Sunday, February 27, 2011

Risk of Nerve Damage in Thyroid Cancer Surgeries Review

While it has become more uncommon in recent decades, nerve damage incurred during surgery for thyroid cancer is still a possibility for people undergoing an operation to remove some or all of the gland. Recently, researchers tried to quantify the incidence of and risk factors for recurrent laryngeal nerve damage.

The recurrent laryngeal nerve (RLN) supplies electrical impulses that make the larynx move, according to Gray's Anatomy. Damage to this nerve can cause hoarseness or even impair a person's ability to speak.

In a recent study published in the Oman Medical Journal, a group of surgeons from Dammam University, Saudi Arabia, found that major thyroid surgeries appear to increase the risk of RLN damage, particularly if a patient undergoes a follow-up surgery.

The team began by stating that RLN damage is quite rare today, noting that injuries to the nerve occur in approximately 1 to 2 percent of all thyroid surgeries. In the study itself, slightly more than 4 percent of participants suffered some form of nerve damage related to the removal of thyroid carcinomas.

Researchers followed 340 patients admitted for thyroid cancer, hyperthyroidism, goiter and other diseases of the thyroid gland. They found that over the course of all observed surgeries, 13 cases of RLN damage occurred.

Most of them involved unilateral damage, or injury to to the RLN affecting just one side of the larynx. This sort of damage can result in a hoarse voice once patients have recovered. Of the 11 patients who had unilateral RLN damage, just one patient suffered a permanently hoarse voice.

Just two participants experienced bilateral RLN injuries, which affect the entire larynx and can more seriously impede the ability to speak. Neither case was permanent.

The study's authors analyzed data on the risk factors associated with these injuries and came to the conclusion that what increases risk of RLN damage the most is secondary surgery. While fewer than 3 percent of primary surgeries ended in RLN injury, more than 21 percent of secondary, or follow-up, surgeries did.

Likewise, total thyroidectomies and a failure to identify RLN damage during the procedure each increased the risk of hindered nerve function.  Surgery is still one of the most effective treatments for thyroid cancer, a disease that takes the lives of nearly 1,700 Americans each year, according to the National Cancer Institute.

Thursday, February 24, 2011

Thyroid Cancer and Genetic Tumor Disorder Study

For a number of years, scientists have been investigating the association between thyroid cancer and PTEN Hartoma Tumor Syndrome (PHTS), a genetic disorder that increases an individual's likelihood of having cancer.

In a new study of the pediatric intersection of the two conditions, endocrinologists from two Massachusetts hospitals found that young patients with PHTS had an estimated 70 percent incidence of thyroid nodules and thyroid cancer.

The group, which was composed of endocrinologists and other healthcare experts from Children's Hospital Boston and Brigham and Women's Hospital, published their findings in the Journal of Clinical Endocrinology and Metabolism.

PHTS is a complex condition caused by the mutation or deletion of a gene that regulates the production of phosphatase and tensin homolog (PTEN), a protein that is a crucial part of the body's natural defenses against cancer.

PTEN proteins help keep the cycle of cell division and death balanced and in working order, moving neither too fast nor too slow. If a person's PTEN gene is damaged or missing, they may be at a high risk for certain forms of cancer, according to the Children's Hospital of Philadelphia (CHP).

By the age of 20, people with PHTS often display a number of noticeable PHTS symptoms, which can include cognitive delays, an enlarged head, skin tags and certain kinds of cancer, the hospital states. The disorder can also lead to severe tumors of the skin, bones and glands.

The CHP notes that the most common cancers associated with PHTS are those of the breast, uterine lining and thyroid gland.  In the new study, physicians detected thyroid nodules or outright thyroid cancer in five out of seven children between the ages of 6 and 12. All seven patients had previously been diagnosed with PHTS.

They concluded that a diagnosis of PHTS should engender an strong clinical suspicion of the presence of thyroid cancer, and vice versa. They added that ultrasound scans may safely be used to search for thyroid nodules in children of all ages.

Nearly 2 percent of annual thyroid cancer cases in the U.S. are diagnosed in people under the age of 20, according to the National Cancer Institute.

SOURCE: endocrineweb

Monday, February 21, 2011

PET Scans May Allow Early Prediction of Response to Targeted Therapy of Thyroid Cancer

Reston, Va. -- Positron emission tomography (PET) can image metabolic changes following treatment with the protein kinase inhibitor vandetanib, helping to define the therapy response or the effectiveness of the therapeutic agent, according to research published in the February issue of The Journal of Nuclear Medicine. Currently being tested in clinical trials, vandetanib inhibits the function of the RET (rearranged-during-transfection protein) proto-oncogene and other protein kinases involved in the development and progression of cancer.

"For the most part, clinical trials have been measuring the effectiveness of vandetanib by changes in tumor size. Based on the activating effects of mutated RET and other protein kinases on numerous intracellular metabolic pathways, we hypothesized that PET imaging could play a role in the early evaluation of response to vandetanib," said Martin A. Walter, MD, lead author of the study "Metabolic Imaging Allows Early Prediction of Response to Vandetanib."

The study examined the usefulness of metabolic imaging to determine response to vandetanib in three ways. First, medullary thyroid cancer cells were used to create an in vitro model. After cultivation, the cells were treated with vandetanib, and changes in the metabolic profile of the cells were successfully monitored by transcriptional profiling and by radiotracer uptake studies.

Using the same untreated cells, the researchers then created an in vivo model by injecting mice with the cancerous cells and treating them with vandetanib. Small animal PET/computed tomography (CT) imaging was performed and was found to reproduce the in vitro findings of metabolic activity after three days.

Finally, a 43-year old patient with biopsy-proven metastasized medullary thyroid cancer was treated with vandetanib. PET scans taken at 12 and 24 weeks after treatment were able to detect metabolic response to vandetanib, consistent with the in vitro and in vivo samples.

"With the increasing number of available treatment options, careful patient selection is necessary to ensure targeted therapy is administered to those most likely to gain clinical benefit," said Walter. "The identification of markers of treatment efficacy is a key factor for the success of these novel treatment approaches."
"Furthermore," he continued, "relating in-vivo PET imaging metabolic data with transcriptional profiling data using cluster analysis is an innovative concept that allows much potential in the field of molecular imaging."

SOURCE: Society of Nuclear Medicine

Friday, February 18, 2011

Genetics and Thyroid Cancer: Know Your Risks

A risk factor is anything that affects a person's chance of getting a disease such as cancer. Different cancers have different risk factors. For example, exposing skin to strong sunlight is a risk factor for skin cancer. Smoking is a risk factor for a number of cancers.

But risk factors don't tell us everything. Having a risk factor, or even several risk factors, does not mean that you will get the disease. And many people who get the disease may not have had any known risk factors. Even if a person with thyroid cancer has a risk factor, it is very hard to know how much that risk factor may have contributed to the cancer.

Scientists have found a few risk factors that make a person more likely to develop thyroid cancer.

Gender and Age:  For unclear reasons thyroid cancers occur about 3 times more often in women than in men. Thyroid cancers can occur in people of all ages, but most cases of papillary and follicular thyroid cancer are found in people between the ages of 20 and 60 years.

Diet Low in Iodine:  Follicular thyroid cancers are more common in areas of the world where people's diets are low in iodine. In the United States, dietary iodine is plentiful because iodine is added to table salt and other foods. A diet low in iodine may also increase the risk of papillary cancer if the person also is exposed to radioactivity.

Radiation Exposure:  Exposure to radiation is a proven risk factor for thyroid cancer. Sources of such radiation include certain medical treatments and radiation fallout from power plant accidents or nuclear weapons. Having a history of head or neck radiation treatments in childhood is a risk factor for thyroid cancer. In the past, children were sometimes treated with radiation for things we wouldn't use radiation for now, like acne, fungus infections of the scalp (ringworm), an enlarged thymus gland, or to shrink tonsils or adenoids. Years later, studies linked these treatments to an increased risk of thyroid cancer.

Radiation therapy in childhood for some cancers such as Hodgkin disease also increases risk. In general, the risk is higher with younger children. Radiation exposure as an adult carries little risk of thyroid cancer.

Several studies have pointed to an increased risk of thyroid cancer in children because of radioactive fallout from nuclear weapons or power plant accidents. For instance, thyroid cancer is several times more common than normal in children living near Chernobyl the site of a 1986 nuclear plant accident that exposed millions of people to radioactivity. Adults involved with the cleanup after the accident and those who lived near the plant have also had a higher rate of thyroid cancer. Children with more iodine in their diet appeared to have a lower risk.

Some radioactive fallout occurred over certain regions of the United States after nuclear weapons testing in western states during the 1950s. This exposure was much, much lower than around Chernobyl. At such low exposures, a higher risk of thyroid cancer has not been proven. If you are concerned about possible exposure to radioactive fallout, discuss this with your doctor.

Hereditary Conditions:  About 1 out of 5 medullary thyroid carcinomas (MTCs) result from inheriting an abnormal gene. These cases are known as familial medullary thyroid carcinoma (FMTC). FMTC can occur alone, or it can be seen along with other tumors. The combination of FMTC and tumors of other endocrine glands is called multiple endocrine neoplasia type 2 (MEN 2).

There are 2 subtypes, MEN 2a and MEN 2b:

In MEN 2a, MTC occurs along with pheochromocytomas (tumors in the adrenal glands, which are located on top of the kidneys) and with parathyroid gland tumors.

In MEN 2b, MTC is associated with pheochromocytomas and with benign growths of nerve tissue on the tongue and elsewhere called neuromas. This subtype is much less common than MEN 2a.

In these inherited forms of MTC, the cancers often develop during childhood or early adulthood and can spread early. MTC is most aggressive in the MEN 2b syndrome. If MEN 2a, MEN 2b, or isolated FMTC runs in your family, then you may be at very high risk of developing MTC. Ask your doctor for information about having regular blood tests to look for problems and the possibility of genetic testing.

Other Thyroid Cancers: People with certain inherited medical conditions are at higher risk for more common forms of thyroid cancer. Higher rates of the disease occur among people with uncommon genetic conditions such as Gardner syndrome, Cowden disease, and familial adenomatous polyposis (FAP).

Papillary and follicular thyroid cancers do seem to run in some families without a known inherited syndrome; this may account for about 5% of thyroid cancers. The genetic basis for these cancers is not totally clear.

Several inherited conditions have been linked to different types of thyroid cancers for more information about your specific risk factors or any questions you may have please speak to your family doctor.

Tuesday, February 15, 2011

Hypothyroid Myopathy: What You Need To Know

One of the most difficult problems my daughter had to deal with early on as a teenager becaming increasingly disabled by a misdiagnosed thyroid condition (which we later learned was a non-functioning thyroid due to Stage II thyroid cancer) was chronic muscles aches and pains. Her complaints of chronic fatigue and muscle cramping and pain were attribute to weight gain and later as fibromyalgia.

After a radical thyroidectomy and over the course of the past 3 years we discovered a pattern of increased muscle pains and aches as her now synthetic hormone levels fluctuated. It has been a nightmare to have a doctor validate how she feels and why. Our own personal research discovered a little known or perhaps a little discussed cause we want to share with you today. 

Hypothyroid Myopathy
Muscle involvement in a variety of forms is a frequent problem in both congenital and adult-onset hypothyroidism. This topic will discuss the clinical manifestations and pathogenesis of hypothyroid myopathy. We will discuss other neurologic manifestations of hypothyroidism separately.

As you may already  know deficiency of thyroid hormone leads to a state called hypothyroidism. Common causes of hypothyroidism include the following:
  • Treatment with radioactive iodine (I131 ) for Graves disease
  • Hashimoto disease - An autoimmune process in which lymphocytic infiltration and fibrous tissue accumulation cause replacement of normal thyroid tissue
  • Drug-induced hypothyroidism - Known to occur with amiodarone and iodine (ie, Wolff-Chaikoff effect)
  • Hereditary disorders of the iodothyronine synthesis pathway (thyroxine [T4] and triiodothyronine [T3])
  • Pituitary tumors and related surgical resections and/or excisions.
  • Thyroid Nodules/tumors and related surgical resections and/or excisions.
Hypothyroidism can cause several symptoms, ranging from mild (eg, fatigue, weight gain, cold intolerance, mental slowing, muscle cramping) to severe (eg, heart enlargement, myxedema coma [rare]).

Without regard to the cause of hypothyroidism, neuromuscular and musculoskeletal manifestations can be observed in many patients with the condition. These manifestations can occur at any time in the hypothyroidism disease process. Usually mild, they include weakness, pain, aching, and stiffness.

Hypothyroid myopathy typically manifests as polymyositis-like myopathy with proximal muscle weakness and an increased creatine kinase level. However, it sometimes manifests as muscle enlargement (pseudohypertrophy); in adults, this condition is called Hoffman syndrome. In children with hypothyroid disease (cretinism), a pattern of proximal weakness and diffuse muscle enlargement is known as Kocher-Debr é -S é m é laigne syndrome.

Several case reports describe rhabdomyolysis associated with hypothyroidism. In these cases, the hypothyroidism is thought to have predisposed individuals to rhabdomyolysis.


Hypothyroidism causes a constellation of changes in the body. The lack of thyroid hormone results in slowed or reduced metabolic function, such as decreased protein turnover and impaired carbohydrate metabolism. These metabolic changes occur in many organ systems, including the muscles. Pain with muscle exertion is characteristic of defective carbohydrate metabolism.

Slowed muscle contraction and relaxation, known as hypothyroid myopathy, may be caused by a shift in the distribution of muscle fiber types from fast-twitch fibers to slow-twitch fibers. A reduction in muscle mitochondrial oxidative capacity and beta-adrenergic receptors, as well as the induction of an insulin-resistant state, may result in these changes.

Evidence from a study by Sinclair and colleagues suggests that a decrease in muscle carnitine in patients with either hypothyroidism or hyperthyroidism may contribute to thyroid myopathy.

The global inhibition of the main oxidative pathways (substrate incorporation, substrate oxidation) and of the respiratory chain within cells also may cause myopathic symptoms. A diminished energetic consumption is related partially to a transition in the myosin isoforms, which express a slower adenosine triphosphatase, and to an impairment of the transsarcolemmal transports. All of these factors may contribute to muscle weakness, fatigue, and exertional pain.

Exercise intolerance could be due to an abnormal recruitment of several metabolic pathways, such as glycolysis, related to the mitochondrial metabolism impairment. An abnormal accumulation of protons and monovalent phosphate ions (which are involved in the actin-myosin interaction), as well as abnormal Ca++ metabolism, also may cause reduced exercise tolerance.

Hyponatremia often is seen in patients with hypothyroidism. The decreased number of Na+/K+ adenosine triphosphatase–dependent pumps could imply an abnormal intracellular Na+ level and explain frequent disorders of membrane excitability.

Myoedema is a phenomenon in which mounding up of muscle tissue occurs after light percussion. Myoedema occurs in approximately one third of patients with hypothyroidism, but it is not entirely specific for hypothyroidism. Myoedema is thought to be caused by delayed Ca++ reuptake by the sarcoplasmic reticulum, which also prolongs muscle contraction. Although not proven, this type of prolongation of muscle contraction is also thought to cause muscle hypertrophy.


United States
  •  In North America, acquired impairment of thyroid function affects about 2% of adult women and about 0.1-0.2% of adult men.
  • Neonatal hypothyroidism occurs with a frequency of 0.02% in the white population. In the black population, the frequency falls to 0.003%. 
  • Of individuals with hypothyroidism, 30-80% manifest neuromuscular symptoms, depending on the severity of hypothyroidism. Weakness is observed in one third of patients with hypothyroidism. Carpal tunnel syndrome, although not part of the myopathy, is a peripheral nerve dysfunction found in 15-30% of patients with hypothyroidism.
  • Neonatal screening programs for congenital hypothyroidism in many areas of the world show that hypothyroidism is present in 1 out of every 4000 newborns. In iodine-deficient areas of the world, the incidence of hypothyroidism is 10- to 20-fold higher.

Mortality has not been shown to be increased in patients with hypothyroid myopathy. Morbidity is significantly increased, reflected in the performance of activities of daily living (ADL) and in patients' quality of life.


No race predilection has been established.


The incidence of hypothyroidism is much greater in women than in men. Myxedema coma is extremely rare, but its incidence is higher in elderly women, especially those older than 60 years.


Hypothyroidism is seen more commonly in women aged 40-60 years; however, it can be seen in persons of all ages.



Neuromuscular symptoms present in 30-80% of patients with hypothyroidism. These symptoms improve or
disappear with correction of the hypothyroid state.

Patients may complain of muscle cramping, proximal symmetrical muscle weakness, muscle stiffness, and exercise intolerance. These manifestations can occur at any time during the presentation of hypothyroidism. 

Slowness of muscle relaxation and of muscle contraction are noted in hypothyroid myopathy.


Deep tendon reflexes are delayed in approximately 85% of patients with hypothyroidism.

Mounding of the muscle after light percussion (ie, myoedema) occurs in one third of patients with hypothyroidism, but it is not necessarily specific to hypothyroidism.

Muscle enlargement, stiffness, and cramping are a constellation of findings seen in individuals with hypothyroidism. In adults, these findings are known as Hoffman syndrome. In children, they are called Kocher-Debré-Sémélaigne syndrome.

Myokymia, which may be related to a low sodium level, may be seen.

Causes   (See Pathophysiology.)

Hypothyroidism can impair mitochondrial metabolism, resulting in decreased muscle energy production. A low thyroid hormone level is the main causative factor.

Certain drugs, such as lipid-lowering medications, may exacerbate myopathy in patients with hypothyroidism.

There are reports of an increased risk for statin-induced myopathy in patients with hypothyroidism.

Lipid-lowering drugs include beta-hydroxy-beta-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors; also commonly called statins, they include following:
  • Atorvastatin (Lipitor) 
  • Fluvastatin (Lescol) 
  • Simvastatin (Zocor) 
  • Pravastatin (Pravachol) 
  • Lovastatin (Mevacor)
Interferon-alfa therapy for hepatitis, as well as hepatitis infection itself, has been reported to cause a number of adverse immunologic and/or autoimmune effects.Thyroiditis, seen in 10% of patients, may induce hypothyroidism.

Information Sources and References:

1. Barohn R. Metabolic myopathies. In: Cecil RL, Goldman L, eds. Textbook of Medicine. 21 ed. Orlando, Fla: Harcourt Health Sciences; 2000.

2. Miyake I, Hiromatsu Y. [Hypothyroid myopathy]. Ryoikibetsu Shokogun Shirizu. 2001;(36):294-7.

3. Scott KR, Simmons Z, Boyer PJ. Hypothyroid myopathy with a strikingly elevated serum creatine kinase level. Muscle Nerve. Jul 2002;26(1):141-4.

4. Deepak S, Harikrishnan, Jayakumar B. Hypothyroidism presenting as Hoffman's syndrome. J Indian Med Assoc. Jan 2004;102(1):41-2.

5. Turker H, Bayrak O, Gungor L, et al. Hypothyroid myopathy with manifestations of Hoffman's syndrome and myasthenia gravis. Thyroid. Feb 2008;18(2):259-62.

6. Tuncel D, Cetinkaya A, Kaya B, et al. Hoffmann's syndrome: a case report. Med Princ Pract. 2008;17(4):346-8.

7. Kisakol G, Tunc R, Kaya A. Rhabdomyolysis in a patient with hypothyroidism. Endocr J. Apr 2003;50(2):221-3. 

8. Sinclair C, Gilchrist JM, Hennessey JV, et al. Muscle carnitine in hypo- and hyperthyroidism. Muscle Nerve. Sep 2005;32(3):357-9. [Medline].

9. Lochmuller H, Reimers CD. Exercise induced myalgia in hypothyroidism. In: Year Book of Sports Medicine. St Louis, Mo: Mosby; 1994:999-1001.

10. Casimiro-Lopes G, Alves SB, Salerno VP, et al. Maximum acute exercise tolerance in hyperthyroid and hypothyroid rats subjected to forced swimming. Horm Metab Res. Apr 2008;40(4):276-80.

11. Cakir M, Samanci N, Balci N, et al. Musculoskeletal manifestations in patients with thyroid disease. Clin Endocrinol (Oxf). Aug 2003;59(2):162-7.

12. Horak HA, Pourmand R. Endocrine myopathies. Neurol Clin. Feb 2000;18(1):203-13.

13. Pourmand R. Metabolic myopathies. A diagnostic evaluation. Neurol Clin. Feb 2000;18(1):1-13.

14. Monzani F, Caraccio N, Siciliano G, et al. Clinical and biochemical features of muscle dysfunction in subclinical hypothyroidism. J Clin Endocrinol Metab. Oct 1997;82(10):3315-8.

15. Ghilardi G, Gonvers JJ, So A. Hypothyroid myopathy as a complication of interferon alpha therapy for chronic hepatitis C virus infection. Br J Rheumatol. Dec 1998;37(12):1349-51.

16. Obolonczyk L, Obolonczyk L, Siekierska-Hellmann M, et al. Side effects during interferon-alpha therapy of hepatitis C with special consideration of thyroid dysfunction. Postepy Hig Med Dosw (Online). Jun 26 2007;62:309-21.

17. Takanami I, Imamuma T, Yamamoto Y, et al. The rapid transformation of hyperthyroidism to hypothyroidism complicated by myasthenia gravis. J Thorac Cardiovasc Surg. Sep 1995;110(3):852.

18. Modi G. Cores in hypothyroid myopathy: a clinical, histological and immunofluorescence study. J Neurol Sci. Apr 1 2000;175(1):28-32.

Saturday, February 12, 2011

Low Thyroid Lab Confusion With TSH, T3, T4, Hypothyroid and Hyperthyroid

Dr. Chris Heimlich of Phoenix, AZ talks about what TSH, T3, T4 and other thyroid lab markers mean and how they relate to low thyroid function or hypothyroid. For More Information or to make an appointment with Dr. Heimlich call 480-991-9355


Wednesday, February 9, 2011

Canadian Football Player Recovers from Thyroid Cancer

Two months after he had surgery to remove his thyroid gland, Canadian football player Anthony Calvillo has reported a steady recovery from thyroid cancer, according to the Montreal Gazette.

The two-time Grey Cup champion and quarterback of the Montreal Alouettes announced his speedy recuperation at a press conference alongside his personal physician and his wife, Alexia, who has also overcome cancer.

The newspaper said that 38-year-old Calvillo had undergone a total thyroidectomy after doctors detected a malignant carcinoma in the gland. He was also treated with a round of radioactive iodine therapy, which destroys cancerous thyroid cells that remain in the body.

The football player announced that he plans to continue playing for the Alouettes, a team that he joined 13 years ago.  Calvillo has the second most passing yards of any quarterback in the Canadian Football league, according to his official team profile. He told the press that he might never have noticed that he had thyroid cancer if he had not been hospitalized in August for a bruised sternum.

CTV reported that doctors noticed a lump in his thyroid while he was being given an extensive physical exam. Biopsies later revealed that the nodule was malignant.  The player's physician, Vincent Lacroix, noted that Calvillo will be taking levothyroxine - which is a synthetic thyroid hormone also known by various brand names, including Synthroid and Levoxyl - as part of his post-operative medical regimen.

Individuals who undergo full thyroidectomies must take thyroid hormone supplements. Without this treatment, they will experience hypothyroidism. This condition is characterized by sluggishness, brittle hair, dry skin, muscle cramps and depression, according to the National Endocrine and Metabolic Diseases Information Service.

For people Calvillo's age who are treated for the disease, the outlook is often good. The mortality rate for thyroid cancer among adults between the ages of 35 and 44 is just over 2 percent, the National Cancer Institute (NCI) reports. Overall, one in 111 Americans will be diagnosed with thyroid cancer in their lifetimes, the NCI states.

Sunday, February 6, 2011

EPA decides to regulate drinking-water chemical linked to thyroid cancer

The U.S. Environmental Protection Agency (EPA) recently announced that it has set a national standard for the allowable level of perchlorate, a chemical linked to thyroid cancer, in tap water.  The agency will likely set the safe level at one part per billion, a level recommended eight years ago by a committee convened by the EPA, the Associated Press reports.

The news source added that this recommended level was later increased to 15 parts per billion under President George W. Bush, whose administration decided not to pass any official public health standards concerning the chemical. The new regulations will supersede that decision.

Perchlorate is a volatile molecule that contributes to the combustion reaction in airbags, fireworks and solid rocket fuel, the agency said. It was formerly used to treat to treat some forms of hyperthyroidism, a condition in which the thyroid gland overproduces hormones.

Since the chemical interferes with the production of thyroid hormone, its presence in drinking water has been associated with hypothyroidism, certain thyroid cancers and glandular disorders in pregnant women and newborns. Extended exposure to perchlorate caused thyroid cancer in laboratory rodents, according to a study conducted by the Centers for Disease Control and Prevention (CDC).

Even if thyroid cancer were not a risk, the agency says that the chemical affects the way that the thyroid takes up iodine, which can, in turn, affect nearly every system in the body.  Once the EPA has finalized the chemical's regulation under the Safe Drinking Water Act, public water systems will be largely responsible for ensuring that the level of perchlorate stays at or below the recommended level.

The agency states that perchlorate may currently be present in the drinking water of more than 16 million Americans.  In the U.S., more than 44,000 people are diagnosed with thyroid cancer every year, according to the CDC.

Thursday, February 3, 2011

Neuropathy Symptons and Thyroid Disease: The Pain is Real

In general  thyroid disease and thyroid hormone imbalance can present with symptoms of peripheral neuropathy and other neurological problems which may not fully resolve with hormone treatment in all patients. This is particularly true for thyroid cancer survivors who may have a unique sensitivity to radio-active iodine therapy and other thyroid cancer treatments for advanced or metastatic thyroid cancer such as external beam radiation and chemotherapy.

In many cases, the neurologic manifestations occur in conjunction with the systemic features of  thyroid  disease and may be noted only incidentally. However, symptoms and signs of neurologic dysfunction may be the presenting feature in some patients and can contribute significant disability. Most of these complications are partially or fully responsive to thyroid replacement therapy in the majority of cases but for some Thyroid dysfunction related neuropathy can become a life long struggle.

Hyperthyroidism and Nerve Pain:
What Thyroid Cancer Survivors Should Know  

Thyroid hormones are  important at a cellular level, affecting nearly every type of tissue in the body, these hormones functions as controllers of the pace of all of the processes in the body. This pace is called metabolism. If there is too much thyroid hormone, every function of the body tends to speed up. It is therefore not surprising that some of the symptoms of hyperthyroidism are nervousness, irritability, increased perspiration, heart racing, hand tremors, anxiety, difficulty sleeping, thinning of the skin, fine brittle hair, and muscular weakness—especially in the upper arms and thighs. More frequent bowel movements may occur, but diarrhea is uncommon.

Thyroid hormone is critical to normal function of cells. In excess, it both overstimulates metabolism and exacerbates the effect of the sympathetic nervous system, causing "speeding up" of various body systems and symptoms resembling an overdose of epinephrine (adrenaline). These include fast heart beat and symptoms of palpitations, nervous system tremor such as of the hands and anxiety symptoms, digestive system hypermotility (diarrhea), considerable weight loss and unusually low lipid panel (cholesterol) levels as indicated by a blood test.

Hyperthyroidism usually begins slowly. At first, the symptoms may be mistaken for simple nervousness due to stress. If one has been trying to lose weight by dieting, one may be pleased with weight loss success until the hyperthyroidism, which has quickened the weight loss,  causes other problems.

Thyroid Related Neuropathy Symptoms

Neuropathy symptoms include those having to do with nerve functions throughout the body. Common neurological symptoms include headaches, numbness or tingling in the hands and/or feet (peripheral neuropathy), abnormal reflexes and muscle weakness and spasms. Thyroid disease is an endocrine gland disorder (hormone related) and all disorders in this category, including diabetes have potential to cause neurological symptoms. In the case of thyroid disease, the hormones produced by this endocrine gland regulate the metabolism in every cell of the body, including those related to nerve function. When a disorder affecting thyroid hormone balance develops or they thyroid gland is surgically removed, the function of the nervous system can be sped-up or slowed down, resulting in nerve-related symptoms.

Treating Thyroid Hormone Imbalances

Hypothyroidism is a condition in which thyroid hormone levels drop below normal. This results in all bodily functions slowing down (hypo-metabolism), including brain-nerve signals (motor responses). It also causes fluid build up in tissues of the body or what is referred to as “myxedema”, which can cause pressure on nerves, resulting in additional symptoms of neuropathy, such as numbness and tingling in the extremities. When thyroid hormones are brought back up to correct levels, these type symptoms improve, as well as myxedema in body tissues affecting nerve signals.

[Hypothyroidism is a common and growing medical condition in the general population that often goes undiagnosed or misdiagnosed for many reasons. Common systemic manifestations include fatigue, constipation, cold intolerance, weight gain, hair loss, dry skin, and hoarseness which are often discussed in blogs and other forums. An often overlooked and more important discussion is a  variety of central and peripheral nervous system manifestations common in patients with hypothyroidism and hyperthyroidism.]

Hyperthyroidism is a condition of abnormally high thyroid hormone levels, which causes all bodily functions to become sped up (hyper-metabolism). Muscle reflexes are hyper-reactive, meaning there is abnormal muscle tension in response to brain-nerve signals. This can result in the adverse effect following physical activity, of severe muscle weakness. Some patients may also experience episodes of muscle paralysis and/or muscle deterioration. Neurological symptoms that accompany hyperthyroid conditions are sometimes referred to as “thyrotoxic myopathy” but will improve significantly with treatment to reduce thyroid hormone levels and treatment for symptoms of an overactive metabolism via anti-thyroid drugs and beta-blockers.

Thyroid cancer survivors can have fluctuations in their thyroid hormone levels ranging from high to low (hyper / hypothyroidism) as a result of the surgical removal of the thyroid gland and how well they respond to hormone replacement therapy, synthetic hormone absorbtion and other individual factors such as co-existing disorders or medical conditions that require the use of other medications among other things.  It is also important to remember that thyroid cancer patients are normally required to remain slightly hyperthyroid to prevent thyroid cancer recurrence.

Thyroid Antibodies: The thyroid hormone imbalances caused by the surgical removal of the thyroid gland and other thyroid diseases are an obvious cause of neurological symptoms but what role does “thyroid autoimmunity” play in these type symptoms? Autoimmune-caused hypothyroidism is called Hashimoto’s thyroiditis and autoimmune-caused hyperthyroidism is called Graves’ disease. Medical research conclusions on studies of thyroid patients has shown that the disease process itself may contribute to neurological symptoms in some thyroid patients in spite of correcting abnormal thyroid hormone levels.

For those patients whose neuropathies do not fully resolve with treatment for thyroid hormone imbalance, another factor in causing symptoms that should be considered is the disease process of thyroid autoimmunity itself. The auto-antibodies sent from the immune system to attack the thyroid gland may also exert negative effects on the peripheral nervous system. Some of this may be the result of inflammation in the body that begins to effect nerve function. With “Hashimoto’s Encephalopathy” for example, which can result from Hashimoto’s thyroiditis in very rare cases, severe and even life-threatening neurological symptoms can develop. It would seem obvious that neuropathies may manifest in Hashimoto’s patients to lesser degrees as well.

Other medical research studies have found that some autoimmune thyroid disease patients have other auto-antibodies present as well, that can directly affect the nervous system. This includes studies that have found mild manifestations of other autoimmune diseases present in thyroid patients including symptoms of Myasthenia Gravis. There is no cure for auto-antibodies but keeping thyroid hormone disorders well-treated can help and some research suggests that supplementing patients with selenium may help to reduce thyroid antibody levels.

Side Effects of Neuropathy

It is important to understand that neuropathy exists in two forms, autonomic and peripheral.
  • Autonomic neuropathy involves damage to nerves that control involuntary functions, such as heart rate, blood pressure perspiration and digestion, states
  • Peripheral neuropathy is nerve damage in motor and sensory nerves that leads to pain, numbness and weakness. Many different conditions, infections, poisonous substances and forms of trauma can cause neuropathy. A patient should be aware of the side effects of neuropathy and know when to seek treatment.

1.  Dizziness and Fainting states that dizziness and fainting are side effects associated with neuropathy. Specifically, damage to autonomic nerves that control blood vessels are affected. Because these nerves are damaged, blood vessels cannot contract and expand to control blood pressure. A patient with an autonomic neuropathy that controls blood vessels may experience dizziness and fainting when standing from a sitting or laying position. This occurs because blood vessels in the lower body do not effectively constrict, or shrink in response to the increase in blood pressure in the lower extremity. This causes blood to pool in the legs, which reduces blood pressure in the brain. Because blood pressure in the brain is reduced, a patient may begin to feel dizzy or faint.

MedlinePlus states that a peripheral neuropathy may cause a loss of sensation. This occurs because damage to sensory nerves result in numbness and an inability to determine joint position, which can cause incoordination. A patient may notice sensory loss that begins in the hands or toes that progressively affects the arms or legs. Sensory loss is a serious medical condition because patients, particularly diabetic patients, may not be able to feet a sore or ulcer developing in the feet. The open sore or ulcer can get infected, which may lead to serious complications. Thus, a patient with a sensory loss should not hesitate to schedule an appointment with the physician so the cause of sensory loss can be determined.

2. Movement Difficulties

Neuropathy may affect nerves that control muscles, states MedlinePlus. Specifically, advanced peripheral neuropathy may affect motor nerves in the hands, arms, feet or legs that results in difficulty moving. In addition, a patient may experience cramps, difficulty breathing, difficulty swallowing, joint instability, lack of coordination and loss of muscle tissue. Peripheral neuropathy should be diagnosed and treated early to avoid further decrease in motor function.

What About When the Pain Doesn't Go Away?

Typically, neuropathy symptoms do usually resolve with proper treatment of  your thyroid condition. When muscle and joint pain does not go away with proper thyroid treatment, however, it's time to ask yourself and your doctor several questions.
  • If you are hypothyroid, are you getting sufficient and proper treatment? Insufficient thyroid hormone replacement, or a need for the additional hormone T3, may be required to resolve muscle and joint pain.
  • If you are receiving optimal thyroid treatment, and still suffering joint and muscle problems, should you get a referral to a rheumatologist, for further evaluation and possible treatment?  In many cases a well  trained rheumatologist can provide a more thorough evaluation of  unexplained muscle aches and pains that does not respond to pain medication. *Rheumatologists are experts in joint and muscle problems, and treat arthritis, some autoimmune conditions, various musculoskeletal pain disorders, fibromyalgia and tendonitis.
*To find a rheumatologist in your area, check the American College of Rheumatology's Doctor Directory

Interestingly, on the subject of fibromyalgia, some practitioners actually believe that fibromyalgia is actually a manifestation of hypothyroidism. Fibromyalgia is a syndrome that features specific tender points in the body, with widespread weakness and fatigue.
  • Is it time to look into alternative therapies? Some patients with chronic joint and muscle pain related to their thyroid conditions have had success with therapies such as massage, acupuncture, bio-feedback,  myofascial and nutritional supplement therapies.

Tuesday, February 1, 2011

Thyroic Cancer and Sexuality

Some of the possible effects of cancer and its treatment on sexuality are described here. Please remember and keep in mind  that it is very difficult to accurately predict how cancer and its treatment will affect you -individually-, and for some thyroid cancer patients and survivors who have difficulty metabolizing synthetic hormones  this can become a life long challenge you may need help with as you adapt to hormonal changes after the loss of a major endocrine gland.

Some people may need to adapt to changes and develop new ways of giving and receiving sexual pleasure. If you have a committed, loving partner, cancer does not mean your sexuality will be destroyed. With support and clear communication, you will often still be able to enjoy a fulfilling sex life no matter what type of cancer you have or the treatment you receive.

There are four main ways that cancer or its treatment can affect your sexuality:

(1) physical ability to give and receive sexual pleasure

(2) thoughts and feeling about your body (body image)

(3) feelings, such as fear, sadness, anger and joy roles and relationships.

The links between these four areas are important. If there is a problem in one of them, it may have an impact on another. When someone becomes ill, it can affect their ability to feel good about themselves sexually, or their physical ability to give and receive sexual pleasure. If this has happened to you or your partner, it might be helpful to understand that some changes will only be temporary.

Even if the changes are long lasting, or permanent, you can find ways to adapt sexual techniques that are no longer possible or discover new ones. You can learn to feel good about yourself sexually despite the cancer and the possible side effects of the treatments.
  • Tiredness - Many people with cancer say that they feel washed out and almost completely without energy for many months or even years. This may be to do with the cancer itself, or sometimes the treatment. This tiredness can make people lose interest in sex during and after cancer treatment.
  • Mismatch in sex drive - In many relationships one partner may be more interested in sex than the other. Cancer can exaggerate this. If one partner has a change in their level of desire, this can be upsetting when there is the added complication of cancer.
How will cancer affect my sex life?

Sexual feelings and attitudes vary greatly among people under any circumstances. This is also true during illness. Some people have little or no change in their sexual desire and energy level because of cancer. Others find that their interest declines because of the physical and emotional stresses of having cancer and getting treatment. Stress may include concerns about changes in appearance; worry about health, family, or money; or the results of treatment side effects, including fatigue and hormone changes.

Some people find that they feel even closer to their partners during this time and have an increased desire for sex. Even though pregnancy may be possible during cancer treatment, it may not be wise because some treatments could cause birth defects. Many doctors tell men and women to use birth control throughout their treatment.

If your sexual desire and energy levels change during treatment, keep in mind that this is normal and can happen for a number of reasons. Some common reasons are stress, fatigue, and other treatment side effects. Body image issues may also play a part. If you have had surgery for a cancer in the pelvic or stomach areas, it may make intercourse difficult or painful for a time. Some women have vaginal dryness, and some men have problems with erections (erectile dysfunction) as a side effect of some treatments. If possible, discuss these concerns with your cancer care team and your partner.

If you were comfortable with and enjoyed a healthy sex life before starting treatment, chances are you will still find pleasure in physical intimacy during your treatment. You may find that intimacy takes on a new meaning and you relate differently. Hugging, touching, holding, and cuddling may become more important, while sexual intercourse may become less important.

Good communication is the key to staying sexually active or resuming your sex life with your partner. Your partner's concerns or fears are normal, and they can have an impact on your sex life. Some partners may worry that physical closeness will hurt the person who has cancer. Others may fear that they might "catch" the cancer or be affected by the radiation or chemotherapy. Catching cancer is not possible, but talking about issues like these can clear up many problems. It will also help you find out what different things you can do to make the sexual contact something you can both enjoy.

A healthy sex life can be hard to maintain when there are so many physical and emotional factors involved. Get as much information from your doctor and other resources as you can so that you understand what you can and cannot do before, during, and after treatment. For more information, you may order the free booklets Sexuality for the Man With Cancer and Sexuality for the Woman With Cancer by calling your American Cancer Society at 1-800-227-2345.