors: surgical and medical management. Surg Oncol 6 (2): 67-92, 1997.

  3. Tsang RW, Brierley JD, Panzarella T, et al.: Radiation therapy for pituitary adenoma: treatment outcome and prognostic factors. Int J Radiat Oncol Biol Phys 30 (3): 557-65, 1994.

  4. Snyder PJ: Extensive personal experience: gonadotroph adenomas. J Clin Endocrinol Metab 80 (4): 1059-61, 1995.

  5. Lillehei KO, Kirschman DL, Kleinschmidt-DeMasters BK, et al.: Reassessment of the role of radiation therapy in the treatment of endocrine-inactive pituitary macroadenomas. Neurosurgery 43 (3): 432-8; discussion 438-9, 1998.

Pituitary Carcinomas Treatment

Standard Treatment Options for Pituitary Carcinomas

Standard treatment options for pituitary carcinomas include the following:

  1. Surgery.
  2. Dopamine agonists, such as bromocriptine, pergolide, quinagolide, and cabergoline, for prolactin (PRL)-producing carcinomas.
  3. Somatostatin analogues, such as octreotide, for growth hormone (GH)-producing and thyroid-stimulating hormone (TSH)-producing carcinomas.
  4. Adjuvant radiation therapy, which does not appear to change the disease's outcome.
  5. Chemotherapy, which is of little benefit.

Some reports indicate that as many as 88% of pituitary carcinomas are endocrinologically active, and adrenocorticotrophin hormone-secreting tumors are the most common.[1] Treatments for patients with pituitary carcinomas are palliative, with the mean survival time ranging from 2 years to 2.4 years, though several case reports of long-term survivors have been published.[2][3][4][5]

Treatment options for patients with pituitary carcinomas include resection and dopamine agonists for PRL-producing tumors; somatostatin analogues for GH-producing and TSH-producing tumors; radiation therapy, and chemotherapy.[1] These treatments are palliative with the mean survival time ranging from 2 years to 2.4 years, though several case reports of long-term survivors have been published.[2][3][4][5]

Current Clinical Trials

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with pituitary tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.

References:

  1. Ragel BT, Couldwell WT: Pituitary carcinoma: a review of the literature. Neurosurg Focus 16 (4): E7, 2004.

  2. Pernicone PJ, Scheithauer BW, Sebo TJ, et al.: Pituitary carcinoma: a clinicopathologic study of 15 cases. Cancer 79 (4): 804-12, 1997.

  3. Sironi M, Cenacchi G, Cozzi L, et al.: Progression on metastatic neuroendocrine carcinoma from a recurrent prolactinoma: a case report. J Clin Pathol 55 (2): 148-51, 2002.

  4. Landman RE, Horwith M, Peterson RE, et al.: Long-term survival with ACTH-secreting carcinoma of the pituitary: a case report and review of the literature. J Clin Endocrinol Metab 87 (7): 3084-9, 2002.

  5. Vaquero J, Herrero J, Cincu R: Late development of frontal prolactinoma after resection of pituitary tumor. J Neurooncol 64 (3): 255-8, 2003.

Recurrent Pituitary Tumors Treatment

Standard Treatment Options for Recurrent Pituitary Tumors

Standard treatment options for recurrent pituitary tumors include the following:

  1. Radiation therapy for postsurgical recurrence, which offers a high likelihood of local control.[1][2]
  2. Reirradiation, which provides long-term local control and control of visual symptoms.[3]

The question and selection of further treatment for patients who relapse is dependent on many factors, including the specific type of pituitary tumor, prior treatment, visual and hormonal complications, and individual patient considerations.

Treatment Options Under Clinical Evaluation for Recurrent Pituitary Tumors

Treatment options under clinical evaluation for recurrent pituitary tumors include the following:

  • Stereotactic radiation surgery.[4][5][6]

Current Clinical Trials

Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with recurrent pituitary tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI Web site.

References:

  1. Kovalic JJ, Grigsby PW, Fineberg BB: Recurrent pituitary adenomas after surgical resection: the role of radiation therapy. Radiology 177 (1): 273-5, 1990.

  2. Tsang RW, Brierley JD, Panzarella T, et al.: Radiation therapy for pituitary adenoma: treatment outcome and prognostic factors. Int J Radiat Oncol Biol Phys 30 (3): 557-65, 1994.

  3. Schoenthaler R, Albright NW, Wara WM, et al.: Re-irradiation of pituitary adenoma. Int J Radiat Oncol Biol Phys 24 (2): 307-14, 1992.

  4. Sheehan JP, Kondziolka D, Flickinger J, et al.: Radiosurgery for residual or recurrent nonfunctioning pituitary adenoma. J Neurosurg 97 (5 Suppl): 408-14, 2002.

  5. Laws ER, Sheehan JP, Sheehan JM, et al.: Stereotactic radiosurgery for pituitary adenomas: a review of the literature. J Neurooncol 69 (1-3): 257-72, 2004 Aug-Sep.

  6. Picozzi P, Losa M, Mortini P, et al.: Radiosurgery and the prevention of regrowth of incompletely removed nonfunctioning pituitary adenomas. J Neurosurg 102 (Suppl): 71-4, 2005.


This information is provided by the National Cancer Institute.

This information was last updated on July 27, 2012.

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