I later tried cutting the dose of Doxy back, but still continued to have intolerable problems in the form of pain, fatigue, and my feet, ankles and toes all swelled, with redness and they were feverish. My ankles felt like bone grinding on bone.

I later swithched to Minocycline. It is said to be better tolerated and better absorbed. I have only take very small doses every other day, like 10 mgs, but along with the heparin, I am in about 95% remission, after being one very sick puppy.

I would start with the minocycline first, if that is ok with your doc. Also, start slow and ramp up. This has worked for me and may save you some pain and suffering.

PS: I am awaiting the results of my Lyme and Babesia tests. I have a STRONG feeling that even if my tests don't come back positive, my LLMD will still diagnose me as such since I have been bitten no less then 15 times that I know of. I have had the maority of symptoms and then some.

Be well,

This form of hyercoagulation is usually due to a chronic infection like the majority of us have. When we have an infection, and this is true even in healthy people we produce fibrin in our blood. In a healthy person this stops when the infection is gone, but in chronic infection the fibrin builds up chronically. Fibrin is a sticky substance and coats the viens somewhat like teflon as it has been discribed.

The fibrin also serves as a protective coating to the pathogens that we have acquired. The teflon like coating makes it nearly impossible for nutrients, oxygen and medication to reach their intended target. You can only imagine the host of problems this situation will bring on. But, in the case of ABX, the fibrin blocks access for the ABX.

This is where the heparin comes in. Heparin disolves that fibrin buildup, making the ABX better able to penetrate, therefore making the ABX more potent. I think it actuallys ays that in some of the literature that comes with heparin, makes certain drugs more potent.

Even though at this point it doesn't appear that heparin kills mycos directly, I do have a sstudy from Japan that indicates, heparin kills Babesia and another that seems to indicate it kills Lyme.

I am hoping that is true and that maybe after being on heparin for 3 years, this is in part the reason I am at 95% remission or symptom free.

I thnk in order to have real blood clots you need to much platelet activity. That doesn't have to be there in order to have this form of hypercoagulation or ISAC. There really is a ton of research on it, and a lot of it is already on my site.

sure you can take doxy, but minocycline is better. it will not make you super sensitive to the sun. in addition it is known not only to not cause candida, but to have an anti yeast/fungal action.
brand name is also clinically shown to be much more effective. patients relapsed when they switched from minocin to generic. there is a good article on using minocin for myocplamsa on dr. mercolas website. he has the largest alternative health site on the web because of the articles he posts. http://www.mercola.com/2000/aug/27/rheumatoid_arthritis.htm http://www.mercola.com/fcgi/pf/2002/jul/3/minocin.htm

I had VERY high levels of fibrin. I had very bad circulation. I was ice cold and either deathly white or a bluish black. I did not bruise.....ever, and I did not bleed. I regularly clogged needles during blood draws.

I started heparin in a nasal spray form and there was immediate and noticable differences. My fibrin levels within about 6 weeks returned to normal. I warmed up, turned pink, and began to bleed and bruise in a normal fashion.

You tell me what happened to the fibrin??? Where did it go? Was it broken down or what? How did it get out of my tiny little capillaries? This happens time and again to people on heparin. I am sure there is some very long explanation that is more precise and scientific, but this has been how it is explained to us wee people. But please tell us in terms we can all understand what it is you are saying heparin does or does not do.

My point was simple, in that heparin stops, prevents or whatever you want to call it, fibrin from building up and removes what had accumulated. This makes the ABX benetrate better, do you argue that point?

[This message has been edited by Jellybelly (edited 15 June 2005).]

myself and both my kids have lyme, so does my brther's whole family ..we've had it chronically adn the kids are being treated by dr. jones et...and none of us have hypercoagulation problems...

just wanted to mention this for hte newbies, so they don't all think they may have this automatically...

Lisa

The ONLY place to get the ISAC panel is from Hemex. You can look at their website at Hemex.com. There are a couple of mainstream medical tests that can be run, that might give a doctor an idea if you might have ISAC, but these will not give you a difinitive answer.

In my family, my daughter and I have/had it. My dad who they thought had Lupus had it REAL bad. My son's color on his feet and hands looks like he might have ISAC, but so far he tests negative. I'd bet my house that he will end up positive if he doesn't get treatment soon.

Another thing to keep in mind, is that you can be a bleeder and still have this form of hypercoagulation/ISAC. The real problem is the buildup of fibrin that coats everything, including pockets of infection.

recommending an herb or med they can buy over the counter because someone might be scared they fall into this category is a dangerous thing ....blood thinning is not for everyone, and can cause many problems if you do NOT have this problem. I also think the number is much less than 75% by the way personally..but that doesnt' matter.

what does matter is that I don't'want newbies running out and getting this otc med to thin their blood IF they don't need to...that could cause many problems in their body...

PLease anyone reading htis...check with your dr. before taking any blood thinners ..ok?

quote:

---

Originally posted by newdurham77:
What do you mean by the fact that "he problem with minocycline is pulmonary nodules and eosinophilia".!

---

thanks!

Nattokinase is considered to be EXTREMELY safe not just by those who use alternatives, but the mainstream medicine crowd are recognizing it to be very safe too.

But as ALWAYS, before people run out and buy anything, they should always learn about it first. Whether you're talking Rife, ABX, Colloidal Silver or whatever. We are all responsible to learn before we use anything.

With that being said, again I have tons of information on Nattokinase if anyone is interested in how it is used and whether or not is believed to be safe. It has been eaten for decades in the Asian culture and is made from soy. The website address is up in one of my first posts.

soy products by the way can't be used by any patient tht has problems with thyroid conditions, makes them worse..just so you know...

im in perimenopausea and can't use any soy stuff...bummer...because i;m hypothyroid, my endocronologist says no way...

here's a good article on it:

Soy's Thyroid Dangers
From Mary Shomon,
Your Guide to Thyroid Disease.
FREE Newsletter. Sign Up Now!

A Look at the Dangers of Soy to the Health of Your Thyroid
Health and nutrition magazines tout the benefits of soy as a cure-all for women's health, hormonal problems, cancer prevention, weight loss, and many other problems. The reality, however, is that promotion of soy may be more a matter of business and marketing, rather than recommendations based on sound scientific evidence.

Isoflavones, the key components of soy that make them so potent as a posible substitute for hormone replacement, mean that soy products, while touted as foods and nutritional products -- often are used and act as like a hormonal drug.

If you have a diagnosed or undiagnosed thyroid problem, or a history of autoimmune disease, overconsumption of soy isoflavones can potentially trigger a thyroid condition. Soy foods can worsen an existing diagnosed thyroid problem in many people. Sponsored Links
Thyroid and Coconut Oil
Research on hypothyroidism, weight- loss, metabolism, & thyroid health www.coconutoil.com

The Graves' Disease Inst.
The International Institute for Graves' and Thyroid Eye Disease www.thyroideye.org

Hypothyroidism?
If you're a woman over 35, your thyroid may not be the problem. www.womentowomen.com
In both cases the symptoms such as fatigue, weight gain, and depression or moodiness are often overlooked and hard to diagnose.

A recent study found that as millions of Americans -- perhaps as many as more than 10 million -- have an undiagnosed thyroid condition. The vast majority of thyroid patients are women over 40. This is the same group that, responding to marketing claims that promote soy as helping to prevent breast cancer, reducing the risk of high cholesterol or heart disease, or as a treatment for symptoms of menopause, are turning to soy foods and isoflavone supplements in vast numbers.

Here is more information regarding soy and its relationship to the thyroid.

FDA's Soy Experts Speak Out Against Soy

"there is abundant evidence that some of the isoflavones found in soy, including genistein and equol, a metabolize of daidzen, demonstrate toxicity in estrogen sensitive tissues and in the thyroid. This is true for a number of species, including humans.

Additionally, isoflavones are inhibitors of the thyroid peroxidase which makes T3 and T4. Inhibition can be expected to generate thyroid abnormalities, including goiter and autoimmune thyroiditis. There exists a significant body of animal data that demonstrates goitrogenic and even carcinogenic effects of soy products. Moreover, there are significant reports of goitrogenic effects from soy consumption in human infants and adults."

Lisa

[This message has been edited by lla2 (edited 16 June 2005).]

When the stressor was over, and I was back home, I happened to scratch my throat and found this rather large lump. Turns out my thyroid was all swollen on one side. I had even been having a sore and horse throat, with knuckles that looked like elephant skin.

Did some quick research and then remembered about soy. I knew that, because just a year earlier my daughter was diagnosed with Hashimoto's. My dad had Grave's, so thyroid issues are probably in my future.

Stopped the soy and thyroid swelling and associated issues subsided. Even though Natto is made from soy, in my case and my daughters it doesn't cause any problems with the thyroid. I think the amount of soy is very tiny, compared to the benefits to those who have hypercoagulation.

Punkin: I was always of the understanding that the tetracycline classes of ABX were used for many of the Mycoplasma subclasses--and it can take over two years of ABX treatment to make a "dent" in the mycoplasmas--tough to treat

Someone on the thread mentioned Garth Nicolson-his website: www.immed.org

And the fluoroquinolones were used specifically for Mycoplasma Pnuemonia

To this who exhibit tendon damage while on the quinolones--zithromax is another viable option-for myco P.

Myco P is a well known sign of immune supression--as it is just about everywhere( airborne--also called "Airplane pneumonia", since it is a common pathogen that is recycled in the jumbos')--not just transmitted by ticks, or other vectors--so it is not just a TBD infection

It is the underlying pathogen that causes "Walking Pneumonia" --but you most likely know that--so not to reiterate.

JellyBelly: I have to chime in and agree with Punkin and Lisa about both heparin, and natto---the information that they shared with you is the same information that I recieved from my hemotologist

Punkins' "Take" on the clotting cascade is correct--as I have Factor V Leiden--which is a genetic mutation---but am "Negative" per the ISAC panel==amazing for someone with active lyme for over 6 yrs.( But there is a reason for that,, since my immune system is/was below par prior to the borrelia infection--my immune system---Thankfully--- doesn't trigger this cascade(ISAC) into activity)

Anyway,

It's been covered pretty well here....but one of the best web-sites around when researching issues relating to the clotting cascade---for the layman
www.factorvleiden.com

And they have a list chat group for any questions--folks are very knowledgeable on that group--quite a few airline pilots, since DVT's are an occupational hazard for anyone with FVL, or any of the other thrombotic mutations ( officially called thrombophilia ) who are involved in alot of air travel.

There are other reputable labs( usually at major teaching university hospitals) that can run the ISAC panel--as this is main line science---hypercoagulation due to chronic infections is well understood by those who are in hemotology

There is artial clotting due to platelet aggregation( think of the explanation that is used in the T.V ad for plavic) Plavic, Pletel, and aspirin therapy is used for this problem

And then there is venous clotting( think DVT's) due to genetic mutations in the clotting cascade--which is usually handled by taking several precautions---

1) no hormone replacement therapy, and no birth-control pills--or the like

2) the need for anti-coagulation therapy during:

Pregancy, certain surgeries, during any treatment therapies using in-dwelling cathaters ( including PICC lines) and certain cases of prolonged air travel--or times of in-mobility

The immune system activated coagulation seen many times in lyme patients resembles "Activated Protein C Resistance", or "APC Resistance" for short

So, if you research this term--you get a good, general discusssion on what is happening to those lyme sufferers who need Heparin/Coumadin therapy

I have had to use LMW heparins on several occassions-- I have suffered from clots due to the factor v leiden( even with a normal ISAC panel)so I just thought I would poke my head in on this thread--and try to help out with my two cents worth--hope you guys don't mind!!!!

But it is true.....If the blood is too "thick" you do have a harder time getting the ABX to penetrate certain types of infectious pathogens, since they do use the fibrin to build their little cystic structures ( sneakly little B*st*rds)--but not all types of pathogens do this. Nor are we sure which strains of borrelia do this, either.

And your own antibodies have a tougher time mobilizing at the scene of the crime ( the infection)

I have read ( and I can't say whether it is true, or not) that heparin can provoke candidia into a "super infection" in those that are prone to those sorts of infections ( my guess is that if you are seriously immune supressed/ have heavy problems with untreated yeast infections--you may want to ask your LLMD about this topic matter prior to starting heparin)

How do people get mycoplasmas? I ask this because several of us at work came down sick. One doc said that she had discovered mycoplasmas in another case where several at work came down sick.

But, when it came to getting the insurances approval for the drug she needed for testing things feel threw the cracks.

Much later, my LLMD tested me for mycoplasma's and I think it came back positive.

I do not think I have had any of the drugs mentioned.

I have a workmen's comp case going on this and need resources to help me explain to the judge why mycoplasmas may be part of this and how it could be work related.

I also would like to understand why several of us came down sick myself. At least 4 of us are still struggling to regain our health.

All of us have been dx with cfs/fibro/stress and told there is nothing that can be done.

Hate to be a Nudge as Punkin says but I really believe you do not understand ISAC. If you do a search and use the word hypercoagulation you will come up with a description of "it" that you are describing, Thrombosis. That may have to do with Factor V Liden or Acitvated Protien C Resistence. etc.

In the case of ISAC it doesn't "have" to do with any of those. Those things may allso be a problem but they don't have to be. I have had ISAC and do not have any of those problems. It has been determined that my hypercoagulation is due to a chronic infection. This has proved true as I have been treating the infections and the hypercoagulation is gone.

You said that ISAC resembles Antiphospholipid Antibodies, and you are right it does resemble it, but it is not the same at all. A similar things happens, differemt cause, involving antibodies that are known. In ISAC you may get micro clots or thickening of the blood in general. ISAC DOES NOT mean blood clots or Thrombosis.

The ISAC panel is NOT used by mainstream medicine at this point. It is a new test developed by Hemex within the last 7-10 years. It is not covered by insurance or at least it wasn't last time I had it done 9 months ago. I do not believe it is approved by the powers that be either. It is more like Bowen's Lyme test, good but not approved. It is possible that some of the teaching hospital/labs are now using the ISAC panel and I do have info from I bleieve it was Vanderbilt that uses some pieces of the ISAC panel, but not all. That is very recent though. It is not used as a general screening test on us. Most doctors don't know about it.

I had dealings with a perinatologist who delivers high risk pregnancies. He deals with APS and he had never heard of ISAC. That was about 18 months ago. He's very good and has been on the Discovery Channel Health a few times.

In ISAC, fibrin is the primary probelm. There are several parts to the clotting cascade, whcih do not have to all fire up in ISAC. Example: I have had very high fibrin levels and T/AT, but my platelet level were just ever so slightly elevated. My daughter had no platelet activity and my dad had very high fibrinogen and very low platelet activity.

You got the same info from your hematologist I gave on heparin, that is awessome. It is slowly hitting the mainstream. What I said about Natto though is even more true. I don't know that I said it on this thread but I have said it numerous times, Natto is hitting the mainstream, big time. I just got a very recent report like 2 months old, that talks about using Natto in certain heart problems. Unlike you, I say a hematologist about 4 years ago, also very respected in the field and she had no clue about ISAC and heparin being used for it. She thought my doctor was a moroon, but she had absolutely NOTHING to offer me as far as my ice cold extremities, white or blue hands and feet. She just took pictures.

Let me just tell you that, I have read and read and read up on ISAC for many years. I know it pretty well and how it works in layman's terms. I am not so sure that you or Punkin have really read up on it as you keep bringing up blood clots, and ISAC by itself has really nothing to do with blood clots, but rather thick, sticky blood. You guys should know that it you are up on ISAC.

And finally I will say it one more time, Heparin does degrade fibrin. If you have info to prove otherwise, we would all love to see it. I have plenty of info on my website to say heparin works in the way I have said.

Mycos are everywhere. Myco Pnuemonia is very common, also known as Walking Pnuemonia. That is likely where the break out in your office came from. For most of the world they get it, it goes away, they move on. But if you are like me, which many are, I got Myco P. and have never been the same. It was the beginning of my downhill slide into the black abyss.

Other strains of Myco are everywhere. It is a very common contaminant in labs. It is often found in vaccinations which is another way in which we can acquire Mycos, vanccinations. Then there is Fermentans, man made, and I don't know how I got that. It does seem to show up more in people with Lyme though, maybe a key, a tick bite.

When going before the judge you might explain it this was. It is already a known fact that just about anyone can get Chicken Pox. Most people get it, it goes away, and they never give it another thought. BUT there are a certain few, that do hear back from the Chicken Pox virus. Many years later under possibly stressful circumstances it can return as Shingles. Very painful.

Chicken Pox actually never leaves in any of us. It is always there, but usually dormant, kept that way by out immune system. Let the right set of circumastances arise, and wham, you may end up with Shingles. They are finding this to be true with many pathogens. Same with Epstein Barr. Most never are bothered again, but they are now realizing it can come back to haunt a certain few.

Hope it goes well with the JUDGE.

Department of Microbiology, Kurume University School of Medicine, Japan.

Fifty strains of Mycoplasma pneumoniae in L cells were tested for susceptibility to macrolide antibiotics. Rokitamycin, a new macrolide antibiotic, was most active against these organisms, with an MIC for 90% of strains of 0.007 microgram/ml. The MICs of erythromycin, josamycin, and kitasamycin for 90% of strains were 0.03, 0.03, and greater than or equal to 0.06 microgram/ml, respectively. Based on these results, rokitamycin is a promising antibiotic for the treatment of mycoplasmal infections, and further clinical investigations are needed.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3124740&dopt=Abstract

:::::::::::::::::::::::::::::
::::::::::::::::::::::::::

Abstract:
This study determined the comparative in vitro potency of the new investigative quinolone gemifloxacin (SB-265805) using low-passaged clinical isolates and type strains of mycoplasma commonly found in the human respiratory and urogenital tracts.
Organisms studied were Mycoplasma pneumoniae, Mycoplasma hominis, Mycoplasma fermentans, Mycoplasma genitalium, Mycoplasma penetrans and Ureaplasma urealyticum, obtained from different geographical regions.
Comparator drugs were levofloxacin, trovafloxacin, grepafloxacin, azithromycin, clarithromycin, tetracycline and clindamycin. MICs were determined using a microbroth dilution method.
The overall range of MICs of gemifloxacin was 0.008-0.125 mg/L for different Mycoplasma spp. and 0.008-0.5 mg/L for Ureaplasma spp.
Depending on the species tested, gemifloxacin showed variable results when compared with the macrolides.
http://www.cfsresearch.org/mycoplasma/treatment/3.htm

::::::::::::::::::::::::::::::
:::::::::::::::::::::::::::::

Gohara Y, Arai S, Kuwano K, Kawashima T, Matsu-Ura I.

Department of Microbiology, Kurume University School of Medicine, Japan.

The antimicrobial activities against Mycoplasma pneumoniae of new quinolones (temafloxacin, ofloxacin, ciprofloxacin, enoxacin, and norfloxacin) and of tetracyclines and macrolides as controls were compared. Among new quinolones, temafloxacin, ofloxacin, and ciprofloxacin were more active than enoxacin and norfloxacin against fifty strains of Mycoplasma pneumoniae, giving MIC50 and MIC90 significantly lower than those of the latter two, by the agar-dilution method. The three more active antibiotics in the above assay were then determined for MICs and MBCs by the broth-dilution method. The MICs of every antibiotic except erythromycin determined by both the methods were very similar each other. The MICs of erythromycin determined by the broth-dilution method were ten-times higher than those determined by the agar-dilution method. Temafloxacin and ofloxacin gave MBCs only about four-times higher than MICs, whereas ciprofloxacin, minocycline, erythromycin and josamycin gave MBCs as much as 15 to 1,000-times higher than MICs. From the MICs and MBCs determined by the two assay methods, it is apparent that temafloxacin and ofloxacin, and to a less extent ciprofloxacin, have more potent mycoplasmacidal activities than do macrolides and tetracyclines.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1318981&dopt=Abstract

:::::::::::::::::::::::::::
::::::::::::::::::::::::::

Treatment

A 2-3 week course of certain antibiotics (erythromycin, azithromycin, clarithromycin, dirithromycin, or doxycycline) is generally prescribed for atypical pneumonia. This disease is infectious for weeks, even after the patient starts antibiotics. A persistent cough may linger for 6 weeks.

http://www.chclibrary.org/micromed/00057430.html

:::::::::::::::::::::::::::
::::::::::::::::::::::::::

Regardless, many physicians and rheumatologists are treating their arthritis, CFISD, fibromyalgia and other mycoplasma infections with long term antibiotic therapy. One of the more popular conventional protocols involves rotating multiple 6 week cycles of Minocycline or Doxycycline (200-300 mg/day), Ciprofloxacin (1,500 mg/day), Azithromycin (250-500 mg/day, and/or Clarithromycin (750-1,000 mg/day) among others.
http://www.rain-tree.com/myco.htm

:::::::::::::::::::::::::::::::::
::::::::::::::::::::::::::::::::

Medical Care:

Antimicrobial therapy is not necessary for mycoplasmal upper respiratory tract infection.
Although pneumonia is self-limiting and is not life threatening in most patients, treat it with appropriate antimicrobials to shorten the duration of illness and, perhaps, to reduce the spread to contacts.
Management of genitourinary diseases in which Mycoplasma species may play a role depends on recognizing the clinical syndromes for which antimicrobial therapy may be appropriate. Consider using antimicrobials that are active against mycoplasmal organisms in nongonococcal urethritis and pelvic inflammatory disease.
Surgical Care: Surgical treatment typically is not needed.

Consultations: Although consultations usually are not needed, in severe cases, ICU admission and consultation with critical care specialists, pulmonologists, and infectious disease physicians may be warranted. In patients who present with extrarespiratory manifestations, consult appropriate subspecialists.

Activity: Activity is as tolerated by the patient.
MEDICATION Section 7 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography

As a result of the lack of a cell wall, beta-lactams are ineffective; neither are trimethoprim and sulfamethoxazole effective. Aminoglycosides are effective in vitro, but efficacy is unknown in vivo. Ketolides are in development but show effective activity against mycoplasmal organisms.

Streptogramins (ie, quinupristin/dalfopristin on the market) are available only as a parenteral formulation; therefore, they are not practical for use in patients with Mycoplasma diseases.

Macrolides are the agents of choice. Alternatively, tetracyclines may be used in patients older than 8 years. Fluoroquinolones may be considered if macrolides or tetracyclines are not suitable choices; however, fluoroquinolones are not approved by the US Food and Drug Administration for use in patients younger than 18 years.

Drug Category: Antibiotics -- Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Whenever feasible, guide antibiotic selection using blood-culture sensitivity.Drug Name
Erythromycin (E.E.S., E-Mycin, Eryc) -- Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections. In children, age, weight, and severity of infection determine proper dosage.
Adult Dose 500 mg PO q6h for 7 d
Pediatric Dose 30-50 mg/kg/d PO divided qid
Contraindications Documented hypersensitivity; hepatic impairment
Interactions Inhibits CYP450 isoenzymes 1A2 and 3A4; coadministration may increase toxicity of theophylline, digoxin, carbamazepine, or cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Caution in liver disease; estolate formulation may cause cholestatic jaundice; adverse GI tract effects are common (administer doses pc); discontinue if nausea, vomiting, malaise, abdominal colic, or fever occur
Drug Name
Tetracycline (Sumycin) -- Treats gram-positive and gram-negative organisms, as well as mycoplasmal, chlamydial, and rickettsial infections. Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s).
Adult Dose 500 mg PO q6h for 7 d
Pediatric Dose <8 years: Not recommended
>8 years: 25-50 mg/kg/d (10-20 mg/lb) PO divided qid
Contraindications Documented hypersensitivity; severe hepatic dysfunction
Interactions Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy; tetracyclines can increase hypoprothrombinemic effects of anticoagulants
Pregnancy D - Unsafe in pregnancy
Precautions Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
Drug Name
Clarithromycin (Biaxin) -- Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Adult Dose 500 mg PO q12h for 7 d
Pediatric Dose 15 mg/kg/d PO divided bid
Contraindications Documented hypersensitivity; coadministration of pimozide
Interactions Toxicity increases with coadministration of fluconazole and pimozide; clarithromycin effects decrease and adverse GI tract effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, HMG-CoA-reductase inhibitors; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; administer one-half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies; caution in children because susp has bitter taste
Drug Name
Azithromycin (Zithromax) -- Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Adult Dose Day 1: 500 mg PO
Days 2-5: 250 mg/d PO
Pediatric Dose <6 months: Not established
>6 months:
Day 1: 10 mg/kg PO once; not to exceed 500 mg/d
Days 2-5: 5 mg/kg/d PO; not to exceed 250 mg/d
Contraindications Documented hypersensitivity; hepatic impairment; do not administer with pimozide
Interactions May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Site reactions can occur with IV route; bacterial or fungal overgrowth may result with prolonged antibiotic use; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function, prolonged QT intervals, or pneumonia; caution in patients who are hospitalized, geriatric, or debilitated
Drug Name
Doxycycline (Vibramycin) -- Inhibits protein synthesis and thus bacterial growth by binding to 30S and, possibly, 50S ribosomal subunits of susceptible bacteria.
Adult Dose 100 mg PO q12h for 7 d
Pediatric Dose <8 years: Not recommended
>8 years: 2-4 mg/kg/d divided PO bid; not to exceed 200 mg/d
Contraindications Documented hypersensitivity; severe hepatic dysfunction
Interactions Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy
Pregnancy D - Unsafe in pregnancy
Precautions Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
Drug Name
Levofloxacin (Levaquin) -- Of the fluoroquinolones (eg, ciprofloxacin, ofloxacin, levofloxacin, sparfloxacin, grepafloxacin), levofloxacin has emerged as the DOC to treat community-acquired pneumonia in adults. Use in children and in women who are pregnant remains restricted because of concern regarding cartilage toxicity, but several clinical trials are ongoing, and such use may be indicated in the future.
Adult Dose 500 mg/d PO
Pediatric Dose <18 years: Not recommended
>18 years: Administer as in adults
Contraindications Documented hypersensitivity
Interactions Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; levofloxacin reduces therapeutic effects of phenytoin; probenecid may increase levofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
http://www.emedicine.com/ped/topic1524.htm

::::::::::::::::::::::::::::::::::::::::::
::::::::::::::::::::::::::::::::::::::::::
::::::::::::::::::::::::::::::::::::::::::

::::::::::::::::::::::::::::::::::::::::::::

Ciprofloxacin (Cipro�)
Levofloxacin (Levaquin�)
Norfloxacin (Noroxin�)
Ofloxacin
Moxifloxacin (Avelox�)
Gemifloxicin (Factive�)
erythromycin
clarithromycin
azithromycin
roxithromycin
http://www.answers.com/topic/mycoplasma-pneumoniae

::::::::::::::::::::::::::::::::::::::
::::::::::::::::::::::::::::::::::::::

Mycoplasmal Infections
Mycoplasmal CDC

Mycoplasma

Autoimmune Debate

:::::::::::::::::::::::::::::::::::::::::
::::::::::::::::::::::::::::::::::::::::

SCIENTIFIC FACTS
VERSUS
FICTION ABOUT MYCOPLASMA
Aristo Vojdani, Ph.D., M.T.

INTRODUCTION
Members of the genus Mycoplasma are the smallest organisms lacking cell walls that are capable of self-replication and cause various diseases in humans, animals, and plants.

Seven different species of mycoplasma have been associated with various infections in humans. The earliest reports of mycoplasma infectious agents in humans appeared in the 1930s, 1940s and finally, in the early 1960s. The definite relationship between Mycoplasma pneumoniae and the primary atypical pneumoniae was established.

Mycoplasma pneumoniae
Today, M.pneumoniae remains an important cause of pneumonia and other airway disorders such as tracheobronchitis and pharyngitis. This organism is also associated with extrapulmonary manifestations such as hematopoietic, joint, central nervous system, liver, pancreas and cardiovascular syndromes.

Mycoplasma genitalium
M.genitalium was originally isolated from urethral specimens of two men with nongonococcal urethritis. This organism could be involved in pelvic inflammatory disease. A DNA probe hybridization assay has indicated that M.genitalium was present in urogenital specimens collected from 60% of male homosexual patients with recurrent or persistent nongonococcal urethritis and 22% of heterosexual men with recurrent urethritis, compared with 9% of men without urethritis.

Ureaplasma urealyticum
Ureaplasma urealyticum is considered to be a commensal organism in the lower genital tract of sexually-active women and has been found at a colonization rate of 40 to 80%. In some colonized pregnant women, ureaplasmas have been considered to be a cause of chorioamnionitis and premature delivery. They are frequently transmitted from mothers to their infants, and this may cause various diseases which includes pneumonia, persistent pulmonary hypertension, chronic infection of the central nervous system and bronchopulmonary dysplasia.

Mycoplasma fermentans, M. pirum, M. hominis, and M.penetrans
Mycoplasma fermentans, M. pirum, M. hominis, and M. penetrans have been proposed as human pathogens and possible cofactors in HIV infection. These organisms may contribute to the variation in the time from infection with HIV to the development of AIDS symptoms.

Mycoplasma fermentans (incognitus)
Mycoplasma fermentans is considered to be a commensal in the human mucosal tissues and has often been found in saliva and oropharyngeal of 45% of healthy adults. Also, M. fermentans organisms have been isolated from the human urogenital tract and are suspected of invading host tissues from a site of mucosal colonization.

Although mycoplasmas are recognized primarily as extracellular parasites or pathogens of mucosal surfaces, recent evidence suggests that certain species may invade the host cells.

The molecular and cellular bases for the invasion of M. fermentans from mucosal cells to the bloodstream and its colonization of blood remain unknown.

Also, it remains unclear whether M. fermentans infection of white blood cells is transient, intermittent or persistent. It is not clear how these stages influence any disease progression. The invasion of host blood cells by M. fermentans is due to inhibition of phagocytosis by a variety of mechanisms, including antiphagocytic proteins such as proteases, phospholipases and by oxygen radicals produced by mycoplasmas.

Mycoplasma fermentans is capable of fusing with lymphocytes and changing their immunological characteristics.

Mycoplasma fermentans cells are able to fuse with Tlymphocytes and change their characteristic of cytokine production. By electron microscopy we have been able to show that M. fermentans can indeed fuse with CD4 (Molt-3) cells and induce production of proinflammatory cytokines such as IL-6 and tumor necrosis factor alpha.

Prevalence of M. fermentans in patients with Chronic Fatigue Syndrome (CFS) and comparison with healthy subjects

Using PCR and genetic probes, we were able to demonstrate that between 30 and 35% of CFS patients and 4 to 8% of healthy controls do carry the Mycoplasma fermentans genome in their peripheral blood mononuclear cells.

While PCR and genetic probes are rapid and sensitive methods for detecting M. fermentans in clinical specimens, the clinical significance of this organism in Chronic Fatigue Syndrome should be determined by further research studies.

We emphasize that M. fermentans is not the etiologic agent for Chronic Fatigue Syndrome. It may serve as a cofactor in the induction of cytokines and other immune abnormalities found in CFS. These abnormalities may compromise the immune system, allowing other agents, whether they be biological, chemical, or both, to exert an effect resulting in symptomatology shown in CFIDS. Therefore, if the genome of this bacteria is detected in the blood cells of patients with chronic illnesses, treatment with antibiotics may be the logical step for its elimination from the blood.

Mycoplasmafermentans in Persian Gulf War veterans

Due to the similarity of symptoms in patients of Gulf War Syndrome and Chronic Fatigue Syndrome, we applied the PCR and genetic probe methodologies to the blood samples of the soldiers and found a similar percentage (32%) to be positive for the M. fermentans genome. Since the percent detection of M. fermentans genome in Persian Gulf War Syndrome is similar to that of Chronic Fatigue, we believe that M. fermentans is a cofactor and not the major cause of illness in the soldiers of the Persian Gulf War.

Claims that HIV genome was inserted in mycoplasma fermentans are unfounded.

In one study, it was suggested that pathogenic mycoplasma genomes were genetically manipulated, and part of the HIV genome was inserted into M. fermentans causing a large number of disease cases among veterans. To prove or disprove this claim, we attempted to amplify various regions of the HIV genome by using primers specific for different regions of the HIV genome in the PCR assay. We also utilized the extremely sensitive method of Southern Blot analysis with probes specific for the HIV genome. Using both methodologies we found no portion of the HIV genome among DNA samples of Gulf War veterans who were infected with mycoplasma. In all cases, we found that only the M. fermentans-specific probe reacted with the DNA samples and the specific probe of HIV did not react. The results of this experiment clearly indicate that the above claim regarding insertion of the HIV genome into M. fermentans is scientifically unfounded.

Mycoplasma and rheumatoid arthritis

The occurrence of various mycoplasma and ureaplasma species in joint tissues of patients with rheumatoid arthritis and other human arthritides can no longer be ignored.
M. fermentans was suggested more than 20 years ago as a cause of rheumatoid arthritis (RA) on the basis of isolation from synovial fluids of a few patients. Recently, with PCR methodology, the M. fermentans genome was found in 40% of synovial biopsy specimens and in 21% of joints of patients with rheumatoid arthritis respectively. This genome was also found in 20% of patients with spondyloarthropathy and psoriatic arthritis and in 13% of patients with unclassified arthritis.
M. fermentans was not detected in any specimens from patients with reactive arthritis, chronic juvenile arthritis, osteoarthritis or gouty arthritis.
Minocycline in rheumatoid arthritis

In two recently-published independent randomized trials, rheumatoid arthritis patients were treated with 100 mg of oral minocycline twice daily or a placebo for a period of 26 weeks. In the minocycline group, more minocycline-treated patients than placebo showed greater than 75% improvement in swollen joint count, tender joint count and in clinical parameters such as serum C-reactive protein (CRP) level and erythrocyte sedimentation rate (ESR). In these studies, the intergroup differences were statistically significant for these findings and the mean changes over time revealed continual improvement in the minocycline-treated patients during the entire period of both studies.

This and other presently-available data on minocycline therapy in rheumatoid arthritis suggest that such treatment may be considered along with disease-modifying anti-rheumatic drugs such as methotrexate, sulfasalazine, gold salts and hydroxychloroquine. However, additional clinical research is necessary to document the long-term efficacy of minocycline in the decreased progression of joint destruction. We believe that such long-term study about the efficacy of minocycline should be conducted on patients who are positive for mycoplasma and chlamydia genome (since we detect the chlamydia trachomatis genome in blood and joint fluid of 20% of patients with rheumatoid arthritis) and not by random selection of arthritis patients. Such selection or comparison between mycoplasma- and chlamydia-positive patients with mycoplasma- and chlamydia-negative individuals may further increase the clinical efficacy of minocycline or doxycycline in future double-blind placebo studies.

The eradication of the pathogenic mycoplasmas from blood and various tissue sites requires an intact functional immune system, which most patients with chronic illnesses do not possess. Therefore, immune enhancement strategies along with prolonged drug therapy may help to eliminate mycoplasma from the human body.

Drs. Baseman and Tully, in Emerging Infectious Diseases, Volume3, January-March, 1997, concluded that "the available data and proposed hypotheses that correlate mycoplasmas with disease pathogenesis range from definitive, provocative and titillating to inconclusive, confusing and heretical. Controversy seems to be a recurrent companion of mycoplasmas, yet good science and open-mindedness should overcome the legacy that has burdened them for decades."

Importance of measuring IgG and IgM antibodies against mycoplasma fermentans

We have developed a specific ELISA assay for measurement of antibodies against mycoplasma fermentans and compared the results to the presence of DNA in the blood. We found that only in about 60% of cases where M. fermentans was positive, antibodies to M. fermentans antigens were elevated significantly. In the other 40% in which the genome was positive, IgG and IgM antibodies were not detected. This may be due to the nature of the M. fermentans cell invasion, the inhibition of phagocytosis, and the lack of immune response to this organism in these individuals.

On the contrary, in about 20% of cases, the M. fermentans genome was absent but antibodies of IgG and IgM isotype were detected in their blood.

The absence of M. fermentans DNA from blood cells and the simultaneous presence of antibodies to this mycoplasma in the serum of the same patients suggests chronic infection of other tissues or cells with Mycoplasma fermentans. Another possibility is that these antibodies are cross-reactive in their nature. This means that antibodies produced against collagen, cartilage, and thyroid in some patients with autoimmune disease may cross-react with mycoplasma antigens and give false positive results. For this reason, we measured antibodies against synthesized peptides corresponding to M. fermentans and were able to reduce the degree of cross-reactivity.

Gold standard for detection of mycoplasmas

The polymerase chain reaction (PCR) for detection of mycoplasma genomes is still the gold standard.
However, confirmation of PCR should be done by southern blot and molecular probes in order to decrease the rate of false positivity and improve false negativity.
Antibodies (IgG, IgM and IgA) against peptide-specific mycoplasma should be performed simultaneously.
As no diagnostic tool is 100% accurate, we suggest that PCR, molecular probe, and IgG, IgM, and IgA antibodies should all be performed to gain the most accurate result.

http://www.immuno-sci-lab.com/mycoplas.html

:::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::

http://www.cfsresearch.org/mycoplasma/index.htm

:::::::::::::::::::::::::::::::::::::::::
:::::::::::::::::::::::::::::::::::::::::

Mycoplasma Treatments

Hate to be a Nudge as Punkin says but I really believe you do not understand ISAC.

Jellybelly: Oh, Dear Heart, I understand hypercoagulation "VERY WELL" Not only as an allied health professional. WHICH, BTW--is not the methodology by which I speak out on this topic matter--I have had two DVT's--one of which traveled to the lung, and became a PE-or Pulmonary Embolism,(which as you may know--if it travels to the chambers of the heart, or makes it way into the brain---you can kiss it all goodbye) so as they say, I have walked the walk, many times over!!!! I am now a coumadin lifer.

The ISAC panel stands for immune system activated coagulation--as you well know

Yes, this is activated by chronic infections, such as borrelia, as WELL as malfunctioning immune status--that is to say that this cascade "CAN"( read: CAN, does not mean that this is happening in everyone!!!!) be activated in persons with ANY type of immune system disturbance--not just those who are fighting chronic, active infections

People who are actively dealing with Multiple Chemical sensitivities(MCS) have also been known to have abnormalities on the ISAC panel--as one example

Mold sufferers (mycotoxins) are another example--still PWC's, but an example of those who are dealing with a different sort of chronic "toxin producing" infections, or toxin producing exposures

I'm going to respond to your posting by referencing each item that we may not agree upon--this is ment in the guise of brainstorming, and sharing information--I am not trying to match wits with you or anyone esle for that matter!

I tend to only post information that have have dealt with on a first hand basis---You can reseach, and read medical journal after medical journal, attend conference after conference---and I'm sure you will agree:

Experince is the best education of them all!

Anyway, back to your posting in response to my orginal posting on this thread:

JellyBelly: If you do a search and use the word hypercoagulation you will come up with a description of "it" that you are describing, Thrombosis.

YIB: The terms Thrombosis and Thrombophilia do have the same basic meaning which is per The American College dictionary:

Thrombosis:
N, The formation, presence, or development of a thrombus

Thrombus: A fibrinous clot formed in a blood "Vessel"( note: not in a artery)or in a chamber of the heart

Thrombophilia ( also called thromboplastic) was a term that was orginally "coined" for those of us who quite literally "love to clot" By Dr. Leiden--who is the German researcher that found the genetic mutations that are behind such clotting disorders as Factor V(FIVE) Leiden, and others that are genetic in orgin. This was presented to the medical community in 1994. These clotting disorders are found in 10-15% of the germanic population ( most carcasians
are of germanic descent) and are not quite as common amoungst african americans, and those of latinio orgin.( Yaah, good for them!!!)

So "Thrombophilia", in essense, is the exact opposite of "Hemophilia"

Hemophiliacs have to recieve Factor Five three times a week, as they produce very little of their own!---

In Factor Five Leiden patients----we produce too much factor five--which is much more complex than just suggesting that our clotting cascade is producing too much fibrogenic matter. But there are some close similiaries to the ISAC, and FVL which I will chat about later in the thread.

JellyBelly: That may have to do with Factor V Liden or Acitvated Protien C Resistence. etc.

In the case of ISAC it doesn't "have" to do with any of those. Those things may allso be a problem but they don't have to be.

YIB: True!

JellyBelly: I have had ISAC and do not have any of those problems. It has been determined that my hypercoagulation is due to a chronic infection. This has proved true as I have been treating the infections and the hypercoagulation is gone.

YIB: Most problems that show up on an ISAC panel are transcient in nature---meaning that they are not genetic in orgin
You may have misunderstood my first posting, if I was not self-explaintory enough, please forgive me---as I have added addition information in my response above

I agree that ISAC, and genetic mutations can be indeed different--but where there is smoke, there can definatily be fire---that is WHY Hemex usually reccomends running the ISAC panel first---to check on the status of active coagulation due to some of my above mentioned co-factors---such as ANY chronic infectious agents, and then--if there is a known reason that is shown within the ISAC panel, (such as something suggestive of genetics comes out abnormal) they will THEN run the genetic screening

There are reasons one does not run the gentic panel unless absolutely needed, one of which is that it is an additional expense to the patient if it is not indicated, the other reason is that it is not a good idea to have a abnormal genetic profile known on your medical records---since this can make it hard to purchase a life insurance policy, or obtain health insurance, disability insurance, ect. if you are self-employed

To mention names: I see the doctors at Gulf States Hemophilia and Thrombophilia at the University Of Texas medical center in Houston, TX. These are world reknown hemotologists---and not once have they *boo-booed* my lyme DX.

They run the ISAC panel first, followed by the Genetic panel if indicated--IN PATIENTS SUCH AS MYSELF---this may NOT be the way they do things on everyone!!!!! I can only speak from my experince!!!!!

Jelly Belly:You said that ISAC resembles Antiphospholipid Antibodies, and you are right it does resemble it, but it is not the same at all. A similar things happens, differemt cause, involving antibodies that are known. In ISAC you may get micro clots or thickening of the blood in general. ISAC DOES NOT mean blood clots or Thrombosis.

YIB: No, JellyBelly, I never said that hypercoagulation resembles the antiphospholidid syndrome---I mentioned that the syndrome that seems most common in patients "With hypercoagulation AND Lyme" resembles APC resistance---Which, BTW resembles Factor V Leiden

How?

Let's go over that again: Activated Protein C resistance creates excessive fibrogen due to infectious agents, just like Factor V Leiden creates excessive fibrogen due to the genetic mutation at the point R506Q mutation on the Factor V gene. It is more complex cascade than that---but this is a good quick, example.

That's where it may have gotten confusing--in the human body--whether it is Factor V Leiden, or APC resistance--they both produce the same effect on the clotting cascade.

There are many dimensions of the clotting cascade---some can be triggered by the hypercoagulation of chronic infections(ISAC) some are not triggered by this factor(Infectious agents).

JellyBelly:The ISAC panel is NOT used by mainstream medicine at this point. It is a new test developed by Hemex within the last 7-10 years.

YIB: The ISAC panel is too main stream medicine--if you are seeing a good hemotologist.

I had mine ran at St. Lukes Episcopal Hospital, at the Texas Medical Center, in Houston, Tx. I have also had an additional panel ran at Memorial Hermman Hospital, also at the Texas Medical Center, in Houston, TX.

When the ISAC panel came back negative( remember, my genetic panel was positive for several genetic clotting mutations--but thank god, the infections did NOT trigger the ISAC reaction in me!! so we have the exact opposite result---and are both borrelia patients) thru these institutions--I had one ran at HEMEX===It came out with exactly the same results as those ran at the Texas Medical Center.

Which I feel is good news---as more people will have access to this type of testing.

JellyBelly: It is not covered by insurance or at least it wasn't last time I had it done 9 months ago. I do not believe it is approved by the powers that be either. It is more like Bowen's Lyme test, good but not approved. It is possible that some of the teaching hospital/labs are now using the ISAC panel and I do have info from I bleieve it was Vanderbilt that uses some pieces of the ISAC panel, but not all. That is very recent though. It is not used as a general screening test on us. Most doctors don't know about it.

YIB: If you have out-of-network benefits thru your health insurer--you maybe able to get some money back on this testing thru HEMEX, but I had to file all the paperwork myself--and someone has to help with diagnosiac codes, ect. You may know someone in medical billing that could assist
you.

I do agree though, most doctors do not know about these disorders---and it does help if you are able to obtain testing thru one of the major medical centers in the country.

JellyBelly:I had dealings with a perinatologist who delivers high risk pregnancies. He deals with APS and he had never heard of ISAC. That was about 18 months ago. He's very good and has been on the Discovery Channel Health a few times.

YIB: Now we are getting somewhere here,

First off, it is sad this specialist had never heard of the ISAC panel---but I may know why

The genetic clotting mutations can, and do become "active" during preganecy-meaning two things

1) Many women will not be able to become preggers if they are not treated with anti-coagulates while trying to concieve

2) All Factor V Leiden pregancies are considered high risk---and all are to recieve anti-coagulation treatment until after the baby is born( usually six-weeks after delivery) This is true with other clotting disorders also

Most FVL pregnancies are induced earlier than the normal gestational period---off-hand, I can't remember the eact time frame in which they typically induce labor

I keep mentioning FVL--because it is the most common genetic clotting disorder--it effects one in five people---and most people do not realize that they carry the mutation until after someone in the family finds out that the carry the mutation---and tell the rest of the family to get checked for it------or you have had more than one clotting episode---or several unexplained mis-carriages.

Those with a positive ISAC panel most likely do not feel well enough to consider starting a family---but they do not require the medical interventions that FVL patients require anyway.

The precautions that I listed in my previous posting with regards to birth-control pills, air-travel, in-mobility, ect., are with regards to those who show positive on the genetic panel---since, FYI--I am seeing quite a few Factor V Leiden/Lyme patients showing up on other chat boards!!!!!

Quite a few!! So I like to present all types of clotting disorders when discussing this topic.

Jelly Belly:In ISAC, fibrin is the primary probelm. There are several parts to the clotting cascade, whcih do not have to all fire up in ISAC.

YIB: I agree with the above---but if there are hidden genetic mutations---other factors can be triggered by the ISAC activation---the fibrin problem can cause other issues. It's the case of an enviromental trigger( infectious agents) triggering genetics---scary, I know!!!!

JellyBelly: Example: I have had very high fibrin levels and T/AT, but my platelet level were just ever so slightly elevated. My daughter had no platelet activity and my dad had very high fibrinogen and very low platelet activity.

YIB: Heparin/coumadin for venous clotting(ISAC panel is venous "micro" clotting/hypercoagulation) ""AND"" DVT's and genetic thromboplastic disorders--these meds do effect fibrin production, coagulation factors, ect.

Plavic, aspirin, pletel, ect., for artial clotting, occlusive disease of the extremities, any clotting disorder that effects the platlets--these meds effect the viscocity of the blood in a different way then heparin/coumidin. They quite literaly render the blood "slipperier", so that there is less stress on the biggest muscle in the body---the heart, as well as less chance of platlet aggregation(clumping)

Some poor folks actually suffer from both problems.

JellyBelly:You got the same info from your hematologist I gave on heparin, that is awessome. It is slowly hitting the mainstream.

YIB: I was dx'.ed in Michigan in 1996!!!!!!!!--that's some pretty old news to me--were are all these doctors who should know about this stuff!!!!!

Now, this is where my profession comes into play--most PharmD's know enough about this to have a rather enlightening conversation about it with the laymen of the world---where are all the doctors' on this one??

JellyBelly: What I said about Natto though is even more true. I don't know that I said it on this thread but I have said it numerous times, Natto is hitting the mainstream, big time. I just got a very recent report like 2 months old, that talks about using Natto in certain heart problems.
Unlike you, I say a hematologist about 4 years ago, also very respected in the field and she had no clue about ISAC and heparin being used for it. She thought my doctor was a moroon, but she had absolutely NOTHING to offer me as far as my ice cold extremities, white or blue hands and feet. She just took pictures.

YIB: I personally don't have a problem with Natto---as I have successfully used natto to help deal with phelbitises that I have had to to IVIG infusions that I recieve every three weeks--and it works

What I was siding with regards to Lisas'
posting: Is that Natto should not be used by those who are hypothyroid, or have soy, or moderate to severe mold, fungial allergies.

There are several persons with FVL who use Natto on the FVL boards---and let everyone know about these precautions--they also will place you in touch with a doctor who researches the Natto--and who very much likes the product---BUT, like every med, or herbal---there are indications for some against usage of the product.

Like every other known agent--it has it's pros and cons---period!

JellyBelly:Let me just tell you that, I have read and read and read up on ISAC for many years. I know it pretty well and how it works in layman's terms.

YIB: JellyBelly, I'm not exactly "green" to this topic--and I have attended quite a few conferences on the subject matter---CEU's, you know!

JellyBelly:I am not so sure that you or Punkin have really read up on it as you keep bringing up blood clots, and ISAC by itself has really nothing to do with blood clots, but rather thick, sticky blood.

YIB: You may want to re-read your own posting---as you mentioned that the positive ISAC can contribute to "Micro Clots", Well, enough "mirco clots" can cause a major clot--if all the "micro clots" have developed in the same region,these micro clots can also cause the bluish extremities that you referred to above!-------

Jellybelly: You guys should know that it you are up on ISAC

YIB: My point is that you should be up on BOTH, the ISAC panel, and the genetics behind hypercoagulation---as you can have "JUST" a genetic panel positive---and still have thick, sticky blood---without a postive ISAC!!!!!!!

JellyBelly:And finally I will say it one more time, Heparin does degrade fibrin.

YIB: No one here was questioning that factoid, JellyBelly! It also does one hella of a job at thinning out the blood in anyone- no one needs to be told that!!--so expertise is needed with heparin usage!

JellyBelly:If you have info to prove otherwise, we would all love to see it. I have plenty of info on my website to say heparin works in the way I have said.

You can disagree all you want, but it is really sad that you are giving people incorrect info,

YIB: JellyBelly, make sure you are correct in your assumptions prior to accusing someone of giving out incorrect information---as my pretense was based on the fact that BOTH TYPES of coagualtion disorders need to be presented here on Lymenet.

Not just the ones in which you wish to refer to.

JellyBelly:and treating hypercoagulation is a VERY important key if it is a problem for you.

YIB: Well, we agree on that statement

JellyBelly: Hypercoagulation is very easily treated

YIB: That statement can be easily mis-constrewed--hypercoagulation can not always be easily treated---and you should know that!!!!

Improperly managed coumidin/heparin levels can lead to bleeds--which are quite dangerous---as you should know--!!!!!!

Quite a bit of knowledge is needed when dealing with the interactions of other medicines/foodstuffs, and anti-coagulation therapy

INRs' bounce all over the place if each and every additional medication is not taken into consideration with regard to heparin/coumidin usage.

JellyBelly: and can make a HUGE difference in how well your ABX therapy will work and how fast your progress is.

YIB: It doesn't have the same effect with regards to the "Faster progress" that you mention above with everyone. Many have been "freed" of the positive ISAC panel with anti-coagulation therapy---and are still quite ill--many yrs, and ABX treatments later.

Too many other viables with this disease---not just coagulation issues----which don't effect everyone with chronic Lyme, or other chronic infections---period---it's just not the blanket statement that you suggest that it is!!!!!!!

I still see that we are talking an apple and an orange though. I am talking ISAC, and your are talking DVTs or Thrombosis.

I have also read up quite a bit on FVL and Protien C and S I believe, it's been about 3 years and I haven't refreshed on it. When Hemex started doing the genetic testing, I was tested for them and I came back negative. I was sure I was going to have FVL. I am fully aware that there will be those who have ISAC that also have Factor V Liden and there will be those who do not have ISAC and still do have Factor V Liden. Let me just remind you that there can be false negatives with the ISAC panel due to length of illness, similar to the way there can be false negatives with Lyme the longer you have been sick.

What I am posting about is not Thrombosis though, that's all. There is no problem there that I can see. I do see your need to explain to people about Factor V Liden, but that doesn't negate that people should look into ISAC. That is all I have been encouraging, look into this form of hypercoagulation.

I do believe that heparin's effect on fibrin was brought into question from the very start of this thread. It was over and over said that everyone should seek a doctors advice in using Natto, and if one is more comfortable asking their doc, then great. Me, I am the one who educated my doctor about Natto and he now recommends it as a first course instead of heparin. Of course we would seek a docs advice in getting heparin, because as far as I know you can't get it without a doctors supervision. No problem there.

I was looking at some info from Berg again today. I will be posting this info later on my thread about ISAC. Berg said "this hypercoagulability produces fibrin deposits that result in 50-95% occlusion - but not immediate thrombosis". ISAC produces more viscous blood with all the excess fibrin, and can make a genetic clotting disorder even more seriouos. All the more reason to find out if you have ISAC and then treat it. It you are a clotter, you don't need an excess of fibrin flowing through your viens. In ISAC the fibrin does not ball up and collect with platelets to form a clot. The fibrin just floats freely and accumulates on eveything, including pathogens. I just read today as to why it doesn't ball up, but I'll have to read it some more before I could explain it to others.

I agree, that drugs like warfarin and coumadin can be dangerous. But I do not agree that heparin carries that same danger when given in the miniscual doses that are given for ISAC. Heparin is VERY stable and has a very short half life. It is gone and out of your system within 12-24 hours which is not true for warfarin and coumadin. My daughter delivered her first child while on heparin, even had an epidural. She was told to stop the heparin when contractions started so that she could have and epidural.

As far as other chemical sensitivities causing ISAC, again I don't have a problem with that. I don't have a problem with most any chronic illness causing ISAC, because I have a gut feeling that most of mans illnesses are caused by some sort of pathogen or chemical. Who knows, maybe even the genetic ones.

As far as the APS, sorry I misunderstood. APS is still similar to ISAC though. Berg calls ISAC a variant of APS. I am familiar with the infertility stuff too. That is where the research came from that lead to discovering ISAC. Knowing that was likely what made it possible for my daughter to have kids at all.

I agree 100% with what you say about genetic testing. We aren't on different sides, just coming in from different angles.

[B]Whew, thanks for going point by point. What I see is that we really don't disagree on anything, but that your are more focused on a certain aspect of clotting then I am talking about, due to your history. That is entirely normal and I am more focused on ISAC because it effects 3 people in my family.

I still see that we are talking an apple and an orange though. I am talking ISAC, and
your are talking DVTs or Thrombosis.

YIB:No, I'm just trying to present both types of hypercoagulation topics---since one can contribute to the other

I have also read up quite a bit on FVL and Protien C and S I believe, it's been about 3 years and I haven't refreshed on it. When Hemex started doing the genetic testing, I was tested for them and I came back negative. I was sure I was going to have FVL.

YIB: I'm glad that you don't have a positive genetic profile---it's a life sentence--while a positive ISAC panel can be transcient.

I am fully aware that there will be those who have ISAC that also have Factor V Liden and there will be those who do not have ISAC and still do have Factor V Liden. Let me just remind you that there can be false negatives with the ISAC panel due to length of illness, similar to the way there can be false negatives with Lyme the longer you have been sick.

YIB: I've heard about the false negatives in the ISAC panel--as Fibrin levels can flucuate in chronic infections--henceforth--if you can afford it--retesting at another lab, or at a later date might be advisable.

What I am posting about is not Thrombosis though, that's all. There is no problem there that I can see. I do see your need to explain to people about Factor V Liden, but that doesn't negate that people should look into ISAC. That is all I have been encouraging, look into this form of hypercoagulation.

YIB: I agree, and I'm not try to negate the importance of ISAC--just add information on top of the knowledge of ISAC.
But I have heard of, and have known people personally who have positive ISAC's---and have had blood clots---and believe it, or not---when tested for the genetic panel--they are negative on the genetics---so I think that it is still pertinent to try to understand both to the best of your abilities( and I know it's hard for someone with alot of cognitive problems from B.B)

I do believe that heparin's effect on fibrin was brought into question from the very start of this thread.

YIB: Not by me, I did post about reading on several chat boards( mostly the CFIDS anti-coagulation groups) about Heparin causing candidia to become more pronounced--with some developing yeast "super infections". But I never questioned heparin/comadins fibrinotic abilities

It was over and over said that everyone should seek a doctors advice in using Natto, and if one is more comfortable asking their doc, then great. Me, I am the one who educated my doctor about Natto and he now recommends it as a first course instead of heparin. Of course we would seek a docs advice in getting heparin, because as far as I know you can't get it without a doctors supervision. No problem there.

YIB: Alot of doctors are unaware of natto's contradictions with soy and fungal sensitivities--as well as it's effect in blocking the receptor capabilities with thyroid medications--but it's just one or two problems that need to be uunderstood--if you don't have those sorts of problems--then the issue is moot

But thyroid problems are fairly common amoung B.B sufferers--so getting the information out to this group is valuable.

I was looking at some info from Berg again today. I will be posting this info later on my thread about ISAC. Berg said "this hypercoagulability produces fibrin deposits that result in 50-95% occlusion - but not immediate thrombosis".

YIB: I agree-but it has happened even in those who show no genetic tendencies( thrombosis)--IMO--I tend to think that it may well have to do with the bodies ability to re-route the circulating blood thru the vascular system by developing new pathways. when occlusions develop in certain sections of the vascular system that already have several occlusions present, or are already overtaxed due to previous areas that had occlusions in the past( and the body had slowly rid the area of such occlusions, but a certain amount of scarring is left behind---areas which are now even more prone to future occlusions) ---or the vascular system can not regenerate new networks fast enough--you can have those "Micro-clots", that you mentioned--which can break free--and possiably travel up to the lung, or heart--and give the patient quite a bit of discomfort.

No, this are not the same as DVT's--and usually are not serious--but still, mind my french," Are a Pain in the arse"

ISAC produces more viscous blood with all the excess fibrin, and can make a genetic clotting disorder even more seriouos. All the more reason to find out if you have ISAC and then treat it. It you are a clotter, you don't need an excess of fibrin flowing through your viens. In ISAC the fibrin does not ball up and collect with platelets to form a clot.

YIB: If you are positive on both profiles--the above mentioned scenerio can take place--not in so many words---but the fibrin can collect on platlets that are already starting to aggregate together--and speed the process up towards a rather unpleasant possiable event.

This is not a common case scenerio--but it can happen--it's not impossiable.

The fibrin just floats freely and accumulates on eveything, including pathogens.

YIB: Like I mentioned above--it can collect on aggregated platlets also--not super common--but it happens.

I just read today as to why it doesn't ball up, but I'll have to read it some more before I could explain it to others.

YIB: I can't think of a better descriptive term for it either-tonight--but balling up isn't what I'm picturing in my mind, either.

I agree, that drugs like warfarin and coumadin can be dangerous. But I do not agree that heparin carries that same danger when given in the miniscual doses that are given for ISAC. Heparin is VERY stable and has a very short half life. It is gone and out of your system within 12-24 hours which is not true for warfarin and coumadin. My daughter delivered her first child while on heparin, even had an epidural. She was told to stop the heparin when contractions started so that she could have and epidural.

As far as other chemical sensitivities causing ISAC, again I don't have a problem with that. I don't have a problem with most any chronic illness causing ISAC, because I have a gut feeling that most of mans illnesses are caused by some sort of pathogen or chemical. Who knows, maybe even the genetic ones.

YIB: The germ-line( at birth) genetic mutations--such as Factor V Leiden, were traced back to muations that happened at the time in which Cro-magnen became Homo-sapien.

These were survivial mutations--too many people lost in child bearing yrs, due to women bleeding to death in childbirth, and due to excessive bleeding when injured due to daily activities, ect.

Somatic mutations( aquired though enviromental, infectious, or other sources of mutations) are just as they sound---aquired though-out the life time

If not caught, and treated (if infectious), or the offending enviromential toxin(s) are not removed--It does look like in several cases these mutations can become permanent--and cause further problems---such as APC resistance---which once activated, will now need to be treated--or problems can result.

Or this mutations can possiably be passed on as germ-line mutations in the next generation born of the aquired mutant parent.

As far as the APS, sorry I misunderstood. APS is still similar to ISAC though. Berg calls ISAC a variant of APS. I am familiar with the infertility stuff too. That is where the research came from that lead to discovering ISAC.

YIB: ISAC does mimick APS, but APCR can sure look like it's kissing cousin too, esp. to the layman, or uneducated doctor.

Knowing that was likely what made it possible for my daughter to have kids at all.

YIB: I'm glad she was able to have children--I was not--and did not find out why, until the FVL was found--and by then--I was well past child bearing age.

I agree 100% with what you say about genetic testing. We aren't on different sides, just coming in from different angles.

It is awesome that you have found other avenues to get the ISAC tests. I would like to know who or where they are so that I can post their locations. I lived in San Diego which is pretty progressive but now one there knew about ISACs that I or my doc ever talked too. Hopefully your sources are less expensive then Hemex. I would like to post that info on my website, also any good hematologists who know about ISAC. I'll share it with my doctor too.

YIB: I'll ask around--and see if it's ok to reccomend anyone esle in the area.

Best of luck on your web-site.

That is one of the reasons I have such a drive to help others learn about ISAC. When there is repeated miscarriage, APS is usually always checked for. Apparently now they are looking at FVL too. But for my daughter, she came back negative for those and her OB had nothing else to offer. It was my doctor an Osteopath who helped us out with the ISAC info and testing.

ISAC can cause soooo many problems still, for those who do not fall into your category. There are negative implications all over the place. I just read that cancer treatments work better when the layer of fibrin is removed from cancer cells. Same idea goes for the pathogens, they can be wearing little fibrin coats, that make ABX useless. Fibrin can hide clusters of pathogens only to be released again at some later time.

I am passionate about this issue, but I will try to be mindful of including a reminder about checking with your doctor. I don't often think about doctors because for the most part, they have offered me nothing to regain my health. Thankfully I found at least one doc in 24 years, that knows what he is doing, getting me my health back. I got a long way by fighting for myself.

PS: I am not looking for your doctors names, there are plenty of docs who will request the testing. You said that there are hospitals in Texas that do the ISAC testing. I am sure you don't have to ask for their permission to give out their names. I would just like to add them to the list of where you can get the ISAC panel done. Everyone's doctors can take it from there. Thanks!

Thanks for your kind words with regards to the having children issue!

Yes, I agree, very important to get the word out about all types of hypercoagulation disorders

With regard to the ISAC panel--and the docs' that use it--maybe HEMEX could tell you who uses their panel frequently?

I'm not sure if that violates any of the thousand new laws that have come into being recently about privacy, ect.

But if it's alright.....

And then, maybe the doctors could be contacted, and asked if it is o.k to refer them?

I have no experince in this area-so I don't know

--but once, on a thyroid yahoo group that I lurk on--patients had referred a local doctor to the "Good Doctors" list

Which just ment that they( the doctors') were willing to use Amour thyroid--and also used clinical judgement in using thyroid preperations--not just using blood tests alone.

One of the doctors was not happy to be placed on the list--and openly asked to be taken off

The patients felt bad for posting his name--since know one ever asked him

Maybe the OPMC watches endocrinologist too!( I'm trying to be funny!!)