Jump to content
ACN Latitudes Forums
  • Trigger-Book-Horizontal-png

jacobsmom

Immunologist, Infectious Diseas Dr and Rheumatologist for PANDAS?

Recommended Posts

We were refered to an infectious diseases dr by an ENT we went in to see recently. Has anyone else been to an infectious disease dr, a rheumatologist, or an immunologist? What does a rheumatologist do? My son has been into so many drs and I am willing to search the earth to help him out but I don't want to create a monster here. Any other PANDAS patients out there who have gone to any of these types of drs and have any of them been helpful? Thank you for your reply!

Share this post


Link to post
Share on other sites

Hi there,

 

We have been to an ID clinic and rheumatologist. We are seeing an immunologist in a few weeks. The ID clinic really just gave the go ahead for long term antibiotic use. They ran some tests that I asked for and then also did the referral to immunology which I also asked for. The rheumatology was also at my request as I was thinking if RFever kids were sent there and there seems so many similarities to Rheumatic Fever and PANDAS - and my son complains of joint pain when sick. They just did a full exam, checked all his joints, heart, and that was it - it was just good for me to feel like I have gone at this at all angles - I do think immunology is probably key. Just my opinion. It is a pain to go to so many doctors, the ID clinic and rheumatolgy were very non invasive appts.

 

Rhuematologists deal with joint issues mostly, lupus, arthritis in kids etc. all also autoimmune related.

 

The appts were helpful in that we were able to cross things off our list!

Share this post


Link to post
Share on other sites

For a long time we had a pediatric rheumatologist who coordinated the care for my son, however he does have a dx of rheumatic fever due to a mitral valve regurg on his ECHO (so he also sees an pediatric cardiologist yearly for follow-up) and a seconary dx of PANDAS as per the NIMH. I found the infectious diseases doctor to be the most helpful and he was also the doctor who recommended the long term prophylactic antibiotics and he is the doctor our family physician goes to if she has questions. We have never seen an immunologist as we live in a smaller center and one was not available to us. As well in the beginning we saw several neurologist...all of them fairly useless (they just wanted to prescribe meds like Orap, etc) and several pediatricians, but it was not till we started going to our pediatric rheumatologist that things improved and we found someone we had good teamwork with.

Share this post


Link to post
Share on other sites

My son went to a ID doc on Monday He had a culture done and it was positive for strep. Even though

he has no symptoms presently she feels that hes a carrier and wants to try to irradicate it with Clindamcin

and Refampin. 10 day course. My son did have a pandas panel done last month and was positive for

extremely high antigens and autoantibodies. Very high. Presently being that he has no symptoms other

than an occassional tick in his wrist am i taking a risk by going on this 10 day course ? Ive been reading

that when finished with antibiotics the symptoms can return with vengence. Is this only true if youve

been on them for a very long time? Im also scheduled to have my sons tonsils adnoids removed in 2

weeks. A doctor in Illonois recommended this and also suggested taking Keflex instead of Clindamicin

and Refampin. He thought it would work much better to erradicate the strep and thought these others

were too strong and would probably not work. Has anyone had any success with any of these?Are there

sideeffects? Has anyone ever successfully erradicated the strep? And had symptoms completely

disappear? Im probably just dreaming that this might happen in our case. I get such mixed opinions

from every doctor i speak with. This one panda expert says its very important to nip it in the bud asap

before puberty because once he goes into puberty the damage cannot be reversed and the ticking and

ocd will stay thru his adult life. Has anyone heard of this happening? He also suggested TA removel

and then if symptoms reappear taking steroids then ivig then keflex for a year. Yikes! One thing im

very confused about is why if you can erradicate the strep whereever it might be ,why would you still

have symptoms? If theres no strep toxins then there would be no antigens for the autoantibodies to

attack the basil ganglia right? or wrong. I find this so confusing. I can understand if he got another

strep infection the symptoms could reoccur but what if he didnt get another strep.? Is it common with

panda children to be carriers? If so when they do have reoccurances with strep are they getting the

strep each time from other people or from themselves? Over and over again. Im so so sorry

for all of these questions but im in a desperate state. Im suppose to start these antibiotics tomorrow

and im afraid if ido it his symptoms will all return when im finished. The doctor is concerned if i dont

do it that the step can end up doing permanent damage to his heart. I thought when a child is a carrier

it doesent do damage . If hes just a carrier why are there such high antigens in his blood? I thought

carriers didnt have this it just stayed in their throats. Would this mean that he may insteas have a true

infection instead of a carrier? Its been 8 Months now of non stop sleuth work

and look at all of these questions i still have. The docs all give me completely different advice. I dont

know who believe or what to do. I hope someone out there can take a moment out there busy schedule

try and answer any of my questions. Id be so very grateful. Has anyone ever seen a child make

a 100 recovery from Pandas or thru supplements, probiotics, cheltion etc have the immune system

straighten itself out and become symptom free?

 

God Bless

 

Dominique

Share this post


Link to post
Share on other sites

dominique,

 

I felt so badly for you with the decision that you were trying to make.

 

My boys both had repeated strep, but I never really thought that either of them fit the PANDAS criteria.

 

I was told at one point that my now 10 yr. old was a carrier, and my oldest (now 14) had his tonsils out due to the strep infections, and the fact that his tonsils were enlarged. That's what I was told was the determining factor. Youngest, they said "no" for, as his were not large.

 

With my oldest son, he didn't have what I recoginsed as tics at the time so I couldn't comment on any improvement in that area. What I feel so badly about, was all of the tylenol (with codein) that I gave him after the surgery. If you decide to have the surgery, you may want to do some reading on tylenol and the relationship with gluathione. My son was one of the kids that had a lot of pain for quite a while, close to 10 days. I would never want to use as much tylenol again, as I did then.

 

I'm wondering if you decided to start the antibiotics?

 

I also wondered if you are giving probiotics?

 

There were a couple of interesting things in these articles, that I thought you might want to read.

 

Streptococcus

 

http://www.cehs.siu.edu/fix/medmicro/strep.htm

 

EPIDEMIOLOGY:

These organisms are widely distributed in nature.

Five to 15% of normal healthy individuals carry S. pyogenes.

Carriage of S. pneumoniae (a solely human organism) is age dependent:

Age % Carriage

Less than 5 40%

5 to 9 30%

10 to 15 17%

adults 6%

adults with children 25%

 

Streptococci are labile organisms that require close personal contact for transmission; S. pyogenes respiratory disease peaks at 6 and 13 years old, showing a seasonal pattern (late winter, early spring).

 

Normal Flora

http://www.cehs.siu.edu/fix/medmicro/normal.htm

 

These are some remarks from Dr. Amy Yaskow (DAN Dr.)

http://www.autismanswer.com/articles/yasko...thimerosal.html

 

I believe that it is likely that the streptococcus permanently resides as part of the bacteria or flora in the nasopharyngeal cavity of these children who are highly susceptible to streptococci. The mucous system in our nasal passages flushes bacteria and viruses into our stomach. It is easy to see how under "compromised conditions", streptococci could survive the stomach and make its way to the intestinal tract. Gastric reflux has been implicated as a factor in ear infections.26 It is not surprising then, to note that in addition to its role in ear infections and strep throat, streptococcus has been implicated in leaky gut.27

 

Gut flora changes play a major role in causing the increased intestinal membrane permeability that is seen with leaky gut. Depletion of glutathione is a common occurrence in leaky gut. Streptococcal infection, or the presence of chronic or recent infection, depletes glutathione levels.28 High glutamate levels also result in the depletion of glutathione.29 Streptococcal infection is also more likely to be an issue in individuals with high glutamate levels, as glutamate is related to virulence in streptococci. Streptococcus flourishes in a high glutamate, low glutathione environment.30,31 Thus, the combined effects of changes in gut flora and depleted glutathione lay the groundwork for leaky gut.

 

http://www.autismanswer.com/articles/yasko...citotoxins.html

 

Amy Yaskow

 

Blood Type/Streptococcal Infection

 

The A-B-O system for blood typing is dependent on the blood group antigens that are expressed on the outer surface of an individuals' red blood cells. Those with blood type A have NAC-gal (n-acetyl galactosamine) as the predominant blood group antigen, and those with type B have galactose as their primary antigen. Those with blood type O have fucose as a predominant antigenic determinant on their red blood cells. In addition, to a lesser extent the NAC-glu (n-acetyl glucosamine) antigen would be accessible to the immune system in those with blood type O due to the limited carbohydrate antigen on the surface of type O red blood cells. It is necessary for the body to discern the difference between self and non-self, and to prevent the immune system from attacking self. As a consequence of this "tolerance" to self, those with blood type O would have a higher tolerance to NAC-glu, and would not have as high a natural tolerance to NAC-gal and galactose as would those with blood types of A or B. Similarly, those with blood type A would have a higher "self-tolerance" to NAC-gal.

 

The major carbohydrate antigenic determinants on the surface of the streptococcus bacteria are predominantly NAC-glu and NAC-gal. As a consequence, persons with blood type O and type A would have an initial greater natural tolerance to infection from streptococcal bacteria. After repeated exposure to the streptococcus bacterium, an immune response would finally be mounted, and targeted against the antigenic determinants on the bacterium. When this happens the immune cells of the body inadvertently launch an autoimmune attack upon body tissue with antigenic determinants that are similar to the antigen on the surface of the streptococci. This reaction to the NAC-glu and NAC-gal on the surface of the streptococci could also lead to an autoimmune type reaction against the NAC-glu/gal in the GI tract. This process has been recognized since the middle 1980's and is known as molecular mimicry.

 

The excessive shedding of NAC-glu and NAC-gal, otherwise referred to as GAG has been described and well characterized by others. Suffice to say that the shedding of GAGs in the GI tract is enhanced with immune activation and inflammation. Following infection and/or inflammation, the body would need to replace GAGs that have been shed, as well as to sulfate them. If there is a sulfur deficiency in the body, this would lead to undersulfated GAGs in the GI tract along with the deficiency of other sulfur related proteins in the body. Nitric oxide has been shown to inhibit sulfation of GAGs. High levels of nitric oxide are a consequence of excitotoxin damage.

 

Generally, bacteria elicit a B cell mediated immune response, and viruses elicit a T cell mediated immune response. However, a large number of extracellular toxins are elaborated by streptoccocci, all of which have the ability to nonspecifically stimulate T cells. Therefore once an immune response is mounted against streptococcus it would involve both T cell and B cells resulting in a major inflammatory reaction.

 

One particular extracellular enzyme produced by streptococcus is a sulfhydryl protease. This protease is capable of cleaving sulfhydryl groups and may lead to a deficiency of available sulfur containing moieties in the body following streptococcal infection. These sulfhydryl groups are involved in the binding and elimination of heavy metals in the body. Streptococcal infection is also known to lead to elevated levels of the inflammatory cytokines NFKB and TNF alpha. In addition, the level of TNF alpha is inversely correlated with glutathione levels. Consequently, high TNF alpha levels as a result of streptococcal infection would result in decreases in glutathione levels.

 

Streptococcal infection is also associated with a wide variety of behavioral disturbances. High levels of TNF alpha (as a result of streptococcal infection) have been implicated in Tourettes syndrome, facial tics, obsessive compulsive behavior, and schizophrenia. On a related note, lithium (the most popular prescription drug for treating the mood swings associated with manic, or bipolar depression) has been demonstrated to act by protecting the brain from over stimulation by glutamate. Excessive levels of glutamate have also been implicated in drug craving and in addictive behavior.

 

Consequently, the net results of streptococcal infection are depletion of Vitamin K levels, decreased glutathione levels, decreased sulfhydryl protein levels, over stimulation of the immune system, increased TNF alpha levels (which trigger OCD, facial tics, etc.), potential autoimmune responses and inflammatory reactions against the GAGs in the GI tract.

 

I hope you have been able to come to a decision that you're comfortable with. :)

Share this post


Link to post
Share on other sites

dominique,

 

Per PM, I just wanted to let you know that there is quite a bit of conversation on this site currently, regarding Amy Yaskow's program. http://health.groups.yahoo.com/group/autisminfo/

 

Her expertise lie in the genetic testing, not patient follow up.

 

These were a couple of people mentioned, as using her program.

 

Dr. Rachel West is in California

 

Nancy Mullen in California

 

Michael Payne Virginia

Share this post


Link to post
Share on other sites

Dominique,

 

I think you will have to join to read the messages here, but just click on this...to take you to this group.

 

http://health.groups.yahoo.com/group/autisminfo/

 

This is where I found the names of the Dr.s, and the remarks regarding Amy Yaskow program.

 

Also, read this thread; http://www.latitudes.org/forums/index.php?...;st=0#entry8355

 

It has a very informative post by Ronna.

Share this post


Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now

×
×
  • Create New...