SForsgren
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posted
Which of the HLA-DRn genes are of most interest to those of us with Lyme. I have heard 2 and 4 and also 3 and 4.
Has anyone had these tests done and did you find the resulting information useful?
Thanks
-------------------- Be well, Scott Posts: 4617 | From San Jose, CA | Registered: Jul 2005
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riversinger
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posted
Hi Scott!
It is more specific than just 1, 2, 3, 4. Each type also has subtypes. I have had the full subtyping done, and found the resulting information has been extremely useful when decoded according to the tables in Mold Warriors.
It completely fit how my body responds to these illnesses, and gave some strategies that I, in particular, need to follow. I have a subtype that is easily damaged in the hypothalamus, as well as one that has difficulty detoxing dead Lyme bacteria. Further testing substantiated that it was correct.
My son also had the typing done, and he has aslighty different type in one of his genes, so has to look out for different things, which also makes sense. However, he is also susceptible to hypothalamic damage, which was supported by his testing as well.
The two doctor's groups I am involved with are both finding this info very helpful with their chronic patients, whether they have Lyme or another chronic condition.
oxygenbabe
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posted
Where did you get the testing done? Thanx.
Posts: 2276 | From united states | Registered: Jun 2004
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riversinger
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posted
Hey, Oxygenbabe! Labcorp does the testing. It is HLA DR DBQ testing, if I remember right. Test code number 012542. This is the testing they do for transplant compatibility.
But you will have to translate the info you get by using the chart in the Mold Warriors book. It doesn't come out in the form used by Dr. S. It is just a confusing mix of numbers. So either you, or your doctor, has to know what to do with it.
It is paid for by insurance if your doctor knows how to bill.
This has been my experience but I don't know what it all means.
HLA- DR4 A positive result indicates the presence of the antigen which has been associated with an increased risk of an adverse reaction to the lyme vacine.
(I don't know if this means even without the vaccine that you are at greater risk such as from the Bb bacteria in general but I would guess that it does. I know there are certain genetic markers that make you more susceptible to chronic autoimmune type illnesses. And believe this is one of those???) Just thinking out loud. In type, whatever....
This is from a Quest Diagnostics lab report.
My 3 oldest had theirs run by Dr J
Theirs were negative and so were their HLA-B27 which is associated with ankylosing spondylitis & Reiter's disease.
But their HLA-DR15 and HLA-DQ6 were positive this types for Narcolepsy and may mean other things.
It seems these are important #'s as these four results are listed on the front of the reports by the Dr for reference.
Posts: 399 | From Texas | Registered: Apr 2005
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posted
I PM'd you the # to call the HLA and Immunogenetics Laboratory for more info. Hope it helps.
Posts: 399 | From Texas | Registered: Apr 2005
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SForsgren
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posted
Thanks everyone for all the information. I appreciate your responses.
-------------------- Be well, Scott Posts: 4617 | From San Jose, CA | Registered: Jul 2005
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lpkayak
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posted
i have the #4 one...and i have severe progressive osteo arthritis in many joints. my doc suggested doing the test because all my lyme symptoms were under control or gone except the joint pain. when we got the results i stopped abx and cleansed for a year. i felt some better after the cleanse - but the arthritis continues to progress and has to be treated like artritis-cosamine , anti inflammatories until surgery is the only answer. i refuse the cortisone shots.
-------------------- Lyme? Its complicated. Educate yourself. Posts: 13712 | From new england | Registered: Feb 2004
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posted
I have the DR4 and band 31 on the western blot Dr K in CT did the testing. He told me that I have chronic autoimmue lyme because of the DR4 gene. He said 30% of the population has this genotype and is waiting to be triggered by lyme, bacteria, mycoplasma, virsues, etc. Lucky me
I was put on plaq, a old arthritis med. I was told that no matter how low that lyme level got, a small amount/level of the band 31 would always trigger the DR4 gene.
Posts: 315 | From USA | Registered: May 2005
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posted
My daughter is DR2 and DQ1 positive. Her first Western Blot had double positives on the 31 and 34 bands. Dr. J in CT said that both her WB results and her HLA results indicate a predisposition to develop an autoimmune reaction to Lyme. In Dec, Dr. J ran a test called Immune Complex, C1q. Her value was 35, with anything over 10.8 being positive so hers sounds kind of high to me. I asked him what it meant and he basically said that it hangs together with her WB and HLA results in painting a picture of someone with an autoimmune reaction. When I asked how we should address it, he said by continuing to treat the Lyme and taking Plaquenil, which she's been on since August. He also said a drop in her Immune Complex number might be the first indication that the autoimmune reaction is resolving. He wants to retest in 3 or 4 months.
I barely understand this autoimmune stuff. I would be really interested to hear others' results and understanding of the Immune Complex test.
Posts: 164 | From USA | Registered: Jul 2005
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minoucat
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posted
I'm pushing this to the top because it occurred to me that the hubby (who has persistant and painful arthritis) and a couple of other lymie friends who are struggling with tx may have this marker.
I'd like to hear about how (IF!) knowing about the gene and subtype helped you address LD/Co or the symptoms.
Riversinger, it sounds as if this knowledge has played a big role for you in some of your choices? Is it continuing to help, do you think?
Lpkayak and littlesprout, have you followed any specific protocols related to your HLA testing, and has it made any difference?
And -- I haven't found any docs locally who are familiar with the Shoemaker/Mold Warriors protocol, and my LLMD isn't real conversant with it either. Are any of you feeling your way through this with non-expert medical advice, and how is it going for you? Was it hard to get the right testing done?
bpeck
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posted
Leslie:
What your Doc is saying is that: If you have band 31 kDa on your western blot, it means that the body has made antibodies to Outer surface protein A ( OspA ) which is a protein in the membrane of the Lyme bacteria.
The protein configuration of OspA closely resembles some of the protiens on the body's own cells (so they call that similarity molecular mimicry). So, the theroy says that when the body's antibodies are attacking Lyme (specifically attacking because they recognize OspA- band 31 ) they can get confused and attack the body's tissues that resemble that protein configuration (and that's called the autoimmune response).
When an antibody and an antigen combine, it's called an immune complex. If too many of these immune/antigen combos (called complexes) are circulating in the body - they can cause problems- in the kidney's for example- they don't filter thru very well - and they can accumulate in other parts of the body as well. Mostly the test for imune complxes is an inflammation marker.
Some researchers are saying that if you are of a specific tissue type ( Like HLA Dr4) then your body's immune system is predisposed to having a flaw in recognizing "self" verses "non-self"..
It's starting to become mainstream thinking that if you show band 31 on a western blot you have a good chance of having what's called autoimmune post Lyme syndrome after all signs of the infection are gone.
Hope this helps. Barb.
Leslie Wrote: My daughter is DR2 and DQ1 positive. Her first Western Blot had double positives on the 31 and 34 bands. Dr. J in CT said that both her WB results and her HLA results indicate a predisposition to develop an autoimmune reaction to Lyme. In Dec, Dr. J ran a test called Immune Complex, C1q. Her value was 35, with anything over 10.8 being positive so hers sounds kind of high to me. I asked him what it meant and he basically said that it hangs together with her WB and HLA results in painting a picture of someone with an autoimmune reaction. When I asked how we should address it, he said by continuing to treat the Lyme and taking Plaquenil, which she's been on since August. He also said a drop in her Immune Complex number might be the first indication that the autoimmune reaction is resolving. He wants to retest in 3 or 4 months.
I barely understand this autoimmune stuff. I would be really interested to hear others' results and understanding of the Immune Complex test.
Posts: 1875 | From VT | Registered: Oct 2002
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Lydie
Unregistered
posted
Antinuclear antibody (ANA) is a pretty basic test to see if autoimmune activity is going on.
I and my two daughters have positive ANA's. Two of us are HLA-DR4 types and continue to be sick, after years of treatment. The other daughter is not HLA-DR4, and is doing fine after 4 months of abx. Her ANA is low, ours is high.
The conclusions seem pretty clear to me, I guess.
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Im hlr4 positive and had the vaccine. The info has done me no good except to help et a diagnosis of chronic lyme/autoimmune dut to having had the vaccine
The info has been no help to the 2 lyme docs Ive seen excet for the above.
My insurance company didnt want to pay for the testing. They said they only pay for that testing for transplant patients.
My lyme doc gave me a hugh stack of papers and I sent them all to the the ins co and they paid without a fight.
Posts: 561 | From connecticut | Registered: May 2004
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posted
My son is HLA DR4 also and he was tested by Dr. K in CT also...You have all explained this much better than it was explained to me by doc...anyway he did say that my son due to this typing they have found a person to be predisposed to developing an autoimmune disorder....well he has autism so I guess there is truth to that...Why the rest of the HLA testing was not done I do not understand but plan on getting more answers to this soon...
I was particularly upset to see that some are not getting better with abx's that have the DR4 typing and the ones that dont are getting better...
If you are an LLMD or make claims to be than shouldnt all the testing be done for HLA genes? and shouldnt everyone who has these positives be treated differently?
Otherwise isnt it just all a waste of time and unfortunate painful herxing?
Sorry this is all just so damned upsetting...Eileen
Posts: 127 | From Rock Tavern, New York | Registered: May 2005
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bpeck
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Eileen:
It should be stressed here that it is still THEORY that people typed as HLADr_ are predisposed to a life of autoimmunity if they contract Lyme.
But the theory has gone main stream with the Dr.s - including the LLMDs.
From what I can read - it does look like the treatment might be swinging in a different direction for people with the HLA DR tissue type (I see more Mino and Plaq - both which have suppressive mechanisms) being used now that was used 5 years ago.
It's complicated- even for the Drs. (and really complicated for some Docs- not everone graduates at the top of their class you know).
Lyme supresses part of the immune system- so over time, other parts of the immune system can become hyper-sensitised - so you really have supression and hyper immunity going on the same time -
Tailored treatment for tissue type? Probably still to early in the research for that to be a main-stream reality. But I think for this tissue type- most LLMDs are using an immune modulator in conjunction with the abx- and choice of abx is probably important too.
Unfortunately - no one has the final answer on tissue type/Lyme.
But I'd hate to see the HLA DR gene get cast in stone as a sure thing to life long autoimmune problems as it has been linked to other autoimmune disorders- if this happens Post Lyme SYndrome will be treated like RA and Lupus... more suppression - and no more looking for a root cause.
We have been doing a trial of Immune Modulation..IVIG....This is a controversial subject and dont really want to be judged on our decision...sorry but I have been already and dont want to go there...anyway...after 6 months at 150mg per month we have seen nothing...Nada...and it is being discontinued as a therapy for the time being...we were told by doc who prescribed this that we should have seen something by now and we have not....
He will be starting minocycline, tini, and diflucan....not all at once...starting slowly...Mepron/Zith caused psychotic behavior and had to be stopped after 5 weeks of treatment...we may very well see the same thing with the new abx's....I am so tired of being in a war zone with my son....
Questran has been helping him these past 3 wks and we are hoping once the new abx's are started it will also help with the herxing....
That is why I really want to get to Dr. S in MD and continue to explore the toxin angle...Eileen
Posts: 127 | From Rock Tavern, New York | Registered: May 2005
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posted
Yes, I am worried about this trend also. They do not understand "autoimmunity" well enough for this to be said a sure thing.
I had no bands below 41, and my joints are much less problem now than neuro symptoms. So, is someone going to say this is autoimmune neuro? Seems to be getting too close to camp A, without enough explanation of finding ketes, blebs, etc in chronic patients.
Have heard of people with apparent autoimmune markers getting normal test results after longterm and apparently successful lyme treatment. Until all of us are tested, including the people who go into a long remission, we are not going to have a good enough basis for this autoimmune stuff. And taking steroids is dangerous for people with infectious diseases.
I have tests results showing one positive ANA, and several negatives. What does this mean? Negative RA factor. Positive for antithyroid antibodies. Does this testing picture add up to something? If I did the HLA typing, would it be any clearer? I am still something of a skeptic on lyme autoimmunity, maybe because the wrong people have been its champions, and because chronic lymies who have had extended treated DO get better in many cases, or get worse when abx stopped. Or respond in some way when a new abx combo started. There are just too many questions left.
Posts: 8430 | From Not available | Registered: Oct 2000
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posted
Eileen, Dr. K in Ct was the doc who finally diagnosed me with chronic lyme/autoimmune due to having had the vaccine.
I saw him for one year and went from antibiotic to antibiotic and never felt better. After a year he told me to be greatful I wasnt any worse off than I am and learn to live with it cuz its "autoimmune" and he knew nothing else to do.
Im now seeing a new doc. Had a pretty good summer but a terrible winter so will see what he says next month.
I know I can be better cuz I have those days and moments of "ME" again and I wont surrender to being a blob who's only triumph is feeding herself.
Dont let "autoimmune" give the docs a reason to dismiss your sons health troubles. Its just a word and they really dont know what it means.
I would love to be close enough to Gigi Dr. in Wash state and try the herbal route under competent direction.
Ive tried local naturopaths before and they just took my money. None of them believed in the lyme stuff either. They all just smirked as I payed the bill and bought all their products that were going to make me stronger and happier. Yeah!!!
Posts: 561 | From connecticut | Registered: May 2004
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Absolutely not going to let this get dismissed....We are just at the beginning of all this...He was dx last June so we are in baby phase I believe....We see a Primary LLMD also who IS treating the lyme but due to the autism wanted us to also see a neuro which Primary is not....
I have had many responses from parents telling me it took years of treatments before they saw improvements so I know it can be awhile...
If you dont mind PM ing me with your new doc....Could even be the Primary LLMD we are also seeing....Thanks Eileen
Posts: 127 | From Rock Tavern, New York | Registered: May 2005
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Can you clarify your understanding of the significane of Immune Complexes related to the HLA DR4 type 'auto-immunity' theory?
I may be making a leap, but I am reading your comment to mean that Immune Complexes are resulrant of the potential problem?
Why I am asking is because after use of Minocycline (for M.Fermentans, and Lyme I guess)
My son and my chronically high Immune Complexes went down to well below 'normal' range and have stayed there.
I am HLA-DR4, and he is not. But we both have had band 31k show up. This is interesting to look at IMO.
I am wondering if this is all connected.
Mo
Posts: 8337 | From the other shore | Registered: Jul 2002
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bpeck
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posted
Lou/Eileen/Sofy:
I has astromical ANAs and other antibodies against self- and I was carrying so many "documented" dx of autoimmune disorders that they changed the dx to "complex autoimmune disorder"......
My Drs. though keep telling me I'm a "rare" case.. i.e. meaning they actually beleive I "had" Lyme that was mis dx as autoimmune disorders..
But I also know- these same Docs will revert to Post Lyme dx (autoimmuneity problems) if I have a relpase.... It's just drummed into them (and some of the LLMDs too).
But in the endn (as far as my therapy) - it only matters what I think. I understand this isn't so easy to say when caring for a child. The stressors are much much greater.
But- the more educated you are in this disease- the better able you 'll be able to handle Dr.s discussions on your son's therapy.
bpeck
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posted
Mo:
It's pretty well established in Lupus that the continual presence of immune complexes (antibody/self) is indicated by a low C3 or 4 (can't remember if it's both 3 & 4 or just one or the other). So a continually low measurement C3 or 4 is considered one of the inflammatory markers.
If you talk to a Lupus Doc- their thinking is: immune system attacks "self" --> never ending immune complexes---->low complement---> high inflammation/w tissue distruction, many symptoms -----> treatment= immune suppression ...
If you ask this Doc why has the immune system gone awry- (s)he'll say.. If you are of a certain tissue type then you're DOOMED if certain pathogens come your way (Lyme is one of them). Then you hear the theroy of Post Bla, Blah, Blah Symdrome. 30 years ago this same Doc would have said " I dunno - the immune system just screws up.
I just don't happen to think this way... If the immune system was this flawed, then natural selection would have weeded out this tissue type long before the the 1940's.
As far as blanket statments about the immune system: I take issue with a group (even if they are researchers) that think they know everything about the immune system- when some of the major discoveries on how the immune system works have only been uncovered in the last 5 to 10 years.. it's a dynamic changing field- . There's lots no one knows. But I'm digressing here-...
Immunosuppresion is a loaded work- although I am VERY against prednesone (it supresses - way upstream) I am not against using HCQ or another (suppressive) modulator because I do recognize the need to quell inflammation inorder to get at the root (bacteria? stealth pathogen) of the problem.
Immune complexes are a consequence of another problem- but they can go on to cause their own set of (infammatory) problems when they accumulate or their numbers get too high in the blood or organs.... then it's all a domino effect- all in the wrong direction.
MY DAUGHTER WAS ALSO TESTED IN FEB. BY DR. J. IN CT. FOR THESE "MARKERS". SHE IS HLA-B27, HLA-DR4 AND HLA-DQ6 POSITIVE.
HLA-B27 IS PRESENT IN APPROX. 7-9 PERCENT OF CAUCASIONS.
HOWEVER, HER ANA SCREEN, C-REACTIVE PROTEIN AND ESR WERE ALL WITHIN THE NORMAL RANGE. I TAKE THIS TO MEAN A GOOD THING.??
MY ONLY UNDERSTANDING ON WHAT THESE RESULTS MEAN, IS THAT IF YOU ARE POSITIVE, YOU HAVE A PREDISPOSITION TO DEVELOPING AN AUTOIMMUNE DISORDER. OTHER LAB TESTING LIKE BUT NOT LIMITED TO ANA, C-REATIVE PROTEIN, ESR, DNA (DS) ABS, DNASE-B AB CAN FURTHER QUALIFY THE HLA RESULTS.
YOU CAN GOOGLE THESE LAB TESTS BY NAME AND GET SOME PRETTY GOOD EXPLANATIONS ABOUT THEM.
LYMEDESIGN
Posts: 263 | From Georgia | Registered: Feb 2006
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riversinger
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posted
quote:Originally posted by minoucat: I'd like to hear about how (IF!) knowing about the gene and subtype helped you address LD/Co or the symptoms.
Riversinger, it sounds as if this knowledge has played a big role for you in some of your choices? Is it continuing to help, do you think?
Hi Minou! As you can see, I have very different gene types than the other folks. The only one they would recognize is the HLA-DQ6. According to Dr. S's typing, I have what he calls post-Lyme and a low MSH gene.
In practical terms, it has made a big change in my treatment. First of all, what I understand the post-Lyme gene to mean is that I don't make antibodies that will clear out the dead Lyme bacteria once the antibiotics have killed them.If I continue to effectively kill the bacteria, but don't have any way to remove the debris, I get sicker, instead of better.
This is what was happening, in fact.
Add on top of this that I have the gene type that gets low MSH. MSH is a hormone that is produced in the hypothalamus, and is involved in everything from immune function to pain control. The hypothalamus is damaged by a build up of the toxins from the dead Lyme, as well as mold and other neurotoxins. The more it is damaged, the less well the immune system works. The less well it works, the more neurotoxins stay in the body, and on and on.
For me, I had to look at a combo of aggressive neurotoxin removal, and a LESS aggressive antibiotic protocol. If I allow too strong of a herx reaction, I could cause even more damage to my hypothalamus than has already occured. I also have enough damage at this point, that I have to be extremely careful to avoid mold exposure, or a new acute Lyme exposure.
I have to watch my actual MSH levels very carefully, and there is the possibility I may need MSH supplementation. This is tough, because so far there is no legal means to acquire this in the US, but it is what I need.
This info pointed to other testing I needed to see what was happening in my immune system. We found I had an overactive complement system, which we have been bringing into line by correcting the neurotoxin levels and treating the nasal staph. Without correcting the overactive complement, you are at risk for autoimmune problems.
It also gave some direction on why I was having problems with shortness of breath, and why I did not respond well to regular exercize. Slowly, once I understood what was happening, I have been working on correcting it.
The HLA testing shows the susceptibility, then more specific testing shows whether you have the problems, in other words, whether the susceptibility has been triggered, how, and what to do about it.
I still have to treat Lyme, the coinfections, and other issues, but this info has changed my strategy on how to go about it, and what might be important.
As far as finding a doctor, that is tough. I am lucky that two practitioners here are very interested in the neurotoxin protocol, and Dr. S is very willing to consult with doctors. It helps if you learn as much as you can, so you understand how to participate in the protocol.
posted
Here is an excerpt from an article on tumor necrosis factor, from the most recent issue of PLOS Pathogens. Can google it, and read the whole thing if you are technically inclined.
Tumor necrosis factor (TNF) is one of the cytokines produced by our immune systems in response to antigens. But microbes have evolved ways of coping with these cytokines.
My impression from this is that "autoimmunity" could be going on at the same time as infectious agent still in evidence. Who knows, maybe this reaction benefits the pathogen.
--------------------------------
Anti-TNF Therapy: Clues from Pathogens?
Although TNF plays a major role in growth regulation, cell differentiation, and response to microbial infections, its inappropriate overexpression has been implicated in the pathogenesis of a wide spectrum of human disorders, such as autoimmunity (e.g., multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease), allergy, septic shock, allograft rejection, and insulin resistance.
TNF derived from mast cells also plays a crucial role in initiation of inflammation, particularly in the case of rheumatoid arthritis [123]. TNF may also exert tumor-promoting activity [124]. A recent study has demonstrated that the PLAD domain of TNFR1 is critical in TNF response, because mutations in PLAD reduce NF-κB activation and cause TNFR-associated periodic syndrome, an autoinflammatory syndrome [125]. Protein therapeutics containing only the PLAD domain can effectively prevent TNFR signaling and potently inhibit arthritis [126].
Many approaches have been investigated to inhibit TNF activity for the treatment of various inflammatory/autoimmune diseases (e.g., rheumatoid arthritis, Crohn disease, and inflammatory bowel disease).
The currently commercially available TNF antagonists are infliximab (a chimeric mouse/human monoclonal anti-TNF antibody), etanercept (a soluble fusion protein combining two p75 TNFRs with an Fc fragment of human IgG1), and adalimumab (a humanized monoclonal anti-TNF antibody).
Although they have shown to be partially effective in clinical trails, still more needs to be learned in terms of the biology of TNF. These current inhibitors need to be delivered at high doses, and some adverse events have been reported, so that the long-term safety of all these molecules is not thoroughly understood [127].
The investigation of TNF inhibition mechanisms by pathogens may provide novel therapeutic insights. In particular, TNF inhibitors derived from viral pathogens, which operate at relatively low concentration within the infected host, offer new therapeutic strategies for reducing the pathologic consequences of excessive TNF expression in inflammatory disorders.
Posts: 8430 | From Not available | Registered: Oct 2000
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posted
while i don't know much about hla tissue typing, i once saw a lot written about this perusing the medical text, 'Harrisons-------" in a good book store over coffee and a pastry.
Posts: 2708 | Registered: Feb 2005
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Lydie
Unregistered
posted
There are many different scenarios, but persistent Lyme infection and autoimmune problems are not at all mutuall exclusive. Autoimmune illness just means the body is attacking itself in some ways, and it is not really a specific illness, in spite of the attempts to label. So, Lyme or other pathogens might trigger autoimmune activity that will go away with antibiotic treatment. For some, the auotimmune stuff might continue past the infection, even when all the pathogens are gone- it's possible. For some of us, the bacteria seem to persist but the autoimmune markers do go down with abx. And, finally, some of us improve to a point on abx but can't get off, and still have positive autommune labs as well.
There is no way to simplfy the mysteries in all this, and a lot of research is needed. Various LLMD's have published writings online about all this: my favorite is "Lyme Disease: A Sensible Pursuit of Answers."
Lou, you certainly seem to have some autoimmune illness going on. Low complements can go away with treatment too, my daughter's did.
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[Pathogenetic-clinical problems of Lyme borreliosis]
[Article in Polish]
Hermanowska-Szpakowicz T, Zajkowska JM, Pancewicz SA, Kondrusik M, Grygorczuk SS, Swierzbinska R.
Kliniki Chorob Zakaznych i Neuroinfekcji, AM w Bialymstoku.
In this article a short review of pathogenesis and clinical manifestations of Lyme disease is presented. As regards pathogenesis, attention was paid to the mosaic protein structure of the B. burgdorfieri spirochete, particularly of outer surface proteins (Osp) that influence the clinical course and diagnosis of the disease. The presence of various atypical spirochete forms: spheroplastic L (without cell walls), cystic, and granular "blebs" may lead to a chronic form of the disease and to a low efficacy of antibiotic therapy.
An important part of the pathogenesis is epithelial damage, stimulating the production of inflammatory cytokines (mainly IL-1, TNF-alpha, IFN-gamma), adhesive molecules and acute-phase proteins. Moreover, in the course of the disease not only an impairment of phagocytosis and chemotaxis was found, but also B. burgdorfieri spirochete binding by antibodies into immunological complexes that may maintain chronic inflammation. In terms of the Asbrink classification, complaints predominating in the clinical picture of an early and late stage of the disease were presented, with an emphasis on neuroborreliosis.
Publication Types:
* Review
PMID: 14560706 [PubMed - indexed for MEDLINE]
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bpeck
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posted
River: That's what I'm talking about- tailored treatment to the individual- and there's alot of different components at work that have to be addressed.
I'm just hoping they continue the research along the tissue typing lines- and don't just stop with "with have an autoimmune gene- you'll have a problem fopr life".
.. I agree autoimmunity is the result of a trigger (maybe pathogen load) but I don't agree it's an immune system just gone whack-o. The ROOT of that problem has to be addressed - not just stop at autoimmunity and feed the patient anti depressants and immune suppressants for life.
I'm glad you're doing better! You've had a long haul. Lucky you found a smart Dr. willing to take the time to figure a few things out -
regards, Barb
Posts: 1875 | From VT | Registered: Oct 2002
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riversinger
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posted
Hi Barb!
You are right, I am lucky. I don't think any one theory has all the answers. Finding a doctor who is willing to find what really works for the individual is a treasure. I am very fortunate to have a committed practitioner who doesn't identify herself with any one type of treatment, just with being a healer.
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