We have all heard of DNA genetic-testing services like 23andMe. After I suffered adverse reactions from the antibiotic Levaquin, I found others who suffered the same fate online. Several suggested that there could be a genetic component as to why some people have severe adverse reactions and some do not.
Seeking answers, I got my kit from 23andMe, spit in the vial and sent it back.
Could a genetic test explain why an otherwise healthy 36-year-old suddenly becomes disabled?
In 2006 I went to my doctor for what was thought to be a cough caused by a sinus infection. My doctor prescribed Levaquin. I was told it was safe, FDA-approved (Food and Drug Administration), and strong enough to kill any infection. After all, Levaquin is an antibiotic, and antibiotics are meant to help people feel better. But I got worse. I was having pain in my muscles and joints. I was suffering from fatigue and brain fog. When I complained to my original doctor and two orthopedic surgeons, they dismissed me and said an antibiotic cannot possibly be the reason I was suddenly disabled.
In the three years following my taking the Levaquin, I suffered three ruptured tendons, each of which needed surgery. Finally, one of my orthopedic surgeons said it was not normal for a healthy 36-year-old to continue to have increasing pain, to be losing the function of a foot or to have three tendon ruptures in three years. He began by asking me to go over my health history. I told him that I am usually pretty healthy, but I had a sinus infection diagnosis less than a month before my tendons started rupturing. He asked me what I was prescribed. When I told him it was Levaquin, he put his pen down and leaned against the exam table, and asked me if I knew that Levaquin was linked to tendon ruptures and that there was a 2008 Black Box warning.
I had no idea. I thought that since it was an antibiotic, it could not be the reason for the tendon ruptures. I felt myself getting angry at how ludicrous it sounded. I went home and researched it, hoping to prove him wrong.
He was right.
When I finally got back my 23andMe test results, my trait report said that I have a cilantro-taste aversion, my eye color is hazel, my hair is thick and dark, and my ancestry is Southern European and Italian. I am predisposed for macular degeneration, blood clots and deficiency of glucose-6-phosphate dehydrogenase (G6PD), an enzyme that regulates various biochemical reactions in the body, 23andMe also reported.
What is most remarkable from my results is that it showed that I had the C677T variant of the methylenetetrahydrofolate reductase (MTHFR) gene mutation. This is a common gene mutation in those who suffer from what the FDA coined as fluoroquinolone associated disability (FQAD), also known as fluoroquinolone toxicity. The theory is that the gene mutation causes toxic buildup and the body cannot detox from it. Perhaps this explains why I am still rupturing tendons and having central nervous system issues, fifteen years after I took Levaquin.
Pharmacogenomics is an emerging field that uses genetic testing to predict how a person responds to medications. Your DNA can determine how fast or slow your body absorbs the drug. It can determine what receptors you have and how many, which can affect your response to a drug.
Because of the antibiotic Levaquin, I went from having a cough to becoming disabled. I often wonder if I had known about pharmacogenomics and been genetically tested before taking the medication, if that data could have helped me and my doctor make an informed decision about what the best course of action would have been.
I didn’t know this in 2006 when I was prescribed Levaquin. But I know now and can make more informed decisions as a result. Helping people identify and get help for FQAD is so important to me that I now work as a patient safety expert and communications lead at the American Society of Pharmacovigilance.