Fluoroquinolone Antibiotics And Nerve Damage...Again!

Today's post from floxiehope.com (see link below) takes yet another look at the danger of fluroquinolone antibiotics (cipro, levaquin and others) but this time from a slightly different angle. There is a little more personal opinion in this article than you may wish for in an objective study but it does provide a string of logic that is difficult to ignore or deny. Definitely worth a read and a discussion with your doctor if you've been prescribed these antibiotics. Remember, there are always alternatives.

Fluoroquinolones and Peripheral Neuropathy – Another Look
October 23, 2014



An article published in the journal Neurology entitled “Oral fluoroquinolone use and risk of peripheral neuropathy: A pharmacoepidemiologic study” found that users of fluoroquinolones are at a higher risk of developing peripheral neuropathy than those in a control group – with those currently using fluoroquinolones at the highest risk. I am thankful to Doctors Etminan, Brophy and Samii for their work! The study quantifies the risk of developing peripheral neuropathy after using fluoroquinolones. The results are:

“We identified 6,226 cases and 24,904 controls. Current users of FQs were at a higher risk of developing PN (RR = 1.83, 95% confidence interval [CI] 1.49-2.27). Current new users had the highest risk (RR = 2.07, 95% CI 1.56-2.74). No risk was observed for current users of finasteride (RR = 1.21, 95% CI 0.97-1.51).”

A review in Neurology Today, about the study, featured some expert comments. Some of those comments, frankly, pissed me off. From the review in Neurology Today –

“Ahmet Hoke, MD, PhD, a professor of neurology and neuroscience and director of the Daniel B. Drachman Division of Neuromuscular Diseases at Johns Hopkins School of Medicine in Baltimore, MD, expressed reservations about the Neurology study, however, because there are so many kinds of peripheral neuropathy, many of them apparently caused by infection. “It is very difficult to know if [fluoroquinolones] are causing the neuropathy, because most of the patients follow a course that is similar to post-infectious peripheral neuropathy,” said Dr. Hoke, who is also the editor-in-chief of Experimental Neurology. “Since these antibiotics are always given to patients who have active infections, we don’t know if the infection or the drug is triggering the neuropathy. It’s more likely that the infection, which may have been there for four or five days before the antibiotic was started, caused this neuropathy.”

Bacterial infections don’t cause peripheral neuropathy. They just don’t. The bacteria that lead to urinary tract infections cannot cause peripheral neuropathy. The bacteria that lead to sinus infections can’t cause peripheral neuropathy either. In the billions of years of life on this planet in which eukaryotic organisms have been suffering from bacterial infections, there is no history of bacterial infections causing peripheral neuropathy. It’s simply false. I would say that Dr. Hoke is lying, but I don’t know his intentions. What I do know is that his statement and his assumptions are wrong.

There is currently a connection between bacterial infections and peripheral neuropathy because antibiotics cause peripheral neuropathy. It is foolish to mistake the effects of a drug given to treat a disease for the symptoms of the disease itself. (Read Anatomy of an Epidemic for a description of how this is done rampantly in the field of Psychiatry.)

Here is the probable mechanism for fluoroquinolone induced peripheral neuropathy:

Synthetic bactericidal antibiotics, including fluoroquinolones, beta-lactams and aminoglycosides, damage mitochondria and lead to an increase in reactive oxygen species (ROS) (source). Damaged mitochondria lead to an insufficient supply of ATP and “Mitochondrial conditions that are due to an insufficiency of ATP, especially in organs that rely on mitochondria for their energy source, include developmental disorders of the brain, optic neuropathy, neuropathic pain, hearing loss, muscle weakness, cardiomyopathy, and lactic acidosis.” (The source for that quote is an FDA document entitled “Disabling Peripheral Neuropathy Associated with Systemic Fluoroquinolone Exposure.”) Of course, the complexity of the biochemical reactions needs more than a couple sentences to explain sufficiently, but the gist of it is that drugs that damage mitochondria can cause peripheral neuropathy. Other people at Johns Hopkins realize this – this article, “Feet First? Old Mitochondria Might Be Responsible For Neuropathy In The Extremities” is out of Johns Hopkins Medicine. Maybe they should pass the memo onto Dr. Hoke.

Dr. Hoke and others – what is the mechanism by which you think bacteria cause peripheral neuropathy? There is none, because they don’t.

Another doctor who reviewed the study, Dr. Wolfe, “noted that infections themselves, such as hepatitis B and C, HIV, and diphtheria, can generate neuropathy.”

Other than diphtheria, THOSE ARE VIRUSES. (If you’re using fluoroquinolones, or any other antibiotics, to treat viral infections you should probably go back to Med School.)

I seriously doubt that viruses can cause peripheral neuropathy either. In the case of HIV, peripheral neuropathy is probably from the mitochondria damaging drugs that are given to patients with HIV. In Mitochondria as a Target of Environmental Toxicants, it is noted that:

“Another example is the nucleoside reverse transcriptase inhibitors (NRTIs) that are used to combat human immunodeficiency virus (HIV) infection. NRTIs act by inhibiting the reverse transcriptase activity required for viral replication. They have been highly successful in treating adults and in preventing transmission of HIV from pregnant mothers to their children, but unfortunately many NRTIs also inhibit the mtDNA polymerase γ. This has resulted mtDNA depletion- and mutation-mediated mitochondrial toxicity, and even death, in patients and in animal models (Benhammou et al., 2007; Blanche et al., 1999; Chan, 2007; Claessens et al., 2003; Divi et al., 2010; Kohler and Lewis, 2007). Similar effects have been observed with nucleoside analogs intended for other viruses as well (McKenzie et al., 1995). Thus, chemicals that damage mtDNA or alter its copy number can have very serious health consequences.”

In “Delayed cytotoxicity and cleavage of mitochondrial DNA in ciprofloxacin-treated mammalian cells” it is noted that fluoroquinolones cause a loss of mitochondrial DNA.

Both NRTIs, used to treat HIV, and fluoroquinolones, used to treat bacterial infections, deplete mitochondrial DNA and lead to peripheral neuropathy. I don’t understand why this is so difficult, or why people have to obfuscate the issue by making false statements about bacteria and viruses causing peripheral neuropathy. Neither bacteria nor viruses cause peripheral neuropathy. The drugs to treat them do.

I shouldn’t know more about drug induced mitochondrial dysfunction and peripheral neuropathy than these doctors. It’s absurd that I do.

Sources:
Neurology, “Oral fluoroquinolone use and risk of peripheral neuropathy: A pharmacoepidemiologic study.”
Neurology Today, “New Support for Association Between Fluoroquinolones and Peripheral Neuropathy”
Science Translational Medicine, “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells”
Department of Health and Human Services Public Health Service Food and Drug Administration Center for Drug Evaluation and Research Office of Surveillance and Epidemiology, Pharmacovigilance Review, April 17, 2013, “Disabling Peripheral Neuropathy Associated with Systemic Fluoroquinolone Exposure”
Johns Hopkins Medicine News and Publications, “Feet First? Old Mitochondria Might Be Responsible For Neuropathy In The Extremities”
Toxicological Sciences, “Mitochondria as a Target of Environmental Toxicants”
Molecular Pharmacology, “Delayed cytotoxicity and cleavage of mitochondrial DNA in ciprofloxacin-treated mammalian cells.”

http://floxiehope.com/2014/10/23/fluoroquinolones-and-peripheral-neuropathy-another-look/