Fluoroquinolones like Levaquin are just Plain Toxic
-InjuryBoard
12/10/2008- Those who are familiar with pain pump cases know that bupivacaine is chondrotoxic. Joint cartilage is composed of cells called chondrocytes, and most of the anesthetic “caines” cause chondrotoxicity that can result in cell death and disappearance of cartilage. It is also evident that fluoroquinolones (quinolones) like Levaquin and Cipro are both chondrotoxic and toxic to tendon cells (tenocytes).
For several years, investigators have known that quinolones act like metal magnets in removing magnesium from tissue. That removal process is called chelating. The problem with quinolones chelating away magnesium is that transmembrane proteins, like integrins, need metals like magnesium to connect cells to a cell matrix (cytoskeleton). That cytoskeleton acts as a scaffold holding chondrocytes in place to make a tough and slippery cartilage. Investigators have found that by “vacuuming up” magnesium, quinolones make pronounced changes to that cell scaffold, and negatively interfere with the normal biological process. These negative changes occur in humans as well as other mammals.
That brings us to the possible reasons why quinolones cause tendons to rupture; according to scientists, those reasons are not yet clear. Presently, however, there are a few things that investigators do know about the effects of quinolones on tendons.
When tendons stretch, tendon cells change shape and become elongated. More importantly, that stretching affects the process of tissue regeneration, such as tendon cell division, DNA synthesis, and cell metabolism. In fact, after 48 hours of stretching, thymidine levels in the cells’ DNA increase. Collagen synthesis also increases. Lastly, cell growth increases. In a sense, tendons use external forces to “engineer themselves" to meet the daily challenges we all give them. What if some chemical or other force deprives those tendons of the opportunity to “engineer” effectively? Let's address the reasons why quinolones such as Levaquin and Cipro interfere with normal tendon tissue regeneration.
Since the early 1990s, investigators have been aware that quinolones trap gyrase-DNA tropoisomerase IV-DNA complexes. It is well known that gyrase-tropoisomerase trapping slows bacterial cell growth down to a crawl. But does the same action occur in cells found in higher species? Evidence shows that it does.
In 2005, a group of toxicologists investigated the effects of Cipro and Levaquin on the tendon forming apparatus and arrived at the following conclusions:
Cipro at 3 mg and Levaquin at 10 mg had equal effect in causing damage at the cellular level;
Both drugs alter integrin receptors (the tissue building blocks mentioned above);
The effects were intensified at higher concentrations (that physicians might prescribe to treat certain resistant infections);
The length of exposure (increased time) and concentration increases the chemicals responsible for cell death (apoptosis);
Both drugs caused the following alterations:
Condensed material in the nucleus;
Swollen cell organelles;
Apoptotic bodies; and
Bleb formation at the cell membrane.
All of the above provides evidence of the following: 1) the two quinolones investigated cause changes in receptor and signaling proteins, which result in changes in tissue composition; and 2) future investigators must consider cell death (apoptosis) as a final event in the process of quinolone induced tendon disease.
However, it is not a stretch to say that what affects tendon and cartilage cells probably affects other cells in the body. Quinaolone drug manufacturers want quinolone based drugs to discriminate between bacterial cells and human cells. The trouble is that quinolones are not prone to such discrimination, and they go beyond bacteriocidal efficacy to attack human tissue cells.
Despite the difference of opinions portrayed in the two preceeding videos, there is no question that quinolones do have an effect on cellular DNA and mRNA composition and processing. For at least three decades, scientists have been investigating the effects of quinolones. They have done so on a molecular level, a cellular level, and across species.
While quinolones might serve as antibiotics of last resort, many investigators have cautioned against physicians prescribing quinolones in a frontline fashion, as they would amoxicillin or similar antibiotics.
If you or a loved one have experienced serious side effects or injury as a result of Fluoroquinolone antibiotics such as tendonitis, torn ligament, or ruptured tendons, you may be entitled to compensation. Contact one of our Fluoroquinolone lawyers today for more information regarding your legal rights. For more information about a potential Fluoroquinolone lawsuit, or Fluoroquinolone side effects, fill out our free case evaluation form or call the toll-free number listed below.