Dna symptoms and conditions

After you read a representative sampling of this website's testimonials, you certainly ask yourself inter alia: Can this be true? Did thousands of people inject an antibiotic from the fluoroquinolone family, which crippled them for longer or for shorter? Most of us, I suspect, never really get beyond the initial litmus test: Did this medicine poison me or save me? (The answer depends, of course, upon the age, gender, medical condition, and most importantly, the DNA make-up of the individual patient. For hundreds of thousands of patients this antibiotic is a boon. For thousands of other misfortunes this antibiotic is a disaster.) But there is another important question here.

Who gains from self-revelation? To be sure individual sufferers gain certain emotional catharsis from posting their adverse drug reactions (ADRs) to levaquin. E-postings are one-way anonymous tracks that form ruts on a well-traveled trail of tears. Unless these postings are hoaxes written by mischievious gnomes, then they consitute prima facie evidence for a causal link between levaquin injection and sundry crippling ADRs.

Curiously, this e-forum cannot be used as a tool for organizing thousands of potential litigants who might coalesce under a class action lawsuit. Yes, we can analyze each other's anonymous revelations to see if they muster our respective sense of the "ring-of-truth" re: levaquin toxicity, and we may contact each other one-on-one, but no-one can harness this intoxicating communication's technology to reach simultaneously all respondents en masse as a bloc.

So, who wins? The emotionally unburdened e-poster who learns belatedly that s/he is not alone and that prescription medicine likely caused more pain than the underlying malady for which s/he is being treated? Or big pharma that continues to manufacture and market a medication that poses downside risk to many consumers who unwittingly incur more damage than therapeutic value?

Indeed, who wins in a forum where consumers anonymously reveal their symptoms and unconfirmed suspicions? The answer is big pharma wins. Pharmaceutical companies data-mine our postings to estimate the frequency and bredth of ADRs about which consumers complain. House statisticians estimate the ratio of active complainants : silent complainants, i.e., the ratio of complaints who show up on this website to the far heftier percentage of complainants who never post on this website because either they are technology-challenged or they are incurious. House actuarians proceed to estimate how much operating profits their employers must set aside to cover losses in out-of-court settlements or in awards made to plaintiffs in class action lawsuits.

I think this is how the game is played in a behavioral sink where billions are made in a deregulated marketplace that allows predators and prey to interact anonymously. Sorry to be such a downer, but I fathom only the desperate plight of tens of thousands of levaquin consumers for whom no monetary award ever will compensate them adequately for their suffering, and the hundreds of millions of dollars at stake in court awards if consumers ever brought to bear their aggregate numbers and draw a bead on their big pharma tormenters.

I think it a true horror and shame that pharmaceutical companies have not devised a test which determines in advance which patient safely may consume levaquin and which patient's DNA places him or her at risk. I suspect the genome technology is available, but would dig too deeply into big pharm's bottom line. The economics of "parachutes-for-everyone" is infeasible. We are all guinea pigs in a B-grade movie featuring Russian roulette, billion-dollar pay-offs, and an FDA that pretends not to know.

Wow! Let me tell you my story: I was first diagnosed with HBP (170/140) during a high school sports physical in the beginning of 8th grade (I was about 14 years old). I was in top shape and a very healthy eater. I had probably (from what I remember) every test done to see what was the cause of this hypertension - and the only thing found was that my kidney's produce too much renin (the hormone that increases BP). I was then put on Lisinopril 10mg. Everything continued good for about 6 years - I also stayed in shape and ate healthy. However, throughout those 6 years, I did notice my curly hair turing straight and my incredibly (can't do nothing with) thick hair started to thin and become stylable. Now...I do know this is my fault, but in the past 2 years my healthy eating habits have slipped, I've gained weight and started smoking - plus have a sit down, don't move kinda job. However, about 1 year ago, I had a slight spike in my pressure and my doctor added a diuretic (HCTZ 12.5mg) to my lisinopril. Ok, that brought the pressure down and all seemed well. Then..... in December 2008, not long ago, I started not feeling well. Thinking I was sick, I went to the doctor's to find my blood pressure to be 190/140. Immediately, my does was increased to 30-12.5mg. That brought a quick drop in my BP down to 110/66 - I was so darn dizzy I could barely function. I was also but on short-term disability because all this caused me to be off work for so long. Unfortunately, when my dose was adjusted to 20-12.5mg and the dizziness stopped I went back to work. Now, I can't go back on S.T.D. for many, many weeks. And....... The past month has been complete HELL!! My hands (mainly fingers) and toes are almost always cold, I've been dieting for over a month and am struggling to lose weight, my hands and feet go numb more often than usual - I never used to find myself waking up in the middle of the night because of pins/needles feeling, my hair is thinner than ever and stick straight - I'm afraid I'm not gonna have any left, I have UNBEARABLE headaches (sometimes all I want to do is sleep and sometimes, like tonight -it's 4:12am- I can't sleep), I have acne like a teenager - mind you, I never had more than 1 to 2 pimples at a time growing up, and that was rare (I was lucky)... Thank god for FMLA, or I would of lost my job since I've spent so much time home since I thought all was good and went back to work. Only wish I could make a dollar again. Now to top it off...I was referred to a nephrologist (kidney specialist) who after seeing me only once for about 30min and reviewing bloodwork from the end of January (I had a high calcium level as well as some others that deal with the kidneys) wants to take away the diuretic (HCTZ) part of my medication (hopefully to reduce the calcium level) BUT DOUBLE MY MG OF LISINOPRIL. HE WANTS ME TO TAKE 20MG TWO TIMES A DAY. I was starting to think all these new symptoms that came on so quick were a result from the increase of lisinopril - now I think I'm sure. I'm not changing my medications until I can talk this over with my PCP - I'm going to ask we try a medication change. Does anyone have any suggestions? Or any suggestions why a 20-year-old has blood pressure as high as 190/140 with no family history of HBP or really any health problems? Any suggestions why the kidneys are producing too much renin? Any meds that drop the pressure and we don't get headaches - I can live with cold limbs and numbness - it's the headaches that are rendering this 24-year-old helpless :(

I was put on Singulair about three weeks ago, and noticed immediately that my mood had changed. I am an adult ,and felt this sense of sadness, anxiety, solitude, not wanting to be around anyone. I took myself off the drug and have tics all over my body and eyelids ,which is driving me crazy! I even had heart palpitations ,which are very distressing. Today it seems to be better, and this is day three off the med. The only way I can explain how I felt on this drug is doom and gloom.

Why does Singulair cause these symptoms? I am going to give my explanation which is only a HYPOTHESIS. This should not be categorized as any thing but an educated guess. This is not backed by scientific research because nobody will do any research that would appear to anger
Merck even if people are suffering in the thousands.

1. The original research that preceded the development of Singulair (montelukast) seemed to focus on the theory that asthma was caused by an unusual immune response to certain pathological stimulus. There are many references to the observation that a high percentage of asthma sufferers are people whose asthma is caused by fungus. Many people suffer from asthma and are told that they are allergic to dust mites. Dust mites can live only because the fungus aspergillus pre-digests the
food source that dust mites can then absorb. Other sources of fungus occur in the home due to dampness or problems with wood rot.

2. The body's immune system fights certain categories of pathogens such as bacteria and fungus by creating nitric oxide which kills them at the site where they try to enter the body. The mast cell is the immune cell that is responsible for the production of nitric oxide. Mast cells are found in the skin, airways, intestines etc. The mast cell is capable of many different types of biochemical functions that are designed to signal other cells or other chemical responses. When the mast cell knows that pathogens
are present and nitric oxide is NOT produced, then it signals other immune cells to be sent to the site of the infection. Thus in the case of asthma, it is known that excessive numbers of eosinophils appear in the airways and these cells create inflammation.

3. Singulair was developed for asthma and later allowed to be prescribed for other reasons. I believe that montelukast probably creates a source of nitric oxide that prevents the mast cell from signalling for other immune cells to arrive at the source of infection. I arrived at that conclusion from studying the chemical structure of montelukast, the chemical structure of the gene cysLT1 receptor, and the chemical structure of the cell wall of fungus which would be what the mast cell uses to determine "what to do in order to kill the fungus."

The researchers who invented montelukast first had to clone the gene-cysLT1 receptor meaning that they had to be able to identify the gene and replicate it. Then by trial and error they had a find a "chemical"
that would bind (connect chemically) to the cysLT1 receptor. The theory would be that montelukast would take the place of the fungus or other pathogen and thus prevent the gene from reacting to produce the
responses that the sick patient with asthma produced. Merck says in the literature that montelukast binds with the cysLT1 receptor in order to prevent the mast cell from signalling the eosinophils to arrive in excessive
numbers that cause inflammation. I believe that montelukast is also causing the production of an amount of nitric oxide that is actually killing the pathogens that are present. For one thing, I would think that it
would be dangerous to incapacitate the immune system in that way without providing a way to kill the pathogens. I don't believe that the asthma response is just allergies to something like dust. Pollen from trees and flowers is loaded with fungus spores.

4. IF, IF, IF, montelukast does actually produce nitric oxide, then it does so by binding with the gene. Any place in the body where a molecule of montelukast encounters the cysLT1 receptor (a gene) then the corresponding molecules of nitric oxide are produced before the liver enzymes break the montelukast molecules up. Nitric oxide is TOXIC and
INFLAMMATORY. So let's look at the symptoms in regard to the location of the cysLT1 receptors. The location of these symptoms would not be places in the body where the mast cells normally encounter fungus or bacteria. The cysLT1 also has other functions in that it communicates with the cysLT2 receptors. Obviously, nitric oxide
should not be produced in these locations because of the signalling effect of nitric oxide on other physiological functions.

a. intestinal pain - the cysLT1 receptors are located in the small intestines
b. leg pain actually caused by vasculitis - cysLT1 receptors are found inside blood vessels- consistent with the fact that montelukast causes
Churg-Strauss
c. some people who didn't have asthma develop asthma - the cysLT1 receptors are in the airways
d. nightmares, depression, neurological damage - when montelukast penetrates the blood brain barrier probably due to unusual conditions of blood pH or electrolyte imbalance then nitric oxide in the brain causes neuron damage and excitoxicity

5. Why do some patients not experience side effects? Probably because genetically they are completely compatible with the model that researchers created when they cloned the cysLT1 receptor gene. I didn't not find any information about whether researchers knew that there are many different variations of this gene.

6. IF, my theory is even close to being correct, then why doesn't Merck do anything about researching these side effects. Maybe because nobody in the company knows how this drug works but the researchers who created it. All of the Merck literature is very vague about any biochemical information.

Again, this is just speculation and hypothesis. I have made an attempt to put this in simplistic language and therefore sacrifice scientific accuracy. But, I think that you will get the point.

SINGULAIR IS VERY DANGEROUS TO PATIENTS WHO EXPERIENCE NEGATIVE SIDE EFFECTS. DOCTORS SHOULD JUST REALIZE THAT
THOSE PATIENTS ARE NOT COMPATIBLE WITH THE MODEL FOR THE DRUG.

Results: DNA was collected from 252 participants: 69% were white, 26% were African American. Twenty-eight SNPs in the ALOX5, LTA4H, LTC4S, MRP1, and cysLT1R genes, and an ALOX5 repeat polymorphism were successfully typed. There were racial disparities in allele frequencies in 17 SNPs and in the repeat polymorphism. Association analyses were performed in 61 whites. Associations were found between genotypes of SNPs in the ALOX5 (rs2115819) and MRP1 (rs119774) genes and changes in FEV1 (p < 0.05), and between two SNPs in LTC4S (rs730012) and in LTA4H (rs2660845) genes for exacerbation rates. Mutant ALOX5 repeat polymorphism was associated with decreased exacerbation rates. There was strong linkage disequilibrium between ALOX5 SNPs. Associations between ALOX5 haplotypes and risk of exacerbations were found.

Conclusions: Genetic variation in leukotriene pathway candidate genes contributes to variability in montelukast response.

http://ajrccm.atsjournals.org/cgi/content/full/173/4/379

Wow, I had no idea that Levaquin affected so many people. My daughter had knee surgery a couple of years ago. They gave her vancomycin before the surgery. She had an allergic reaction to the stuff. She also found out from one of the nurses that levaquin is related to vancomycin.

I had a total hip replacement 3 years ago and they gave me vancomycin just before the surgery. I was laid up in the hospital for a week. When I arrived home I noticed that my skin was really itchy (mostly my arms). Whenever I scratched it left whelps and turned extremely red. Now after 3 years my skin is still itchy, but not as frequent as it used to be. Has anyone had this problem with their skin?

I wanted everyone to be aware of the relation between vancomycin and levaquin.

Good luck to all.

I am getting mine removed FRIDAY!! And Friday can't come soon enough. I am kinda bummed tho for having to go back on the pill but I can't hack this ANY LONGER!!! One of my friends works for a GP and I went to him because of some of my side effects. The flu like symptoms minus having the flu (had it for at least 2 to 3 mos now) NO sex drive (causing trouble with my marriage. Hubby is taking it WAY to personal), swelling in my hands, feet, legs, and face. (my face will feel flush and BAM I'm swollen!!) VERY BAD MOOD SWINGS!!! Very Bad isn't the word for it!! There are no words to explain my moods!! ANYHOW..... I sent this to my friend to read and she pulled it up at work. Well the GP said that this isn't a reliable place to go for information on the side effects. "There are NO positive side effects to anything." Which is true BUT he seems to think going to Web MD or some sight like that is more reliable than here. And that this sight shouldn't scare me and he wouldn't urge me to have it removed after reading this. (OH YEAH I forgot to mention joint pain, I have HORRIBLE joint pain in my hands, wrists, elbows, knees, ankles, and feet. The worst of it is in my wrists and elbows) Back to what I was saying. To that (this sight not being reliable) I say go to Web MD and post there too! I pray that I can get back to me after this comes out!! I hope it don't take too long either! I MISS the old me and HATE the new me!! But FRIDAY HURRY UP AND GET HERE. And for anyone who has had it removed........ anything I should be repaired for??? Thanks for your time!