Introduction

This document is a summary of my personal experience with Fluoroquinolone Toxicity (FQT) and how it appeared to negatively affect my Thyroid Hormone (TH) and Iodine homeostasis and metabolism.  Because it’s a summary, much detail has been left out that that could answer questions that might arise.  Additionally, because TH/Iodine metabolism is such a complex subject, I knew I couldn’t possibly write up these ideas in such a way that all audience members will understand in a summary.  So I tried to take a “middle of the road” approach.  For some people, the information herein will be too simplistic.  For other people, the information may be too complex.  For most people, there will be huge gaps in connections of information, leaving my interpretations open to question.  Some of my statements will have to be taken at face value until/unless I can provide additional information in later writings.  My hope is to fill in some gaps and provide more detail over time.  Additionally, I do encourage anyone who is interested to research some of these issues on your own.

For internet search reasons, I wanted the words “Thyroid Hormone” in the title of this document along with “Fluoroquinolone Toxicity”.  This is because most people have heard of “thyroid gland” problems, or “thyroid hormone” problems and can relate somewhat to this.  However, I believe that I developed more than just a “simple thyroid problem” due to the fluoroquinolone antibiotic I took.  I believe that in my case, damage or abnormalities with Iodine metabolism and/or Tyrosine metabolism greatly contributed to the severity and chronicity of my floxing syndrome.  “Thyroid Hormone” is nothing more than iodine moieties attached to tyrosine residues, and so in that way, anything that affects Iodine or Tyrosine metabolism will most likely affect thyroid hormone metabolism as well.  For the purposes of this paper, I will use the term “TH/Iodine” to encompass all of these, however.

This document takes quite a “thyrocentric” view of things, meaning I explore and describe my symptoms all through the lens of “TH/Iodine” metabolism problems.  For this reason, it’s as much a description about “thyroid related problems” as FQT-related problems.  Also for this reason, it may be of interest to thyroid patients who are not flox victims as well.  Having said that, I believe that thyroid issues were not my only issues as a result of being floxed.    Over the years, I ended up exploring numerous possibilities, and wrote about some of them here, here, and here.  I don’t spend a lot of time with these in this paper, as this particular document is geared towards the thyroid related issues, ie, the “thyrocentric view”.

FQT in its severest form, which is what I have experienced, is a multi-organ, whole body systemic toxicity.  There may be one single underlying mechanism to account for this; for example, mitochondrial damage or depletion, or one receptor, enzyme, or signaling process which occurs throughout most or all of the body and is damaged, therefore causing such widespread damage throughout the body.  Another possibility is that FQ’s negatively affect more than one mechanism, and I suspect this is most likely the case.   It’s rare if not impossible for any drug, especially a synthetic one, to target one and only one enzyme or mechanism throughout the body.  Even if it did, that one enzyme may be involved in a multitude of functions, or at the very least start a “domino effect” of all kinds of other unintended mechanisms.  There are many valid proposed hypotheses of FQT Damage which already exist, such as DNA, oxidative, mitochondrial, and GABA/Glutamate receptor damage.  Although these mechanisms and more may easily be contributing to FQT, I believe there are others with more knowledge than I addressing these issues.  So I won’t be focusing on these areas in this document.  There are no doubt potentially innumerable places within the human body where FQ’s can exert their damage.  In my case, I believe the Cipro I took negatively affected my TH/Iodine metabolism and homeostasis, and because it happened to me, there may be others that this has happened to as well.

I personally believe that underlying endocrinopathies of any type may play a large part in many cases of FQT, and that the robustness of the various endocrine and neuro-endocrine systems at all levels (genotype, phenotypic expression, environmental influences) may be one determinant of who recovers from FQT versus who becomes chronic.  A healthy thyroid axis and gland, for example, can probably withstand the temporary insult the FQ’s probably cause, and the person will either not feel the effects of the drug while taking it, or recover over time if they do.  Those with pre-existing thyroid conditions, or a subclinical or “silent” unknown thyroid condition may be much more susceptible to the immediate, delayed, and long term adverse effects of these drugs.  The same may be true of those with any underlying endocrinopathy, not just thyroid-related ones.  Additionally, as compensatory mechanisms kick into action once one system is adversely affected, this in itself can cause a host of problems and issues as well as obscure the origin of the initial insult and problem.

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 the endocrine disorders can:  hyper and hypoadrenocorticism (cortisol), diabetes (insulin), hyper and hypo parathyroidism (calcium/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.  Prednisone, the synthetic version of our body’s natural steroid cortisol, is usually given in supra-physiological immunosuppressive doses – and may mimic a “Cushingoid state” of hypercortisolism, thereby potentially increasing susceptibility to FQ-induced tendon pathology greatly.   Tendon pain and tendinopathies are a major hallmark of FQ toxicity in general.   Regardless of what other symptoms occur with FQT, the severe localized as well as systemic tendon pain that can occur, sometimes with resultant ruptures, is distinctive, idiosyncratic, and virtually unique to FQ antibiotic use alone.   For this reason, I felt that the tendon issues were key in looking for unifying mechanisms of FQ-induced damage.  And I still believe that whatever can be learned here, can provide big clues as to what is going on systemically as well. The hormones in endocrine and neuroendocrine systems are by their very definition systemically acting, which is probably why there are such broad and wide spread systemic effects.  The receptors, transporters, enzymes, and signal transduction processes involved in endocrine and neuroendocrine metabolism are located everywhere in the body, and that includes “brain cells” in the CNS.  Interestingly enough, receptors for thyroid hormone, cortisol, sex hormones, and even Vitamin D and xenobiotics all belong to a “superfamily” of receptors which share homology and a lot of “crosstalk”, each modulating and being modulated by the others.   Cytochrome P450 enzymes are present in most tissues of the body, and play important roles in hormone synthesis and breakdown (including estrogen and testosterone synthesis and metabolism), cholesterol synthesis, and vitamin D metabolism.   I suspect the FQ’s are major endocrine and neuroendocrine disrupters in general, leading to something similar to a Polyglandular Endocrine Deficiency Syndrome either temporarily or permanently.   And this includes the thyroid gland and axis.

I had no indication prior to taking the FQ of any “thyroid problems” or any other health conditions that I was aware of.  However, in hindsight, I do believe I had an underlying susceptibility, genomically, phenotypcally, and subclinically, to both TH/Iodine related pathologies and Myasthenia Gravis -like (MG) related pathologies, that the FQ unmasked with catastrophic swiftness and devastating consequences.  If I hadn’t taken the FQ, I think there’s a good chance I’d be fine today, living my life as a healthy, athletic, in-pretty-good-shape-50-something, still blithely unaware of the horrific phenomenon of “getting floxed”.  The worst mistake I ever made in my life was taking a fluoroquinolone antibiotic, because it effectively ended any quality of life for me.

 

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