The Fluoroquinolone community has known for a very long time that delayed adverse events to fluoroquinolones (FQ’s) were a reality, even though when I initially entered into the community 13 years ago, “delayed reactions” as they were called then, were considered rare and terrible.

The flox report which, at the time over a decade ago, was a breakthrough piece of research put together by citizen scientists. It characterized these ‘delayed reactions’ as a more dreadful pathology that was rarer and very chronic.  Since then however, much has changed and a good portion of the data in the flox report is now outdated.

With the benefit of over a decade of 20/20 hindsight, anecdotal information has been showing us that delayed adverse events, or what I call FQ late effects, are more commonplace than once was thought.  And now, current academic research that is tricking in from various parts of the globe, is starting to lend credence to our own community collected anecdotal data, reinforcing what many in the community have suspected all along.

Recent Research

Recently researchers out of India and Switzerland studying FQ’s as therapy for Tuberculosis noticed a high incident of joint pain andFluoroquinolone Joint Pain tendon injury when the FQ’s were involved in the treatment.   The paper titled “High Incidence of New-Onset Joint Pain in Patients on Fluoroquinolones as Antituberculous Treatment” published January 17, 2020 focused on “joint pain incidence during antituberculous treatment among patients diagnosed with tuberculosis visiting the outpatient clinic over a duration of 1 year, as well as assessed their link with fluoroquinolones.”

While I appreciate the all current academic studies that focus on FQ’s adverse events, the finding that FQ’s can cause joint damage and pain is nothing new.

I believe the important point is contained farther down in the article.

There were 260 patients total. Group A had 140, group B had 81, and group C had 39.

  • Group A received the drug pyrazinamide alone and 24 of the 140 patients or 17% experienced joint issues.
  • Group B received a fluoroquinolone alone and 32 of the 81 patients or 40% experienced joint issues.
  • Group C received both pyrazinamide and a fluoroquinolone and 20 of the 39 patients or 51% experienced joint issues.

For me the main takeaway is what they call the median latency to the onset of joint pain or the time it took for the problem to appear.

The median latency to the onset of joint pain 138 days group B, and 88 days in group C.

This study showed that those receiving FQ’s had a higher incident of joint problems and a delayed onset time of up to 138 days or 4 ½ months!

Delayed Permanent Peripheral Neuropathy

Research from the University of Dundee published on April 29, 2019 has shown that FQ’s increase a patient’s risk of suffering a serious,FQ Peripheral Neuropathy potentially permanent, and delayed onset nerve damage event by almost 50 percent (source).

Their nested case-control study showed that current use of systemic FQ antibiotics increased the risk of peripheral neuropathy (PN) by 47%.  The greater the cumulative exposure the higher the risk, with males and those over the age of 60 at greatest risk .

The most damning evidence was their finding that there was a significant increase in the relative incidence of PN within 30 days of oral FQ therapy, which remained significant for up to 180 days following exposure!

Additionally, the PN risk may increase by approximately 3% for each additional day of FQ exposure.

Delayed Carpal Tunnel

The study “Fluoroquinolone Use and Risk of Carpal Tunnel Syndrome: A Pharmacoepidemiologic Study” published in April of 2017

Fluoroquinolone Carpal Tunne;l

Woman holding wrist

discusses FQ usage and the risk for Carpal Tunnel Syndrome (CTS).

The study found that any use of FQ within the year prior to CTS diagnosis was associated with a 34% and 36% increased risk of CTS in the primary and sensitivity analyses, respectively.

Their findings may suggest a possible delayed response with FQ use and the development of CTS.

The Veracity of Anecdotal Data

My adverse event to the FQ’s did not manifest itself for several months after ingestion.  It took me retooling, so to speak, investigatory skills from my career in law enforcement, to track down the suspect, Levaquin.

Since then I have interacted with hundreds.  Some of these individuals are very smart, and like me, they pieced together their own clues.  The connected the dots and re-established the cause and effect linkage.

I have to admit that data collection is difficult.  It is tough to weed out confounding data and separate fact from fiction.  There is a certain percentage, where after careful examination, another pathology can be assumed, and then there are those who are using it for personal gain, which confounds the processes a little further.  But all in all, after a while a fairly accurate picture emerges and I wrote about this in the article The Fluoroquinolone’s Inconvenient Truth.

Despite the fact that there are detractors to the veracity of our anecdotal information, others withing the academic and professional medical fields recognize the accuracy of the data and are using it.  

Just Scratching the Surface

Academic research is just now incidentally scratching the surface on the subject of delayed adverse events, or late FQ effects.  This data is showing up and honest academic researchers that are not under the thumb of conflicting interests, are starting to report the connections. Connections that many people suspected all along.

The adverse events of FQ’s are disparate and by all definitions, outrageous. They range from permanent nerve damage, tendons large and small spontaneously rupturing, organ failure, psychosis, and dozens more.  Most doctors consider this broad ranging adverse event pathology from an antibiotic outrageous and when you throw in delayed onset…. they find it preposterous.

Regardless, we are starting to see these delayed adverse events emerge in the data.    If researchers would just look, they would find these correlations which are normally overlooked because the cause and effect are separated by a very subjective period of time. 

Resistance is Still Strong

I believe that the medical community is rife with cognitive dissonance. Cognitive dissonance is a universal human phenomenon and it is based on the assumption that people want consistency between their expectations and reality. Because of this, they contort their thinking into knots to make that happen. In the case of FQ adverse events, it is to preserve the notion that our efforts help rather than hurt, so their impulse is to attribute the harm to something other than their intervention.

This cognitive dissonance is re-enforced in the paradigms taught in medical schools that are all tacitly funded by the pharmaceutical companies with conflicts of interest (source).  Unfortunately, many doctors never break out of this sphere of influence.

For instance, a pro FQ propaganda piece surfaced in May of 2019.  Titled, “Oral fluoroquinolones carry small risk of peripheral neuropathy,” the authors write “there are no strong hypotheses regarding the pathomechanisms of fluoroquinolone-induced neuropathy.”

Many medical professionals, based on their indoctrinated training, simply can’t wrap their heads around a differential diagnosis to include the FQ’s.  Many still deny the possibility outright or at the very least call it extremely ‘rare.’

After all, will the average practitioner suspect peripheral neuropathy in a patient prescribed the FQ’s six months earlier?

Or, will they connect carpal tunnel or joint issues in patient who received FQ’s months or years earlier?  What about heart problems, CNS issues, etc…?

 The answer to these questions in most cases is No, they will not make the connection.  If the patient doesn’t connect the dots, then the facts are lost in time and because of this, delayed adverse events, such a peripheral neuropathy and others, do not get reported accurately.

I will concede years ago connecting these delayed adverse events to a pharmaceutical was very difficult.  Medical science’s knowledge about things such as DNA and mitochondria was limited. Today, we know much more and when you look to the DNA and mitochondria you will find your pathomechanisms for a whole host of delayed onsets pathologies.

Expect more to come.