autoimmune thyroid Archives

Fluoroquinolone Antibiotics and Thyroid Problems: Is There a Connection?

Published on March 19, 2024

66104 views

One Fateful Day – And a Journey into the Enigmatic World of Thyroid Related Problems Begins

I remember the day of March 19, 2010 very well. That was the last day I ever went jogging. That was the last day I could have hopped on my bike and ridden 50 miles if I wanted to. That was the last day I ate my favorite breakfast of a 3-egg omelet topped with cheese and veggies, with 3 pieces of whole wheat toast slathered in butter and jam, 3 pancakes on the side, and at least a quart of milk. That was the last day I worked in my profession, brought home a paycheck, and was self sufficient financially. It was the day before I started taking Ciprofloxacin, a fluoroquinolone (FQ) antibiotic, for a simple UTI. And it was the last day I was a normal person with a normal life.

By March 25, 2010 – six days later — I was completely bedridden with severe pain in what felt like every tendon in my body, along with peripheral and central neurological symptoms and other symptoms from the side effects of that drug. These adverse effects are collectively called “Fluoroquinolone Toxicity Syndrome” (FQT), or “floxed” for short. And although I didn’t realize it then, my physical, professional, financial, and personal life as I knew it was over. Within a few days and a few pills, I joined the ranks of the chronically disabled, those with “chronic invisible illnesses”, and “Romney’s 47%”. It’s five long years later, and I still struggle with the aftermath of taking those few pills. I regret every single day since then that I ever even considered a fluoroquinolone antibiotic for a simple UTI.

So what does all this have to do with the thyroid gland? Well, like most victims of this toxicity, all my extensive traditional medical testing during the acute phase of the reaction, as well as for the first year and a half after, gave normal or negative results. Astoundingly enough, despite being severely disabled and feeling essentially non-functional, according to the medical profession, I was the picture of health on paper. Until I finally decided to do more than a TSH test to check my thyroid status. That’s when I discovered I had all the anti-thyroid antibodies. And that’s really when my journey into the enigmatic world of “thyroid problems” began in earnest.

Having the antibodies for both Hashimoto’s Thyroid Disease and Grave’s Thyroid Disease makes for an astounding array of symptoms. Many of them appeared to mimic or overlap my symptoms of Fluoroquinolone Toxicity. Naturally, as a result of these observations, and my experiences with these conditions, I started questioning as to how much fluoroquinolone antibiotics caused severe endocrine disruptions, in particular of the thyroid axis.

The Thyroid Fluoroquinolone Epidemic: Where Is the Research?

There is a lot of published research available showing how damaging the FQ’s are too many different body systems and cellular processes, but almost none of it includes the thyroid system or the endocrine system in general. I suspect that someday, studies will be published showing the association between fluoroquinolones and thyroid abnormalities. Until then, it will be up to patients themselves to try and figure out if this association exists for themselves. In my case, my suspicions were further strengthened when I found that thyroid hormone medications, both T4 and T3, dramatically and profoundly affected all my floxing symptoms. Even more interesting to me, iodine alone did the same. I also found it interesting that a significant number of flox victims reported hormonal disruptions of all types post flox, such as with sex hormones, adrenal hormones, thyroid hormones, dysglycemias presumably in association with insulin hormone, and Vitamin D, which is also considered a hormone. This was also true of me after I was floxed. Eventually, I created a website* summarizing my observations, experiences, interpretations, and hypotheses on these possible correlations.

I had several intentions in creating the website, and one of them is to start the conversation about this potential link between fluoroquinolones and thyroid related problems, hopefully leading to unbiased studies and research in this area. I believe it is sorely needed. According to the U.S. Preventive Services Task Force Clinical Guidelines:

“The annual number of dispensed prescriptions of levothyroxine sodium in the United States increased by 42% over a 5-year period, from 50 million in 2006 to 71 million in 2010. In 2013, there were more than 23 million new prescriptions and refills for a single name brand of thyroid hormone in the United States, making it the most commonly prescribed drug in the country.”

This implies there are a lot of “thyroid problems” out there. According to several news investigations airing across the country, the FQ antibiotics are one of the top five drugs prescribed in the US each year. In our current day and age, we are bombarded by many substances which are known or suspected endocrine disrupters, including affecting the thyroid system. Could the epidemic of FQ usage be contributing to the epidemic of thyroid-related problems resulting in patients receiving thyroid medication for life? It would not surprise me if this were the case. I hope association studies, along with causation studies, will be done someday. Until then, those of us with thyroid disorders are on our own in looking at FQ antibiotic usage history and questioning this association for ourselves.

In my case, it was pretty clear cut that the acute symptoms I experienced right after starting the antibiotic were actually caused, or at a minimum, triggered by the antibiotic. My flox symptoms were pretty classic for these reactions all around, and there is plenty of research, as well as anecdotal stories, to substantiate this. But were my symptoms also “thyroid related”? In other words, did the antibiotic affect my thyroid system, either primarily and directly, or secondarily through a “cascade effect”, and at least some of these floxing symptoms I experienced were actually “thyrotoxic” symptoms as well? I think the answer is yes. These are the issues that I explore in my website, and I will briefly present here.

Tendon Pain and Ruptures: A Link between FQ Antibiotics and Endocrine Disorders?

One of the most well known adverse effects of FQ antibiotics are tendon problems. Most flox victims will experience some level of tendon pain at some point in time during their flox reaction. Regardless of what other symptoms occur with FQT, the severe tendon pain that can occur, sometimes with resultant ruptures, is distinctive, idiosyncratic, and unique to FQ antibiotic use alone. It is a hallmark of FQT. So much so, that an FDA “Black Box Warning” about it exists for all fluoroquinolone antibiotics.

It turns out there just aren’t a whole lot of things in life, either natural or synthetic, that can cause sudden spontaneous tendon ruptures or severe tendon pain and tendinopathies –but all of the endocrine disorders can. This includes: hyperadrenocorticism (cortisol), diabetes (insulin), parathyroid disorders (calcium/PTH/Vitamin D), hyper and hypothyroidism (tyrosine/iodine/thyroid hormone), hyper/hypo sex hormones (estrogens/testosterone), and probably other steroid and sex hormones and their metabolites as well (see references). A specific genetic metabolism disorder of tyrosine, which is a major component of thyroid hormones, can also cause spontaneous tendon rupture later in life as a first manifestation of this disorder. Many rheumatic diseases also often have an associated, if not underlying, endocrine component (especially thyroid related). Additionally, conditions that at first glance appear to be unrelated, such as chronic renal failure, often have a high association with endocrinopathies, in particular, parathyroid hormone abnormalities. The parathyroid glands are intimately associated with the thyroid gland via proximity alone; if thyroid gland architecture is destroyed, presumably these glands could be affected too.

I took a fluoroquinolone antibiotic and developed severe, systemic tendon pain, Type 2 Diabetes, and two Autoimmune Thyroid Disorders. A legitimate question could be: Are fluoroquinolone antibiotics severe endocrine disrupters, which, among other symptoms, can result in tendon pain, tendinopathies, and tendon rupture?

I then found that the thyroid hormone medications T4 and T3, as well as iodine alone, profoundly affected my tendon pain and other symptoms, capable of making these symptoms dramatically better — or much worse. This, too, seemed to support the argument that the fluoroquinolones had somehow damaged my thyroid system, as supplying exogenous hormone in the form of medication now could make such dramatic differences in my symptoms.

One of my hypotheses is that people with healthy and normally functioning thyroid glands or other endocrine systems can probably withstand these dramatic changes in the hormonal axes that may be occurring while on the FQ – at least, up to a point. For people who don’t react at all to these drugs, they probably never even feel the fluctuations, as their hormonal axes can automatically adjust rapidly. But I would suspect that anyone with any underlying genetic predisposition, or possibly harboring a subclinical, latent, or silent endocrinopathy might be “pushed over the edge” into full blown clinical pathology. This is actually what I think may have happened with me, even though I had no overt indications of any kind of thyroid or endocrine disorder prior to taking the Cipro.

Additional Links To Consider Relating Fluoroquinolones to Thyroid System Damage

I don’t profess to even begin to know the millions of ways fluoroquinolones could possibly exert their damaging effects on the thyroid or endocrine system in general. However, that didn’t stop me from thinking about this problem. As I said, I hope research studies will be initiated in this area sooner than later. In the meantime, I came up with several mechanisms of FQ-Induced Thyroid Pathology to consider as possibilities, to narrow down the search. Additional unintentional targets of fluoroquinolones that I considered could have thyroid-related repercussions included targets such as mitochondria, acetylcholine, steroid receptors and hormone response elements and their common pathways, selenium dependent enzymes and proteins, halogenated peroxidase enzymes, iodine receptors located on most or all cells as well as on the thyroid gland, and more. I think one of the more interesting observations is the fact that new fluoroquinolone derivatives are now being considered for use as “tyrosine kinase inhibitors” (TKI’s). TKI’s are relatively recent chemotherapy drugs developed to fight cancer – and one of their adverse effects appears to affect the thyroid system with some rather alarmingly high statistics. From my perspective, there appeared to be striking similarities between thyroid abnormalities occurring with TKI’s and the thyroid abnormalities I suspect may occur with the FQ’s.

Fluoroquinolone Antibiotics: Consider the Risks

Thyroid disorders, especially autoimmune based ones, are no joke. Autoimmune Thyroid Disorders are not simply disorders of the thyroid gland; in my opinion, they are systemic disorders, affecting many or all of the cells and tissues in the body, which is why there can be such widespread and potentially devastating symptoms. There are numerous environmental stressors that contribute to thyroid disease and endocrine disease, and the fluoroquinolone antibiotics may be one of them. Fluoroquinolones exert many damaging effects, and if they are damaging the thyroid axis directly or indirectly via a cascade effect, actually causing anti-thyroid antibody production, or even if they are triggering or unmasking a subclinical or silent condition in susceptible patients to an active pathological condition, this is of serious concern – or it should be. A “silent” condition means just that – you don’t know you have that predisposition. I can say from my own experience that taking a fluoroquinolone antibiotic is a hell of a way to find out. It is Pharma’s responsibility to provide adequate warnings and risks of this possibility, and the medical profession’s responsibility to make sure adequate testing rules out these antibodies along with other potential risk factors, before prescribing a fluoroquinolone antibiotic. Sadly, neither of these things is happening right now. Until it does, I think anyone considering taking a fluoroquinolone antibiotic for a simple infection, such as uncomplicated UTI or sinusitis, should be aware of the risk factors and possible alternatives.

Based on what I’ve learned in the past several years, I believe anyone with pre-existing endocrinopathies of any type (whether they’re known or not), to be at increased risk for these adverse reactions. I also believe that anyone who has experienced any kind of flox reaction has now gotten a warning sign, and is at increased risk of developing an overt or clinical endocrinopathy as a result of being floxed at any time after. One of the few supportive pieces of evidence for this hypothesis is buried in Table 3, Page 136 of a Mayo clinic paper here. Note the at risk population includes people with autoimmune or endocrine disorders (diabetes, thyroid, parathyroid) and steroid usage (ie, Prednisone, inhalers, anabolic steroids, etc.).

The best approach, of course, is to stay away from these drugs altogether if at all possible. In my opinion based on my own experience, developing a lifelong severe thyroid disorder – or any other disorder — to solve a short term problem such as an uncomplicated infection with a fluoroquinolone antibiotic, isn’t worth the risk.

References and Resources

Share Your Story

If you have been injured by a fluoroquinolone antibiotic, please share your story. Send us a note here, for more information.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

Laboratoires Servier, CC BY-SA 3.0, via Wikimedia Commons

*The website is no longer available.

This post was published originally on Hormones Matter on May 7, 2015; links have been updated where appropriate.

A Call for Improved Thyroid Treatment Options

by Thyroid Change

Published on February 11, 2014

3456 views

Did you know that there is a controversy regarding the treatment of thyroid disease? Harvard Health estimates that more than 12 million Americans have thyroid disease, many of whom don’t even realize it. Thyroid patients insist that current treatment standards leave too many patients suffering from a lack of diagnosis or ineffective treatment. Both patient populations are left with a diminished quality of life, yet there are few doctors willing to step outside of the current guidelines. In an effort to change this situation a team of patients created ThyroidChange, a nonprofit organization dedicated to improving the treatment of thyroid disease.

What is Thyroid Dysfunction?

The thyroid is a gland in your body which is located at the base of your neck. Go ahead, touch it! Just above your collar bone and just below your “Adam’s apple.” This gland is shaped like a butterfly with two lobes which stretch around your trachea – hence its nickname the butterfly gland. This gland is key to your body’s metabolism. The hormones it secretes kick-start the energy in every cell of your body like a spark plug in your engine or flint to a match. Without appropriate amounts of thyroid hormones, whether too high or too low, the function of your body is greatly impacted. There are over 300 symptoms of insufficient thyroid hormone and they represent dysfunction in every major organ. Thyroid dysfunction is so common that you or someone you know is probably impacted or will be in the future.

Thyroid hormone is a broad term. The thyroid secretes many hormones, but the two most important for this conversation are thyroxine (T4) and triiodothyronine (T3). The pituitary gland located in your brain senses the level of hormones in that area of your brain, and sends out thyroid stimulating hormone (TSH) which excites your thyroid and causes it to release hormones. T3 is used immediately by various cells and T4 is called the storage hormone because it cannot be used by the cells. It is stored to later be converted to the useable and valuable T3. When a patient does not have sufficient levels of T3 in their blood stream, physicians expect a patient’s TSH level to increase, demonstrating the demand for more hormone by the pituitary gland. If a patient’s thyroid is producing too many hormones, the TSH lab value should decrease to tell it to “decelerate” its production.

An individual whose thyroid gland makes too much thyroid hormone is hyperthyroid. Some patients are rendered hyperthyroid due to an autoimmune disease called Graves’. One can also have cancer of the thyroid gland. Treatments for these can vary, but inevitably it leads to a lifetime of hypothyroidism.

One who has insufficient T3 available to their cells is called hypothyroid. The leading cause of insufficient thyroid hormone is the autoimmune disease, Hashimoto’s Thyroiditis. This disease causes one’s own body attacks their thyroid gland making it inefficient.

What is the Current Treatment standard? Why is it Flawed?

The flawed TSH test is used to diagnose and treat individuals. A physician will run the TSH and if the value is above a particular threshold, the physician will declare a patient hypothyroid. The physician will usually prescribe levothyroxine which is synthetic T4. The dosage will be determined by the TSH lab value. Once it hits a number determined by the physician, the patient will be determined as “euthyroid” or “good as new.”

How many disorders are you aware of that have one lab test and one prescribed treatment? Even though there is research demonstrating that the TSH lab test is flawed and that there are alternative treatments to effectively treat thyroid disease, thyroid patients have difficulty accessing these research-proven methods. We have not even begun to discuss that a majority of hypothyroidism is caused by an autoimmune disease that is seen as insignificant and is not necessarily tested for when a patient is being treated for the resulting hormone imbalance.

What is the Change Being Sought by Thyroid Patients?

One can plainly see that current treatments are solely based on T4 substitution and the ability of an individual’s body to convert the prescribed hormone to the active hormone T3. Patient experience shows that if a patient continues to complain about lingering symptoms, physicians focus on current guidelines which promote the flawed TSH lab value instead of drawing additional labs. This further testing may well demonstrate that a patient is lacking the necessary T3 to function properly, but as so few physicians are willing to perform this, many patients continue to suffer.

In a person with low Free T3, raising T4 doses will not alleviate symptoms. These patients are often prescribed drugs such as antidepressants and cholesterol-lowering drugs to mask the symptoms of insufficient T3. (If you are on one of these medications, have you had your thyroid tested? If you are on thyroid medication, have you had your Free T3 tested?). Adding medications increases side effects and does not restore balance to the patient’s hormones. Simple blood tests can demonstrate to a physician why symptoms persist after the employment of current treatment guidelines. Tests such as Free T4 and Free T3 can indicate how much Free and useable T4 and T3 are in a person’s bloodstream. These tests in combination with antibody testing can help to shed light on a patient’s persistent symptoms.

As per the current guidelines in the treatment of hypothyroidism, based on TSH testing most patients are sufficiently relieved of their symptoms by T4-only treatment. Those who are not in the majority are left to struggle for a doctor willing to listen and run extended lab tests. Complicating this further, many doctors and patients are not only unaware of additional lab work, but also of the many treatment options that one can use to treat thyroid disease.

Levothyroxine or synthetic T4 will restore health in some patients. There are also various T3-containing treatment options such as natural thyroid extract and synthetic T3 which can be used to supplement or substitute T4 treatment. Each patient is unique. We need to make sure that each patient has access to the treatment approach to best restore his or her health. ThyroidChange is about patients advocating for other patients.

Who is ThyroidChange?

ThyroidChange is a nonprofit organization advocating for the use of extended lab testing (Free T4, Free T3, TSH, Reverse T3 and thyroid antibodies) and access to various treatment options to suit the individual patient. We host a petition to appeal for such changes and this has garnered more than 16,000 signatures worldwide, demonstrating that there is indeed a genuine need for change in thyroid treatment. Our community unites patient advocacy groups in an effort to gain better care for thyroid patients and to raise awareness of this widespread problem. ThyroidChange also aims to work with medical oversight agencies in order to create a unified standard of care for thyroid patients to increase patient access to effective, modern treatment.

Please help this effort by visiting www.ThyroidChange.org to sign the petition and unite for better thyroid care, or contact ThyroidChange to discuss how you can support this initiative.

autoimmune thyroid