By Gary M. Pepper, M.D. (This article is for educational purposes only and is not intended as medical advice or treatment) During the Covid-19 pandemic my medical practice has been operating as normally as possible. The other day a young woman arrived wearing a surgical mask with a stack of medical records in hand, for a new patient appointment. Her difficulties began 6 weeks prior with intense tenderness in the right side of her neck just above the clavicle (collarbone) which varied in intensity over the course of about 10 days. Evaluation by her primary care physician uncovered newly elevated thyroid hormone levels. During our discussion she recalled a respiratory tract infection starting a week before the neck pain developed. Still complaining of lung congestion she denied fever or shortness of breath. Sitting comfortably, the thyroid was no longer tender but was slightly enlarged and unusually firm. Reading on it will become clear why my preliminary diagnosis is sub-acute thyroiditis, an inflammation of the thyroid following a viral respiratory tract infection, possibly Covid-19.
The nature of interaction between the thyroid and coronavirus is unknown but we are on the verge of finding out as we investigate cases like this. Until then, our understanding of how other viral infections affect the thyroid can provide grounds for speculation. A good place to start is with Hashimoto’s thyroiditis, also known as chronic lymphocytic thyroiditis. This is a common thyroid disease most often diagnosed in middle-aged women although it can occur in both sexes and all ages. As an autoimmune disease Hashimoto’s results when immune cells and the antibodies they produce attack the thyroid gland. Normally immune cells, known as lymphocytes, with their antibodies are protective against viral and bacterial infection. In autoimmune thyroid disease a population of the affected individuals immune cells begin to destroy thyroid cells instead. Technically this is an inflammatory reaction but unlike many inflammations, Hashimoto’s is generally painless. Being painless, Hashimoto’s can exist for many years before it is detected by routine blood tests for thyroid levels or is discovered on physical exam presenting as an enlarged and lumpy (nodular) thyroid gland.
The development of Hashimoto’s is thought to involve inherited (genetic) factors but also likely requires an environmental trigger such as a virus to initiate clinical disease. The genetic nature of Hashimoto’s is manifest in the occurrence of the disease in multiple members within a family. The type of viral infection promoting this disease is unclear. Some studies point to Epstein Barr virus, commonly called EB virus as a potential trigger for Hashimoto’s activation. EB virus is extremely wide spread found in over 95% of the world’s population. In humans, it generally exists in an asymptomatic state from childhood to old age. In certain individuals, EB virus can create serious illnesses such as mononucleosis or cancers of the lymphoma type. Evidence that EB virus plays a significant role in autoimmune thyroid disease includes finding of the EB viral genetic material (RNA) in the thyroid tissue of 80% of those with Hashimoto’s and 62% of those with Grave’s (hyperthyroidism). 90% of all lymphomas involving the thyroid occur in those with Hashimoto’s, and as just mentioned lymphoma is a characteristic cancer related to EB viral infection.
Why do some people and not others develop the more severe form of EB disease such as lymphoma or autoimmune thyroid disease? The likely explanation is that as mentioned above, genetic factors result in susceptibility to more aggressive complications of the viral infection. Many infectious disease experts are speculating similar genetic factors account for the extreme variability between individuals of complications of Covid-19.
Another form of thyroid inflammation that unlike Hashimoto’s is often painful, is sub-acute or DeQuervain’s thyroiditis. This thyroid disorder tends to occur days to weeks after an upper respiratory illness. The onset is often accompanied by fatigue, generalized muscle pain, low-grade fever and throat pain, which can radiate upward to the ears. At the onset of this disorder thyroid hormone levels are elevated due to destruction of thyroid cells releasing hormone into the blood. Many of the presenting symptoms of sub-acute thyroiditis are those of elevated thyroid levels such as rapid heart rate, sweating, and weight loss. These symptoms usually resolve in a few weeks and in 15-30% of patients due to thyroid tissue destruction permanently under active thyroid function (hypothyroidism) results.
Substantial evidence exists for involvement of viral infection in the development of sub-acute thyroiditis. For example, the occurrence of sub-acute thyroiditis is more frequent in summer when Coxsackievirus infection is most common. Virus particles similar to mumps and flu have also been found in the thyroid of people with sub-acute thyroiditis and outbreaks of this thyroid disease have occurred during mumps epidemics. Some experts believe that sub-acute thyroiditis is a post-viral illness, meaning the body’s immune response persists even after cleansing the body of the virus but in a misdirected manner, attacking molecular targets on the thyroid cells that bear similarities with the virus structure. Interestingly, the occurrence of sub-acute thyroiditis is more common in those with Hashimoto’s.
The presence of HTLV-1 viruses has also been associated with development of autoimmune thyroid disease including both Hashimoto’s thyroiditis and Grave’s disease (hyperthyroidism). Evidence for this involves finding antibodies to HTLV-1 virus in Hashimoto’s and Grave’s patients. About 6% of those with Grave’s and 7% of Hashimoto’s having these antibodies. Since 95% of people with antibodies to HTLV-1 never develop any symptoms, screening people for this infection is currently not being done.
A common question in my medical practice is whether those with Hashimoto’s have increased vulnerability to Covid-19 infection? There have been no formal studies of this as yet but in a poll of the 10 endocrinologists in my group none felt that Hashimoto’s was a risk factor for suppression of the immune system which could result in more severe viral complications. Also, there is no compelling evidence that those with Hashimoto’s have impaired ability to fight infections. Of great interest, a study published in 2022 reports that several cases of Grave’s disease or overactive thyroid function have resulted after SARS-CoV-2 vaccination
Studies indicate that low levels of thyroid hormone can result in impaired immune function without any link to underlying Hashimoto’s. This relationship should motivate those with hypothyroidism to check that their thyroid hormone levels are optimized to help maintain immune function. There is disagreement in the medical community regarding what exactly constitutes best thyroid hormone levels and how to achieve those levels when medication is required. Concerned individuals should discuss this matter with a qualified health care provider and valuable information on this topic can be found at www.metabolism.com.
Another question in the wake of the coronavirus pandemic is whether the virus induces pathological changes in the thyroid such as seen with Hashimoto’s thyroiditis, Grave’s disease or sub-acute thyroiditis. If infection by this virus does affect the thyroid the clinical signs and symptoms could take weeks after recovery from Covid-19 to become apparent. As detailed by the case reported at the beginning of this article, initial symptoms of sub-acute thyroiditis include pain in the throat often radiating upward to the ears, swelling in the lower neck, and tenderness in this area. During the early phase of sub-acute thyroiditis symptoms of elevated thyroid levels can also occur including excessive sweating, persistently feeling hot, rapid heartbeat, shakiness, and unexplained weight loss. Similarly, Grave’s disease can cause these symptoms but without the accompanying tenderness in the thyroid area. If enough damage is done to the thyroid by the inflammation within a few more weeks symptoms of low (hypo) thyroid levels may develop such as feeling unusually cold, muscle cramps, unexplained weight gain, fatigue, constipation and facial puffiness. Individuals are encouraged to consult with their health care professional if experiencing these or other unusual symptoms to determine if they represent a medical disorder.
By Gary M. Pepper, M.D. (This article is for educational purposes only and is not intended as medical advice or treatment)
During the Covid-19 pandemic my medical practice has been operating as normally as possible. The other day a young woman arrived wearing a surgical mask with a stack of medical records in hand, for a new patient appointment. Her difficulties began 6 weeks prior with intense tenderness in the right side of her neck just above the clavicle (collarbone) which varied in intensity over the course of about 10 days. Evaluation by her primary care physician uncovered newly elevated thyroid hormone levels. During our discussion she recalled a respiratory tract infection starting a week before the neck pain developed.Â Still complaining of lung congestion she denied fever or shortness of breath.Â Sitting comfortably, the thyroid was no longer tender but was slightly enlarged and unusually firm.Â Reading on it will become clear why my preliminary diagnosis is sub-acute thyroiditis, an inflammation of the thyroid following a viral respiratory tract infection, possibly Covid-19.(more…)
Update from the 15th International Thyroid Congress, Orlando Florida, October, 2015 By Gary Pepper, M.D. Â Â Â Â I just returned from Orlando, Florida, where I attended the 15th International Thyroid Congress and want to provide a report of my experience, to readers of metabolism.com. This was truly an international event with an estimated 50% of the attendees from outside the U.S. Organizers of this event describe it as, â€œRenowned experts in thyroid function and biology, diagnosis and management of thyroid disease, and novel therapies for treating thyroid cancer are gathering at the 15th International Thyroid Congress (ITC) to present, discuss, and debate the latest advances in thyroidology. Held every five years, the ITC is a collaborative meeting of the four world thyroid associations; the ATA (American Thyroid Association), Asia-Oceania Thyroid Association (AOTA), European Thyroid Association (ETA), and Latin American Thyroid Society (LATS).â€ I was particularly excited to be attending this conference this year since my colleagues, Drs. Paul Cassanova and Kathryn Reynolds and I were presenting our study on the use of combination T3 plus T4 for the treatment of underactive thyroid (hypothyroidism). Here are some papers I found to be of particular interest; (more…)
A few weeks ago a new patient arrived at my office to discuss treatment for her thyroid disease. She was diagnosed with an under active thyroid several years prior but treatment with Synthroid was unsuccessful. She stopped using the medication on her own, at least a year ago. Blood tests obtained by another doctor a month before her visit with me, were diagnostic of hypothyroidism (low thyroid levels with elevated TSH) . During our session she described typical symptoms of hypothyroidism including fatigue, feeling unusually cold, dryness of the skin, brittle nails and puffiness around the eyes. On exam her thyroid was enlarged and had a gritty texture typical of Hashimotoâ€™s Thyroiditis. Her sister and mother also had thyroid disease, increasing the likelihood of the diagnosis of Hashimotoâ€™s. Since her latest thyroid blood tests were only a few weeks old I felt comfortable beginning her on thyroid hormone replacement, in this case, Armour Thyroid, which I prefer due to its excellent clinical effectiveness.
My new patient was also on a number of supplements and vitamins including a non-prescription â€œmetabolic complexâ€ given to her recently by her chiropractor. By law in the U.S. supplements like these do not possess thyroid hormone and, in my experience, have no impact on thyroid hormone levels, either to increase or decrease them. As a precaution, we obtained a new set of thyroid hormone levels along with the test for Hashimotoâ€™s Thyroiditis (anti-thyroid antibody panel).
Several days later, the patient called complaining she was â€œallergicâ€ to the Armour Thyroid, developing jitteriness, anxiety, feeling flushed and a rapid heart rate. My first thought was she received the wrong dose of medication but a quick check of her records indicated this was not the issue. I called the lab and was surprised to learn the TSH at the time of her visit was already low, indicating excess thyroid levels or hyperthyroidism. What could have caused the sudden switch from hypo to hyper thyroidism? Rarely, patients with Hashimotoâ€™s Thyroiditis can convert to hyperthyroidism, an event I call the Zombie Thyroid because the thyroid comes back from the dead. More likely was that one of her supplements contained actual thyroid hormone, so I asked the patient to get me the labels from these products. In the meantime, I instructed her to stop the Armour Thyroid and the supplements until I could figure out what was happening. Her allergic symptoms resolved in a few days.
Examination of the supplementsâ€™ labels indicated that one manufactured in New Zealand did in fact have thyroid extract in it. It had so much thyroid hormone in it that the patient was already becoming hyperthyroid at the time she first came to the office. Signs and symptoms of hyperthyroidism didnâ€™t develop until she started taking Armour Thyroid along with the supplement. The mystery was solved but I am left feeling much less secure that my patients will not injure themselves with products obtained from outside the country either via the internet or from practitioners who provide it, perhaps unwittingly.
As I have in the past, I urge everyone to avoid medications and supplements produced outside the country which can contain active ingredients with potential health hazards. Always check with a physician before beginning a supplement which is obtained from the internet or mail order.
Gary Pepper, M.D. Editor-in-Chief, metabolism.com
This information is for educational purposes only and is not intended as medical advice or treatment. Some details of this case have been altered to protect the patientâ€™s identity.
Periodically, I update metabolism.com with interesting problems from my medical practice. Last week I was reminded of a particular thyroid disease which is little known and deserves more attention. In my patient’s case, she had an inactive thyroid (hypothyroid) due to Hashimoto’s thyroiditis for several years which, on its own switched to become an over-active thyroid (hyperthyroid). I call this event a “Zombie Thyroid”. Don’t bother trying to look this term up since ‘Zombie Thyroid’ is my own terminology. A Zombie Thyroid is, of course, one which returns from the dead. Most times when the thyroid is destroyed by either natural forces or by human intervention, the destruction is complete and irreversible. Rarely however, a thyroid which ceased function for years resumes producing thyroid hormone and may even becoming “hyper” or over-functioning. Such was the case of my patient last week. Confusion may result because the newly risen thyroid begins adding thyroid hormone to the blood of someone already taking thyroid hormone replacement for hypothyroidism (under-functioning thyroid). Recognizing the Zombie Thyroid can take months or years due to the rarity of the condition and the subtlety of the changes that occur on blood testing.
The Zombie Thyroid occurs in the setting of either autoimmune thyroid disease such as Hashimoto’s thyroiditis or a structural thyroid disease, multinodular goiter. Hashimoto’s is the most common cause of naturally occurring hypothyroidism in women under the age of 60 years. Hashimoto’s occurs when the body creates an antibody to the thyroid, resulting in destruction or impairment of the thyroid tissue. It is thought that the thyroid can ‘return from the dead’ if the body begins to produce more of another type of antibody that results in stimulation of the thyroid tissue. The switch from under active to over-active can take months or years. During this time the combination of taking thyroid hormone pills for Hashimoto’s plus the new supply of the body’s own thyroid hormone production can result in disturbing and seemingly unexplainable high thyroid levels. Once it is clear that the thyroid is producing thyroid hormone again it is possible to make appropriate adjustments in medication to return the situation back to normal.
Another situation involving the Zombie Thyroid is seen in elderly people who have had an enlarged and lumpy (nodular) thyroid for years. Some of these “multinodular goiters” produce adequate amounts of thyroid hormone but others can be associated with thyroid hormone deficiency (hypothyroid). When the multinodular goiter causes hypothyroidism, the patient will be treated with thyroid hormone replacement just like the Hashimoto’s patient. Over time the nodules may slowly begin to wake up and begin producing thyroid hormone. If the patient is already taking thyroid hormone due to the previous diagnosis of hypothyroidism, the combination of the two sources of thyroid hormone can result in excess or “hyper” thyroidism. In the elderly the doctor may suspect the elevated thyroid hormone levels are the result of a medication error perhaps due to the patient’s forgetfulness. If no action is taken serious complications of hyperthyroidism can develop such as irregular heart beat, congestive heart failure, excessive fatigue, and mental or mood impairment. Some elderly patients become withdrawn and lose weight mimicking depression, a situation known as “apathetic hyperthyroidism”. Recognition of the Zombie Thyroid is essential to restoring the thyroid levels and the patient’s clinical status back to normal.
Don’t let yourself or loved one become a victim of this ‘back from the dead’ thyroid. Alertness is the key to recognizing and treating the Zombie Thyroid. Ask your own physician for advice if you suspect this condition.
This article is for educational purposes only and is not meant as medical advice. The disclaimer of metabolism.com applies to this and all my blogs.
Gary Pepper, M.D., Editor-in-Chief, metabolism.com
The mission of the The Thyroid Project is to encourage sharing of information and experience between the public and the medical community about the treatment of hypothyroidism (low thyroid function). For at least the past few decades there is a growing awareness of â€œsomething missingâ€ in the way suffers of hypothyroidism are treated for their disease.
Too many patients, as documented in an on-line study of 12,000 individuals conducted by the American Thyroid Association published in June 2018, (https://doi.org/10.1089/thy.2017.0681) , complain of persistent symptoms of hypothyroidism despite what their doctors believe is successful treatment with levothyroxine (brands include Synthroid, Unithroid, Tirosent, Levoxl). We believe something needs to be done to resolve this conflict between patients and their doctors.
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