Thyroidcancerhelp Yahoo Group
Dr. Ain served as one of the first ThyCa medical advisors and has been the ThyCa listserve medical advisor for over 12 years. He now runs his own Yahoo listserve to service thyroid cancer patients’ specific questions. The group is called ThyroidCancerHelp. To open the ThyroidCancerHelp Yahoo group in a new browser window, please click this link.
Please find below, answers to the most common questions on ThyroidCancerHelp (to date) which have been arranged alphabetically. Use the alphabet below to browse topics. To search key words, use your browser's FIND function. The original questions and answers are archived on ThyroidCancerHelp which any member may access.
Disclaimer
The information contained on this site is intended for educational purposes only. It is not intended, nor should it be construed, as specific medical advice or directions. Any person viewing this information is advised to consult their own physician(s) about any matter regarding their medical care.
TOPICS (answers only)
A B C D E F G H I L M N O P R S T U V X Z
99m-Tc is not used in thyroid cancer patients
99mTc-pertechnetate should not be used in patients with known thyroid carcinoma. It is only used for scanning thyroid glands in patients with thyroid glands that are still in their neck. Although convenient for the nuclear medicine physician, it is generally inferior to radioactive iodine for scanning thyroid glands.
—ThyroidCancerHelp, July, 2007
A
Age of diagnosis as a risk factor
There are a number of epidemiologically studies performing something termed "multivariate analysis" to try to see what patient features have predictive value in determining outcome risk.
The many, many published studies are usually retrospective and thus limited in their power; however, a majority have determined common risk factors: Tumor size: the bigger the tumor the higher the risk; Tumor invasion: if it invades tissues outside of the thyroid beware; Distant metastases: seems obvious, but if it spreads to your lungs or brain, it's not good; Male sex: on average, men who get thyroid cancer have worse outcomes than women with the same extent of disease; Patient age: dedifferentiated tumors are more likely to be discovered in older people. There is a difference between studies in the particular age. Some studies say that it is 45 years, some say 50 years, some say older. Since I'm in my 50's, I'd prefer not to refer to this age as "older."
There are a number of other factors, but I think that the picture is clear.
—ThyroidCancerHelp, August, 2007
Alcohol ablation of recurrent tumor
When searching for the site(s) of residual/recurrent thyroid cancer, known to be present because of increased thyroglobulin, many methods are often used. Ultrasound is very useful in the neck region, particularly since more than half the time, there is persistent disease in this region. When a suspicious node or mass is found, particularly when verified by fine needle aspiration biopsy, there are several approaches. In most circumstances, we advise that an experienced surgeon approach the lymph node compartments in that region of the neck, not only to remove the particular mass/node but also to remove additional lymph nodes that often contain disease not made evident on the ultrasound. If these sites of disease had already been confirmed as no longer taking up radioactive iodine, follow-up treatment with external beam radiation is often a consideration.
Injecting alcohol (ethanol ablation) into the cancer-containing lymph node or mass to destroy it is a method that we sometimes apply when the patient is too fragile to tolerate another surgical procedure or the site of the tumor is in a region that is not easily approached by surgery. It has limitations in that it presumes that the ultrasound has been definitive in defining all of the tumor sites in that region. It also requires fairly definitive confidence in the biopsy diagnosis that the site contains tumor. There are often many alternative approaches to dealing with this problem and each of them have their strengths and weaknesses.
—ThyroidCancerHelp, October, 2007
Amifostine and XRT
Amifostine should not be used with I-131 therapy. On the other hand, although it might be helpful to decrease salivary gland damage when used with external beam radiotherapy, there are a number of issues with its use that should be carefully discussed with the radiotherapist.
—ThyroidCancerHelp, September, 2007
Anaplastic thyroid cancer: A primer
Much of my research is on the cell biology and treatment approaches for anaplastic thyroid cancer (ATC). It is very important to have the pathology re-checked by an experienced thyroid pathologist since it is very common that less-experienced (in thyroid cancer) pathologists make errors in this diagnosis. There are several points that should be made concerning this type of thyroid cancer:
1) There is sufficient evidence to say that anaplastic cancer is a terminal dedifferentiation of a pre-existing papillary or follicular thyroid cancer. In my experience, the most likely type of cancer to undergo an anaplastic transformation is tall cell variant papillary thyroid cancer, although other types can do so. There are a number of genetic changes in the thyroid cancer that are thought to underlie this process. Typically, anaplastic thyroid cancer arises in the context of a pre-existing differentiated cancer that has not been excised or treated for a very long time. Sometimes this cancer has independently spread through the body and there might end up being “two types” of thyroid cancer existing simultaneously in the same person. We tend to focus exclusively on the anaplastic thyroid cancer since this is the most dangerous one. In the very rare (unfortunately) individuals who survive their anaplastic cancer more than two years, we consider the ATC to be “cured” because in nearly all cases (if correctly diagnosed as ATC) they would not have survived for two years if the ATC was still present. In such rare cases, the patient now needs to have their papillary or follicular cancers (that had been clinically ignored) independently dealt with, using I-131 scans and therapy. In some particular circumstances, this may be done after only a year, especially if the thyroglobulin is significantly increasing despite suppression of TSH with levothyroxine.
2) Typically, ATC does not make thyroglobulin (or very little, if any). If there is ATC present, the thyroglobulin actually represents the co-existing papillary or follicular thyroid cancer and does not reflect the presence or absence of ATC tumor. We tend to ignore the thyroglobulin level until we are confident that the ATC has been dealt with and it is time to deal with the underlying papillary or follicular cancer.
3) Appropriate treatment of ATC requires an excellent surgeon to do as complete a removal of the thyroid tumor and as much of the thyroid gland as is possible. Following this surgery, it is VERY necessary to undergo a full course of external beam radiotherapy (XRT), often using a hyper-fractionated approach. At this time it is important to do a complete “tumor staging”. This consists of CT scans of all major areas of the body (contrast SHOULD be used in the context of ATC). This is for the purpose of searching for any evidence of tumor sites in the body. It is exceedingly rare for anyone with ATC to avoid having such tumor show up. These CT scans should be repeated every 3 weeks for the first 3 months, then monthly thereafter (until tumor sites are found or two years pass; the second year, the CT scan interval can be every two months).
4) When these CT scans document evaluable sites of ATC tumors (usually in the lung or liver), then it is time to undertake chemotherapy. There are no chemotherapy drugs with excellent and reproducible activity against ATC cells. Of all of the available standard drugs, taxanes (paclitaxel (taxol) and taxotere) have the greatest activity, but it is not for sure in any particular patient. None of these drugs can be given without significant potential side effects and it is unreasonable to take them unless they demonstrate their effectiveness in the patient. For that reason, it is important to avoid giving them unless there are clear and objective clinical endpoints. That is why my best advice is to wait until there is objective evidence (for example CT scans showing new lung nodules) so that the benefit of these drugs can be verified by seeing the nodules shrink or disappear. In the absence of such objective clinical endpoints, a significant number of patients would get toxic effects of therapy without benefit and with no idea of when to stop the treatment. Considering the consequences of toxicities from ineffective chemotherapy drugs, it's better to wait than to "spin your wheels in the mud."
5) Alternatively, there are occasionally clinical trials for ATC; however, most such trials still require the presence of "evaluable" disease before starting their experimental agent. It is critical to enlist the assistance of an oncologist to search the National Cancer Institute PDQ Database to see if there are any reasonable clinical trials that might be appropriate.
6) Every week or so, I receive phone calls from physicians around the globe to discuss their patient with ATC and ask for suggestions and education regarding treatment options. Although I do not typically see such patients in my own practice, it is a very reasonable opportunity to have your physician(s) contact me at 800-888-5533 (PHYSICIANS ONLY) to discuss the situation.
7) The final message is that "time is clearly of the essence." Waiting (sometimes even by a week or more) can limit the treatment options and alter the outcome. You should use your primary care physician to call specialists directly. Scheduling clerks and nurses generally have absolutely no inkling of the urgency of this matter. Any medical or surgical referral should evolve through a direct telephone call from your physician to the consultant so that the issues are clearly understood and so that there is as little delay as humanly possible.
—ThyroidCancerHelp, February, 2008
Antiangiogenesis in thyroid cancer
Antiangiogenic therapy is indeed a viable direction to treat rapidly proliferative non-iodine-avid thyroid cancers. My laboratory has been pursuing this direction for several years. We've just published a reasonably successful clinical trial using thalidomide
for this purpose: Ain KB, Lee C, Williams KD 2007 Phase II Trial of Thalidomide for Therapy of Radioiodine-Unresponsive and Rapidly Progressive Thyroid Carcinomas. Thyroid 17:663-670.
In addition, we've been very impressed with the results, so far, in our ongoing clinical trial using lenalidomide (Revlimid; a derivative of thalidomide). The "answer" to this clinical problem will likely eventually involve multiple new medications.
—ThyroidCancerHelp, September, 2007
Anti-angiogenesis, research into
It is most unfortunate that sometimes thyroid cancer spreads to parts of the body that make them particularly dangerous and difficult to treat. It is also very true that thyroid cancers tend to be highly vascular, that means that they induce the body to provide many blood vessels to feed such tumors. This can make surgery very difficult and dangerous, particularly when the tumor involves bones or regions in the spinal cord or brain.
My laboratory has been involved in research in this area for nearly a decade, trying to find drugs that will block the formation of feeding blood vessels to these tumors and cause the tumors to stop growing. Our studies have been reasonably successful, resulting in a successful clinical trial using thalidomide as an antiangiogenesis (against the growth of new blood vessels) drug to keep metastatic thyroid cancers from growing (Ain KB, Lee C, Williams KD 2007 Phase II trial of thalidomide for therapy of radioiodine-unresponsive and rapidly progressive thyroid carcinomas. Thyroid 17:663-670.). Although promising, thalidomide was not the best drug considering its side effects.
We systematically tested other agents, particularly new drugs that had been chemically modified from thalidomide, using human thyroid cancer tumors grown in nude mice in our laboratory (these mice are genetically altered so that their immune systems do not reject the human cells). We found that lenalidomide (Revlimid) was particularly effective and have been conducting a phase 2 clinical trail with this drug for nearly two years. The preliminary results will be reported at an oncology meeting in late May, but are excellent enough to warrant additional clinical trials in the near future. Unfortunately, it seems that thyroid cancer metastases at different body sites respond differently, with the most responsive tumors being in the lungs or liver.
Antiangiogenesis drugs have not yet been used pre-operatively to permit the surgery to be performed easier, partly because they do not destroy existing blood vessels, but rather keep tumors from recruiting new blood vessels. Because of this, we frequently have the radiologist thread a tube into the blood vessels that feed some of these tumor sites and try to block the blood vessels by injecting special substances, a process called embolization. There is another class of experimental drugs called "tumor vascular-targeting agents" that are intended to destroy existing blood vessels feeding tumors. Unfortunately, there is not yet sufficient effectiveness of this drug approach.
Research efforts continue at my lab and at other labs. We are all working hard to increase the number and effectiveness of our treatment options. For some patients, the answers will not come soon enough.
—ThyroidCancerHelp, January, 2008
Anti-thyroglobulin antibodies (a primer on)
Around 20% of thyroid cancer patients have auto-antibodies against their own thyroglobulin. These antibodies tend to interfere with the accurate measurement of thyroglobulin. The typical medical condition associated with anti-thyroglobulin antibodies is called Hashimoto's thyroiditis.
Hashimoto's thyroiditis is very common, afflicting nearly 20% of women and 10% of men. For that reason, it is very common to have coincidental thyroid carcinoma and Hashimoto's thyroiditis. One of the hallmarks of Hashimoto's thyroiditis is the production of antibodies directed against parts of the thyroid, particularly the thyroperoxidase enzyme and thyroglobulin.
Antibodies against thyroglobulin interfere with the ability of all currently known blood tests to accurately measure the actual thyroglobulin level. They tend to make the tests register a lower thyroglobulin level than actually exists. As you know, thyroglobulin levels are extremely important to ascertain the presence of thyroid cancer after a person has had a total thyroidectomy and radioactive iodine therapy. For this reason, a low or immeasurable thyroglobulin level, in the presence of anti-thyroglobulin antibodies, does not provide any confidence for the absence of thyroid cancer. On the other hand, when thyroglobulin levels are elevated in the presence of anti-thyroglobulin antibodies, particularly when these levels increase in response to hypothyroidism, this is believable evidence of the presence of thyroid cancer.
The body's immune system is carefully programmed to produce antibodies against foreign invaders, such as bacteria, viruses, and toxins. When vaccines are given to people, they consist of inactive samples of the virus or toxin that are injected to produce an antibody response from the white blood cells. These vaccine-stimulated antibodies protect the person against that specific virus or toxin. The white blood cells retain a memory regarding the production of this particular antibody, the "amnestic response," which permits them to rapidly make antibodies whenever the virus enters that person. Unfortunately, when the white blood cells endure a long period of time without seeing that particular virus, they "forget" how to make that specific antibody. That is the reason why booster shots are given to restore the vaccine's protection [for example, the tetanus vaccine].
If you understand this, you could see how a thyroid cancer cell, making thyroglobulin, can function as producing "booster shots", enhancing anti-thyroglobulin antibody production in patients with Hashimoto's thyroiditis and thyroid cancer. For those patients who are truly free of this thyroid cancer, the absence of these "booster shots" permits the memory of the white blood cells making this antibody to fade and the antibody go away.
This is the reason how we can use the persistence of anti-thyroglobulin antibodies to suggest the persistence of thyroid cancer, and the loss of these antibodies to suggest the absence of remaining thyroid cancer. Likewise, should these anti-thyroglobulin antibodies suddenly appear (provided that this is not due to lab error) it is likely to signify a proliferation of persistent thyroid cancer cells.
—ThyroidCancerHelp, September, 2007
Anti-thyroglobulin antibodies (persistence of)
The presence of measurable thyroglobulin in the blood, for people who have had their thyroid glands and thyroid cancers removed surgically and have had the remains of those items properly destroyed with radioactive iodine, indicates persistent/recurrent thyroid cancer. Unfortunately, nearly one quarter of thyroid cancer patients produce antibodies against their own thyroglobulin that interferes with all laboratory tests seeking to measure the thyroglobulin level. Most of the time, these antibodies cause the thyroglobulin level to appear lower than it actually is.
Over time (several years), if all thyroid cancer has been effectively eliminated, consequent to successful treatments and good fortune, the level of anti-thyroglobulin antibodies will diminish and disappear as the "memory" B-lymphocytes start to "forget" their blueprint for making anti-thyroglobulin antibodies. The loss of those antibodies, with zero thyroglobulin levels, is very reassuring that there is no evidence of persistent thyroid cancer. Likewise, the persistence of these antibodies, is suggestive of persistent disease (although it may take 2 to 4 years for the antibodies to disappear in the absence of disease).
—ThyroidCancerHelp, July, 2007
Armour thyroid extract: do not use
Thyroid cancer patients should not be on desiccated thyroid extract (Armour thyroid). Permit me to quote one of my earlier postings from long ago:
Levothyroxine (T4) is the major product of the thyroid gland and is essentially a prohormone with minimal (if, debatedly, any) activity of its own. It has a long and stable half-life in the blood (one week) and is transported into cells where it is converted into T3, which directly interacts with receptors which bind DNA and regulate genes. All of this has been well-studied and constitutes a vast medical and molecular biology literature. For patients without thyroid glands, the ingestion of a pure levothyroxine product provides ALL of the necessary thyroid hormone products consequent to normal metabolic and enzymatic bodily processes.
There is absolutely no conceivable role for taking Armour thyroid extract or mixtures of T3 and T4. Most of my colleagues and I would be happy if the FDA removed these items from production. Thyroid extract is a mixture of T4, T3, thyroglobulin, and many other breakdown products with erratic pharmacokinetics and nearly impossible to accurately titrate for suppression of TSH. There is no magical or supernatural or any advantage to this animal product. Armour thyroid provides a mixture of hormones that are produced in pigs, not in humans. The only reasonable medication is pure levothyroxine (choose your brand). Cytomel is useful for the first four weeks of the six-week levothyroxine withdrawal period in preparation of I-131 scans and or therapy. It also has very limited utility for supplemental treatment of myxedema coma unresponsive to levothyroxine. (A medical study from a couple of years ago suggesting T3 supplementation of levothyroxine therapy for hypothyroidism is not generally accepted by thyroidologists, for many good reasons, and has been debunked in multiple follow-up clinical trials.)
There is nothing gained by choosing medications based on "natural" extracts or processes. Such items, frequently found in "Health Food" stores, are often dangerous, impure, untested, and of unproven value. Their designation as a "natural" product merely protects their manufacturers from having to justify their purity, safety, and efficacy to the FDA (which is empowered to protect us from "pharmaceuticals" only), permitting great financial profits at the expense of the public. Many new drugs, such as Taxol (from the Yew tree), and old drugs, such as penicillin (from mold), come from sources in nature. In comparison to "Health Food" shenanigans, these natural products are stringently purified and tested prior to making them available as medications. It is possible that a few of the "natural" products may have a fraction of a percent of a useful agent, mixed in with far larger quantities of toxic and useless "natural" chemicals. Next time you go to these unregulated "Health Food" stores, consider that the poison on the darts used by various native peoples did not come from a drug store. Finally, in the wake of experience with "mad cow" disease in England and the known presence of prion diseases in cows, sheep, humans, and other mammals, anyone who would knowingly take an animal product over a chemically pure synthesized compound should have their head examined (for spongiform encephalopathy).
—ThyroidCancerHelp, July, 2007
B
Barium and iodine
Swallowed barium will not interfere with radioactive iodine scans or therapies. On the other hand, sometimes radiologists use an oral contrast agent that contains stable iodine and WILL interfere. Make certain that "barium" truly is barium.
—ThyroidCancerHelp, July, 2007
BRAF mutations in papillary thyroid cancer
The recent discoveries regarding BRAF gene mutations have to do with a protein in cells that controls certain biochemical pathways related to cell growth and behavior. A portion of patients with papillary thyroid cancer have a mutation of this gene that causes its regulatory pathway to be excessively "turned on" possibly accounting for more aggressive tumor behavior. These are just a few of many discoveries regarding various tyrosine kinase pathways that are likely to be exploited in future new therapies. Aside from analyzing for such mutations in needle biopsies of thyroid nodules (something that may be done in the future) or looking for these mutations in resected tumors for prognostic information, analyses for such mutations do not yet have any direct clinical application.
—ThyroidCancerHelp, January, 2008
Breast feeding and thyroid cancer
In a person that is free of any evidence of persistent thyroid cancer (clean I-131 whole body scans with no measurable thyroglobulin, as well as clean chest CT scans and clean neck ultrasounds) and is not planning to have radioactive iodine scanning for at least a year or more, breast feeding is fine and of no ill consequence to the child or to the mother. On the other hand, lactating women should not undergo radioactive iodine scans or therapy until their child has been completely weaned and the breasts have had sufficient time to completely "dry up."
—ThyroidCancerHelp, June, 2007
Biopsies (don't ask too much from)
Fine needle biopsies of thyroid nodules are not capable, nor intended, to do much more than determine whether there is a reasonable likelihood that a nodule is malignant. To demand more details than that is similar to demanding that the cover of a book reveal everything that is written inside.
Sometimes a biopsy is able to reveal that a tumor is an anaplastic cancer, a medullary cancer, or a thyroid lymphoma. In such circumstances, knowing that it is anaplastic can prompt a careful evaluation for disease extent prior to the surgery to permit proper treatment planning. Likewise, knowing that it is a medullary thyroid cancer can prepare the surgeon to do a very complete bilateral neck dissection, necessary for the best chances for treatment. If it is a lymphoma, the surgery can be avoided and the treatment would be very effective using just external beam radiotherapy and chemotherapy. For most other thyroid cancers, papillary and follicular and the respective variants, merely knowing that the nodule is an adenocarcinoma is fully sufficient and dictates the need to remove the thyroid gland surgically.
It is important to avoid demanding more information from a procedure, than the procedure is able to provide, particularly if such information is of no additional benefit.
—ThyroidCancerHelp, August, 2007
Biopsies—thyroid surgery
A biopsy of a thyroid nodule is a wonderful tool, but imperfect and limited. It's inappropriate to ask more of this technique than it is equipped to deliver. There are only three reasonable outcomes of a thyroid biopsy that has been properly performed and contains sufficient numbers of cells to evaluate: clearly benign, clearly malignant, and indeterminant/suspicious. Only patients with those nodules that are clearly benign by biopsy should avoid having thyroid surgery.
—ThyroidCancerHelp, September, 2007
Bone metastases from misdiagnosed thyroid cancers
There is a classic type of thyroid cancer mismanagement that is much too often repeated. It starts with the misdiagnosis of a follicular thyroid carcinoma as a benign follicular adenoma. Many years later, the follicular carcinoma, that had already been metastatic to distant sites in the body before the surgery, grows large enough to be discovered. Sometimes it is discovered as a tumor growing on a rib or in the spine. Sometimes it is found as a tumor growing in the brain or in the lung. Once this metastatic tumor is found and biopsied, revealing itself to be a thyroid cancer, the proper steps are crystal clear. Unfortunately, it seems that such clarity is not apparent to some physicians.
There is NO ROLE for any further thyroid scans on the remaining thyroid lobe. It needs to come out ASAP, regardless of whether it harbors additional cancer or is completely normal thyroid tissue. This is because it is impossible to effectively administer radioactive iodine for therapy or scans if it is left in place. Next, if there is a tumor on bone, it should be surgically removed. This is necessary, even if it is fairly extensive, if at all possible. Likewise, large tumor masses in the lungs (if localized to a small portion of one lung) or tumor masses of any size in the brain should be removed or subjected to stereotactic radiosurgery ("gamma knife"). External beam radiation for bone metastases, instead of surgery, is usually inappropriate.
Once there is surgical clearance of macroscopic disease, the stage is set for radioactive iodine therapy (ideally, high dose therapy utilizing dosimetry). Knowing this in advance, the wise physician will assiduously avoid any use of CT contrast dye. Instead, MRI scans with gadolinium can be equally effective without interfering with I-131 treatment. I could, and have, write entire chapters on the management of this problem. Very, very sadly, as in the case above, the treating physicians have no inkling of the appropriate course.
—ThyroidCancerHelp, August, 2007
C
Calcitriol is preferred over Zemplar
There is no reason that I can imagine for someone with hypoparathyroidism to be treated with Zemplar (paricalcitol). It has the same mechanism of action as calcitriol and is just as useful, but far more expensive. The retail price (in Kentucky) for 30 pills of 1 mcg Zemplar is $235.00. The retail price for 30 pills of 0.5 mcg calcitriol (equivalent to 2 mcg Zemplar) is $60.00. There is no reason to pay more than four times as much for no added benefit. The appropriate dosing interval of both Zemplar and calcitriol is once per day.
Many people with hypoparathyroidism have only a partial parathyroid hormone deficiency, requiring less calcitriol and calcium than someone with complete deficiency. When the vitamin D analog (calcitriol) dosage is excessive, less calcium is needed; however, this is usually at the expense of an excessive phosphate level. The best ratio is to use the least dose of calcitriol and sufficient calcium (taken three to four times daily) to keep the IONIZED calcium in the low normal range.
—ThyroidCancerHelp, October, 2007
"Capsules" in thyroid cancer pathology reports: A primer
To avoid current and future confusion, I'll briefly discuss the issue of "capsules" as it pertains to thyroid cancer pathology.
Capsulation refers to the fibrous (collagenous) tissue that encircles and encloses a structure. There are two, very different, types of capsules when discussing thyroid cancer pathology: tumor capsule (covering the thyroid tumor inside the thyroid) and thyroid capsule (covering the entire thyroid gland).
Some thyroid tumors are covered by a "capsule" of fibrous tissue. In the case of FOLLICULAR thyroid tumors, it is important to note whether any of the tumor cells have penetrated into and through this tumor capsule. If there is even a single area of tumor capsule invasion OR a single area in which the tumor cells have invaded into a vein or artery (vascular invasion), then the tumor is known as a FOLLICULAR CARCINOMA. If not (requiring the ENTIRE tumor to be carefully examined) it is called a FOLLICULAR ADENOMA. This is also the way that Hurthle cell neoplasms are characterized: even a single instance of capsular or vascular invasion distinguishes a Hurthle cell carcinoma from a Hurthle cell adenoma. This is a very tedious and meticulous assessment, if done properly. PAPILLARY CARCINOMAS are NOT distinguished as being cancers based on tumor capsular invasion and the presence or absence of a tumor capsule merely adds to the description of the papillary cancer.
On the other hand, the THYROID CAPSULE is often not much of a definitive capsule, often comprised of a very thin layer of fibrous tissue, but it can be very important in discerning behavior of thyroid cancers. Thyroid cancers of any type (papillary, follicular, medullary, etc.) that "eat their way" through the thyroid capsule are frequently found to be particularly aggressive. If there is extensive thyroid capsular invasion, particularly if the tumor also invades surrounding muscle or vital structures (esophagus, trachea, nerves, etc.) then there is a higher risk of distant spread of the tumor (lung, bones, liver, brain, etc.).
Thus, sometimes the assessment of invasion of the tumor capsule can add to the diagnostic classification of the tumor, whereas the assessment of thyroid capsular invasion provides important prognostic information.
If a thyroid tumor is described as non-encapsulated, it merely means that this particular tumor has no evidence of a fibrous capsule. It is very different from a description of having a capsule that has been invaded. Do not confuse these issues.
ALL of the variants of papillary thyroid cancer are dealt with in the same fashion in regards to the tumor capsule. The presence of absence of a tumor capsule is merely descriptive for all of the papillary variants, since the diagnosis of malignancy for such cancers is based on the appearance of the cell nucleus, not on whether there is invasion of the tumor capsule. Also, there is NO difference in the prognostic risk between encapsulated and non-encapsulated follicular variants of papillary thyroid cancer. The determinants of risk are related to the size of the tumor (bigger is worse), the extent of nodal metastases (more is worse), and the presence of invasion through the THYROID capsule into surrounding tissues (such invasion is worse).
—ThyroidCancerHelp, November, 2007
CT contrast dye and radioactive iodine
It is completely inappropriate to use CT contrast dye in any person planned for radioactive iodine scanning or therapy within 8 months. The stable (non-radioactive) iodine from the CT dye can persist within a person for 2 to 12 months and it is totally unpredictable how long it will take to clear in any particular individual. To find out if one has cleared the stable iodine from a preceding contrast dye exposure, you should follow a strict low iodine diet for one week and collect a complete 24 hour urine for the last day of that week, having this analyzed for urine iodine (by the Mayo Clinic Laboratory in Rochester, MN). Optimal 24 hour urine iodine values total 50 micrograms for the entire 24 hour sample; however values under 100 mcg are sufficient.
There is NO NEED for contrast dye for a CT scan of the chest, unless the physician is specifically looking within the mediastinum (the area around the heart). If contrast dye is necessary for a body area (such as the liver) then an MRI is better, since MRI dye (gadolinium) does not contain stable iodine.
It's quite sad to compromise the effectiveness of a treatment regimen with radioactive iodine, merely to take a picture with a CT scan. On the other hand, if a person is adequately prepared for this radioactive iodine scan (elevated TSH and low iodine diet) and has a negative study despite an elevated thyroglobulin, it is very likely that the tumor is unable to concentrate iodine and this particular modality should be abandoned.
—ThyroidCancerHelp, June, 2007
CT contrast dye exposure before thyroid surgery
Physicians are often well-intentioned in their efforts to "help" patients, but unfortunately their efforts end up counterproductive. Ultrasounds permit assessment of nodules without contrast and biopsies are the only way, short of surgery, to appropriately assess thyroid nodules. If CT contrast dye has been used and thyroid cancer (necessitating radioactive iodine therapy) is later discovered, then it's a matter of weighing a delay in I-131 treatment until the urine iodide levels are low enough or proceeding ahead. The only way to make such choices is to consider the findings at the time of surgery. Until that time, all speculation is useless.
—ThyroidCancerHelp, October, 2007
CT contrast dye (oral vs. intravenous)
I have evaluated patients after oral (likely the same as rectal) iodinated contrast material, as well as those who have received betadine skin preparations during their surgery. The data shows that these sources of stable iodine are handled much like dietary iodine and are cleared by two weeks. On the other hand, intravenous stable iodine from contrast dye can remain for many months.
—ThyroidCancerHelp, September, 2007
CT contrast dye, PET scans, and I-131
CT scan contrast dye can interfere with radioactive iodine uptake for 2 to 10 months. The only way to verify that sufficient time has passed to eliminate such interference is by following a low iodine diet for one week and obtaining a 24-hour urine iodide measurement (done by the Mayo Clinic labs) on the last day of the diet. A total urine iodide level of less than 100 mcg shows that the interference has passed.
18-FDG, used for a PET scan, will not interfere with I-131; however, any iodinated contrast used for the CT fusion component certainly will. Oral contrast will interfere for only 2 weeks; but IV contrast will interfere for 2-10 months.
—ThyroidCancerHelp, September, 2007
CT scan contrast dye and radioactive iodine use
Here is the simple information on this:
Even a single use of iodinated CT contrast dye (and ALL intravenous CT contrast dye IS iodinated, without ANY exception) can cause non-radioactive (stable) iodine to persist in the blood in sufficient amounts to interfere with radioactive iodine scans or therapies for 2 to 12 months. If such dye has been used, inadvertently or unavoidably, we can determine when it has passed out of the system by measuring the iodine in a 24-hour urine sample while in the final day of a one-week low iodine diet.
CT scans of most parts of the body (with the exception of the chest) usually require contrast dye for optimum sensitivity. CT scans of the chest DO NOT need such dye because it is easy to evaluate the lungs for nodules (air-solid interface) without such contrast dye. For other body parts, MRI scans are perfectly fine and can freely use gadolinium contrast dye without any interference problem. Alternatively, ultrasounds are likewise useful for selected body areas.
On the other hand, should there be a medical emergency, such as the need to do a cardiac catheterization (using iodinated contrast dye) to avoid an impending heart attack or the need to find the sources of bleeding with a contrast CT scan after a motor vehicle accident, common sense suggests that the issue of radioiodine interference is secondary in consideration.
—ThyroidCancerHelp, June, 2007
CT scan dye contains IODINE
ALL CT scan contrast dye contains massive amounts of stable (non-radioactive iodine). A CT scan contrast dye without iodine has never been seen on this planet yet. A single dose of this contrast dye has the potential to interfere with all radioactive iodine scans and therapies, regardless of whether hypothyroid or Thyrogen preparation is used, for 2 to 10 months.
Unless it is an emergency, such as chest pain evaluation with a cardiac catheterization or an automobile accident needing a CT scan with contrast to evaluate internal bleeding, there is no need for contrast dye to be used if radioiodine is to be used within the critical interval. Necks can be evaluated with ultrasound or MRI (gadolinium contrast is OK). Chest CT scans do not need contrast to be informative. Abdomen and pelvis studies can be done with MRI. There is no excuse to senselessly waste exposure to radioactive iodine and compromise clinical care for optional diagnostic CT scans.
—ThyroidCancerHelp, September, 2007
Cytomel and levothyroxine combined for chronic therapy: DO NOT USE
I DO NOT advise taking levothyroxine and Cytomel (liothyronine) together in combination as chronic therapy. This is very ill-advised for any thyroid cancer patient. In addition, many well done studies have proven it to be of no advantage for hypothyroid patients.
The ONLY valid use of Cytomel in any foreseeable clinical situation is for the hypothyroid preparation for radioiodine scanning and therapy or for the transition from a hypothyroid state back to being on thyroid hormone.
—ThyroidCancerHelp, August, 2007
Cytomel doses (don’t make up missed)
Unlike levothyroxine, that has a long half-life of a week, Cytomel has a very brief half-life. For that reason, you should not "make up" missed doses of Cytomel.
—ThyroidCancerHelp, September, 2007
Cytomel is well tolerated
It is exceedingly rare that a patient cannot tolerate Cytomel as part of the levothyroxine withdrawal preparation for radioiodine scanning or therapy. Usually, the problem is that they are being given the wrong dosage of Cytomel. Although most people feel fine on 25 mcg twice daily, this may be too much for some people. In such cases, I have them split the tablet, making the dose 12.5 mcg, and take the pill three times daily (or more rarely, twice daily). This is taken for 4 weeks after thyroid surgery or stopping levothyroxine; then the Cytomel is stopped for 2 weeks (while on the Low Iodine Diet) prior to receiving I-131 for scanning or therapy or both.
Although it is possible that less time than 6 weeks from stopping levothyroxine (or thyroid surgery) is adequate to get the TSH higher than 30, this is VERY variable between people. In my very busy practice, it's not possible to schedule people months in advance with variable and uncertain lengths of preparation. Cytomel (used as described above) is useful for my scheduling, for nuclear medicine scheduling, for patients to work out with their employer, and to clearly define the time that driving and working will not be possible. It is very rare for this 6 week preparation to fail to elevate the TSH appropriately and my patients find it easier to have a limited period of hypothyroidism, rather than a drawn out period that is far longer without Cytomel.
I delayed answering the question regarding the article in Clinical Endocrinology (Vol 67, p839, 2007) by Leboeuf et al, until I had a chance to read it. I find it totally unconvincing and poorly done. In this study, the authors used an outdated psychological assessment scale (the Billewicz score) and seemed to show that patients on Cytomel with normal TSH levels were equally "hypothyroid" as patients off of all thyroid hormones with TSH values as high as 60. Unfortunately, their findings do not jibe with clinical experience and seem to be an artifact of using an inappropriate and insensitive assessment test. It's very important to assess the medical literature critically by carefully reading the entire paper, not just the brief abstract.
—ThyroidCancerHelp, December, 2007
Cytomel (liothyronine) is not appropriate chronic thyroid hormone therapy
Cytomel (liothyronine) is NOT appropriate chronic thyroid hormone replacement therapy. It's primary role is as a temporary thyroid hormone treatment during the early phase of levothyroxine withdrawal for radioiodine scans or therapy. It has such a brief lifespan in the blood, that your body is exposed to a roller-coaster of too much to too little hormone throughout the day and night. It is far more likely to evoke thyrotoxic problems and is not useful for the long-term suppression of the TSH level that is the hallmark of thyroid cancer management.
—ThyroidCancerHelp, June, 2007
D
Dr. Ain (direct help from)
I am happy to provide education and advice regarding any thyroid cancer (particularly anaplastic thyroid cancer), provided that the physician takes the initiative to call me directly, via my PHYSICIANS-ONLY paging service at 800-888-5533.
It is not possible for patients or their families to directly make appointments to see me. My practice has been closed to new patients for over a year. The only exceptions have been patients whose surgery has been performed by our surgeons at the University of Kentucky, patients entering my experimental clinical trials (referred via their physicians) or special
situations that are discussed with the physician. I am hopeful that I can re-open my practice in the future after I have been successful recruiting another physician to join me. At this time, the straw has nearly broken the camel's back.
—ThyroidCancerHelp, September, 2007
Dosimetry (an explanation of)
The most commonly used type of radioactive iodine dosimetry is a method for determining the maximal dose of radioactive iodine that can be administered to a particular person at a particular time that has a reasonable likelihood of being safe for that person (in terms of toxicity).
It involves preparing a person with a hypothyroid withdrawal and low iodine diet, then administering a small tracer dose of radioactive iodine (I-131) to swallow. Blood samples are obtained at specific intervals over 5 days and whole body radiation counts are obtained at the same intervals. Data obtained by measuring the radioactivity of the blood samples and body counts are entered into specific computations to model the radiation dose to the bone marrow and lungs, making sure that safe limits are defined. These calculations define a "safe" upper limit for the treatment dose.
The choice of whether to administer the maximal I-131 dose defined by the dosimetry study is a clinical decision of the physician based upon the nature and extent of the thyroid cancer being treated. Some times a lower dose is administered if the physician feels that a maximal dose is not necessary or safe for some reason. Sometimes the dosimetry study reveals that a dose that the physician was planning to give would be too high for safety in a particular patient. Thus the dosimetry calculation can sometimes make the physician choose an administered dose lower than previously intended.
The determination of what a patient should be given for a particular thyroid cancer treatment need remains an individual decision of the physician and is strongly influenced by the training and experience (or lack thereof) of that particular physician. Even among physicians who are considered "experts" in the field, the choice of treatment dose can differ by more than 10-fold for any particular circumstance. This is unfortunate and confusing for patients; however, I do not foresee any likelihood of a consensus regarding this that is based on valid principles. The best suggestion is to carefully choose your physician.
—ThyroidCancerHelp, October, 2007
E
Elevated thyroglobulin=persistent tumor
The presence of measurable thyroglobulin levels, even as low as 2, indicates the presence of persistent thyroid cancer.
There are FOUR common errors made in the followup of thyroid cancer: 1) permitting measurable thyroglobulin to be present without fully searching for the tumor source; 2) presuming that any persistent thyroid cancer MUST be in the neck despite the fact that it can spread to anywhere in the body; 3) presuming that thyroid cancer ALWAYS takes up radioactive iodine. (Sometimes, unfortunately, it loses this ability and will not respond to radioactive iodine for either therapy or scans. Sometimes it is "invisible" to the tracer dose of radioiodine, but able to be "seen" or treated with a larger treatment-level dose); and 4) placing any reliance in the assertions of any surgeon that he/she "got it all." (It requires a mass of at least 2,000,000 thyroid cancer cells in a lump for a surgeon to be able to see it and remove it during surgery. All thyroid cancer tumor masses of 1,000,000, 100,000,10,000, etc. etc. are too small to be seen by any human (or bionic) surgeon.)
As long as interference from non-radioactive iodine is ruled out, the presence of thyroglobulin in the blood should instigate a full assessment of the entire body using a variety of radiological techniques and sometimes using PET scans. Frequently, even after such efforts, the site of the persistent thyroid cancer remains undiscovered. In such situations, maintaining excellent suppression of the TSH with levothyroxine (keep TSH < 0.1) and maintaining a reasonable schedule (avoid bankruptcy or spending all your life in the CT scanner) of continued studies to search for this tumor is the best course with our current state of knowledge.
—ThyroidCancerHelp, June, 2007
External beam radiation (coping with)
External beam radiotherapy to the neck is no picnic. I tell my patients that it is a difficult mountain to climb, but at some point they'll reach the top, have an easier descent, and then reach level ground. It's VERY important to keep well hydrated, maintain nutrition, medications, and appropriate analgesia for a very painful sore throat. The course of radiation is typically given over a month. Each month following, there is considerable improvement in symptoms. For roughly two thirds of my patients, there is very little left of any side effects one year later. For the rest, there may be thickening of the neck tissues (that improves with stretching exercises), prolonged neck tenderness, or sometimes unusual sensations when rapidly bending the neck.
The key purpose of the radiation therapy is prevent disease progression and spread: a much more dangerous consequence than the effects of the radiation. It's very important to maintain communication with the radiation therapist and make use of his/her expertise in preventing or relieving side effects.
—ThyroidCancerHelp, December, 2007
External beam radiation vs. I-131 therapy
For differentiated epithelial thyroid cancers (papillary, follicular, and their variants), external beam radiotherapy is not typically advised unless there has been definitive previous demonstration of loss of radioiodine uptake in that particular person. Sometimes, when the surgeon notes a greater extent of residual disease than indicated by diagnostic radioiodine scanning (particularly when the thyroglobulin is discordantly elevated), a course of external beam radiation could follow the radioiodine therapy; however, it should not precede radioiodine therapy because it is likely to imperil the effects of radioactive iodine.
For tumor tissues that concentrate and retain radioactive iodine very well, an appropriately-dosed radioactive iodine treatment can impart >300 Gray of radiation per gram of tumor; however, the best that external beam radiation can do is little more than 60 Gray per gram.
—ThyroidCancerHelp, September, 2007
External beam radiotherapy for recurrent iodine non-avid local disease
When there is definitive macroscopic tumor recurrence in the neck that is definitely not able to concentrate radioactive iodine, it is best removed with surgery. As soon as there is sufficient wound healing, it is my practice to proceed with external beam radiotherapy (XRT). This is based upon the following factors: 1) XRT works best on microscopic tumor, rather than macroscopic tumor; 2) the surgeon is intrinsically unable to remove microscopic residual disease during the surgery and this is almost certainly still there; 3) should sufficient time elapse for the thyroglobulin levels to again rise, it is quite possible that there would be recurrent macroscopic disease that would require ANOTHER surgery prior to effective XRT (the situation would entirely recur again); and 4) if successful XRT is completed and later on the thyroglobulin increases, attention would be able to be focused upon other distant sites of potential tumor metastases.
Many physicians have very different ideas and approaches to this situation. Some are very meek about using XRT and need to be forced into it by rising thyroglobulin levels. I don't share such issues because I have a significant amount of experience with the successful application of this approach. Of course, in life and in medicine, there are no guarantees.
—ThyroidCancerHelp, August, 2007
F
Focal invasion vs. diffuse invasion
In its application to pathology, "focally" means that something occurs at a distinct and particular spot. This is the opposite of "diffusely", meaning that it occurs in a dispersed or widespread location. When this is applied to the assessment of thyroid capsular invasion, it refers to the tumor having grown through the fibrous layer that overlies the thyroid gland. This shows early invasive tendencies of the tumor and is a feature suggesting aggressiveness. Of course, if the tumor is diffusely invasive, this is a much worse situation.
—ThyroidCancerHelp, October, 2007
Follicular variant papillary thyroid cancers
Papillary thyroid cancers comprise a variety of subtypes, among them: follicular variant papillary thyroid cancer. This variant of papillary cancer shows a follicular pattern under the microscope, but has special features seen in the nucleus of the cancer cells that properly classifies it as a papillary thyroid cancer. Before 20 years ago, many of these types of thyroid cancer were incorrectly classified as follicular thyroid cancers. They behave the same as typical papillary thyroid cancers and the follicular appearance does not, by itself, suggest it to be any more aggressive.
Of course, those people with larger thyroid cancers, invasion of blood vessels, and spread to lymph nodes have a situation that suggests a greater risk for recurrence or spread of the tumor or of resistance to treatment. Nonetheless, just having those features does not mean that there will be difficulty in responding to therapy or that the treatment won't work. It means that nothing should be taken for granted and that there should be careful follow-up and verification of response, each step of the way. No one is ever "cured" of their thyroid cancer. Instead, we want to keep monitoring and evaluating each patient on a regular basis until they die of old age (a preferred endpoint). Since many of my patients are much younger than me, I tell them that I'll take care of them until one of us dies of old age (and they'll likely have to switch horses later in the race).
Interference with radioactive iodine therapy from non-radioactive (stable) iodine from CT scan contrast dye can occur if the dye had been given BEFORE the radioactive iodine, NOT after the radioactive iodine. However, the effects of this dye upon subsequent radioactive iodine scans or therapy may persist for 2 to 12 months.
—ThyroidCancerHelp, July, 2007
G
Graves' disease and thyroid cancer
The stimulation of thyroid tissue or involvement of eye muscle tissue that is seen in Graves' disease is consequent to auto-antibodies. The suppression of TSH used for treating thyroid cancer should not exacerbate the eye disease. On the other hand, since Graves' disease auto-antibodies can act on the TSH receptors, working just like TSH does, it is likely that suppressing TSH with thyroid hormone will not be quite as effective. This is because Graves' disease antibodies function just like TSH and they cannot be suppressed by thyroid hormone.
—ThyroidCancerHelp, September, 2007
H
Hair loss in female thyroid cancer patients (causes)
Although men have the advantage in regards to hair loss, because it is far more common for them and reasonably socially acceptable, it is clearly not appreciated or acceptable for women. Sometimes hair loss in women is due to autoimmune disease that targets the hair follicles. Sometimes, hair loss is caused by situations in which androgenic hormones are elevated, such as in polycystic ovary syndrome. Sometimes hair loss is "idiopathic", which simply means that we don't know why.
Thyroid hormone can transiently affect the hair, particularly when it is precipitously changed, such as during hypothyroid preparation for radioiodine therapy or scans. In that case, usually any hair that is lost is regrown and there isn't a net loss of hair. Merely being on higher than normal doses of levothyroxine, to suppress TSH and keep thyroid cancers from growing, does not alter the amount of hair on the head. If there is persistent thyroid cancer in the lung, unresponsive to radioactive iodine yet kept from growing because of the suppressive levels of levothyroxine, it would be terrible to decrease the levothyroxine and have no benefit in terms of preventing hair loss.
There are some women who need to be on a beta blocker (such as metoprolol, atenolol, propranolol, etc), often used to prevent rapid heart beat and nervousness from suppressive doses of levothyroxine. Very rarely, a beta blocker drug can cause significant amounts of hair to fall out. In such very unusual individuals, the hair will grow back within 2 to 6 months after stopping the beta blocker. This is so rare, that most physicians do not know about this unusual side effect. Never stop beta blockers suddenly (they need to be tapered slowly under a physician's guidance) to prevent the heart from beating severely fast.
Lastly, radioactive iodine DOES NOT cause hair loss at all. Any hair loss that seems to be associated with this is actually from the changes in thyroid hormone levels (see above).
—ThyroidCancerHelp, July, 2007
Hashimoto’s disease and thyroid cancer, co-existing
There are several studies, performed between 1998 and 2002 that analyzed prognostic features in patients with both thyroid cancer and Hashimoto's thyroiditis (AKA chronic lymphocytic thyroiditis). Most of them found that patients who had both of these diagnoses in their thyroid gland seemed to have a slightly less aggressive course of their disease; however, the effects are minimal and there are certainly patients in that category with very aggressive tumors. On the downside, if the person has Hashimoto's thyroiditis, then they have a greater chance of having anti-thyroglobulin antibodies that would impede the use of the thyroglobulin assay and complicate their disease status assessment.
—ThyroidCancerHelp, January, 2008
Hashimoto’s thyroiditis and suspicious nodules
Hashimoto's thyroiditis often proves to be a clinical dilemma. It is VERY common, involving almost one fifth of women and one tenth of men, much more common than thyroid cancer. When a gland has multiple nodular regions consequent to Hashimoto's thyroiditis, it is difficult to discern a difference from a gland with malignant nodules by its appearance on radiographic or nuclear studies.
The fine needle biopsy must be relied upon to provide this distinction. When the biopsy is interpreted as clearly benign, the issue is easy. When the biopsy is shown to reveal cancer, the decision for surgery is clear. However, in the presence of suspicious or indeterminate biopsy results and bilateral thyroid nodules, sometimes it is most appropriate for an experienced surgeon to perform a total thyroidectomy. In this way, the appropriate surgery for the cancer has been done. On the other hand, if there is no cancer (as long as the surgery has not caused any complications) there is a reasonable outcome since such a gland would be expected to eventually need thyroid hormone replacement treatment anyway.
—ThyroidCancerHelp, October, 2007
Hurthle cell adenomas (diagnosing)
Benign Hurthle cell adenomas are difficult to verify because they require the pathologist to fully document the ABSENCE of any evidence of tumor capsule or tumor blood vessel invasion (to make sure it's not a cancer). It is usually wise, for this type of diagnosis, to have an outside pathologist (preferably one with well-known expertise in thyroid cancer) to review the slides for a second opinion (a very, very good investment).
—ThyroidCancerHelp, July, 2007
Hypoparathyroidism and phosphorus
Hypoparathyroid patients do not typically need to limit their phosphorus intake in their diet unless their blood chemistry shows elevated phosphorus levels. Phosphorus levels and ionized calcium levels should both be monitored regularly by your physician to properly regulate your therapy. It is insufficient
to merely look at the total calcium level.
—ThyroidCancerHelp, December, 2007
Hypoparathyroidism: a primer
It's unfortunate that some physicians do not pay attention to appropriate management of hypoparathyroidism, nor teach their patients the necessary techniques and information regarding it. I do not know of any treatment that will affect basal ganglia calcifications consequent to hypoparathyroidism, but it's not clear that these are necessarily causing any attributable symptoms.
Below, is my "primer" on treating hypoparathyroidism. I hope that is proves helpful:
Therapy for hypoparathyroidism can sometimes be difficult. The usual dose of calcitriol (Rocaltrol®) is 0.5 mcg daily, but very rarely it can be increased to 0.75 mcg daily. Some patients need only 0.25 mcg.
The most important component of treatment is the oral calcium therapy. I use calcium carbonate (TUMS are a good source) because it is 40% calcium (500 mg of calcium carbonate contains 200 mg elemental calcium), whereas other calcium compounds are usually 20% or less calcium by weight. It is very important to split the calcium dose into every 8 hour or every 12 hour dosing. Sometimes it needs to be taken 4 times daily, but NEVER take all of the calcium together as a single dose. This is because the calcitriol works by helping the intestines absorb this oral calcium. Thus, it is important to split the dose so that there is always some calcium in contact with the intestines or the full 24 hours of each day. The dose must NOT be varied from day to day. Consistency is the essence of therapeutic success.
The quantity of oral calcium may vary from person to person. It's determined by measuring the IONIZED calcium on a consistent dosing of calcium carbonate and calcitriol (for at least 2 weeks) and making adjustments as needed. Some of my patients do well on as little calcium carbonate as 1000 mg (400 mg elemental calcium, equivalent to 2 regular TUMS) twice daily. Others may require as much as 5 TUMS (2500 mg calcium carbonate = 1000 mg elemental calcium) taken four times daily (total 4000 mg elemental calcium per day). Most people with hypoparathyroidism require something in between these extremes.
The target for therapy is an IONIZED calcium in the low normal range. This sometimes results in an elevated phosphorus, because the hypoparathyroid kidneys retain phosphorus in the blood and the calcitriol causes the intestines to also absorb more phosphorus into the blood. High phosphorus levels (which should be monitored by blood tests) are NOT good, particularly since they can cause kidney problems and make it more difficult to keep the calcium level up. For that reason, it is best to avoid dairy products as a source of calcium since they contain equally high phosphorus levels. Sometimes people have to analyze their diet to refrain from too many foods containing high phosphorus (a bit difficult to do since its in many otherwise "healthy" foods). Over time, the therapeutic regimen for treating the hypoparathyroidism should become second nature and easy, with almost never having any low calcium symptoms.
—ThyroidCancerHelp, July, 2007
Hypoparathyroidism (more on)
Paricalcitrol (Zemplar®) is an analog of calcitriol (Rocaltrol®) and is not particularly different in any way, aside from a slightly longer half-life and a greater cost. I find no reason for its use in my own practice and it would not be expected to produce any different effects or results.
One problem with some hypoparathyroid patients is that there is insufficient use of calcium carbonate. It is very rare for the dose of calcitriol to exceed a total of 0.5 mcg per day (I have only one patient on a dose as high as 1.0 mcg per day). Often a patient is not taking sufficient calcium on a regular basis. The dose of calcium carbonate can often be as high as 2000 mg taken four times daily (8000 mg per day, equivalent to 3,200 mg elemental calcium per day).
If such doses of medications are necessary to keep the IONIZED calcium levels normal, it is very unlikely that there would be any recovery of endogenous parathyroid function.
—ThyroidCancerHelp, August, 2007
Hypoparathyroidism (onset of)
Usually, hypoparathyroidism stemming from damage to parathyroid glands during thyroid surgery, reveals itself within a day or two from surgery.
Often the blood supply to these glands is temporarily compromised or the surgeon may have "re-implanted" a removed gland to a different location and the gland may not have resumed effective functioning for a number of days or weeks. In such cases, calcitriol and calcium therapy can be gradually tapered as the person becomes able to sustain their proper calcium levels without such help.
If there is permanent hypoparathyroidism, usually shown as continued need for medication beyond 4-6 months from the surgery, then it is very unusual for someone to recover their parathyroid function later on, although I have a few patients whose parathyroid glands recovered 1-2 years later. In situations in which all four glands have been removed, there is no such spontaneous recovery.
Late onset, months or years later, of hypoparathyroidism is very unusual and should suggest a need to investigate other causes, such as Vitamin D deficiency.
—ThyroidCancerHelp, August, 2007
Hypothyroidism (abnormal lab tests from)
When people are made hypothyroid for radioactive iodine and scanning, there are many blood tests that are caused to be abnormal due to the hypothyroidism. These transient abnormalities normalize after thyroid hormone treatment has been resumed for a month or more. Among these tests are: elevated cholesterol levels, elevated liver enzyme tests, lowered sodium, and slightly increased creatinine levels. It is usually inappropriate for such test abnormalities to prompt any diagnostic studies or therapeutic interventions unless extremely severe and associated with other clinical indications for disease.
—ThyroidCancerHelp, October, 2007
Hypothyroidism after scan/treatment without Cytomel
If, for some reason, a person chooses to be taken off of levothyroxine for 6 weeks before a radioactive iodine scan or therapy without using Cytomel to support them for the first 4 weeks, then they would be considered hypothyroid by 10-14 days after stopping the levothyroxine.
—ThyroidCancerHelp, November, 2007
Hypothyroidism and carpal tunnel syndrome
Carpal tunnel syndrome is a situation in which the nerves that pass through the ventral aspect of the wrists, the "carpal tunnel", are compressed by swelling of these tissues and the nerve damage causes pain and difficulty with finger movement and sensation. During periods of significant hypothyroidism, the extra swelling of the body tissues can exacerbate this carpal tunnel syndrome, making a minimal problem much more symptomatic and obvious. Typically, hypothyroidism itself does not create a carpal tunnel syndrome without there having been some pre-existing compromise of the nerves in the wrist. The treatment for this problem often starts with splinting of the wrists at night, but usually progresses to a surgical treatment in which the constricting tissues at the wrist are "released" by the surgeon.
—ThyroidCancerHelp, March, 2008
Hypothyroidism and driving
The following warning is verbally given to all of my patients, as well as a written copy, for when they stop their Cytomel in the hypothyroid preparation for I-131 scanning or therapy:
Please note that you will become significantly hypothyroid at this time and you are advised to avoid driving or operating dangerous machinery. Sometimes my patients do not heed this warning and this has been responsible for some auto accidents. Please note that auto accidents may involve other people besides the hypothyroid driver. It would not be wrong to call a severely hypothyroid driver an "impaired driver", similar to drivers taking some prescription medicines, alcohol, illicit drugs or other similar items which affect their driving abilities. Likewise, my hypothyroid patients who are nurses, pharmacists, physicians, or other professionals with like responsibilities, are advised to be aware of these problems when prescribing medicines, running IVs or making important decisions. A word to the wise SHOULD be sufficient.
Much is often said concerning whether people feel capable of driving while hypothyroid, despite our warnings to refrain. There is also the legal issue to consider. Should a hypothyroid driver be in an accident, particularly with loss of life occurring, even if absolutely blameless for causing the accident, they could be legally defenseless. Should an opposing attorney or prosecutor find out that the driver was hypothyroid, innocence would be hard to prove. This would be similar to finding the driver with an illegal blood alcohol level, despite an accident which they did not contribute towards. Likewise, should the insurance company find out about the hypothyroid status of the driver, it might be difficult (if not impossible) to obtain financial payments which would
have otherwise been easily obtained. There are may aspects of good common sense to consider regarding this issue.
It is both stupid and unethical to choose to drive a motor vehicle while you are impaired from hypothyroidism. Regardless of a cavalier attitude towards your own safety, such a situation would make you a societal menace, fully capable of drifting across the center line of the road and "taking out" a busload of children. The physician who knowingly prepares a patient for radioactive iodine scanning or therapy using hypothyroid withdrawal has an ethical duty to warn the patient not to drive or operate dangerous machinery. In fact, if the physician becomes aware that the patient is still doing dangerous activities while impaired, he/she has a duty to warn others. For example, when one of my patients was seen still working as a school bus driver despite TSH levels in \ the 100's, I was forced to contact the school district and had her suspended. In another case, a patient was still driving trucks loaded with tons of coal down Kentucky mountain roads while severely impaired. When the coal mine supervisor was not sufficiently impressed to have him stop, the state police were happy to oblige my telephone call. It is sad that there are some people that are so self-centered and uncaring of others that they would get behind the wheel and place innocent bystanders, including their own children passengers, at risk of death…. For a full discussion of the ethical issues, please see the forth-coming December, 2007 issue of THYROID. Dr. M. Sara Rosenthal will have a scholarly analysis of this problem in that issue.
—ThyroidCancerHelp, November, 2007
Hypothyroidism and temperature sensitivity
During periods of hypothyroidism, ALL body tissues are affected and perform suboptimally. After restoration of thyroid hormone levels, these body tissues recover their normal function. It would not prove fruitful to attempt to ascribe persistent symptoms of any sort to previous hypothyroidism if thyroid hormone levels are no longer low.
There are often a variety of causes for the sensation of fluctuating sensitivity to temperature. One cause that is sometimes related to thyroid cancer therapy is the consequence of radioactive iodine causing perimenopausal women to move into menopause a little sooner than if they had not been treated with radioiodine. For younger women, with normal ovarian function, the causes of temperature sensitivity changes are not so clear.
—ThyroidCancerHelp, February, 2008
Hypothyroidism, asymptomatic
Hypothyroidism, in preparation for radioactive iodine scans and therapies, is handled extremely differently by different people. Some feel as if they are on the brink of collapse, while others may not perceive too much difference. This is similar to the different responses of people when they drink alcohol; some can drink half a bottle of wine without much effect while others get tipsy after one glass. The hypothyroid preparation period may produce different symptoms from the first week to the second week, depending upon the length of time since the levothyroxine was stopped and Cytomel initiated. Nonetheless, it is very important to remember that, despite the absence of severe symptoms, hypothyroid individuals should not consider themselves safe drivers. For an academic discussion of this, please see Dr. M. Sara Rosenthal's recent publication:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieveanddb=PubMedanddopt=Citationandlist_uids=18177258
—ThyroidCancerHelp, January, 2008
Hypothyroidism (recovery is slow)
Once a person has become sufficiently hypothyroid for radioactive iodine scans or therapy, it takes some time to get back to normal. Even if the full dose of levothyroxine is re-started at 24 hours after the radioactive iodine treatment (and it should be), it takes a full month before thyroid hormone levels start to approach normal. It should not be a surprise to still feel tired and exhausted within only a week after starting levothyroxine.
To help with this, I usually start the full dose of levothyroxine and also a tapering schedule of supplemental liothyronine (Cytomel) over the first three weeks to boost the person into feeling better faster.
It is important to avoid operating motor vehicles until at least two weeks after starting levothyroxine since a severely fatigued hypothyroid driver is unlikely to be a safe one.
—ThyroidCancerHelp, August, 2007
Hypothyroidism slows down the gastrointestinal system
Although gastrointestinal issues can affect any of us at any time, there are certain ones that are more common during the period of time that thyroid hormones are stopped for radioactive iodine scans or therapies. The rate at which food is transported from the stomach to the small intestines, then through the small intestines and into the large intestines, and then finally out, is partly dependent on thyroid hormone.
When there is too much thyroid hormone, people note frequent bowel movements and sometimes feel that things just run right through them.
When there is too little thyroid hormone, such as during hypothyroid preparations, everything slows down. It is very common to have gastroesophageal reflux during this time. I often advise patients to sleep with the head of the bed elevated. The stomach takes longer to empty itself into the small intestine and this causes bloating, fullness, and again reflux. The slow transit of stools through the large intestines can cause significant constipation, bloating, and much odoriferous gas. Everything gradually gets better when the thyroid hormone levels
are restored.
—ThyroidCancerHelp, July, 2007
Hypothyroid preparation (duration of)
Proper hypothyroid preparations involve stopping levothyroxine for six weeks, with the first 4 weeks taking Cytomel twice daily. With this method, a person is only off of thyroid medication for the two weeks preceding the scan/therapy week (a total of just under 3 weeks off of thyroid hormone). Those patients undergoing a dosimetry study, for the purpose of implementing high dose (>200 mCi) radioactive iodine therapy, are off of their thyroid hormone for an additional week (for a total of 3 and 1/2 weeks) before thyroid hormones are resumed.
I cannot understand the reason why a patient would be denied the temporary support with Cytomel¨ (liothyronine) for the first 4 weeks or why they should be further delayed in resuming their medications under most circumstances. Please note that thyroid hormone therapy can be resumed 24 hours after radioactive iodine treatment, even though the post-therapy whole body scan may be performed at 2-10 days later, because this scan images radioiodine taken by the tumor during the first day only.
—ThyroidCancerHelp, August, 2007
Hypothyroid preparations and emotional changes
The usual method of hypothyroid withdrawal is to stop the levothyroxine 6 weeks before the scan or therapy, putting the patient on Cytomel for the first 4 weeks. This is to avoid hypothyroid symptoms for the first month. The usual dose of Cytomel is 25 mcg twice daily. Some people need a bit less (half the dose, 12.5 mcg, three times daily, for example). If this Cytomel dose is being taken, there should not behypothyroid symptoms for the first 4 weeks.
Cytomel produces a "roller-coaster" effect in some people with peaks and troughs of levels in the blood. This can cause some people to have mood swings. If this occurs, I often suggest that the person split the 25 mcg pill in half and take 12.5 mcg in FOUR doses spread out during the day.
Certainly, when the Cytomel is stopped, for the last 2 weeks of the 6 week withdrawal, as well as during the week of scanning and for 10 days after, while thyroid hormone levels are being restored (a total of around 4 weeks), there is a significant time of hypothyroidism. Although some people may have changing emotions during this period, most are somewhat depressed. It's a very good idea to warn family members and caregivers about the emotional effects of this period so that they can make allowances for inappropriate behavior and can give their greatest support.
—ThyroidCancerHelp, July, 2007
Hypothyroid symptoms can actually be from sleep apnea
There are a number of very common traps that people fall into. One of the most common is the assumption that tiredness always is a symptom of a problem with thyroid hormones.
The suppressed TSH is proof positive that each cell of your body is getting more than sufficient amounts of thyroid hormone. The proper question should be: "What else could be causing me to be tired?"
In a large number of cases, the answer is that the tiredness is caused by insufficient deep (REM) sleep caused by sleep apnea syndrome. The difficulties in getting sufficient oxygen while sleeping causes your brain to "wake you up" out of REM sleep, while not actually reaching a conscious state. The result is severe chronic sleep deprivation, often feeling as bad or worse than hypothyroidism. The answer is to have a formal sleep lab study performed and there are a variety of treatments once this diagnosis is confirmed.
There are a number of other causes; however, I've found sleep apnea to be severely undiagnosed and very common, particularly in overweight or snoring individuals.
—ThyroidCancerHelp, July, 2007
Hypothyroid symptoms DO NOT always come from Hypothyroidism
Nearly ALL of the symptoms that can be felt with hypothyroidism can be seen in totally unrelated conditions that are have normal thyroid hormone levels and are NOT hypothyroidism. They include: sleep deprivation (from sleep apnea syndrome), obesity, physical deconditioning, dry skin from heating systems, fibromyalgia, depression, etc., etc., etc.
The key to proper diagnosis and treatment is to first EXCLUDE hypothyroidism by verifying normal TSH and free T4 levels, then looking elsewhere for the correct cause of the symptoms.
—ThyroidCancerHelp, August, 2007
Hypothyroid, using antidepressant medications while
Hypothyroid preparation for radioactive iodine decreases liver function and kidney function in a temporary fashion. This means that many medications that are metabolized by the liver or excreted by the kidney may require dosage adjustments during such a period. For most medications, this temporary state of affairs does not require and changes; however, for others it may be important. For that reason, when using antidepressants or other medications, it's good to remind your physician of the temporary metabolic changes so that the medication can be more carefully monitored or adjusted if necessary. Antidepressant medications will continue to provide the desired activity, but people feel much better after restoring their thyroid hormone levels.
—ThyroidCancerHelp, October, 2007
I
I-123 as a scanning agent (I do NOT advise using)
I DO NOT advise using I-123 as an imaging agent for thyroid cancer. Its radiokinetics are much inferior to I-131 and it is far less informative. The issue of "tumor stunning" that is mentioned above is not very significant a problem and can be dealt with in far more effective ways than compromising the whole body scan with I-123…
[continued from another posting]:
The reasons why I-123 is not the best agent for imaging thyroid cancer using whole body scans follow:
1) The very brief half-life of I-123 results in significant loss of signal in target tumor metastases by 48 hours after dose administration, the optimal time for clearance of non-target tissues. This results in a poor signal-to-noise ratio at that time. The opportunity to view at 72 hours is completely lost with this isotope. To compensate for the rapid decay of I-123, images are often taken at 24 hours; however, there is far too much background at that time to distinguish key areas, such as diffuse pulmonary uptake or to distinguish abdominal/pelvic sites from overlying stool. These factors overcome the minimal enhancement of the image due to the better gamma emissions from this isotope. I-131 provides better imaging using proper techniques.
2) The idea of tumor stunning, meaning that the tracer dose of I-131 used for imaging will impair the subsequent uptake of the treatment dose of I-131, may be largely mythical, consequent to imaging technique. This has recently been demonstrated by an excellent analysis of Dr. Sissonand and associates; [Sisson JC, Avram AM, Lawson SA, Gauger PG, Doherty GM 2006 The so-called stunning of thyroid tissue. J Nucl Med 47:1406-1412]. For the very rare circumstance when an actual impairment of treatment effect is considered evident in a particular case, it is a very simple process to deal with. Merely avoiding administering the treatment dose until at least 6 months later (using a separate hypothyroid and low iodine diet preparation) will permit a treatment without any preceding scan. For the vast majority of patients, there is no need to fear this phenomenon.
Although a complex issue, not very well appreciated by most nuclear medicine physicians, the use of I-131 for both scanning and therapy is the best lesson to learn.
—ThyroidCancerHelp, September, 2007
I-131 dosing, determinants of
The amounts of radioactive iodine given for therapy are, unfortunately, quite arbitrary and based more on habit than on science. For many years, the most common dose was 29 mCi because this was the highest dose that did not require hospitalization. Many
considered this to be standard and higher doses were considered "high". This is despite excellent studies that suggested that a minimum of 100 mCi was necessary to definitively ablate a thyroid remnant after surgery.
In my practice, I use 100 mCi as the minimum dose for small tumors that are not invasive and have no spread to any site outside of the thyroid bed (where the thyroid used to be). Local spread in lymph nodes in the neck is treated with 150 mCi. Invasive disease in the neck is treated with 200 mCi (provided that the patient has normal kidney function, otherwise the dose may need to be lower). When there are metastases (spread tumor) outside of the neck (such as bones or lung or liver), I perform a "dosimetry study" that tells me what is the highest dose that is "safe" for the patient. This can be as high as 900 mCi for a single dose or as low as 120 mCi (for example, in an elderly woman with poor kidney function).
What one doctor considers a "high" dose, others (such as myself) might consider it to be a "low" dose. There is no consistency between physicians or institutions.
As far as using Salagen prior to and during radioactive iodine treatment, this is not an approach that has been demonstrated to be of benefit. In fact, there is evidence that stimulation of saliva during radioactive iodine therapy is likely to increase the chance of salivary damage, not prevent it. {See: Nakada K, Ishibashi T, Takei T, Hirata K, Shinohara K, Katoh S, Zhao S, Tamaki N, Noguchi Y, Noguchi S 2005 Does lemon candy decrease salivary gland damage after radioiodine therapy for thyroid cancer? J Nucl Med 46:261-266}.
LIthium therapy during radioactive iodine treatment may enhance the treatment by prolonging the retention of the radioactive iodine in the tumor in the small percentage of tumors that release the I-131 too quickly; however, to do this it must be continued for 5 days after the I-131 is given, not 24 hours. {See the study I participated in: Koong SS, Reynolds JC, Movius EG, Keenan AM, Ain KB, Lakshmanan MC, Robbins JR 1999 Lithium as a potential adjuvant to 131I therapy of metastatic, well differentiated thyroid carcinoma. J Clin Endocrinol Metab 84:912-916}.
—ThyroidCancerHelp, June, 2007
I-131 preparation for aggressive thyroid cancers (initial)
When there is a new diagnosis of tall cell variant papillary thyroid cancer, following appropriate total thyroidectomy surgery and modified node resections, it is very important to have the optimal approach to radioactive iodine scanning and therapy. In addition, it is very useful to have a full "tumor staging" work-up (being very careful to avoid contrast dye for xrays and CT scans; gadolinium for MRIs is fine).
In our hands, a staging work-up consists of a high resolution CT scan of the chest (performed WITHOUT ANY contrast), a metastatic bone survey (plain xrays of all of the bones of the body; "bone scans" do not work for thyroid cancer), and (if the tumor is particularly large or invasive) an MRI of the abdomen (using gadolinium contrast). This presumes that there are no symptoms of possible disease outside of the neck. Additional studies may be done if there are specific symptoms. If the patient mentions back pain or sensation changes or weakness of the arms or legs, we do a screening MRI of the entire spine to make sure that there are no tumors pushing on the spinal cord. If the patient notes severe headaches or has evidence of a seizure or visual changes, we do an MRI of the head (with gadolinium).
Preparation for the first I-131 whole body scan is critical. Despite the advances made with Thyrogen, radioactive iodine dose for dose is far more effective with a hypothyroid (thyroid hormone withdrawal) preparation than with Thyrogen; particularly important when dealing with potentially aggressive tumors.
A very careful low iodine diet is critical for 2 weeks before the radioactive iodine scans and treatment and is continued until 24 hours after the radioactive iodine therapy dose is administered. Although the ThyCa website has a free "recipe exchange" that can be downloaded, it doesn't really qualify as a professionally prepared cookbook and contains a number of inaccuracies and inappropriate restrictions. The best information can be found in Norene Gilletz's "The Low Iodine Diet Cookbook" available on Amazon or at www.lidcookbook.com.
If there has been previous exposure to iodinated contrast dye for CT scans or angiograms, going on a low iodine diet for one week and getting a complete 24-hour urine collection on the last day of the diet, permits this urine to be analyzed for total iodine. An excellent low iodine preparation will render the total 24-hour urine under 50 micrograms of iodine; however values under 100 mcg are acceptable. If much higher than this, the diet and urine collection should be repeated monthly until the stable iodine has cleared.
If the tumor was originally invading through the capsule (covering) of the thyroid gland and into the muscles or vital structures of the neck, we would plan to do a dosimetry study so that we could be prepared to treat with a maximally tolerated safe radioactive iodine dose if the tumor has spread outside of the neck. On the other hand, in institutions where dosimetry is not available, some physicians might administer a dose as high as 200 mCi without doing a preceding whole body scan. ALL radioactive iodine therapies MUST be followed by a whole body scan (we find the best time at 48 hour after the treatment) within 2-7 days after the treatment to show where the tumor is in the body that has taken up some of the radioiodine dose.
—ThyroidCancerHelp, July, 2007
I-131 scans can be misinterpreted: uptake in stomach and intestines
It is important to realize that the interpretation of an I-131 whole body scan (WBS) is not always performed properly, even by trained nuclear medicine physicians. I am often required to get to the bottom of situations in which perfectly clean WBSs are misinterpreted. Some common errors include: 1) mistaking salivary gland uptake for tumor sites; 2) mistaking radioactive saliva coating the esophagus for tumor sites; 3) mistaking gastric uptake for tumor; 4) mistaking hepatic "blush" for liver metastases (organified radioiodine from tumors other sites of the body is taken up by the liver without tumor being present in the liver); 5) kidney/ ureter/bladder uptake sites mistaken for tumor sites; 6) radioactive stool scattered in the small and large intestine being mistaken for tumor sites; 7) stool in the appendix or colonic diverticula mistaken for tumor sites; 8) radioactive perspiration or saliva on the skin mistaken for tumor sites; 9) physiological breast uptake or fibrocystic breast uptake mistaken for tumor metastases; 10) benign cysts in the neck/ kidneys/ lungs/ liver/ etc. mistaken for tumor metastases; 11) sucking on a pigtail with radioactive saliva that lays across the neck mistaken for tumor metastases; 12) pulmonary bronchiectasis mistaken for tumor metastases to the lungs; 13) etc. and etc. and etc.
Although it is quite possible to have thyroid cancer metastases in this situation, it is even more likely that the scan has been misinterpreted. When we see such unusual scans, we will do the appropriate maneuvers (from having the patient take a shower to wash the skin, to chewing on a lemon to disperse radioactive saliva, use laxatives to dissipate radioactive stool, or to performing extra lateral chest views to move a woman's breasts out of the way, etc., etc., etc.). If all of the reasonable and known causes of false-positive WBSs are effectively dealt with, THEN we investigate the site of activity with additional scanning and radiological studies.
—ThyroidCancerHelp, July, 2007
I-131 (tearing of the eyes: nasolacrimal duct blockage from)
It is now a well known complication of radioactive iodine therapy (in around 5-10% of patients) to have blockage of the small tube that normally carries tears from the inner corner of the eye to the interior of the nose, the nasolacrimal duct. The presence of this duct is why your nose tends to run when you've been crying or tearing excessively.
The portion of the nasolacrimal duct that is nearest the eye can become scarred and block the passage of tears into the nose. The symptoms of this are a continuous tearing and tears running down your cheeks, even when you're not crying. Only very experienced ophthalmologists are able to deal with this effectively. Sometimes they can put a thin probe into the duct and open it up. Sometimes they need to place a hollow tube into the duct, called a stent, to keep it open. It's unfortunate that many physicians are unaware of this issue.
—ThyroidCancerHelp, July, 2007
I-131 therapy doses and the lung (more on)
The limits of radioactive iodine in the lung are based on the specific radioactive iodine retained in the lung at 48 hours for a single dose, not the cumulative dose. For example (during the preceding tracer dose study), if there is 30% of the administered dose retained in the body at 48 hours and 50% is in the lungs, then (based on the 80 mCi limit) one could safely tolerate a 533 mCi treatment dose. On the other hand, there is an independent limit based upon the dosimetric assessment of the red marrow exposure (see my earlier posting about dosimetry) that usually is reached before one reaches the lung limit.
There are MANY reasons to be short of breath, from emphysema to asthma, and the questioner provides no information about the dosimetric parameters of their therapy. For that reason, it is not possible to comment about the very unlikely chance that any of the pulmonary problems are related to the radioactive iodine therapy.
—ThyroidCancerHelp, December, 2007
I-131 therapy (high dose) is best for distant disease
Unfortunately, one of the common problems encountered when physicians of varying expertise treat distantly metastatic thyroid cancer is the use of radioactive iodine doses that are too low to achieve a useful clinical response. In my practice, patients with distant disease (outside of the neck) that is able to take up radioactive iodine, are evaluated with a radioactive iodine dosimetry study. This method permits me to determine the maximal dose of radioactive iodine that can be given with reasonable safety to that specific patient at that specific time. This dose can range from 120 mCi to 950 mCi as a single dose, based on the dosimetry results. I find this approach to be the most effective one.
Sadly, most patients are not able to reach a physician capable of this dosimetry method of calculating I-131 therapy. Despite this, many physicians can often provide effective treatments with empiric doses of 200 to 250 mci I-131. The most important thing is to avoid the use of repetitive low dose (<200 mCi) therapies that fail to resolve the disease and cause greater side effects in the end.
—ThyroidCancerHelp, July, 2007
I-131 therapy (hypothyroid vs. Thyrogen preparation for)
There are a number of features of radioactive iodine therapy that distinguish the effects of injecting Thyrogen from a hypothyroid preparation.
First, when a person is hypothyroid, the kidney functions at one third the normal activity. In the hypothyroid person, a dose of radioactive iodine circulates longer in the blood before it is passed out in the urine. Since any tumor cells do not instantaneously take up the radioactive iodine, the longer that the radioiodine circulates, the more of it is able to be taken into the tumor.
Second, the effects of TSH, whether injected (Thyrogen) or produced by hypothyroidism, are also not instantaneous. That is, the thyroid cancer cells take several days to fully respond to the TSH, synthesize more iodine transporters, and produce more enzymes needed to hold on to the radioactive iodine, once it is taken into the cancer cell (organification). The brief time that Thyrogen is on board, prior to getting the radioactive iodine dose is a compromise necessitated by the expense of the injections, and the logistics of administering it for longer periods of time. Hypothyroidism exposes the thyroid cancer cells to greater TSH effects.
Truly, there are many people who may be adequately treated with protocols being devised using a Thyrogen preparation. Nonetheless, it is an inferior compromise to a well-done hypothyroid preparation. In minimal and well-responsive tumors, the differences may not be significant; however, in potentially aggressive thyroid cancers, every advantage of a hypothyroid preparation should be used.
—ThyroidCancerHelp, July, 2007
I-131, which thyroid cancers do not require it
It is not necessary to perform radioactive iodine therapy and whole body scanning for EVERY case of thyroid cancer. Those cases that do NOT routinely get radioiodine therapy are unifocal (single) papillary cancers (usual papillary, follicular variant of papillary, occult sclerosing papillary) that are present inside the thyroid gland (do not penetrate the thyroid capsule) and are do not have any clinically obvious local or distant metastatic disease. For such patients, we generally advise them to perform regular (monthly) neck self exams, take an appropriate dosage of levothyroxine to keep the TSH only slightly suppressed (just below or at the lower edge of the normal range) and make certain that their primary care physician provides regular check-ups. We also obtain a baseline thyroglobulin measurement (when the TSH is at the target level) for future comparison (and have their primary care physician check it yearly with routine labs). For most such patients, this is sufficient management.
On the other hand, should the tumor be an aggressive variant of papillary cancer (tall cell, columnar cell, Hurthle cell), extend through the thyroid capsule, reflect any other type of radioiodine-responsive histology (follicular, Hurthle cell, insular, etc.), or exhibit any evidence of lymph node metastases or distant disease, we would assertively treat with radioactive iodine (our minimal dose is 100 mCi for only thyroid bed remnant) and use radioiodine scanning as part of long-term follow-up.
—ThyroidCancerHelp, November, 2007
Insular thyroid cancer: dealing with persistent local disease
Some important information has been omitted from the question above. I'll have to make some assumptions: 1) the "nodes" in question are in the neck; 2) the CT scans were performed with iodinated contrast; and 3) although the results of the radioiodine scan performed 2-7 days after the last radioiodine therapy (the "post-therapy whole body scan") results were not given, I presume them to have been negative.
Insular thyroid cancer is often a very aggressive tumor. Although it may sometimes take up radioactive iodine and be responsive to such therapy, it frequently fails to take it up or loses this ability later in the course of the disease, making radioactive iodine therapy or scans useless. A problem with assessing radioactive iodine uptake in these tumors is that they are very sensitive to the effects of non-radioactive (stable) iodine which prevents the radioactive iodine from going into the tumor cells, sometimes falsely making appear unresponsive to radioactive iodine. CT scans of the neck are usually performed with iodine (stable) contrast dye and its effects on preventing radioactive iodine uptake can sometimes persist for more than 6 months. This possibility always needs to be taken into account.
On the other hand, PET scans present a bit of a "Catch-22" (read Joseph Heller's book). If tumors (or lymph nodes) "light up" on a PET scan, this can be supportive evidence that they contain cancer cells; however, tumors that "light up" on PET scans are usually more rapidly growing and less likely to take up radioactive iodine than those that are not. It would be good to have a fine needle biopsy that shows thyroid cancer cells, but sometimes this may be difficult to do if the local physicians are not sufficiently skilled in the technique.
As mentioned in earlier postings on this site, when there are lymph nodes in the neck that contain thyroid cancer (based on their increase in size, elevated thyroglobulin levels and positive uptake on the PET scan) usually the best course of action is to have an excellent surgeon perform an appropriate modified neck dissection, then to have external beam radiotherapy to the neck and superior mediastinum (the mid upper part of the chest). Although there may be other sites of metastatic tumor (for example: lungs or bones), it is important to deal with tumor in the neck in this fashion because this is a particularly vital part of the body.
—ThyroidCancerHelp, July, 2007
Iodinated contrast dye (decision when to use)
In all of my patients with thyroid cancer, I suggest that they approach the issue of CT scan contrast dye with common sense. If they have an emergency situation, then contrast dye should be used without question, such as: chest pain requiring cardiac catheterization with dye, ruptured cerebral aneurysm requiring an angiogram, or automobile accident with CT scans to assess for internal bleeding. On the other hand, if the contrast dye is to be used for an optional study, particularly if it can be delayed until after the consideration of radioactive iodine use is dealt with, then it should be delayed. If alternative radiographic techniques, such as ultrasound or MRI can be substituted with adequate utility, then this could be considered. Above all use common sense.
—ThyroidCancerHelp, October, 2007
Iodine contrast: you can't make it go away faster
Iodinated contrast will take anywhere from 2 to 12 months to clear. There is NOTHING that can be done to accelerate this process; not diuretics, not selenium, not a low iodine diet. Unfortunately, a little bit of knowledge is dangerous. Areas of the world with endemic iodine deficiency are also usually selenium deficient and both deficiencies go hand in hand; however, they do NOT cause each other. Please do not take well-intentioned, but completely wrong, advice.
The appropriate thing to do, when exposed to such iodinated contrast, is to do a one-week low iodine diet and collect a 24-hour urine sample for total iodine on the last day. If the amount of iodine is less than 100 mcg total, then there will not be significant interference. If the amount of iodine is much higher, I have my patients repeat the one-week-LID-with-urine-study for the next month. Eventually, the iodine will drop sufficiently to proceed with radioiodine plans.
—ThyroidCancerHelp, August, 2007
Iodine isotope choice for scanning
I do not use I-123 for scanning thyroid cancer patients because I find that it has less sensitivity for detecting tumors, particularly when using delayed imaging to reduce non-specific background from the scans. I do not find it to be of any advantage and it is far more expensive than I-131. The issue of "stunning" (having the scan radioiodine dose interfere with the tumor cell taking up the subsequent treatment dose of radioiodine) is highly over-rated and does not occur very frequently in my practice (although we use very sensitive procedures to look for it).
In the rare circumstances when radioiodine scans are positive, and the subsequent treatment dose effectiveness is reduced by "stunning," it is very easy to remedy the matter by performing a radioactive iodine treatment 6—12 months later without doing a preceding scan. Such remedies are not needed very often at all.
Thyrogen stimulated scans are generally less sensitive for detecting thyroid cancer metastases than identically performed scans using a hypothyroid preparation. For that reason, I typically refrain from using Thyrogen until a hypothyroid-prepared scan is completely clean (with undetectable thyroglobulin) and I am confident that the tumor does not show features suggesting it to be particularly aggressive. Not all physicians agree with this approach. In my large practice population of thyroid cancer patients, I generally perform equal numbers of Thyrogen-prepped scans and hypothyroid-prepped scans, each approach tailored to the individual features of each patient.
—ThyroidCancerHelp, June, 2007
Iodine uptake in breasts
Normal female breasts are able to concentrate radioactive iodine in the same ductal tissues that produce milk. In young healthy breasts, this can often be confusing on radioactive iodine scans of the chest. Often I have to get lateral views of the chest to make sure that the regions that mildly "light up" are actually breasts and not in the underlying lung. The iodine uptake is even greater in the breasts of actively lactating women; however, such women should never be given radioactive iodine.
—ThyroidCancerHelp, October, 2007
L
Levothyroxine and alcohol
There is no problem [having] alcohol while taking levothyroxine. It will not interfere with absorption in any way and at any time.
—ThyroidCancerHelp, October, 2007
Levothyroxine and calcium (taking)
The timing of medications should be as optimal as possible within the practical context of living a normal life. I suggest that people take their levothyroxine as soon as they wake up in the morning so it is as far removed from breakfast (when the first calcium dosage is taken) as is practical for their daily routine. The time from the levothyroxine to the breakfast may be anywhere from 20 minutes to two hours, depending on how fast people get dressed and out the door to work. It's not necessary to wait a full 5 hours (unless one is waiting to take iron supplements or cholestyramine; medications that block levothyroxine absorption much worse than calcium). That small difference is usually sufficient. The key is consistency, so that the levothyroxine dose titration takes care of any minor issues arising from the calcium.
—ThyroidCancerHelp, December, 2007
Levothyroxine and coffee
[A recent study found impaired absorption of levothyroxine when taken with coffee.] Taking levothyroxine WITH hot coffee/espresso will impair the effects of the levothyroxine; however, I suspect that this is not due to impaired absorption from caffeine. It has already been well established that levothyroxine is quite heat-sensitive. I suspect that the temperature of the stomach contents will be sufficiently elevated by a cup of hot coffee to degrade the hormonal content of a levothyroxine pill that is also in the stomach. Their results suggest that the coffee should not be taken within 30 minutes of the levothyroxine; after 30 minutes there isn't any effect of coffee on impairing the levothyroxine levels. Unfortunately, this possibility could have been addressed by comparing the ingestion of COLD coffee and levothyroxine with the ingestion of HOT coffee and levothyroxine. Regardless of the mechanism of this effect, it supports the advice that I've been giving my patients for many years.
Take your levothyroxine as soon as you wake up, so that it is as far from when you typically eat breakfast/drink coffee as your routine will permit. It is likely that there would be at least one half hour from the time that one takes the levothyroxine until the coffee meets one's lips.
—ThyroidCancerHelp, March, 2008
Levothyroxine: a primer
With reference to estrogen therapy, applying to both oral and transdermal treatment: Taking estrogens (of any sort) do not necessarily alter the daily dosage of levothyroxine (of any brand).
Their effect on total thyroid hormone levels in the blood is due to their influence on raising the levels of thyroxine binding globulin (TBG; a protein made by the liver which transports levothyroxine in the blood)[Ain KB, Mori Y and Refetoff S (1987) Reduced clearance rate of thyroxine-binding globulin (TBG) with increased sialylation: a mechanism for estrogen-induced elevation of serum TBG concentration. J Clin Endocrinol Metab 65, 689-696]. Since the rate of disposal and metabolic consumption of levothyroxine is only dependent upon the portion which circulates "free" (unbound to TBG and other related proteins), any alteration in TBG levels ultimately results in a new steady-state without clinically affecting the treatment.
Everyone on thyroid hormone therapy has their medication adjusted based on the intracellular concentration of thyroid hormone, which is reflected by the TSH. Usually the dosages of estrogens used in modern medications are not high enough to cause any change in the daily dosage of levothyroxine and there will not be any change in the TSH. The bottom line here, as in the quoted posting above, is to monitor the TSH.
On the other hand, estrogen levels and other physiological changes associated with pregnancy frequently cause significant re-adjustments in the daily dosage of levothyroxine. Some women require their levothyroxine dose to be increased to 150% of previous dosages. After delivery, they usually need to return to their original dosage. This is why it is critical to have the TSH level measured monthly while pregnant.
In reference to general principles of taking levothyroxine, including the effects of iron medications:
The mean suppression dose of levothyroxine is 2.0 micrograms per kilogram (2.2 lbs) per day. For example, a 165 lb person would average 150 micrograms daily to suppress their TSH. Of course, there is a wide range of variation and there are many factors which are involved.
1. Levothyroxine (Synthroid, Levoxyl, Levothroid, etc) is exquisitely sensitive to heat. If exposed to the sun-heated interior of a parked automobile, or a shelf above the stove, or left sitting on the radiator, such pills will forever lose their potency, even if later cooled down. Women (in particular) often make the mistake of carrying the pill bottle in their purses, which are often exposed to wide fluctuations in temperature.
2. Absorption is best on an EMPTY stomach: usually best in the early AM at least one hour before eating breakfast.
3. If a pill is missed, always make it up. For example, if you forgot to take your pills over a weekend, on Monday you should take all 3 doses together. Since the half-life of levothyroxine is one week, such a thing is not only NOT dangerous, but very necessary to avoid losing TSH suppression.
4. Titration of doses to suppress TSH but not cause tachycardia or other evidence of thyrotoxicosis can be difficult in some patients, sometimes requiring dose changes of as little as 10%. For that reason, even missing one pill per week without making it up would cause a variation of more than 14% of the weekly dose. For that reason, NEVER miss your pill, or make it up if you do (as in #3 above).
5. Iron-containing medications and iron-containing vitamins will bind to levothyroxine and interfere with absorption. So will sucralafate (Carafate), cholestyramine, large doses of aluminum hydroxide gels (Maalox, etc), very large doses of calcium, and soy milk/protein supplements. If any of these items must be consumed, they should be taken 5 hours away from the levothyroxine dose. [note: estrogens and birth control pills do NOT interfere]
6. KNOW YOUR PILLS. Not too infrequently, my patients may be given the wrong dose or the wrong pill by the
pharmacist. Check your pills BEFORE you leave the pharmacy. Do not look at the label. Examine the pill itself. Note the characteristic color and numbers on the pill which denote the correct strength. Check the expiration date and ask for the date from the stock bottle. Levothyroxine pills degrade at around 5% of the dose per year by just sitting in the bottle under PERFECT storage conditions. Never use OLD pills (over one year old) if you have access to fresh ones. There have been situations reported when the stock medication dispensed by the pharmacy had been transported long distances in hot truck vans before it had reached the pharmacy, rendering all of the medication badly degraded despite appearing as "new" pills.
7. If you are the least bit forgetful, buy a day-of-the-week pill dispenser and use it religiously.
8. If these precepts are followed PRECISELY, your physician should be able to lower your daily dose to the lowest dose which suppresses your TSH (I prefer TSH < 0.10) to avoid stimulation of hibernating thyroid carcinoma cells. This will also permit the least long-term side effects (however minor) of TSH suppression.
—ThyroidCancerHelp, July, 2007
Levothyroxine dosing and pregnancy
Pregnant patients taking levothyroxine (either for hypothyroidism or thyroid cancer) frequently need to increase their doses (sometimes by as much as 50%) during the later half of their pregnancy. This is not due to the increased body weight per se, but rather due to an expanded "volume of distribution", that includes: the placenta, amniotic fluid, and other factors. TSH levels should be obtained each and every month during the pregnancy. Although it is not necessary to keep the TSH suppressed during the pregnancy, anytime the TSH rises to 2.0 or higher, the dosage of levothyroxine should be increased appropriately. I tell my patients to work with their obstetrician to make certain that the TSH is drawn each month and that the patient is told of the result, only contacting me if the TSH is at 2.0 or higher for a dosage change.
After delivery, the levothyroxine dosage generally needs to be reduced to the pre-pregnant dosage, even if the excess body weight from the pregnancy persists. It is best to wait at least 5 weeks (6—8 weeks are optimal) after making any alteration in the levothyroxine dosage before checking the free T4 and TSH levels for verification.
—ThyroidCancerHelp, January, 2008
Levothyroxine for scans/therapies (waiting six weeks off)
ALL levothyroxine pills of EVERY BRAND, including all generics, have the same half-life of 7 days. This means that when you stop your pills, after one week, the level of thyroid hormone has fallen to 50% of where it had been. After another week, it is 50% of the 50% (or rather 25% of the original level). Likewise, after a third week, it is 50% of 25% (or rather 12.5% of the original level). In this fashion, it typically takes 6 weeks to be rid of most of the thyroid hormone. For the first 4 weeks of this time, my patients are taking Cytomel (liothyronine) 25 micrograms twice daily, so that they feel well. For the last 2 weeks of the 6-week preparation, they are off ALL thyroid hormones and are instructed not to drive motorized vehicles or to perform dangerous tasks that require full mental concentration.
My schedule averages 6 patients getting hypothyroid-prepped whole body scans, 5 patients getting Thyrogen-prepped whole body scans, and 1 or 2 patients getting full dosimetry studies every week. We need to schedule around 50 patients every month and such schedules are made from 2 to 12 months in advance. In very small thyroid cancer practices there are usually only a few hypothyroid scan patients per month and it is possible to check weekly TSH levels, after the first month, to see if there are unique patients whose TSH levels have risen above 30 earlier than the typical 6 weeks. In my own practice, to do this would be a logistic nightmare and impossible to arrange. This "6-week rule" is a practical consequence of the usual pharmacokinetics of levothyroxine.
—ThyroidCancerHelp, July, 2007
Levothyroxine preparations (composition of)
Levothyroxine tablets (as Synthroid®) contain the following: synthetic crystalline
L-3,3',5,5'-tetraiodothyronine sodium salt [levothyroxine (T 4 ) sodium and the inactive fillers: acacia, confectioner’s sugar (contains corn starch), lactose monohydrate, magnesium stearate, povidone, and talc. The following are the color additives by tablet strength: Strength (mcg) / Color additive(s)
25 / FD andC Yellow No. 6 Aluminum Lake
50 / None
75 / FD andC Red No. 40 Aluminum Lake, FD andC Blue No. 2 Aluminum Lake
88 / FD andC Blue No. 1 Aluminum Lake, FD andC Yellow No. 6, Aluminum Lake, D andC Yellow, No. 10 Aluminum Lake
100 / D andC Yellow No. 10 Aluminum Lake, FD andC Yellow No. 6 Aluminum Lake
112 / D andC Red No. 27 and 30 Aluminum Lake
125 / FD andC Yellow No. 6 Aluminum Lake, FD andC Red No. 40 Aluminum Lake, FD andC Blue No. 1 Aluminum Lake
137 / FD andC Blue No. 1 Aluminum Lake
150 / FD andC Blue No. 2 Aluminum Lake
175 / FD andC Blue No. 1 Aluminum Lake, D andC Red No. 27 and 30 Aluminum Lake
200 / FD andC Red No. 40 Aluminum Lake
300 / D andC Yellow No. 10 Aluminum Lake, FD andC Yellow No. 6 Aluminum Lake, FD andC Blue No. 1 Aluminum Lake
—ThyroidCancerHelp, October, 2007
Levothyroxine, resuming after radioiodine therapy
I advise patients to terminate the low iodine diet at just over 24 hours after the administration of the I-131 therapy dose, the same time that I resume their levothyroxine therapy. Most of the critical re uptake and re-circulation of I-131 from the bloodstream to thyroid cancer cells in completed within the first 24 hours of dose administration. Thus there is no advantage to maintaining the same degree of hypothyroidism or low iodine diet status for more than one day after treatment. Any uptake seen in the post-therapy scan is consequent to tumor uptake from the first day of treatment and will not be affected despite resuming levothyroxine and a normal diet. In addition, even when the full levothyroxine dose is taken, it requires another week before the TSH becomes appreciably lower and a full 4 weeks before it starts to suppress.
Although other physicians may do differently, it is unlikely that they have carefully evaluated the radiokinetics of I-131 in the body.
—ThyroidCancerHelp, July, 2007
Levothyroxine suppression (no significant risk of) to cause osteoporosis
There have been a number of studies performed to evaluate whether suppressive doses of levothyroxine used to treat thyroid cancer can increase the risk of osteoporosis. Some of the studies are well done and many are not. One of the better studies is:
Reverter, J. L., S. Holgado, et al. (2005). "Lack of deleterious effect on bone mineral density of long-term thyroxine suppressive therapy for differentiated thyroid carcinoma." Endocr Relat Cancer 12(4): 973-81.
ABSTRACT: The effect of subclinical hyperthyroidism on bone mineral density is controversial and could be significant in patients with differentiated thyroid carcinoma who receive suppressive doses of levothyroxine (LT4). To ascertain whether prolonged treatment with LT4 to suppress thyrotropin had a deleterious effect on bone mineral density and/or calcium metabolism in patients thyroidectomized for differentiated thyroid cancer we have performed a cross-sectional study in a group of 88 women (mean +/- SD age: 51 +/- 12 years) treated with LT4 after near-total thyroidectomy and in a control group of 88 healthy women (51 +/- 11 years) matched for body mass index and menopausal status. We determined calcium metabolism parameters, bone turnover marker N-telopeptide and bone mass density by dual-energy X-ray absorptiometry. No differences were found between patients and controls in calcium metabolism parameters or N telopeptide except for PTH, which was significantly increased in controls. No differences were found between groups in bone mineral density in femoral neck (0.971 +/- 0.148 gr/cm(2) vs 0.956 +/- 0.130 gr/cm(2) in patients and controls respectively, P = 0.5). In lumbar spine, bone mineral density values were lower in controls than in patients (1.058 +/- 0.329 gr/cm(2) vs 1.155 +/- 0.224 gr/cm(2) respectively, P < 0.05). When premenopausal (n = 44) and postmenopausal (n = 44) patients were compared with their respective controls, bone mineral density was similar both in femoral neck and lumbar spine. The proportion of women with normal bone mass density, osteopenia and osteoporosis in patient and control groups was similar in pre- and postmenopausal women. In conclusion, long-term suppressive LT4 treatment does not appear to affect skeletal integrity in women with differentiated thyroid carcinoma.
There are some studies that suggest that there might be some increased risk for osteoporosis in post-menopausal women receiving suppressive levothyroxine therapy; however, this increased risk is likely very small (if present) and is likely mitigated by estrogen therapy.
—ThyroidCancerHelp, August, 2007
Levothyroxine suppression therapy and liver enzymes
Although appropriate adjustment of the levothyroxine dosage, to keep the TSH suppressed to under 0.1 with the smallest dose possible, is not typically associated with changes in liver enzymes, sometimes there is a slight elevation of some of the transaminases (including ALT). The most common enzyme to be elevated is a slight elevation of Alkaline Phosphatase.
On the other hand, sometimes primary liver disease can cause independent elevations of liver enzymes, sometimes starting low and increasing with time. For that reason, it is very reasonable for a physician, noting a slight elevation, to want to check these tests later on to make sure that the elevation is still minimal or transient, rather than much higher and demonstrating hepatitis.
—ThyroidCancerHelp, October, 2007
Levothyroxine suppression therapy and menopause (titrating)
Sometimes, despite careful adjustment of the levothyroxine dosage so that the TSH is under 0.1 using the minimal dosage that will do so, one still has mild thyrotoxic symptoms. If so, then a beta blocker will often prove very helpful. Sometimes, the symptoms have nothing to do with the thyroid hormone and instead are consequent to coincident menopausal symptoms. Careful consideration of these factors usually permits a resolution to such symptoms.
—ThyroidCancerHelp, September, 2007
Levothyroxine: the reason for the brand-name
In the United States, generic levothyroxine preparations are fine for treatment of hypothyroidism. The problem is that there are several different companies that make this generic and if a generic levothyroxine is prescribed, the particular generic is randomly switched from company to company based on the "price of the day." Although most levothyroxine pills are consistent within the same brand or company's product, they are not the same between brands or companies. That is: Sandoz levothyroxine 150 mcg is not equal to Synthroid 150 mcg is not equal to Levoxyl 150 mcg is not equal to Unithyroid 150 mcg is not equal to Levothyroid 150 mcg is not equal to nameless generic 150 mcg.
The differences are usually small and of no concern to people with simple hypothyroidism. On the other hand, in order to take the precise dosage that suppresses the TSH <0.1 without causing thyrotoxic symptoms, the change between different brands or companies is too much of a difference to rely on the adequacy of the dosage. Since it is not possible to compel or prescribe a specific company's generic be used at each pharmacy refill, the only way that one can be sure that the refill will be the exact same dosage and content of levothyroxine is to use a "brand name" drug. It doesn't matter which one, as long as it is the same one each time.
Pharmacies can be a big problem. They have a tendency to try to substitute generics, even when the prescription is clear that it is not permitted. This is because they make a greater profit with generic levothyroxine than with brand name pills. The only way to be certain that you have the correct pills is to open the bottle at the pharmacy counter and check the pill itself, noting the brand name and dosage (usually written right on the pill).
—ThyroidCancerHelp, June, 2007
Liothyronine (T3) therapy, temporary
Under extenuating circumstances, Cytomel (liothyronine or T3) can be taken for a few weeks to restore reasonable thyroid status for surgical procedures; however it should be given in divided doses (2 or 3 times daily) and averaging a total of 50 micrograms per day. Stable treatment with levothyroxine should be initiated as soon as appropriate.
—ThyroidCancerHelp, October, 2007
Lithium for radioactive iodine therapy (the use of)
There is a small subset of thyroid cancer patients with metastatic t