Several months ago, Dr. Linda Martin, Dr. Alan Redd, David Melvin, and John Fratti submitted an abstract for the United Mitochondrial Disease Foundation (UMDF) Symposium June UMDF Symposium 1517th to June 20th in Washington, DC. We are pleased to announce that, after being peer-reviewed by the UMDF Abstract Review Committee, their abstract was selected as a poster for the Symposium. Their abstract will be presented in the course syllabus book distributed to conference attendees, and will be printed in the post-conference issue of the journal Mitochondrion.

The UMDF Mission is “to promote research and education for the diagnosis, treatment, and cure of mitochondrial disorders and to provide support to affected individuals and families.” It is wonderful that the Fluoroquinolone (FQ) Community will be represented at an event specifically held to “promote research and education” about an issue that has affected so many in the FQ Community.

Additionally, it is great that so many physicians, researchers, patients, family members, and others will be exposed to information about possible Mitochondrial Toxicity resulting from FQ consumption through the publication of their Abstract in the syllabus book and journal Mitochondrion.

UMDF Symposium

Speaker at UMDF Symposium

Below is from the abstract:

Linda Martin, Alan Redd, David Melvin, John Fratti
Institution: Not applicable; authors present from a patient perspective
Title: Fluoroquinolone Antibiotics and Possible Mitochondrial Toxicity

A pharmacovigilance Food and Drug Administration (FDA) document dated April 17, 2013, states that commonly prescribed Fluoroquinolones (FQ), may result in possible mitochondrial toxicity. The FDA document describes how mitochondrial toxicity is implicated in serious neurodegenerative diseases, including ALS, Alzheimer’s, and Parkinson’s. Although Charles Bennett, M.D., and the Southern Network on Adverse Reactions (SONAR) submitted a Citizen Petition to the FDA in June 2014 asking the FDA to place warnings of possible mitochondrial toxicity on the FQ labels, the FDA has not yet acted. Because the number of adults with mitochondrial disease appears to be increasing, and because the number of adults with neurodegenerative diseases is increasing, it is important to discuss potential relationships between FQs and mitochondrial disease in adults.


FQs are widely prescribed antibiotics. Levofloxacin, ciprofloxacin, and moxifloxacin are three of the most common FQs. The FDA has approved FQs for the treatment of a wide range of infections.

Consistent with United Mitochondrial Disease Foundation (UMDF) symptom description for mitochondrial disease, those who experience FQ adverse events report new onset of muscle, brain, cardiac, endocrine, gastrointestinal, and/or neuropsychiatric symptoms. Research conducted by SONAR at the University of South Carolina and the pharmacovigilance FDA report of 17, 2013 FDA report both indicate that FQs may result in mitochondrial toxicity. Mice given human equivalent doses of ciprofloxacin developed mitochondrial dysfunction and brain inflammation. The published literature shows that FQs mutate and deplete mitochondria. It is important for physicians and patients to be aware that one source of adult-acquired mitochondrial disease or dysfunction may be the consumption of FQs. Moreover, FQs could exacerbate existing cases of mitochondrial disease. Because there has been relatively limited attention given to adult FQ induced mitochondrial disease or dysfunction, our research provides an under-reported and under-recognized phenomenon.

SONAR submitted the following text from a Citizen Petition to the FDA in June 2014, requesting that the following additional Black Box Warning be placed on the Levaquin label:

Fluoroquinolones may cause mitochondrial toxicity. Mitochondrial toxicity has been implicated in conditions such as peripheral neuropathy, hepatoxicity, glucose disturbances, phototoxicity, developmental disorders of the brain, optic neuropathy, neuropathic pain, hearing loss, muscle weakness, cardiomyopathy, lactic acidosis, Parkinson’s, Alzheimer’s, and amyotrophic lateral sclerosis (ALS).

Our research involves collaboration among pharmacovigilance experts, basic scientists, and patients. This represents a unique approach to evaluating FQ toxicity, a possible cause and or aggravation of adult mitochondrial disease or dysfunction.

Stay vigilant, stay informed, and stay tuned to My Quin Story for timely updates on our interactions with the FDA, the Citizen Petitions, UMDF, and upcoming information on FQ community related research.