Fluorchinolone-Nebenwirkungen

metrogirlblogger August 29, 2017 at 6:30 am Reply
Hi, Reychop. I am interested to know your insight into DNA damage through metronidazole; I know a lot of people who believe they suffered DNA damage because of this drug. However, fluoroquinolones cause mitochondrial DNA damage completely on their own. This isn’t something Lisa or other floxies need to theorize–it’s been proven through multiple studies and even the FDA admitted it on an drug assessment document in 2013 (and yet they left it off of the official FDA label). They know fluoroquinolones cause systemic DNA damage and all it takes is one pill to trigger these affects. That’s why drugs like Cipro, Levaquin, Avelox and other “floxie” drugs have 5 black box warnings a piece.

I’m actually not a floxie–I suffered a serious adverse reaction to metronidazole in 2015. I’ve never taken a fluoroquinolone, but I’ve researched it a lot to gain better understanding into ADRs in general. The effects of these drugs are deadly and disabling on their own.

Now, back to metronidazole. I am curious to know your theories about this, if you’ve uncovered some medical literature about its DNA effects, because the research into metronidazole is quite limited. That being said, I know, as do many in our support group, that metronidazole is a serious neurotoxin. Again, we don’t need to guess–the medical literature is out there. The drug causes lesions to the back of the brain. These are mainly on the cerebellum, but can also affect the basal ganglia and brain stem. In fact the brain stem is the second-most hit region after the cerebellum. Also, the nerves can get damaged (peripheral neuropathy). Most metronidazole victims complain about:

*Altered mental state. Usually horrible, constant panic attacks, loss of emotional control, depression, crying spells, lowering of stress threshold, extreme insomnia, derealization, depersonalization.

* Motor control issues. Usually gait disturbance (ataxia), dysarthria, hand tremors, leg twitches, (rarely) nystagmus. Seizures can happen but they are quite rare for this.

* Peripheral neuropathy. Sometimes only in hands/feet–sometimes everywhere.

* Autonomic dysfunction. This is one medical literature is missing badly. This include dysphagia, respiratory issues, digestion issues (complete loss of appetite is a very common issue, where you take two bites of something and can’t eat anymore), heart rate/blood pressure issues, salivation issues (many people now have a white tongue/mouth due to salivation dysfunction), heat/cold intolerance, loss of equilibrium. Some of are people with the worst cases have been diagnosed with autonomic dysfunction.

* Neck pain, light/sound sensitivity, headaches and/or head pressure (usually at the back of the head but sometimes all over the head), severe brain fog, extreme weakness and fatigue.

The symptoms are usually worse in the mornings and slowly improve as the day continues.

Any of these sound familiar? It’s due to brain damage; there are case studies, systematic reviews and a warning on the FDA label (although the warning is grossly simplistic) that no one bothers to look at even when patients present with symptoms.

I am sorry you’re going through this–I truly am. It’s a nightmare I wouldn’t wish on anyone. Most people do recover from metronidazole toxicity–about 65%. Others improve (about 29%–I’m in this group). About 3% is unknown and the remaining 3% have permanent cognitive impairment.

I am hoping you make a full recovery–that is the most common result. And yes, I’m certain this will make you a better doctor. In fact, it has the opportunity to make you a great one because you now know this problem firsthand.

If you want to learn more about metronidazole, I do have a blog at:

http://www.metrogirlblog.wordepress.com. It’s a little outdated (no mention of ANS issues, that’s something that’s become more apparent in the last several months), but still some good information and links. And let me know about the information you have about metronidazole DNA damage–there are some people in our support group who are leaning towards this theory, and I’m sure they’d love to learn.

Thanks,
Erin

Jahre anhaltende oder innerhalb von Monaten abklingende Beschwerden beruhen möglicherweise auf peripherer axonaler Degeneration infolge Bindung von Metronidazol an neuronale RNA und Behinderung der Proteinsynthese (BRADLEY, W.G. et al.: BMJ 1977; 2: 610-1). Die Behandlung mit Metronidazol sollte möglichst kurz erfolgen und eine Kombination mit anderen potenziell neurotoxischen Mitteln gemieden werden.

By using a novel SL/DS methodology in the model organism yeast, we discovered that the antimalarial drug CQ inhibits thiamine transporters and consequently causes thiamine (vitamin B1) deficiency and growth defects. This mechanism of action (MOA) is conserved in human cells and possibly also in other organisms. Given that both thiamine deficiency and treatment with CQ cause retinal, neurological, and cardiovascular disorders in humans, our results suggest that thiamine deficiency might be a root cause of some of CQ's adverse effects, which might be preventable with concomitant dietary thiamine supplementation. Such a MOA by CQ could also be responsible for its therapeutic effects against malarial parasites, which need exogenous thiamine for survival. Such a possibility needs to be investigated before dietary thiamine supplementation can be used to prevent CQ's adverse effects.

Thiamine is also depleted in those exposed to formaldehyde, and by long-term use of the following prescription drugs: phenytoin, penicillins, cephalosporins, aminoglycosides, tet- racycline derivatives, loop diuretics, fluoroquinolones, sulfonamide derivatives, and trimethoprim.25

Drug-Nutrient Interactions
Thiamine can be depleted by long-term use of the following prescription drugs: pheny- toin, penicillins, cephalosporins, aminoglycosides, tetracycline derivatives, loop diuretics, fluoroquinolones, sulfonamide derivatives, and trimethoprim.25

Subclinical thiamine deficiency
Although frank thiamine deficiency is rare today, large segments of the world’s population continue to subsist on marginal or sub-marginal intakes of thiamine (Sauberlich, 1967; Kawai et al,1980; Lonsdale et al,1980; Anderson et al,1985; Barrett et al,1992). People exposed to subclinical
10
Thiamine deficiency and its prevention and control in major emergencies
thiamine deficiency are predisposed to manifest frank beriberi under appropriate circumstances, occasionally in epidemic proportions (Tang et al, 1989; Rolfe et al,1993). These population groups with endemic subclinical deficiency are frequently difficult to identify because of the lack of quick and simple means of assessing subclinical thiamine deficiency.
Body storage of thiamine is minimal, the liver being the main extra-muscular storage site. In young and healthy non-alcoholic individuals, subjective symptoms appear after 2 to 3 weeks of a deficient diet (Brin,1963). Characteristic early symptoms include anorexia, weakness, aching, burning sensation in hands and feet, indigestion, irritability and depression. After 6 to 8 weeks the only objective signs at rest may be a slight fall in blood pressure, and moderate weight loss. After 2 to 3 months apathy and weakness become extreme, calf muscle tenderness develops with loss of recent memory, confusion, ataxia and sometimes persistent vomiting (Anderson et al,1985).
Mild thiamine deficiency can be seen in people who have high carbohydrate intakes and low thiamine intakes e.g. in people whose staple food is polished rice, especially if their diet contains anti-thiamine factors (tea, coffee, betel nuts, raw fermented fish) and in population groups who consume large quantities of refined carbohydrates in the form of sweetened carbonated drinks and candies. High alcohol intakes and continuous high-calorie intravenous feeding can lead to detectable thiamine deficiency. At risk are also groups whose minimum thiamine needs are markedly increased because of raised physiological or metabolic demand (Anderson et al,1985):
• pregnancy and lactation
• heavy physical exertion
• intercurrent illness (cancer, liver diseases, infections, hyperthyroidism)
• surgery
and wherever absorption is reduced by:
C regular high blood alcohol levels
C gastrointestinal disease; dysentery, diarrhoea, nausea/vomiting.
The symptoms of mild thiamine deficiency are vague and can be attributed to other problems, so that diagnosis is often difficult. Marks (1975) reported that a useful sign of mild and moderate thiamine deficiency is myotactic irritability. Anorexia, which is one of the early symptoms of subclinical thiamine deficiency, is regarded to be a protective phenomenon since a high-carbohydrate diet is most dangerous in the presence of thiamine deficiency (Lonsdale et al,1980).
The symptoms of mild thiamine deficiency clinically improve by the administration of thiamine. Lonsdale (1980) however, reported that in his patients who were biochemically thiamine deficient and who had symptoms considered generally to be those of neuritic dysfunction, the reversal of the metabolic disturbance occurred much slower than is generally associated with vitamin deficiency states.
Abnormal biochemical thiamine status has been associated with reduced growth in the young (Neumann et al, 1979), chronic ill-health in young or middle aged adults (Lonsdale et al, 1980), falls and fractures in old age (Older et al, 1982), impaired reaction to stress such as surgery (Alvarex et al, 1982), lactic acidosis, renal dysfunction, endocarditis, arrhythmias, sudden death in adults (Campbell, 1984; Anderson et al, 1985) and with the Sudden Infant Death Syndrome (Jeffrey et al, 1985). Experiments have also shown that thiamine deficiency predisposes to infection (Anderson et al, 1986).