The following discussion of hypothyroidism is intended to be understandable and practical.  I’ll first present a glossary of terms and then a description of hypothyroidism in adults: symptoms, causes, testing, and treatment.  Then I have sections on special groups with hypothyroidism: pregnant women, newborn infants, and children.  I first published this online as a Google “Knol”.


Thyroid gland refers to the endocrine organ located in the low anterior (front) of the neck. The thyroid gland secretes two forms of thyroid hormone (T4 and T3) to regulate the body’s metabolism.   The thyroid gland weighs only about 15 grams (0.5 ounces) and is shaped something like a butterfly, with wings (lobes) flanking the trachea (windpipe) and connected to each other in front of the trachea.  Figure1:  http://www.med.umich.edu/1libr/aha/aha_thyroidg_art.htm

T4, thyroxine, levothyroxine (synonyms) refers to the form of thyroid hormone that has 4 atoms of iodine in each molecule.  T4 is the main hormone secreted by the thyroid gland.  Over 99% of T4 circulates in the bloodstream attached to proteins (eg, thyroid binding globulin, TBG).  The unattached T4 is known as free T4 (FT4, free thyroxine) and only that tiny portion of T4 can leave the circulating blood to enter cells.

T3, triiodothyronine (synonyms) refers to the form of thyroid hormone that has 3 atoms of iodine in each molecule.  T3 is secreted by the thyroid gland and also made from T4 in other cells that can convert T4 to T3Over 99% of T3 circulates in the bloodstream attached to proteins (eg, thyroid binding globulin, TBG).  The unattached T3 is known as free T3 (FT3) and only that tiny portion of T3 can leave the circulating blood to enter cells.  FT3 is active thyroid hormone and works by entering a cell’s nucleus (center) and binding to certain receptors (like a key in a lock) to regulate the activity of genes. T3 receptors are found in nearly every cell of the body, from the brain to the skin, such that thyroid hormone’s effect is extremely widespread and profound.

TSH (Thyroid Stimulating Hormone) refers to a hormone that is produced by the pituitary, a small endocrine gland that lies at the base of the brain. TSH stimulates the thyroid gland to produce T4 and T3.  The normal pituitary gland secretes more TSH when thyroid hormone levels are too low (hypothyroidism).  The TSH level is elevated when the thyroid gland fails.


Symptoms of Hypothyroidism in Adults

Most adults with hypothyroidism complain of fatigue, weight gain, and feeling cold. There are many symptoms of hypothyroidism that vary considerably among individuals and most people with hypothyroidism will have only a few of them.

Common Symptoms of Hypothyroidism: slow heart rate (bradycardia), high blood pressure, cold intolerance, fatigue, depression, mental dullness, puffiness in face or extremities, thyroid enlargement (goiter), headache, slow speech, hoarse voice, heavy menstrual periods, joint and muscle pains, tingling feeling (paresthesia), carpal tunnel syndrome, hair breakage and thinning, brittle nails, decreased perspiration and dry skin, skin pallor or yellowing, weight gain.

 Uncommon Symptoms of Hypothyroidism in Adults:  

Trouble swallowing (dysphagia), breast milk secretion when not nursing (galactorrhea), shortness of breath, pneumonia, weight loss from decreased appetite, absent menstrual periods (amenorrhea), psychosis, sensitivity to narcotics and reduced consciousness. and coma. 

Causes of Hypothyroidism in Adults

Hashimoto’s thyroiditis (autoimmune thyroiditis) is the most common cause of hypothyroidism. Dr. Hakaru Hashimoto, a Japanese surgeon, first described the condition in 1912.  It’s an autoimmune condition in which the body’s immune system is turned against the thyroid.  White blood cells      (B lymphocytes) invade the thyroid gland, such that the condition is also known as chronic lymphocytic thyroiditis. The thyroid gland may enlarge and develop a rather firm “rubbery” texture.  The blood contains antibodies (immune proteins) that are directed against the thyroid gland.  Such antithyroid antibodies are found in about 10% of most adult populations.  Hashimoto’s thyroiditis is usually a chronic condition that can eventually damage the thyroid to cause hypothyroidism.

Painless thyroiditis,also known as Hashitoxicosis, is an acute autoimmune inflammation of the thyroid gland that releases stored thyroid hormone and initially causes hyperthyroidism, followed by hypothyroidism, due to thyroid damage.  Frequently, the thyroid recovers normal function.  The condition is termed postpartum thyroiditis when it occurs in women within 6 months after delivery.

There is a very strong genetic predisposition to autoimmune thyroiditis. http://www.jautoimdis.com/content/2/1/1  Hashimoto’s thyroiditis can also occur during treatment with lithium, amiodarone, interferon therapy, and immuno-chemotherapy with immune checkpoint inhibitors.  Dietary iodine supplementation also appears to increase the risk of autoimmune thyroiditis. http://www.ncbi.nlm.nih.gov/pubmed/12849065?dopt=Abstract

When Hashimoto’s thyroiditis causes hypothyroidism, it is usually permanent.  However, up to 11% of patients with hypothyroidism may experience a remission after several years.


Rarely, hypothyroidism can resolve and may even go on to hyperthyroidism due to Graves disease.  Graves disease is an autoimmune thyroiditis in which antibodies stimulate the thyroid’s TSH receptors, causing the thyroid to produce excessive amounts of thyroid hormone.  In Graves disease, there is usually concurrent Hashimoto thyroiditis. Rarely, hypothyroidism may alternate with hyperthyroidism.

Although autoimmune thyroiditis can occur at any age and in either sex, it typically affects women.  The sexual disparity is striking, with a female: male ratio of 10:1.   Other autoimmune conditions also tend to be more common in women and the reason for this is not understood.  One debated theory is that, during pregnancy, fetal cells enter the mother and might cause an autoimmune reaction, but autoimmune disease occurs even in women who have never been pregnant.




Usually, autoimmune thyroiditis is an isolated condition.  However, individuals with autoimmune thyroiditis are somewhat prone to develop other autoimmune conditions.  Some degree of Sjöegren’s syndrome (dry eyes & mouth) is fairly common.  Celiac disease, an autoimmunity against the intestine provoked by gluten (wheat), is also more common.   Vitiligo (patches of white skin) can also occur.  In polyglandular autoimmune syndromes, patients with autoimmune thyroiditis have other autoimmune endocrine deficiencies, such as adrenal insuffiency, hypoparathyroidism (low serum calcium), or type 1 diabetes mellitus,

Other causes of hypothyroidism include surgery, radioiodine treatment or exposure (nuclear fallout), chronic hepatitis C, Reidel’s thyroiditis, and certain drugs  (lithium, propylthiouracil, methimazole, sulfonamides, amiodarone, interferon alpha, interferon beta, interleukin-2).  Iodine deficiency can cause hypothyroidism and goiter.  Certain foods (turnips, cassava) can aggravate iodine deficiency and are known as goitrogens.  Hypopituitarism can cause hypothyroidism, due to a deficiency of TSH.

Tests for Hypothyroidism

When the thyroid gland fail, lower levels of thyroid hormone are sensed by the pituitary gland, which secretes more Thyroid Stimulating Hormone (TSH).   An elevated serum TSH level is the most sensitive test for hypothyroidism (except with hypopituitarism)  In hypothyroidism, the serum free T4 (FT4) level is usually low or low-normal.

To screen for Hashimoto (autoimmune) thyroiditis, blood is assayed for antithyroid antibodies: anti-thyroperoxidase (TPO) antibodies and anti-thyroglobulin (TG) antibodies.


Factors that can cause misleading testing for hypothyroidism:

When a serum TSH level is elevated, the test should be repeated before embarking on long-term thyroid hormone replacement.  Certain factors can cause a misleadingly elevated serum TSH that may be mistaken for hypothyroidism: recovery from an illness, acute psychiatric crises, sleep deprivation, and strenuous exercise just before testing.  Heroin or amphetamines can also elevate serum TSH.  Misleadingly elevated serum TSH levels may also be caused by spurious test results resulting from laboratory error or from circulating antibodies that interfere with the TSH antibody assay method or block the TSH receptor.

Misleadingly low serum total T4 levels occur with malnourishment and factors that reduce serum protein levels, such as cirrhosis and nephrotic syndrome. Other conditions that can lower TBG and result in a misleadingly low serum total T4 include anabolic steroid abuse and familial TBG deficiency.  Serum free T4 (FT4) levels are normal in these conditions and the FT4 assay is superior to the total T4 assay.

However, misleadingly low serum FT4 levels can also occur and can result from laboratory error or can be seen in severe illness, particularly congestive heart failure.  Certain drugs also cause low FT4 levels without hypothyroidism: high-dose corticosteroids (eg, prednisone, dexamethasone), anti-seizure drugs (eg, carbamazepine, phenytoin, phenobarbitol), and therapy with T3 (Cytomel).  In these conditions, the serum TSH is not elevated.

 Other Laboratory Findings in Hypothyroidism:

Certain other laboratory tests can also be abnormal in patients with hypothyroidism: hyponatremia (low serum sodium), elevated liver enzymes, elevated serum prolactin levels, and anemia.  High serum lipids are commonly sen: high LDL cholesterol, high triglycerides, and high lipoprotein(a).  In patients with autoimmune thyroiditis, serum ANA levels are usually elevated and are nonspecific, i.e., not usually indicating systemic lupus erythematosis.


Treatment of Adults with Hypothyroidism 

History:  Treatment for hypothyroidism first became available in 1892, when sheep’s thyroid was fried and eaten to treat this condition.  This was not particularly palatable.  In 1900, a thyroid preparation was first introduced in the United States as dessicated (dried) sheep’s thyroid that had been freed from fat, cleaned, dried, and powdered.  It could be made into tablets whose dosage was measured as weight in an old measurement called grains, where 1 grain (not to me confused with the word gram) is equivalent to 60 milligrams (mg).  However, the original desiccated thyroid preparations differed in potency from batch to batch, although it has become more reliable and continues to be available.  Synthetic thyroxine was developed to be a more reliable thyroid medication and that is the type of thyroid preparation in greatest use today.

Synthetic thyroxine (T4) is thyroid medication that is preferred by most clinicians for treating patients with hypothyroidism.  There are several thyroxine formulations and many dosage strengths.  Most formulations have accurate amounts of thyroxine in their tablets.  However, the bioavalability (absorption) of the different manufacturer’s thyroxine formulations can differ slightly. Therefore, it’s best for hypothyroid patients to be consistent and to take the same brand name of thyroxine or the same manufacturer’s generic thyroxine.

Beginning therapy with thyroxine:  There is no mandatory starting dosage of thyroxine.  Generally, for pregnant women, or patients with severe hypothyroidism, a full replacement dosage of thyroxine is given immediately.  For children and otherwise healthy younger adults, near-replacement doses are begun from the outset.   However, for older patients with suspected coronary disease, the replacement dosage should be lower and increased as tolerated.  If angina occurs, the dosage is reduced until coronary intervention can restore coronary artery perfusion.

Monitoring Treatment of Hypothyroidism:

Serum TSH (thyroid stimulating hormone) levels are used to monitor the adequacy of thyroxine replacement. While receiving optimal thyroxine replacement therapy, most people’s symptoms of hypothyroidism resolve fully.  Serum TSH levels are generally kept between 0.4 – 2.0 mcg/dL.  Although serum TSH levels are very useful to determine the optimal replacement dosage of thyroxine, it is important not to rely entirely on this test.

Some hypothyroid individuals who receive thyroxine replacement continue to have symptoms typical of hypothyroidism (particularly fatigue), despite having serum levels of TSH and FT4 that are solidly normal.  In such cases, it is important to screen for other conditions, such as concurrent illness (eg, anemia, diabetes, hypercalcemia, electrolyte abnormalities, celiac disease, adrenal insufficiency, hypogonadism, depression). Medications can cause fatigue (eg, oral statin drugs for treatment of high cholesterol, oral beta blockers, beta blocker eye drops for glaucoma, etc).  In the absence of such conditions, a serum T3 (FT3 in women who are pregnant or receiving oral estrogens) may be obtained.  If the serum T3 or FT3 level is low or low-normal and there are no contraindications (eg, angina, atrial fibrillation), a careful increase in thyroxine replacement is reasonable and may be continued if symptomatic relief is obtained.  But if thyroxine is given such that serum TSH levels are suppressed, the serum T3 or FT3 (for women who are pregnant or taking oral estrogen) level should be monitored, keeping them in the lower half of the normal reference range.  Careful clinical monitoring is also required for symptoms or signs of hyperthyroidism. Periodic bone mineral densitometry may be followed, thyroid hormone replacement does not cause osteoporosis as long as they are clinically euthyroid (no signs of excess thyroid).  Individuals receiving doses of thyroxine that suppress serum TSH may be at an increased risk for clinical hyperthyroidism (eg, atrial fibrillation), particularly with menopause or withdrawal of oral estrogen therapy.

Since the normal thyroid secretes both T4 and T3, there have been studies comparing T4 to combined T4/T3 thyroid preparations, which have yielded conflicting results.  Such combined T4/T3 preparations include Armour Thyroid (dessicated animal thyroid), Nature-Throid, and Liotrix (synthetic, unavailable in USA).  The main problem with giving combined T4/T3 preparations is that the T3 component peaks a few hours after taking the pill, with transiently elevated serum T3 levels.  Nevertheless, some patients subjectively prefer the T4/T3 prepatations in 5:1 or 10:1 ratios.   A Dutch double-blind study of 141 hypothyroid individuals found that their patients often preferred the T4/T3 preparation, and during such treatment, the serum TSH levels were often suppressed.

Medications that Interact with Thyroid Hormone Therapy:

Certain medications can interact with thyroid hormone replacement treatment for hypothyroidism.  Care must be taken when thyroid hormone is taken with the following medications:

Amiodarone: inhibits conversion of T4 to T3; rely on serum TSH levels.

Antacids (aluminum or calcium): reduces thyroxine absoption.

Anti-tuberculous antibiotics: increase liver break-down of thyroxine.

Rifabutin (Mycobutin)

Rifampin (Rifadin, Rimactane)

Anti-sex hormone chemotherapy for breast cancer or prostate cancer:  reduces estrogen and liver TBG production, reducing thyroxine dosage requirement:

Leuprolide (Lupron, Lupron Depot): reduces estrogen and liver TBG production, reducing thyroxine dosage requirement:

Anti-seizure medications: increase liver break-down of thyroxine

Carbamazepine (Tegretol)


Primidone (Mysoline)

Phenytoin (Dilantin)

Chemotherapy: may cause ovarian failure, reducing estrogen levels and liver TBG production, reducing thyroxine dosage requirement.

Cholesterol-lowering bile acid-binding drugs: reduces thyroxine absorption

Cholestiramine (Questran)

Colestipol (Colestid)

Didanosine (ddi, Videx anti-HIV therapy): reduces thyroxine absorption

Digoxin (Lanoxin): thyroxine increases thyroxine clearance.

Estrogens (oral): increases liver production of Thyroid Binding Globulin

Oral contraceptives and oral estrogen replacement therapy:  increase in hepatic production of thyroid binding globulin (TGB) may increase thyroxine dose requirement.

Imatinib chemotherapy (Gleevec): increases liver metabolism of thyroxine

Iron supplements: reduce thyroxine absorption

Proton Pump Inhibitors (PPIs): may cause atrophic gastritis and reduce the           absorption of thyroxine (omeprazole, lansoprazole, pantoprazole, etc)

Raloxifene (Evista): reduces thyroxine absorption

Sucralfate (Carafate): reduces thyroxine absorption

Warfarin (Coumadin): dosage requirement may change (usually drops), due to changes in hepatic metabolism and  clotting factors caused by thyroxine threapy.


Pregnant Women with Hypothyroidism:

Hypothyroidism is a very common condition and unsuspected maternal hypothyroidism appears to cause a 3.8% increase in miscarriage rate. http://www.ncbi.nlm.nih.gov/pubmed/11126160?ordinalpos=25&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

During pregnancy, the developing baby receives the mother’s thyroid hormones, which cross the placenta.  The baby is particularly dependent upon maternal thyroid during the first trimester when the fetal thyroid has not fully developed.  Maternal hypothyroidism can adversely affect the intellectual development of the baby. http://www.ncbi.nlm.nih.gov/pubmed/10451459?ordinalpos=69&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Therefore, screening for hypothyroidism is reasonable for all women who are planning to become pregnant or who have become pregnant.   Screening is mandatory for women with symptoms of hypothyroidism (see above) or who have a personal or family history of thyroid or autoimmune disorders.  Screening for hypothyroidism is done with a blood test for TSH.

Iodine deficiency is surprisingly common and can cause hypothyroidism during pregnancy.  This can be prevented by ensuring adequate dietary iodine with iodized salt and tea or by taking one prenatal multivitamin daily.  The multivitamin should contain 150 mcg iodine, the recommended daily requirement during pregnancy.  Excessive iodine supplements should be avoided, as this can cause the baby to develop a goiter.

Women with known hypothyroidism should have prenatal thyroid function testing to ensure they are euthyroid (normal thyroid levels) before becoming pregnant.  During pregnancy women’s thyroxine requirements predictably increase by as much as 50%.  Therefore, at the diagnosis of pregnancy the dosage of thyroxine is increased empirically by 20-30%.  It is prudent to monitor TSH levels every 6 weeks and adjust the thyroxine replacement to ensure that they are doing well clinically and to keep the TSH level below 2.0  µU/mL Following delivery, the thyroxine dosage may be tapered back gradually over several weeks to the prenatal dosage.


Newborns with Hypothyroidism:

About 1 in 3000 newborn infants are born with hypothyroidism, which is known as congenital hypothyroidism.  Hypothyroid infants may appear lethargic and have a hoarse cry. They may nurse poorly and have abdominal bloating, constipation, and vomiting.  They may also have hypothermia, a large posterior fontanelle and neonatal jaundice that persists for more than 3 days. They may develop a large tongue and a bulging around the belly button (omphalocele). However, hypothyroidism is often not clinically recognized at birth, so a mandated screening process tests all newborns for congenital hypothyroidism, usually with blood obtained from a heel stick and absorbed onto filter paper.  The blood specimen is sent to a central laboratory to assess for inborn errors of metabolism and for TSH and/or T4.  TSH levels fluctuate a great deal during the first few days of life, so there may be false positive and false negative results.

Transiently low T4 levels (with normal TSH) are commonly seen in babies who are not hypothyroid, but who are premature, low birth weight, or who are sick from other causes.  Such babies’ low T4 levels usually rise into the normal range after their recovery and there are no adverse sequelae.  However, repeat testing is advisable, since permanently low FT4 with low or normal TSH levels can be seen with congenital hypopituitarism, which is rare but must be suspected in babies with an abnormally slow growth.

Low neonatal T4 with a high TSH usually indicates hypothyroidism.  About 10% of such babies have temporary hypothyroidism; when this is suspected, at age 3-4 years, thyroxine replacement may be held for 3-4 weeks and the FT4 and TSH repeated to see if they are now normal.

Most babies with hypothyroidism have a permanent condition.  The causes of this include an absent thyroid (thyroid aplasia), an underdeveloped thyroid (thyroid hypoplasia), or an abnormally located (ectopic) thyroid under the tongue (lingual thyroid) or on the side of the neck.  Congenital hypothyroidism can also be caused by thyroid enzyme defects.

When screening tests (T4 and TSH) indicate hypothyroidism, confirmatory blood tests are drawn immediately and the baby is treated with thyroxine while the test results are pending.  Frequent monitoring of the FT4 and TSH levels is important and the FT4 level should be kept in the upper range of normal.  Thyroxine may be not be properly absorbed by the intestines of babies who receive concurrent soy formula or iron preparations.

When babies are diagnosed with hypothyroidism by newborn thyroid screening testing and treated with thyroxine, their growth and intellectual development will be entirely normal.   However, when congenital hypothyroidism is untreated, the baby’s brain gradually suffers irreversible damage that results in a condition known as cretinism.


Children with Hypothyroidism:

Children who develop hypothyroidism typically have a diminished growth velocity and become shorter relative to peers of their age.  The eruption of adult teeth may be delayed.  Hypothyroid children may be somewhat overweight but often do not look particularly sick or have physical complaints. When hypothyroidism develops after age 2 years, permanent mental deficiency does not typically occur.  In fact, hypothyroid children may sometimes be good students because they lack some of the normal hyperactivity of childhood and pay attention in class. However, with more severe hypothyroidism, children can develop problems with cognitive and attention deficits that may seem like a new learning disability.  They may complain of feeling fatigued and cold and may appear depressed and lethargic.  Their skin may be dry and they may be constipated.  Girls may develop the onset of menstrual periods before age 10 years (precocious puberty) and may have heavy, painful, and irregular periods.  These symptoms reverse with treatment of their hypothyroidism.

Thyroxine replacement therapy is given to children with hypothyoidism.  Because of their increased metabolic rate, children and adolescents with hypothyroidism often require a greater relative doses of thyroxine than do adults.  Autonomous adolescents may neglect to take their thyroxine medication regularly and some supervision may be required.






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UCSF Compassionate-Use Protocol for 131I-MIBG Therapy: Tips for Patients with Metastatic Pheochromocytoma and Paraganglioma

Tips about MIBG Therapy for Patients & Family

University of California San Francisco


I-131 (131I) is a radioisotope also known as “radioiodine”.  Metaiodobenzylguanidine (MIBG) is a compound that most paragangliomas and pheochromocytomas actively absorb.  The 131I radioisotope can be chemically attached to MIBG to produce 131I-MIBG, a compound that these tumors absorb, thereby radiating them from the inside.

131I-MIBG (MIBG) was first used as a cancer treatment at the University of Michigan.  Since then, several medical centers around the world have administered MIBG therapies.  We administer MIBG under a UCSF Comprehensive Cancer Center compassionate use protocol.

Preparing for MIBG Therapy

You will require different types of scans to determine the exact location and size of the tumors.  Scans with a small dose of MIBG (“MIBG scan”) will determine whether the tumors will likely absorb sufficient MIBG to shrink them and make them less active.

You will also require blood and urine tests to determine whether you meet “inclusion criteria” (ie, whether treatment would be reasonably safe for you).   Certain additional blood and urine tests measure compounds secreted by the tumor, thus acting as “tumor markers”, reflecting the current activity of your tumor.  You will be asked to collect a “24-hour urine for fractionated catecholamines, fractionated metanephrines, and creatinine.”  Please follow instructions in collecting an accurate 24-hour urine.

Men should consider banking sperm before having MIBG therapy.   Women who are menstruating may receive a medication to reduce menstruation after MIBG therapy.

Medications to Avoid Before MIBG Therapy

Certain drugs interfere with the uptake of MIBG by a pheochromocytoma.  You will be given a list of medications to avoid.  Such medications include labetalol, phenothiazine-derived anti-nausea medications, tricyclic antidepressants, and decongestants.  But check with your UCSF physician before taking a new medication.


Important Documents before MIBG Therapy

Before you can receive MIBG therapy, you’ll sign the “Consent Form”, which explains the possible side effects of the treatment.  The Consent Form must be signed by you and by the physician explaining it to you prior to UCSF Nuclear Medicine ordering the dose of MIBG from a nuclear pharmacy (one week before the scheduled treatment).   You will be given a copy of the signed Consent Form and another document known as the “Patients’ Bill of Rights”.

HIPAA is an acronym for “Health Insurance Portability & Accountability Act of 1996”. Under this US law, you must give signed consent before your health information can be used for research purposes.  You will need to review and sign the HIPAA document before receiving MIBG.

Scheduling MIBG Therapy

Nuclear safety regulations restrict the frequency of MIBG treatments at UCSF.  The UCSF pediatric cancer group also uses MIBG to treat neuroblastoma, a different tumor that arises in children.  They must also reserve treatment dates for their patients, so we use a mutual scheduling coordinator. Your UCSF physician will contact the MIBG scheduling coordinator for a prospective treatment date that will be assigned to you.

We realize that all this will appear to proceed at a frustratingly slow, glacial pace.  Also, additional delays can occur, due to the complex logistics that are explained above. We ask for your understanding if your therapy is rescheduled.  This therapy is usually given on a Friday.  You will be admitted on Thursday afternoon before the treatment on Friday morning.  Expect to stay about one week in the hospital, although the duration of your hospitalization cannot be accurately predicted in advance.  See below.

Where You and Your Family/Friends Can Stay in San Francisco

A list of places to stay around UCSF can be obtained from your UCSF physician.  One place to stay near UCSF is the Stanyan Park Hotel at 750 Stanyan Street: 415-751-1000; www.stanyanpark.com.  Family or friends who wish to stay in the area during your hospitalization must remember that their visiting times are limited by radiation safety regulations.  So family/friends sometimes elect to stay elsewhere in the Bay Area and come in to UCSF for visits.  After discharge from UCSF after MIBG therapy, you may not be able to stay at a public hotel unless your radiation levels are sufficiently low.

What to Bring for Your Hospital Stay

You can wear regular street clothes to the hospital.  You will take them off and store them in a closet to wear after you’re discharged. Bedclothes may become contaminated during radioisotope therapy such that you would need to leave them behind. The hospital provides those wonderful hospital gowns that open in the back.  Some patients like to bring additional bedclothes or slippers but need to be prepared to leave them behind. Bring some toiletries: disposable toothbrush, toothpaste, floss, and mouthwash. The hospital supplies hand soap, towels, and washcloth. Bring your favorite shampoo & conditioner in small travel bottles. There is a sink in the room and shower in your bathroom that you will be able to use on Thursday night and after your bladder catheter is removed on Monday.

You may become rather bored and lonesome since, following the treatment and until you’re discharged, you won’t be allowed to leave your room and loved ones can visit only briefly. So wrap a favorite photograph in cellophane and bring it with you to place on your windowsill or your bedside table. The cellophane keeps it from getting contaminated.  The room has a bedside telephone and television.  Cell phone reception is poor from lead-shielded rooms, but some people have gotten a signal through the window.  So you may bring your cell phone and try it out in the room once you’re there.  Bring a little extra cellophane in case it works and you want to use it.

Most patients have brought laptop computers, wrapped in cellophane; the hospital provides a patient wi-fi system that gets a signal into the lead-shielded room.  Some patients bring iPods or iPhones (wrapped in cellophane), loaded with their favorite songs, along with disposable earphones.  You may wish to bring magazines and paperback books to read.  If you need to wear glasses, bring an old pair; after you’re discharged, you’ll probably be able to wash them sufficiently to bring them home.

Admission Day

On Thursday afternoon before the treatment, you’ll be scheduled to see your                     UCSF physician for a pre-admission examination.  You’ll be given an admission packet that contains protocol orders and information about you and the treatment.  You will then go to UCSF Admissions, which is on the first floor of UCSF Hospital near the Emergency Department.  On your way, stop at the adjacent Gift Shop and purchase some sour lemon drops that can relieve dry mouth and salivary gland discomfort that you may experience after the treatment.  UCSF Admissions will arrange for you to be escorted to 11-Long where a nurse will show you your room, which is one of 3 lead-shielded rooms on that floor.  UCSF Radiation Safety personnel will have your room ready, with the bed and floors wrapped in plastic. Give your admission packet to the nurse to place in your chart.

Later that afternoon, when you’ve settled into your room, your UCSF physicians and nurses will visit you there.  You will have a team of doctors assigned to you.  The team consists of residents, interns, and medical students.  These young doctors are a very select group and they sleep in the hospital to be available for emergencies.  One of them will be assigned to be particularly responsible for you. They will review your history and examine you.   You have a rare tumor and they’ll want to learn more about it and how it has affected you.

On Thursday evening, your will receive your first doses of medications to protect your thyroid against any circulating free 131I from the 131I-MIBG.  You’ll be provided with liquid potassium iodine (KI); your doses will be placed by your bedside and your nurse will instruct you when to take them.  It’s best to take these medications mixed in water or juice.  If it upsets your stomach, please tell the nurse.

A phlebotomist will come by your room to draw admission blood work.  The nurses will start 2 peripheral (arm) intravenous lines on Thursday night.  One line will be used infuse intravenous fluids for several days.  The other line will be used for the infusion of the isotope the next morning; it will be removed after the infusion.

You may possibly need to have a bladder catheter.  If that is the case, it will be inserted Thursday evening and a nurse will pre-medicate you before inserting it.  The bladder catheter will drain into a lead-shielded container by the bedside; from there, it is pumped through a tube to the toilet in your bathroom that has been converted to run constantly.  If you’re anxious or have trouble sleeping, you may ask the nurse for a medication to help you sleep.

Treatment Day

On Friday morning, your nurse will beginning giving you Zofran (ondansetron), an anti-nausea medication that you will take twice daily during your hospital stay.  If you have a bladder catheter or are judged to be at risk for venous clotting, you may receive the first of three daily injections of enoxaparin (Lovenox), an anticoagulant.  This reduces your risk of deep vein thrombosis and pulmonary embolism.

Later on Friday morning, UCSF Radiation Safety personnel will arrive to be sure that the room is safe for the isotope injection.  The nurse will give you a light sedative/anti-emetic.  The UCSF Nuclear Pharmacist will bring the isotope in a lead-shielded container, along with the infusion pump.  He will connect the isotope to your intravenous line.  Before starting the infusion, your family/friends will have a chance to wish you well before leaving the room.  They will receive radiation safety instructions while you are receiving the MIBG.

The infusion of MIBG takes between 1-2 hours.  Your blood pressure and heart rate will be monitored regularly with an automated blood pressure cuff.  If your blood pressure rises excessively, you may be given a capsule (nifedipine) to chew and swallow.

Despite having received prophylactic anti-nausea medication, you may experience some break-through nausea or headache several hours after receiving MIBG.   If you feel nauseated, call the nurse with your call button that is clipped to your bed. Your nurse can give you additional anti-nausea medication. If you develop a severe headache, ask the nurse to call your UCSF physician.

What You’ll Eat in the Hospital

UCSF Food Service will request your meal preferences.  The food isn’t bad, but it isn’t a 4-star restaurant.  Also, after the treatment, Food Service observes radiation precautions and leaves your meal tray outside your door for your nurse to bring to you.  The tray usually gets sufficiently cold to be unappetizing.  If it’s really cold, your nurse may be able to reheat it for you.  You might not have much appetite, so it may not matter.  But consider bringing some favorite snack foods with you.  Also, friends/family are allowed to bring more appetizing food from home, restaurants or the UCSF Cafeteria that is located on the 2nd floor; take the Moffitt elevators, not the Long elevators.  You’ll have no unusual food restrictions.

Your Hospital Stay

Your bed will be in a special lead-shielded room, designed to protect others from radiation.  There will be a portable shield between your bed and the door, next to the bed. Lead aprons don’t work for this sort of radiation, so it’s important that visitors observe radiation precautions and stay on the other side of the lead shield when in the room.  See below.

You will be required to take an oral liquid medication to protect your thyroid gland against radioactive iodine: potassium iodide (KI).   Your nurse will place the KI by your bedside in calibrated syringes and your nurse will remind you to take it every 4 hours, except between midnight and 6AM.  If the KI upsets your stomach, please alert us.

If you develop a dry mouth or discomfort in your salivary glands in your cheeks, you may suck on sour lemon drops.  In the first few days after 131I-MIBG, your lymphocyte count will be low, making you prone to yeast infections.  Tell your doctor if you develop a rash in your groin area or a sore tongue.

You may have a bladder catheter. In that case, it’s important that here not be any leaking; inform your nurse if there is.  The bladder catheter drains into a lead-shielded container; be careful not to pull your catheter out of the container.  While the catheter is in your bladder, you will not be able to leave your bed except for bowel movements for which you’ll use a commode placed by your bedside. Your catheter will be removed about three days after receiving MIBG, but your intravenous line will remain attached.

If you do not have a bladder catheter, you’ll be allowed to walk around the room.  You can roll around the portable IV pole with its bags of intravenous fluids.  But stay back behind the lead shield when a visitor is in the room.  You’ll need to use the toilet in the bathroom; please sit down while going to the bathroom.  You’ll be able to shower and that will feel good; please don’t urinate in the shower, since that would contaminate it.  Several days after MIBG, you will be taken to Nuclear Medicine for a scan to see where and how well the isotope has been absorbed by your tumor.

Radiation Safety Instructions for Family/Friends

Family or close friends (≥ 18 years) will be allowed to visit you with permission from you and UCSF Radiation Safety.  However, nobody who is pregnant or possibly pregnant may visit you after MIBG is administered.  Visitors can receive radiation safety instructions from UCSF Radiation Safety during the infusion of MIBG on Friday. If they do not receive the initial instructions, your nurse can instruct them later.   They will be instructed in how to use a radiation meter and log their name, time, and meter readings before and after visiting you.  They will need to wear a gown, booties, and gloves for protection from radioactivity contamination while in your room.  They will also need to stay on the other side of the lead shield away from you while they are in your room.  They will also need to check their hands and feet with a Geiger counter when leaving the room. All visitors must check in with the nursing station before entering your room.  The amount of time an individual visitor will be allowed in your room will be decided by UCSF Radiation Safety and posted on your door.  Visiting times are minimal on Friday and Saturday after MIBG treatment, but increase daily.

Your Discharge From UCSF

Your day of discharge from the hospital will be determined by your radiation level and by your physical condition.  Both your UCSF physicians and UCSF Radiation Safety must agree that you are ready for discharge.  The typical hospital stay has been 6-8 days, but some patients have needed to stay up to 12 days.  On the day of discharge, Radiation Safety will explain radiation precautions; they will give you a detailed radiation precautions instruction sheet.  They will also give you a wristband that indicates that you have received radioisotope therapy. A nurse will take out your intravenous line.  A pharmacist will review your medications. Your doctor will give you a discharge protocol that will explain your discharge plan and follow-up.  To protect your thyroid, you will receive a prescription for KI (ThyroShield) with instructions to take a dose daily until 30 days after MIBG.

After your discharge following MIBG, you will need to observe radiation precautions to reduce radiation exposure to your family/friends and the general public.  If you will be flying home, you may not be permitted to fly home until your radiation levels have fallen, due to the sardine-like way the airlines pack people into their planes.  Other patients choose to stay in the San Francisco for a few days before returning home in order to be nearby UCSF, particularly if they’re not feeling completely well.  You will not be able to sleep in a hotel room until your radiation is below a safe level.  However, you can stay with family in the area, as long as they receive radiation precautions.  Remember that you will not be allowed to sleep with someone for at least a week after your discharge.

Follow-up After MIBG

It is important that you follow your radiation safety guidelines.  You’ll also need to follow your discharge protocol and see your hematologist/oncologist regularly.  You’ll have blood drawn twice weekly for about 6 weeks or until your blood counts have normalized.  Your platelet count will drop about 3 weeks after receiving MIBG, often low enough to make you prone to bruising and bleeding; you may need platelet transfusions.  Your absolute neutrophil count (ANC) will drop about 3-4 weeks after    MIBG, often low enough to make you prone to infection; you may need injections of GCSF (Neupogen) and prophylactic antibiotics.  Your red blood count may fall low enough that you may require blood transfusions. If you develop any shortness of breath, bleeding, bruising, fever, or any signs of infection, contact your hematologist/oncologist immediately.

About 3-4 months after MIBG, your tumor will be reassessed with scans, blood tests, and possibly a 24-hour urine test if you have a secretory tumor.  MIBG exerts its effect over many months and regular lifetime follow-up is required.

The Complex Logistics of MIBG Therapy

This therapy requires the cooperation of many individuals: yourself, your referring physicians, and UCSF physicians.   We also need the help of UCSF Nuclear Medicine, Nuclear Pharmacy, Radiation Safety, Nurses, the MIBG scheduler, and UCSF Admissions/Bed Control.  We must also obtain authorizations from your insurance company.  MIBG therapy also requires the continued approval of the MIBG Site Committee, the UCSF Committee on Human Research (CHR), the UCSF Comprehensive Cancer Center (CCC) Protocol Committee, the US Food and Drug Administration (FDA), and the US Nuclear Regulatory Commission (NRC).

We obtain the MIBG from an East Coast licensed nuclear pharmacy, which must be up-and-running to synthesize the isotope in the dosage ordered.  Each dose is custom-ordered at least one week before the scheduled treatment.  The MIBG is then delivered to a shipping company that flies the frozen isotope in a lead-shielded container to San Francisco where it is delivered to UCSF.  The MIBG must then be thawed and assayed in a special lead-shielded room by the UCSF Nuclear Pharmacist.  The complex logistics of MIBG therapy are similar to launching a rocket!  So please be patient if a delay occurs.

Dealing with a malignancy is always terrible, even under the best circumstances.  But we hope that these tips will familiarize you and your family with what to expect about MIBG treatment in order to improve your experience at UCSF.

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5 Questions and Answers on Male Hypogonadism and Testosterone Deficiency

Male Hypogonadism (testosterone deficiency) is a hormone disorder in which the body does not produce enough testosterone. This condition affects 10% of all adult men and the majority of older men.

This post will review the symptoms, causes, and treatments of male hypogonadism, and will answer some typical questions from patients with this condition.

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Addison’s Disease

The adequacy of glucocorticoid replacement (hydorcortisone, prednisone) must be assessed clinically. A WBC (white blood count) with differential (the percentage of lymphocytes and polymorphonuclear (PMN) leukocytes) can help, since patients whose replacement dose is too high tend to have a relative lymphopenia (lower percent lymphocytes), while those on excessive doses tend to have a higher percent PMN leukocytes.

Patients receiving fludrocortisone (Florinef) can be assessed for adequacy of replacement by assessment of blood pressure and serum sodium (Na) and potassium (K). Sometimes these can be normal but patients may be under-replaced and not feeling completely well; assessment of plasma renin activity may help, since it tends to be elevated in patients who are not receiving adequate fludrocortisone.

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Hypothyroidism: Diagnosis & Treatment

Google and the UCSF Department of Medicine commissioned me to write a Knol entitled “Hypothyroidism.” I’ve included some excerpts here, but you may wish to see the entire knol, which provides more details and includes sections on hypothyroidism in children and pregnant women as well as myxedema crisis.

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Journal of Clinical Oncology Paper

This paper was published in the Journal of Clinical Oncology in September, 2009. My colleagues and I describe our experience treating 50 patients with high-dose 131I-MIBG for their malignant pheochromocytoma or paraganglioma.

Phase II Study of High-Dose [131I]Metaiodobenzylguanidine Therapy for Patients With Metastatic Pheochromocytoma and Paraganglioma (PDF)

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Embolization of a large secretory paraganglioma

My colleagues and I presented two papers at the Second International Symposium on Pheochromocytoma at Queens College, Cambridge University in October 2008. We describe the successful pre-operative embolization of a large secretory paraganglioma.

Poster: Embolization of a large secretory paraganglioma (PDF)

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UCSF MIBG Protocol

Here are the files for the UCSF Phase II high-dose 131I-MIBG compassionate use protocol for treatment of patients having malignant pheochromocytomas or paragangliomas.

    In order for 131I-MIBG therapy to achieve a remission for patients with malignant pheochromocytoma, the tumors must have sufficient uptake of MIBG on diagnostic scans to allow enough131I-MIBG to enter tumor cells. Treatment doses up to 500 mCi131I-MIBG can be given without cryopreserved blood stem cells. At higher doses, there is a significant risk of severe suppression of the bone marrow. However, peripheral blood stem cell leukophoresis and cryopreservation has made it possible to treat patients with malignant pheochromocytoma more aggressively with 131I-MIBG, since peripheral blood stem cells may be collected in advance and reinfused in the event of prolonged myelosuppression following high-dose 131I-MIBG therapy.

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    Diabetes Caused By Protease Inhibitor Therapy for HIV/AIDS

    Protease inhibitors refer to a group of medications used to stop replication of the HIV (human immunodeficiency virus) retrovirus. They are very effective medications and remain an essential element in the HIV/AIDS cocktail of drugs, also known as “HAART” (Highly Active Antiretroviral Therapy). AIDS is an acronym for “acquired immunodeficiency syndrome”.

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    Acromegaly & Gigantism

    Acromegaly refers to the clinical syndrome caused by excessive growth hormone (GH) in adulthood, after the closure of epiphyses (bone growh plates). GH produces many of its effects through the stimulation of insulin-like growth factor (IGF-I), produced in the liver and at epiphyses. Symptoms of acromegaly typically include the growth of hands and feet, the growth of jaw and brow, with coarsening of facial features. Bones grow thicker and the growth of spinal bone can cause spinal stenosis and serious neurologic problems. Affected individuals are usually very sweaty, and also have increased muscle mass and reduced subcutaneous fat. Carpal tunnel syndrome is common. Diabetes and hypertension commonly occur. Untreated patients have a reduced life expectancy due to cardiovascular complications.

    Gigantism refers to excessive growth in stature during childhood and adolesence, caused by excessive growth hormone. Affected children are much taller than expected for their age. Without treatment, such children eventually develop acromegaly in addituion to their gigantism.

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    Background: Prolactin is a peptide hormone that is produced and released from the anterior pituitary. The pituitary is an autonomous prolactin factory. The pituitary will produce increased amounts of prolactin automatically unless it is inhibited from doing so by dopamine, a hormone secreted by the adjacent hypothalamus; dopamine travels down the pituitary stalk to the pituitary gland.

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    Hemoglobin A1c Testing

    Hemoglobin A1c: Hemoglobin is composed of a tetramer of globin chains; two of the chains are alpha-globin (chromosome 16). Most adults have hemoglobin that is largely comprised of two alpha chains combined with two beta chains (chromosome 11) (alpha2beta2), called HbA. The exons that encode beta-globin are adjacent to those encoding delta-globin and gamma-globin. About 2% of most adults’ hemoglobin is a variant (alpha2delta2), called HbA2. Less than 1% of most adults’ hemoglobin in fetal hemoglobin (alpha2gamma2), called HbF. A portion of HbA becomes glycosylated during its formation; a stable variety of glycosylated hemoglobin is called HbA1c.

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    Hyperparathyroidism therapy with cinacalcet

    The tiny parathyroid glands are located in the neck and are usually located adjacent to the thyroid gland, hence the term “parathyroid”. There are usually four parathyroid glands, but there can be more, and they can sometimes lie in locations away from the thyroid, sometimes elsewhere in the neck or even in the chest (mediastinum).

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    Introduction to Pheochromocytoma and Paraganglioma

    Pheochromocytomas are uncommon tumors that arise from cells of the sympathetic nervous system and may secrete catecholamines (adrenalin). Such tumors are usually found within one or both adrenal glands (90%), but may arise in other areas of sympathetic nerve cells, and are then called paragangliomas. About 10% are found to be malignant at the time or immediately after the primary tumor is discovered. Another 5% of individuals with pheochromocytomas are later found to have malignant or recurrent disease. Interestingly, about 10% of such patients do not have hypertension at all or may have hypertension only during surgical procedures or very intermittently at which time a hypertensive crisis can occur.

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    Graves Disease Symptoms & Treatment

    Graves disease is the most common cause of hyperthyroidism in the United States.  Other causes of hyperthyroidism include multinodular goiter, toxic solitary nodules of the thyroid, and functioning thyroid cancer.  Rare causes for hyperthyroidism include TSH-secreting pituitary tumors, struma ovarii, and hCG-secreting trophoblastic tumors of the ovary or testis.  All of the latter conditions cause increased thyroid radioactive iodine uptake on scanning.  Hyperthyroidism without increased thyroid radioiodine uptake can be caused by subacute thyroiditis, an acute phase of Hashimoto thyroiditis,  thyroid hormone intake, and iodide-induced hyperthyroidism (due to kelp, amiodarone, x-ray contrast,  or potassium iodide).

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