Millions use fluoroquinolone antibiotics annually to prevent bacterial infections. But the drugs are associated with several serious and potentially deadly side effects, including tendon rupture, worsening of a neuromuscular/autoimmune disease, nerve damage and heart complications.
If you're suffering from heart problems after taking a fluoroquinolone antibiotic like Cipro, Levaquin or Avelox, you could be eligible for compensation.
Fluoroquinolones are a popular class of antibiotics that kill bacteria or prevent their growth. They are used to treat a variety of infections, with newer drugs in the class developed with a broader range of indications and effectiveness. But these medications have also been associated with several serious side effects and toxicities, some of which can be deadly.
Several fluoroquinolones have been removed from the market, including grepafloxacin in 1999, removed worldwide after adverse reports of cardiac episodes, and sparfloxacin (brand name Zagam) removed from the U.S. market in 2001, mostly due to poor sales performance.
The FDA, over the years, has strengthened the drug labeling for remaining fluoroquinolones with the addition of three black box warnings, the agency’s most serious type of warning, from 2008 to 2016.
Tendons are flexible bands of tissue (fibrous structures) that connect muscles to bones, according to the National Institutes of Health (NIH). They aid muscles in the movement of bones. When a tendon becomes severely swollen (inflamed), the condition is called tendinitis.
Tendinitis is often referred to in combination with the body part involved in the injury, such as Achilles tendinitis, when the condition affects the heel. Other commonly affected areas include the elbow, knee, shoulder, thumb and wrist.
Tendinitis is typically an acute condition, meaning it comes on suddenly, is generally severe and lasts for just a short time. When the symptoms of tendonitis last for more than six months, it becomes a condition called tendinosis (or chronic tendinitis), which means the tendon has experienced damage at a cellular level (tendon degeneration).
Tendinosis may lead to an increase in tendon repair cells causing reduced tensile strength and increasing the risk of tendon rupture. A tendon rupture occurs when part or all of the tendon is torn. If untreated, this can result in permanent disability.
The first published report of a tendon injury associated with the use of fluoroquinolones was published in New Zealand in 1983, according to the Journal of Clinical and Aesthetic Dermatology. Many anecdotal case reports and case-controlled studies reporting similar findings came out after the publication, most originating in France.
A World Health Organization (WHO) survey in Australia found that ciprofloxacin was the cause of 90 percent of fluoroquinolone-induced tendon injuries. But other reports have also indicated norfloxacin, pefloxacin, ofloxacin and levofloxacin in such injuries. As a result, in July 2008, the FDA required all fluoroquinolone manufacturers to include a black box warning indicating the increased risk of tendon rupture in patients taking these medications.
The drug label addition also advised patients and health care providers that this risk is even greater for individuals over the age of 60, in those who have received kidney, heart or lung transplants, and with the simultaneous use of steroid therapy.
Tendinitis primarily results in pain and soreness around a joint. Other symptoms of the condition may vary depending on the cause and location of the injury.
Tendinitis can be diagnosed following a physical exam, which will look for signs of pain and tenderness when the muscle attached to the tendon is moved in various ways; or if the tendon is inflamed, the skin covering it may be warm and red. Other tests might include an ultrasound, X-ray or MRI.
Treatment is intended to relieve pain and reduce inflammation. Resting the affected tendon as it heals is often recommended as well. This can be accomplished by using a splint or a removable brace. Applying heat or cold to the affected area can also assist with recovery and offer some relief from any pain or discomfort.
Steroid injections can be administered into the tendon sheath when necessary to control pain.
Patients may undergo physical therapy (PT) to stretch and strengthen the tendon as well as the attached muscle. PT may also be effective in restoring the tendon’s ability to function properly, improve healing and prevent future (or repeat) injury. In some more severe cases, surgery may be needed to remove the inflamed tissue from around the tendon.
Approximately 50 percent of patients with tendinitis in their heel as a result using fluoroquinolones recover within 30 days, after discontinuation of the drug and the start of PT, according to the Journal of Clinical and Aesthetic Dermatology. Another 25 percent of those same patients will have symptoms that persist longer than two months.
Early diagnosis is key in preventing tendon rupture.
Myasthenia gravis is a neuromuscular disorder and an autoimmune disease that causes weakness in voluntary or skeletal muscles, such as those responsible for facilitating breathing and moving parts of the body, including the arms and legs, as well as eye movement, facial expressions and swallowing.
A neuromuscular disorder involves the muscles and the nerves that control them, while an autoimmune disease occurs when a person’s immune system mistakenly attacks otherwise healthy tissue. In people with myasthenia gravis, the body produces antibodies (proteins made by the immune system when it suspects harmful substances in the body) that block the nerve cells and muscle cells from communicating via neurotransmitters (or chemicals that brain cells — neurons — use to send messages).
The name myasthenia gravis, which is Latin and Greek in origin, means “grave, or serious, muscle weakness,” according to the National Institutes of Health (NIH). The condition is likewise characterized with muscle weakness that worsens after various movements and periods of activity and improves with rest.
Myasthenia gravis can affect people of all ages, but it is most commonly diagnosed in young women and older men.
Exposure to fluoroquinolones may result in the worsening of myasthenia gravis in patients, according to a 2011 study published by the National Institutes of Health (NIH). The authors of the study concluded that health care professionals should be aware of this serious link between the drug and the disease and carefully weigh the benefits to the risks associated with fluoroquinolones when treating infections in patients with myasthenia gravis.
The study, designed to evaluate post-marketing adverse event reports submitted to the FDA and case reports published in scientific literature, identified a total of 37 cases that reported myasthenia gravis exacerbation following the use of fluoroquinolones.
In February 2011, the FDA necessitated a black box warning, advising consumers that taking ciprofloxacin, a type of fluoroquinolone, may worsen muscle weakness in people with myasthenia gravis, causing severe difficulty breathing or even death.
The onset of myasthenia gravis may be sudden and symptoms are not always immediately recognized as resulting from the disorder. The first noticeable symptom is often weakness of the eye muscles. In some, however, the first signs may be difficulty swallowing and slurred speech.
The degree of muscle weakness associated with the condition can vary greatly from one person to another, ranging also from a localized form affecting a limited area of muscles to a severe or generalized form affecting many muscles, including those involved in breathing.
Autonomic (involuntary or unconscious; relating to the autonomic nervous system) muscles of the heart and digestive tract are typically not affected.
There is no known cure for myasthenia gravis. Treatment can allow for some patients to have periods without any symptoms (called remission), but this is usually only temporary. Available treatments can assist in the control of symptoms to allow for a relatively high-quality (normal or near-normal) life for individuals suffering from the condition.
Eye surgery may also be recommended to treat the eye muscles, if affected.
Most patients with myasthenia gravis have a normal life expectancy. However, sometimes the severe weakness associated with myasthenia gravis can cause respiratory failure, which necessitates emergency medical intervention, as it can potentially result in death.
Peripheral neuropathy is “very common,” affecting about 20 million Americans, according to the National Institutes of Health (NIH). It occurs when the peripheral nervous system is damaged by injury (physical trauma), illness or exposure to certain drugs, like fluoroquinolones.
Peripheral nerves carry information to and from the brain as well as signals to and from the spinal cord and to the rest of the body. When a person has peripheral neuropathy, these nerves don’t work properly. NIH compares the disorder of the peripheral nerves to “static on a telephone line,” with the nerves distorting or interrupting the messages between the brain and the rest of the body.
The condition can occur because of damage to a single nerve (mononeuropathies), a group of nerves (polyneuropathy) or it can affect nerves throughout the entire body. Some peripheral neuropathies are due to damage to the axons (or the long, slender projection of the nerve cell), with others caused by damage to the myelin sheath (a fatty white substance that coats and insulates the axon), or a combination of the two.
In 2013, the FDA announced it was strengthening warnings in the labels for fluoroquinolones to better describe the disabling side effect of peripheral neuropathy. Previous warnings about this serious nerve damage were not strong enough or clear enough, the FDA said. Specifically, the federal agency said older labels failed to explain fully that neuropathy damage can happen immediately after taking the drugs and can be permanent. The FDA told doctors and consumers to discontinue the medication immediately if symptoms of nerve damage surface.
FDA data shows a continued association between the drugs and the crippling nerve disorder, which occurs in the arms and legs. In fact, the onset of peripheral neuropathy after starting fluoroquinolone therapy was rapid, often within a few days. In some patients, the symptoms had lasted for more than a year, even after users had stopped taking the drugs. Several patients were continued on fluoroquinolones despite their showing signs of the disorder. The FDA ultimately concluded peripheral neuropathy can occur at any time during treatment with fluoroquinolones and can last for months to years after the drug is stopped, or can be permanent.
A study published in 2014 by the peer-reviewed journal Neurology further supported the FDA’s findings. The study showed long-time users of fluoroquinolones had twice the risk of developing peripheral neuropathy, while new users had a slightly greater risk. Researchers said, “Clinicians should weigh the benefits against the risk of adverse events when prescribing these drugs to their patients.” Researchers studied more than 30,000 men in the U.S. from 2001 to 2011.
Fluoroquinolones can cause nerve damage that lasts for months to years after the drug is stopped.
Symptoms of peripheral neuropathy vary depending on what nerves are damaged (i.e. motor, sensory or autonomic). Motor nerves control voluntary movement of muscles used for walking, grasping things or talking; sensory nerves transmit information that results in feeling from touch or pain from injury; and autonomic nerves control organ activity activities that are automatic, such as breathing, digesting food, and heart and gland functions.
In some cases, all three types of nerves can be affected.
Damage to the nerves interferes with the messages coming from the brain to the rest of the body. These confused messages can wreak havoc on the types of sensations someone feels. For example, a person may feel severe pain in response to sensations that should not cause pain, like feeling pain from bed sheets, or numbness in fingers and toes. The nerves in the hands and feet are the first to be affected.
There are over 100 different kinds of neuropathy. Each type has its own symptoms, prognosis and treatment. Typically, a doctor starts by performing a physical exam and asks about the patient’s health history and symptoms. The doctor may also recommend blood tests to look for causes of nerve damage.
After doctors diagnose a specific type of nerve damage, they discuss treatment options. First, they will address the cause such as hormones, vitamin deficiencies or exposure to toxic medications. Sometimes, eliminating the issues that caused the damage allows nerves to regenerate.
“Peripheral nerves have the ability to regenerate axons, as long as the nerve cell itself has not died, which may lead to functional recovery over time,” according to the National Institute of Neurological Disorders and Stroke. “Correcting an underlying condition often can result in the neuropathy resolving on its own as the nerves recover or regenerate.”
Adopting a healthy diet and exercise can help manage symptoms. Exercise, for example, can reduce cramps, improve muscle strength and prevent muscle from wasting away. A doctor may recommend supplements or injections to people who have low levels of B12 or other vitamins. Anyone with diabetes should become more knowledgeable on how to control blood sugar, and people who drink alcohol should stop.
Some people participate in therapy to learn exercises to improve their muscle strength and control. Doctors may recommend using a wheelchair, braces and splints to improve movement or even help a patient regain the ability to use an arm or leg that has nerve damage. Orthopedic shoes are another option and can help prevent foot injuries in people who can’t feel pain.
In many cases, doctors may have to prescribe strong drugs including pain killers, antidepressants and anticonvulsants. Antidepressants and anticonvulsants tend to be the medications that are most effective at reducing neuropathic pain. Antidepressant medications can include Elavil (amitriptyline), Cymbalta (duloxetine hydrochloride) or Effexor (venlafaxine). Frequently used anticonvulsant medications include gabapentin, pregabalin, topiramate and carbamazepine.
These drugs typically do not bring back loss of feeling and are generally prescribed to people with neuropathy to reduce pain in the feet, arms and legs. They have their own laundry list of side effects. Opioid pain killers can also leave some people addicted.
Some people may turn to alternative medicine to supplement their treatment. These therapies may include acupuncture, alpha-lipoic acid, fish oil supplements, amino acids and herbs, such as curcumin, geranium oil and evening primrose oil.
Topical medications — such as topical lidocaine, an anesthetic agent, and capsaicin, a substance found in hot peppers that modifies peripheral pain receptors — may also improve neuropathic pain. Another non-invasive method is transcutaneous electrical nerve stimulation (TENS). It involves attaching electrodes to the skin and releasing an electrical current. The efficacy of this therapy in treating peripheral neuropathy has not been tested in controlled clinical trials. However, some studies have shown it improves symptoms of diabetic neuropathy.
How well a patient does depend on the cause and extent of the nerve damage. Sometimes, even with treatment, nerve damage can be permanent. Long-term (chronic) pain is likely, with numbness in the feet often leading to skin sores that are hard to heal, which, in rare cases, require amputation.
The lining of the aorta is made up of collagen. Scientists suspect that fluoroquinolones break down collagen in the body. Two 2015 studies published in JAMA and BMJ medical journals reveal a connection between fluoroquinolones and collagen damage that may lead to aortic aneurysms.
An aortic aneurysm is a bulge in the aorta, which is the artery responsible for carrying blood from the heart through the chest and torso.
According to the JAMA study, fluoroquinolones were associated with a two-fold increase in risk of dissection and aneurysm within 60 days of using the drug. Authors said, “Clinicians should continue to be vigilant for the appearance of aortic aneurysm and dissection in high-risk patients treated with fluoroquinolones.”
The BMJ study found nearly a three-fold increase in the risk of aneurysm. Authors of this study followed about 1.7 million patients and found one third of them received a prescription for a fluoroquinolone. “Reducing unnecessary fluoroquinolone treatments or prolonged treatment courses might have possibly prevented more than 200 aortic aneurysms in this population,” study authors said.
Aortic aneurysms were the primary cause of 9,863 deaths in 2014, and dissections and ruptures are the cause of most deaths from aortic aneurysms, according to the Centers for Disease Control and Prevention.
Aortic aneurysms weaken the aortic wall and are more likely to burst. They can occur in the abdomen (abdominal aortic aneurysm) or in the chest (thoracic aortic aneurysm). These weak spots are extremely dangerous, and once they burst, a patient has a 50 percent chance of survival.
Aneurysms often have no symptoms. These bulges may be found while testing for other conditions on a CT scan or ultrasound of the heart. When the thoracic aneurysm ruptures, people have difficulty breathing, severe chest pain or severe back pain or may lose consciousness.
A ruptured aneurysm is an emergency situation and must be treated immediately. Doctors may prescribe surgery or an aortic stent.
Dissection interrupts the blood flow to other organs by blocking other blood vessels that feed them. This can lead to stroke, paralysis, kidney failure and other problems. All dissections can lead to death, and it is extremely important to catch them early. Doctors typically use CT scans to diagnose them. Treatment may or may not require surgery to replace the dissected portion of the aorta.
In May 2017, the FDA updated a 2016 safety alert to include new information regarding aortic aneurysm and aortic dissection. The agency said it found cases submitted to the FDA and published in medical literature do not support reports that fluoroquinolones may result in aortic aneurysm and aortic dissection.
“FDA will continue to assess safety issues with fluoroquinolones and will update the public if additional actions are needed,” the agency said.
In July 2018, the agency required fluoroquinolones to strengthen their label warnings to include the risk of hypoglycemic comas. The FDA took the action after a review found 13 deaths and nine patients rendered disabled after experiencing hypoglycemic comas while taking the drugs. In total, the review found 67 instances of hypoglycemic comas between 1987 and 2017.
At the same time, those warnings were strengthened, the FDA also required uniform drug labels for all fluoroquinolones regarding mental health side effects. These risks include:
Please seek the advice of a medical professional before making health care decisions.
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