hshbmom
Frequent Contributor (1K+ posts)
Member # 9478
posted
This rare chronic inflammatory disorder sounds like it shares many symptoms with Lyme disease. In addition, it causes mouth & genital ulcers, and recurring skin ulcers that lead to scarring.
I met a person recently with this...the person's young child has migraines of no known cause.
Of course I wonder if this could be another case of Lyme in our area.
-------------------- --Lymetutu-- Opinions, not medical advice! Posts: 96222 | From Texas | Registered: Feb 2001
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david1097
Frequent Contributor (1K+ posts)
Member # 3662
posted
I'll throw in my .02 worth here.
What you describe is a Syndrome. In other words a set of symptoms that occur together but have no known cause.
There are lots of syndromes, some end up having a cause identified over time, some do not. So what do you do?
If you note, as with many "auto immune" diseases, the treatment is to use steroids. Here is the trick with those: If the symptoms get better during the use of the steroids but over time get worse after several courses of steroid use STRONGLY SUSPECT AN INFECTIOUS PROCESS. The steroids suppress the immune functions and will let an infection get worse, while at the same time masking the symptoms. This may lead to the need for ever increasingly high doses of steroids in order to relieve the symptoms.
On the other hand, if steroids produce relief until another flare up and the long term trend is to have the symptoms level about the same during the flare ups and between then I think the likelihood of infection is much much less.
Keep in mind this is only my suggestion and should not be considered as fact.
So what is all the stuff about auto immune diseases anyway?
Consider the following;
lets say a person gets infected by something and say that something when broken apart (ie it dies ) produces a chemical (ie protein or protein fragment) that has a vague similarity to the chemical structure of human tissue. Now the human immune response to the dead organism is to make an antibody that looks for a chemical that matches the description of the dead organism. Which part is used for a description may vary. Its like the police looking for a suspect, they might have a description of the eyes, the hair, a scar , a tattoo, the height etc. They do not need the full description to try to catch the guy.
Now in the disease case, lets assume that the description is not exact, just like the police they will catch a bunch of people that are sort of correctly described but not the right one. In the body this process is much more draconian as the police would catch and question the person but the immune system catches and kills... no questions needed.
When an antibody is produced the pattern for it is stored in special cells. These will often stay with you for life. Now if the antibody uses a description that sort of matches your tissue, you have a problem since the immune system will keep picking up and killing the tissue that sort of looks like the suspects. This is what causes the auto immune inflammatory response.
What is interesting is that the auto immune response might come and go resulting in flare ups. It is quite possible that this could be triggered by an outside antagonist, dust, pollen some sort of air pollution, or any number of other things, including viruses and bacteria that result in antibody production or immune system modulation. In many cases, without the poor description of the bad guy, most of these things may be perfectly harmless. When these ``harmless'' things get detected by the immune system they might trigger the "police" response to step up and continue using the bad description resulting in and attack on the bodies tissues, resulting in a flare up.
Interestingly, type 1 diabetes is thought by many to be a faulty ``mistaken identity: immune response against the islet cell in the pancreas. Many people describe a "flu" before developing the disease. In the diabetes case the police are very through and kill all the potential offenders, no insulin is produced as a result.
In the case of lyme, I think that this mistaken identity is also partly to blame for the "post lyme syndrome" as described by the IDSA panel of ``experts''. By this I means that I strongly believe that the immune system encodes an antibody to the lyme that also captures normal tissue, BUT here is the critical thing, I also believe that it is the persistence of Lyme that even in small amounts is sufficient to be detected by the immune system and then trigger a response.
With this model, it is possible to have a very small bacteria load cause MAJOR problems. This disproportionate effect is well described by many and is at the heart of the how long on antibiotics controversy. Basically the IDSA says that the short term treatment will decrease the bacteria load to insignificant level as that SHOULD not create any problems or symptoms... They are probably right in this regard. Most of the lyme does get killed by heavy does of ABX as happens with most bacterial infections and treatment.
BUT HERE IS THE IMPORTANT POINT.. The longer you have lyme, the more likely it is that the alteration of the bacteria will produce an protein that mimics tissue. This in effect may be part of the method that allows lyme to evade the immune system... that is it eventually morphs into something that looks like your own tissue so as to not appear as an offender to the immune system... sort of trying to blend in with the population. Once an antibody is produced to this look alike, you are in trouble since now your own immune system AMPLIFIES the symptoms due to even a small number of bacteria. What is even worse is that tissue damage may precipitate an immune response and worse yet, the inflammatory response appears prompt any bacteria that are sleeping to want to come back from the deep sleep and multiply. The result... relapse.
So what do you do? You are in a very tough spot. The ILADS approach is to keep hitting the bacteria with long term antibiotics in an attempt to keep the bacteria sleeping or kill them when they come out. The IDSA approach is to let the patient suffer until they get much worse then either write them off or retreat due to relapse.
ILADS is driven by quality of life, IDSA by cost of treatment... NONE OF THE APPROACHES RESULTS IN A CURE ONCE THE ANTIBODIES ARE PROGRAMMED AS IT IS ALMOST UNIVERSALLY AGREED THAT YOU CANNOT TOTALLY ERADICATE BORRIELA ONCE INFECTED. All you can do is keep it at low enough level to not result in I being noticed. As quality of life is important to me, I will stick with the ILADS approach any day.
Anyway, my hands are getting tired and will stop now... those are my personal thoughts on the subject, I hope that they provide some insight.
[ 08. April 2007, 11:26 AM: Message edited by: david1097 ]
Posts: 1184 | From north america | Registered: Feb 2003
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