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dcmom

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Hi all-

 

I am certainly tempted to homeschool- but my situation is complicated by the fact that she has an older sister. Her sister had H1N1 first, Julia caught it from her. Also- I don't think I would be ready to homeschool both- so right now it is a wait and see.....

 

I don't know why the relapse after pex. Two thoughts: either unfortunately her immune system has "memory" from those autoantibodies, and they will be created anytime her immune system is activated- in which case IVIG will be our next step. Or, since she only had 3 rounds of pex (Swedo did 5 rounds) ALL of the bad antibodies were not removed.

 

Buster?

 

 

Eileen

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I think it is the memory thing since we know Carter's antibodies were gone due to the numbers after pEX and they were at 500 and 700 during the relapse. We are preparing for IVIG here. I found someone willing to do it with guidance from Latimer. We are better but still not right.

Hi all-

 

I am certainly tempted to homeschool- but my situation is complicated by the fact that she has an older sister. Her sister had H1N1 first, Julia caught it from her. Also- I don't think I would be ready to homeschool both- so right now it is a wait and see.....

 

I don't know why the relapse after pex. Two thoughts: either unfortunately her immune system has "memory" from those autoantibodies, and they will be created anytime her immune system is activated- in which case IVIG will be our next step. Or, since she only had 3 rounds of pex (Swedo did 5 rounds) ALL of the bad antibodies were not removed.

 

Buster?

 

 

Eileen

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Hi Mommd- I unfortunately also think it is the memory thing, and I guess that is why this becomes chronic for a lot of our kids. But I also want to throw something else out there- Carter's numbers (I assume are ASO and AntiDnase?) could also come from an underlying infection. These are not thought to be the antibodies that attack the brain, right? Was he on full strength abs the whole time since pex? Either way, the IVIG will help that also.

 

Right now, Julia is pretty good- eating, sleeping, doing homework, dressing, bathing, no rages, etc. However, she is still struggling with "stuff" that was not there before pandas, or post pex (before the flu). For example, this morning when we got to school, she almost couldn't go because a tag in her tights was bothering her-however unlike in full blown pandas, she did get it together and keep the tag (without any prompting from me- i told her I would take her home to get changed). So there are low level issues there. She still has two more days of 1/2 tablet of steroid left. I am hoping she holds steady after the steroids.

 

I am hoping to avoid IVIG- as long as everything holds, we will re evaluate in January with probable trips to Dr T and Dr B.

 

Please keep me posted on Carter's progress....

 

Eileen

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Mom MD and DC Mom:

 

As you know we recently saw Dr. K for a second IVIG treatment and we spoke a little bit about PEX. He did say he felt it important to follow-up PEX with IVIG. Apparently, IVIG helps mediate the bone marrow as well as..... wash away deposits in the Basil Ganglia. Not sure what he meant by 'deposits'..... I think he explained it to me at the time but my memory is a little fogging and I'd hate to misquote.

 

-Wendy

 

 

I think it is the memory thing since we know Carter's antibodies were gone due to the numbers after pEX and they were at 500 and 700 during the relapse. We are preparing for IVIG here. I found someone willing to do it with guidance from Latimer. We are better but still not right.
Hi all-

 

I am certainly tempted to homeschool- but my situation is complicated by the fact that she has an older sister. Her sister had H1N1 first, Julia caught it from her. Also- I don't think I would be ready to homeschool both- so right now it is a wait and see.....

 

I don't know why the relapse after pex. Two thoughts: either unfortunately her immune system has "memory" from those autoantibodies, and they will be created anytime her immune system is activated- in which case IVIG will be our next step. Or, since she only had 3 rounds of pex (Swedo did 5 rounds) ALL of the bad antibodies were not removed.

 

Buster?

 

 

Eileen

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I agree. We are in no way as bad as we were before the PEX but we are still having issues. We are waiting to get dosing info from Latimer and then are planning to move forward here in Charlotte. I have already confirmed with the doctor and hospital that we can do it here. We have an appointment with Latimer on the 11th ( a phone consult). It is interesting though. My son's symptoms now are much milder. We are not seeing as much chorea but more mood swings and OCD. Very interesting.

Thanks...I will keep you posted.

Mom MD and DC Mom:

 

As you know we recently saw Dr. K for a second IVIG treatment and we spoke a little bit about PEX. He did say he felt it important to follow-up PEX with IVIG. Apparently, IVIG helps mediate the bone marrow as well as..... wash away deposits in the Basil Ganglia. Not sure what he meant by 'deposits'..... I think he explained it to me at the time but my memory is a little fogging and I'd hate to misquote.

 

-Wendy

 

 

I think it is the memory thing since we know Carter's antibodies were gone due to the numbers after pEX and they were at 500 and 700 during the relapse. We are preparing for IVIG here. I found someone willing to do it with guidance from Latimer. We are better but still not right.
Hi all-

 

I am certainly tempted to homeschool- but my situation is complicated by the fact that she has an older sister. Her sister had H1N1 first, Julia caught it from her. Also- I don't think I would be ready to homeschool both- so right now it is a wait and see.....

 

I don't know why the relapse after pex. Two thoughts: either unfortunately her immune system has "memory" from those autoantibodies, and they will be created anytime her immune system is activated- in which case IVIG will be our next step. Or, since she only had 3 rounds of pex (Swedo did 5 rounds) ALL of the bad antibodies were not removed.

 

Buster?

 

 

Eileen

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I think you are making the right choice..... Fantastic News. I can't wait to hear more about how he is doing.

 

-Wendy

 

I agree. We are in no way as bad as we were before the PEX but we are still having issues. We are waiting to get dosing info from Latimer and then are planning to move forward here in Charlotte. I have already confirmed with the doctor and hospital that we can do it here. We have an appointment with Latimer on the 11th ( a phone consult). It is interesting though. My son's symptoms now are much milder. We are not seeing as much chorea but more mood swings and OCD. Very interesting.

Thanks...I will keep you posted.

Mom MD and DC Mom:

 

As you know we recently saw Dr. K for a second IVIG treatment and we spoke a little bit about PEX. He did say he felt it important to follow-up PEX with IVIG. Apparently, IVIG helps mediate the bone marrow as well as..... wash away deposits in the Basil Ganglia. Not sure what he meant by 'deposits'..... I think he explained it to me at the time but my memory is a little fogging and I'd hate to misquote.

 

-Wendy

 

 

I think it is the memory thing since we know Carter's antibodies were gone due to the numbers after pEX and they were at 500 and 700 during the relapse. We are preparing for IVIG here. I found someone willing to do it with guidance from Latimer. We are better but still not right.
Hi all-

 

I am certainly tempted to homeschool- but my situation is complicated by the fact that she has an older sister. Her sister had H1N1 first, Julia caught it from her. Also- I don't think I would be ready to homeschool both- so right now it is a wait and see.....

 

I don't know why the relapse after pex. Two thoughts: either unfortunately her immune system has "memory" from those autoantibodies, and they will be created anytime her immune system is activated- in which case IVIG will be our next step. Or, since she only had 3 rounds of pex (Swedo did 5 rounds) ALL of the bad antibodies were not removed.

 

Buster?

 

 

Eileen

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Hi Eileen,

 

Fundamentally we don't know but there could be several answers. My guess is it is one of the following:

  1. There was still strep (or a strep exotoxin) in the body and a T-cell got activated causing inflammation and then bound with a B-cell to produce antibodies.
  2. That the BBB was still open and the B-cell got across or a macrophage got back presenting neuronal tissue
  3. That there was some residual antibodies and the BBB got opened due to some other illness
  4. That there was a re-exposure to strep and while the antibiotics prevented a full out infection, he had a response

Based on our experience, I'd say it was #4. Our dd always went into an exacerbation when her sister was colonized with strep.

 

Buster

 

Hi all-

 

I am certainly tempted to homeschool- but my situation is complicated by the fact that she has an older sister. Her sister had H1N1 first, Julia caught it from her. Also- I don't think I would be ready to homeschool both- so right now it is a wait and see.....

 

I don't know why the relapse after pex. Two thoughts: either unfortunately her immune system has "memory" from those autoantibodies, and they will be created anytime her immune system is activated- in which case IVIG will be our next step. Or, since she only had 3 rounds of pex (Swedo did 5 rounds) ALL of the bad antibodies were not removed.

 

Buster?

 

 

Eileen

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Thanks Buster!

 

Julkia's relapse was caused by H1N1, that I know, the pandas issues started about 24 hours after her fever subsided. So I guess that is what may have opened the BBB, then the million dollar question is whether there were some residual antibodies still there, or whether the immune system memory made more of these bad autoantibodies. Obviously the first option would be better, the second option would indicate a chronic situation that will need ivig.

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Thanks Buster!

 

Julkia's relapse was caused by H1N1, that I know, the pandas issues started about 24 hours after her fever subsided. So I guess that is what may have opened the BBB, then the million dollar question is whether there were some residual antibodies still there, or whether the immune system memory made more of these bad autoantibodies. Obviously the first option would be better, the second option would indicate a chronic situation that will need ivig.

Yup, and frankly I don't think anyone knows the answer. We too are hoping it is the first and not the second. PEX only removed a percentage of antibodies -- but doesn't get them all... it's logically a dilution effect. So that sort of leads me to think there were some still there... and just a closed BBB due to lack of inflammation... but no science behind that statement. Just trying to see explanations that might explain what we're seeing.

 

Buster

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Buster,

 

As you know, I've been reading up on the exotoxins of the S. Pyogenes. I think the following is important to statement #1 and why PEX is so immediately successful. BUT, if not ALL the toxins are removed you get a slow progression of symptoms and exacerbation with exposure. IVIG would essentially resolve any remaining toxin after PEX. Just a mother's perspective with NO MEDICAL training. BUT, I intend to drill DR. LEWIS about the following.

 

Characteristically, Streptococcus pyogenes is a Gram-positive facultative anaerobic bacterium. It is not motile, and does not produce spores. It occurs as long chains of cocci, and occasionally in pairs. Streptococcus pyogenes is classified as Group A streptococcus. Group A streptococci typically have a capsule composed of hyaluronic acid and are beta-hemolytic, which is true for Streptococcus pyogenes.[1] Beta-hemolytic streptococci produce a toxin that forms a clear zone of hemolysis on blood agar, demonstrating its ability to destroy red blood cells. This hemolysis is attributed to toxins formed by Group A streptococci called streptolysins. Streptolysins can destroy not only red blood cells, but also the white blood cells responsible for fighting off bacteria and disease, as well as other body cells.[2]

 

Several factors add to Streptococcus pyogene’s ability to cause disease. These factors include its production of exotoxins and streptokinase, the M proteins on its surface, and its hyaluronic acid capsule. Streptococcus pyogenes produces three types of exotoxins. These toxins are responsible for causing fever and scarlet fever rashes; they also increase the risk of endotoxic shock and depress antibody synthesis.[3] Streptococcus pyogenes also produces streptokinase, a toxin that digests blood clots to assist in the invasion of wounds. The cell wall of Streptococcus pyogenes contains M proteins, which are a major factor behind its virulence. M protein is heat and acid resistant, it aids in the attachment to host tissues, and helps the cell to resist phagocytosis. Host immunity to Streptococcus pyogenes results from the development of antibodies specific to M protein.[4] The hyaluronic acid capsule of Streptococcus pyogenes is chemically similar to human connective tissue, which allows it to go unrecognized as an antigen by the host’s body, further helping the bacteria to avoid phagocytosis

 

-Wendy

 

 

Hi Eileen,

 

Fundamentally we don't know but there could be several answers. My guess is it is one of the following:

  1. There was still strep (or a strep exotoxin) in the body and a T-cell got activated causing inflammation and then bound with a B-cell to produce antibodies.
  2. That the BBB was still open and the B-cell got across or a macrophage got back presenting neuronal tissue
  3. That there was some residual antibodies and the BBB got opened due to some other illness
  4. That there was a re-exposure to strep and while the antibiotics prevented a full out infection, he had a response

Based on our experience, I'd say it was #4. Our dd always went into an exacerbation when her sister was colonized with strep.

 

Buster

 

Hi all-

 

I am certainly tempted to homeschool- but my situation is complicated by the fact that she has an older sister. Her sister had H1N1 first, Julia caught it from her. Also- I don't think I would be ready to homeschool both- so right now it is a wait and see.....

 

I don't know why the relapse after pex. Two thoughts: either unfortunately her immune system has "memory" from those autoantibodies, and they will be created anytime her immune system is activated- in which case IVIG will be our next step. Or, since she only had 3 rounds of pex (Swedo did 5 rounds) ALL of the bad antibodies were not removed.

 

Buster?

 

 

Eileen

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Hi Wendy,

 

Gosh, so much to talk about and so little good science here....

 

Let's start with the known...

 

Yes, GABHS can produce all the exotoxins you mention plus the super-antigen/exotoxins named Spe A through Spe Z as well as a bunch we haven't found yet. Different GABHS strains produce different exotoxins.

 

For the moment, let's assume that the exotoxins cause the inflammation. So either the immune system can't get rid of the GABHS and so there continues to be exotoxins causing strep -- or-- the exotoxins aren't getting removed and so they just keep causing inflammation.

 

The improvement (anecdotally) by so many on high dose azith and augmentin leads me to think it really is the strep and not the exotoxins that aren't getting removed. The antibiotics really don't have a lot to do with exotoxins. Yes, the azith can modulate Th1/Th2 response, but largely augmentin and azith don't do a lot to exotoxins themselves.

 

 

So, this makes me think that the real culprit is either:

  1. there is some strep that's gone intracellular and like a virus (e.g. chicken-pox) can come out under stress or other illness
  2. a reinfection has occured and the T-cells go nuts and a B-cell finds a tiny, tiny bit of the antigen (GABHS)
  3. there's leakage across the BBB and the T-cells go nuts and a B-cell finds a tiny, tiny bit of neuronal cells that look like GABHS

I keep coming back to why does PEX, IVIG and prednisone all seem to work and why does high-dose antibiotics work. IVIG will close #3, pred will close #3 and slow down the T-cell recruitment. Antibiotics helps #1 and strangely can prevent T-cells recruitment in #2. PEX breaks the cycle and assuming no more GABHS, removes the offending antibodies. Also, and this may be really really significant, a lot of times blood thinners are used (Warfrin) with PEX. In reading about this, the blood thinners prevent T-cells from collecting on the epithelial hand holds. This might mean that the concentrated breach in the BBB is cleared by not letting the T-cells congregate. Literally this might be what is going on. If so, then PEX is essentially closing the BBB too.

 

So, my gut (wish I had more good science to play with and why I thought that paper on T-cell crossing the BBB was SOOO cool) is that the real culprit is the BBB and any inflammation that causes a breach in the BBB is really at fault here because the B-cells are recognizing neuronal cells just as much as GABHS.

 

I'd be really interested if you get good insight from your immunologist....

 

Buster

 

 

 

Buster,

 

As you know, I've been reading up on the exotoxins of the S. Pyogenes. I think the following is important to statement #1 and why PEX is so immediately successful. BUT, if not ALL the toxins are removed you get a slow progression of symptoms and exacerbation with exposure. IVIG would essentially resolve any remaining toxin after PEX. Just a mother's perspective with NO MEDICAL training. BUT, I intend to drill DR. LEWIS about the following.

 

Characteristically, Streptococcus pyogenes is a Gram-positive facultative anaerobic bacterium. It is not motile, and does not produce spores. It occurs as long chains of cocci, and occasionally in pairs. Streptococcus pyogenes is classified as Group A streptococcus. Group A streptococci typically have a capsule composed of hyaluronic acid and are beta-hemolytic, which is true for Streptococcus pyogenes.[1] Beta-hemolytic streptococci produce a toxin that forms a clear zone of hemolysis on blood agar, demonstrating its ability to destroy red blood cells. This hemolysis is attributed to toxins formed by Group A streptococci called streptolysins. Streptolysins can destroy not only red blood cells, but also the white blood cells responsible for fighting off bacteria and disease, as well as other body cells.[2]

 

Several factors add to Streptococcus pyogene’s ability to cause disease. These factors include its production of exotoxins and streptokinase, the M proteins on its surface, and its hyaluronic acid capsule. Streptococcus pyogenes produces three types of exotoxins. These toxins are responsible for causing fever and scarlet fever rashes; they also increase the risk of endotoxic shock and depress antibody synthesis.[3] Streptococcus pyogenes also produces streptokinase, a toxin that digests blood clots to assist in the invasion of wounds. The cell wall of Streptococcus pyogenes contains M proteins, which are a major factor behind its virulence. M protein is heat and acid resistant, it aids in the attachment to host tissues, and helps the cell to resist phagocytosis. Host immunity to Streptococcus pyogenes results from the development of antibodies specific to M protein.[4] The hyaluronic acid capsule of Streptococcus pyogenes is chemically similar to human connective tissue, which allows it to go unrecognized as an antigen by the host’s body, further helping the bacteria to avoid phagocytosis

 

-Wendy

 

 

Hi Eileen,

 

Fundamentally we don't know but there could be several answers. My guess is it is one of the following:

  1. There was still strep (or a strep exotoxin) in the body and a T-cell got activated causing inflammation and then bound with a B-cell to produce antibodies.
  2. That the BBB was still open and the B-cell got across or a macrophage got back presenting neuronal tissue
  3. That there was some residual antibodies and the BBB got opened due to some other illness
  4. That there was a re-exposure to strep and while the antibiotics prevented a full out infection, he had a response

Based on our experience, I'd say it was #4. Our dd always went into an exacerbation when her sister was colonized with strep.

 

Buster

 

Hi all-

 

I am certainly tempted to homeschool- but my situation is complicated by the fact that she has an older sister. Her sister had H1N1 first, Julia caught it from her. Also- I don't think I would be ready to homeschool both- so right now it is a wait and see.....

 

I don't know why the relapse after pex. Two thoughts: either unfortunately her immune system has "memory" from those autoantibodies, and they will be created anytime her immune system is activated- in which case IVIG will be our next step. Or, since she only had 3 rounds of pex (Swedo did 5 rounds) ALL of the bad antibodies were not removed.

 

Buster?

 

 

Eileen

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Its got to be both and why the combo of treatments is working.

 

With Kawasaki's patients almost ALL antibiotics via IV at acute phase have been tired (perhaps long term antibiotics have not been used) and even IV antibiotics by Dr. K on some PANDAS children to no avail..... its the IVIG 'they think' that does the trick for Kawasaki's. Dr. K's concern is they are not using prophylaxis antibiotics with Kawasaki's as a preventative similar to RF and possibly why WITH a history of Kawasaki's Disease some children are now considered PANDAS. The IVIG treatment my younger son had at day 5 of illness broke the fever within 24 hours and they announced him cured. His aneurysm was a 4 on a scale of 1 to 10 that resolved in 6 months. The combo of steroid and IVIG has also been used to great success for Kawasaki's (although not sure of long term results). Daily baby aspirin is also prescribed (as a blood thinner) until aneurysm resolve themselves (makes you wonder).

 

 

Anyway, the science gets above me at times so I remain hopeful to communicate my intuition to Dr. Lewis effectively. It feels just out of my reach of understanding but so close to knowing why!!!!!!

 

 

 

Hi Wendy,

 

Gosh, so much to talk about and so little good science here....

 

Let's start with the known...

 

Yes, GABHS can produce all the exotoxins you mention plus the super-antigen/exotoxins named Spe A through Spe Z as well as a bunch we haven't found yet. Different GABHS strains produce different exotoxins.

 

For the moment, let's assume that the exotoxins cause the inflammation. So either the immune system can't get rid of the GABHS and so there continues to be exotoxins causing strep -- or-- the exotoxins aren't getting removed and so they just keep causing inflammation.

 

The improvement (anecdotally) by so many on high dose azith and augmentin leads me to think it really is the strep and not the exotoxins that aren't getting removed. The antibiotics really don't have a lot to do with exotoxins. Yes, the azith can modulate Th1/Th2 response, but largely augmentin and azith don't do a lot to exotoxins themselves.

 

 

So, this makes me think that the real culprit is either:

  1. there is some strep that's gone intracellular and like a virus (e.g. chicken-pox) can come out under stress or other illness
  2. a reinfection has occured and the T-cells go nuts and a B-cell finds a tiny, tiny bit of the antigen (GABHS)
  3. there's leakage across the BBB and the T-cells go nuts and a B-cell finds a tiny, tiny bit of neuronal cells that look like GABHS

I keep coming back to why does PEX, IVIG and prednisone all seem to work and why does high-dose antibiotics work. IVIG will close #3, pred will close #3 and slow down the T-cell recruitment. Antibiotics helps #1 and strangely can prevent T-cells recruitment in #2. PEX breaks the cycle and assuming no more GABHS, removes the offending antibodies. Also, and this may be really really significant, a lot of times blood thinners are used (Warfrin) with PEX. In reading about this, the blood thinners prevent T-cells from collecting on the epithelial hand holds. This might mean that the concentrated breach in the BBB is cleared by not letting the T-cells congregate. Literally this might be what is going on. If so, then PEX is essentially closing the BBB too.

 

So, my gut (wish I had more good science to play with and why I thought that paper on T-cell crossing the BBB was SOOO cool) is that the real culprit is the BBB and any inflammation that causes a breach in the BBB is really at fault here because the B-cells are recognizing neuronal cells just as much as GABHS.

 

I'd be really interested if you get good insight from your immunologist....

 

Buster

 

 

 

Buster,

 

As you know, I've been reading up on the exotoxins of the S. Pyogenes. I think the following is important to statement #1 and why PEX is so immediately successful. BUT, if not ALL the toxins are removed you get a slow progression of symptoms and exacerbation with exposure. IVIG would essentially resolve any remaining toxin after PEX. Just a mother's perspective with NO MEDICAL training. BUT, I intend to drill DR. LEWIS about the following.

 

Characteristically, Streptococcus pyogenes is a Gram-positive facultative anaerobic bacterium. It is not motile, and does not produce spores. It occurs as long chains of cocci, and occasionally in pairs. Streptococcus pyogenes is classified as Group A streptococcus. Group A streptococci typically have a capsule composed of hyaluronic acid and are beta-hemolytic, which is true for Streptococcus pyogenes.[1] Beta-hemolytic streptococci produce a toxin that forms a clear zone of hemolysis on blood agar, demonstrating its ability to destroy red blood cells. This hemolysis is attributed to toxins formed by Group A streptococci called streptolysins. Streptolysins can destroy not only red blood cells, but also the white blood cells responsible for fighting off bacteria and disease, as well as other body cells.[2]

 

Several factors add to Streptococcus pyogene’s ability to cause disease. These factors include its production of exotoxins and streptokinase, the M proteins on its surface, and its hyaluronic acid capsule. Streptococcus pyogenes produces three types of exotoxins. These toxins are responsible for causing fever and scarlet fever rashes; they also increase the risk of endotoxic shock and depress antibody synthesis.[3] Streptococcus pyogenes also produces streptokinase, a toxin that digests blood clots to assist in the invasion of wounds. The cell wall of Streptococcus pyogenes contains M proteins, which are a major factor behind its virulence. M protein is heat and acid resistant, it aids in the attachment to host tissues, and helps the cell to resist phagocytosis. Host immunity to Streptococcus pyogenes results from the development of antibodies specific to M protein.[4] The hyaluronic acid capsule of Streptococcus pyogenes is chemically similar to human connective tissue, which allows it to go unrecognized as an antigen by the host’s body, further helping the bacteria to avoid phagocytosis

 

-Wendy

 

 

Hi Eileen,

 

Fundamentally we don't know but there could be several answers. My guess is it is one of the following:

  1. There was still strep (or a strep exotoxin) in the body and a T-cell got activated causing inflammation and then bound with a B-cell to produce antibodies.
  2. That the BBB was still open and the B-cell got across or a macrophage got back presenting neuronal tissue
  3. That there was some residual antibodies and the BBB got opened due to some other illness
  4. That there was a re-exposure to strep and while the antibiotics prevented a full out infection, he had a response

Based on our experience, I'd say it was #4. Our dd always went into an exacerbation when her sister was colonized with strep.

 

Buster

 

Hi all-

 

I am certainly tempted to homeschool- but my situation is complicated by the fact that she has an older sister. Her sister had H1N1 first, Julia caught it from her. Also- I don't think I would be ready to homeschool both- so right now it is a wait and see.....

 

I don't know why the relapse after pex. Two thoughts: either unfortunately her immune system has "memory" from those autoantibodies, and they will be created anytime her immune system is activated- in which case IVIG will be our next step. Or, since she only had 3 rounds of pex (Swedo did 5 rounds) ALL of the bad antibodies were not removed.

 

Buster?

 

 

Eileen

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Also, and this may be really really significant, a lot of times blood thinners are used (Warfrin) with PEX. In reading about this, the blood thinners prevent T-cells from collecting on the epithelial hand holds. This might mean that the concentrated breach in the BBB is cleared by not letting the T-cells congregate. Literally this might be what is going on. If so, then PEX is essentially closing the BBB too.

 

Wow, thank you. This makes me wonder problems about heparan (hep sulfate), Antiphospholipid syndrome too. Also, wonder if the blood thinning effects of fish oil could be helping in some instances?

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Not only fish oil but motrin is also a blood thinner.

 

 

 

Also, and this may be really really significant, a lot of times blood thinners are used (Warfrin) with PEX. In reading about this, the blood thinners prevent T-cells from collecting on the epithelial hand holds. This might mean that the concentrated breach in the BBB is cleared by not letting the T-cells congregate. Literally this might be what is going on. If so, then PEX is essentially closing the BBB too.

 

Wow, thank you. This makes me wonder problems about heparan (hep sulfate), Antiphospholipid syndrome too. Also, wonder if the blood thinning effects of fish oil could be helping in some instances?

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