kim

Mary made a remark on another thread that made me wonder about something in relationship to strep. This statement from the first article made me wonder about strep, that seems so hard to clear in some kids http://www.msnbc.msn.com/id/20825107/ My oldest son has also had a couple of go arounds with staph. I don't think this is what you were referring to Mary, but I did think it was a good opportunity to share a big concern of mine regarding the notion that we can "vaccinate away" disease. Many of the abstracts here are pointing out the danger of serotype replacement with the use of Prevnar and also the increase in staph. You have to wonder how many strains of pneumococcal bacteria are being replaced with other strains. Also, are we trading some cases of pneu. for MRSA staph? I don't think many parents are made aware of these concern when the vaccines are recommended, so I thought I'd share. There is lots of info contained in these articles. A couple are just random things that I have read recently. Near the bottom there are a few with aluminum and thimerosal info that are recent. All bolding Mine. Edit...If abstracts make your head spin, this article which is posted near the bottom, really sums it up. http://insidevaccines.com/wordpress/2008/0...ugate-vaccines/ http://www.whale.to/m/pneumococcal.html Erdem Cantekin, Ph.D., is Professor of Otolaryngology, University of Pittsburgh. An internationally recognized authority on otitis media and has studied causes and treatments for ear infection and sinusitis in his 25 year career. An early, outspoken critic of the overuse of antibiotics to treat ear infections, Dr. Cantekin has published more than 150 articles and abstracts in the medical literature on eustachian tube function, ear tube surgery, antibiotic resistance and conflicts of interest in biomedical research and manufacturer sponsored medicine. Cantekin discussed the new Prevnar vaccine for pneumococcal, as endorsed by the American Academy of Pediatrics. "The alleged benefits for this new vaccine are greatly exaggerated and the risks are significant," said Cantekin. "The bacteria pneumococcus, with more than 90 serotypes, is a common pathogen. Though pneumococcus causes various diseases the carriage rate and serotype distribution rates in different groups are not know. Also, it is not known how pneumococcus transmutes itself into a pathogen. The role of pneumococcus in the microbiological balance is not known. It does contribute to 3,000 cases a year of meningitis, 50,000 a year of bacteremia, 500,000 cases of pneumonia, and seven million cases of otitis media or ear infections." http://cat.inist.fr/?aModele=afficheN&cpsidt=15841788 A trial with a 7-valent pneumococcal-conjugate vaccine in children with recurrent acute otitis media showed a shift In pneumococcal colonisation towards non-vaccine serotypes and an Increase In Staphylococcus aureus-related acute otitis media after vaccination. We investigated prevalence and determinants of nasopharyngeal carriage of Streptococcus pneumonlae and S aureus in 3198 healthy children aged 1-19 years. Nasopharyngeal carriage of S pneumonlae was detected In 598 (19%) children, and was affected by age (peak Incidence at 3 years) and day-care attendance (odds ratio [OR] 2.14, 95% Cl 1.44-3.18). S aureus carriage was affected by age (peak incidence at 10 years) and male sex (OR 1.46, 1.25-1.70). Serotyping showed 42% vaccine type pneumococci. We noted a negative correlation for co-colonisation of S aureus and vaccine-type pneumococci (OR 0.68, 0.48-0.94), but not for S aureus and non-vaccine serotypes. These findings suggest a natural competition between colonisation with vaccine-type pneumococci and S aureus, which might explain the Increase in S aureus-related otitis media after vaccination. http://jb.asm.org/cgi/content/abstract/188/13/4996 Results Among 790 children screened, 43% carried S pneumoniae and 10% carried S aureus. Staphylococcus aureus carriage among S pneumoniae carriers was 6.5% vs 12.9% in S pneumoniae noncarriers. Streptococcus pneumoniae carriage among S aureus carriers was 27.5% vs 44.8% in S aureus noncarriers. Only 2.8% carried both pathogens concomitantly vs 4.3% expected dual carriage (P = .03). Risk factors for S pneumoniae carriage (attending day care, having young siblings, and age older than 3 months) were negatively associated with S aureus carriage. Conclusions Streptococcus pneumoniae carriage, specifically of vaccine-type strains, is negatively associated with S aureus carriage in children. The implications of these findings in the pneumococcal vaccine era require further investigation. http://www.thaindian.com/newsportal/uncate...o_10093089.html New Delhi, Sep 7 (IANS) Raising questions over India’s decision to include a new pneumonia vaccine in the national immunisation programme, a report in a WHO bulletin has said the vaccine has “no effect” on the disease and on the contrary increases the risk of asthma among vaccinated children.The report, published in the September edition of the WHO Bulletin, claimed that Pneumococcal Conjugate Vaccine (PCV), the latest addition to India’s immunisation programme, is ineffective in tackling pneumonia among children and hence does not justify the huge amount of money the government will spend on it. http://jac.oxfordjournals.org/cgi/reprint/50/suppl_3/59.pdf However, immunization can also place selective pressure on the nasopharyngeal flora, promoting the emergence of new pathogens. A shift towards non-vaccineserotypes has been observed among vaccinees in several studies. 109 In South Africa, the carriage of non-vaccine serotypes was increased from 24% in controls to 36% in the vaccines group. A significant increase was seen in the carriage of serotypes 7 and 15, important causes of invasive disease.109 http://jama.ama-assn.org/cgi/reprint/292/6/716 Pneumococcal conjugate vaccines reduce nasopharyngeal carriage of vaccine- type S pneumoniae. Our finding of an inverse relationship between vaccinetype S pneumoniae and S aureus may imply an upcoming shift, not only toward nonvaccine S pneumoniae serotypes17 but also toward higher S aureus carriage rates in children. This would be particularly disturbing in light of the emergence of community-associated methicillinresistant S aureus.5,6,18 This possibility is supported by a recent report of an increased rate of S aureus culturepositive draining ears in vaccinated children compared with controls. Our study suggests a protective role of S pneumoniae carriage against S aureus carriage. Studies measuring the effect of vaccination on S pneumoniae epidemiology should also examine concurrent changes in S aureus. http://www.pubmedcentral.nih.gov/articlere...i?artid=1112059 Why are there so many serotypes of proteins that cause blood coagulation? From our results, we presume that antigenic variation in staphylocoagulases might be useful to evade the host immune response and/or to adapt to the different staphylocoagulase-prothrombin binding sites of mammalian species. Vaccines against the type b capsular polysaccharides of Haemophilus influenzae (Hib) have been used to reduce the incidence of invasive diseases caused by H. influenzae in industrial countries. However, as the use of the vaccines increased, the number of non-Hib strains in clinical isolates has also increased (29, 33, 49). The possibility of “serotype replacement” has been raising concerns. It can be postulated that staphylocoagulases changed their antigenicities by altering amino acids to evade the host defense system. http://www3.interscience.wiley.com/journal...403042/abstract? Neonatal jaundice: a risk factor for infantile autism? http://www.theaustralian.news.com.au/story...5-23289,00.html Overwhelming infection linked to many SIDS deaths http://insidevaccines.com/wordpress/2008/0...ugate-vaccines/ Sisyphus and the Conjugate Vaccines FINDINGS: We noted no reduction of AOM episodes in the pneumococcal vaccine group compared with controls (intention-to-treat analysis: rate ratio 1.25, 95% CI 0.99-1.57). Although nasopharyngeal carriage of pneumococci of serotypes included in the conjugate-vaccine was greatly reduced after pneumococcal vaccinations, immediate and complete replacement by non-vaccine pneumococcal serotypes took place.” and “Conclusions: Streptococcus pneumoniae carriage, specifically of vaccine-type strains, is negatively associated with S aureus carriage in children. The implications of these findings in the pneumococcal vaccine era require further investigation http://www.nvic.org/doctors_corner/lawrenc...ingredients.htm Aluminum is a heavy metal with known neurotoxic effects on human and animal nervous systems. It can be found in the following childhood vaccines – DTaP, Pediarix (DTaP-Hepatitis B-Polio combination), Pentacel (DTaP-HIB-Polio combination), Hepatitis A, Hepatitis B, Haemophilus influenzae B (HIB), Human Papilloma Virus (HPV), and Pneumococcal vaccines.[2] In 1996, the American Academy of Pediatrics issued a position paper on Aluminum Toxicity in Infants and Children which stated in the first paragraph, “Aluminum is now being implicated as interfering with a variety of cellular and metabolic processes in the nervous system and in other tissues.[3] http://www.newsrx.com/articles/1130878.html September 10, 2008 - Researchers from Novartis, Department of Immunology describe findings in vaccines - European Journal of Immunology via Newsrx - "Despite the fact that alum has been injected into billions of people, its mechanism of action is not fully understood." http://www.ageofautism.com/2008/09/stunning-new-li.html I'm a stay-at-home mom in NC with a degree in Computer Information Systems. I didn't know anything about medicine until after my first child was born. When she turned 8 months old she started doing a myoclonic head jerk, and dystonic head postures, which could have meant a brain tumor or movement disorder. Her neurologist didn't know what it was after the MRI, EEG, and PET scan was fine. So I decided to educate myself, and I learned way more about medicine than I ever wanted to know. She was finally diagnosed with stereotypical disorder (usually seen in children with autism, but she did not have any other autism symptoms). Well, after that diagnosis I have been very leery of vaccines and autism, and have spent hundreds of hours reading about the subject. I first read about children having low glutathione levels and thin bones study on Dr. Green's website. The chart http://vaccines-rvb.blogspot.com/ After reading some of the above articles, this almost made me LOL http://www.thetimesnews.com/news/shot_1775...ool_clinic.html "We all need immunizations to keep us healthy," Burns said. There have been six cases of pertussis - whooping cough - reported in Alamance County since 2003

Carolyn, I just couldn't be happier to hear your news! Just a little prayer for you and baby ******** Life presents some with special challenge that sometimes shape in ways never imagined It can be part of what makes someone really special bringing an understanding beyond what is common In Carolyn Lord, I believe this work has been done her child will know this is no ordinary mom With strength wisdom and love with no bounds may a healthy new life begin in her arms A new little soul has been sent from above Keep your arms around them dear Lord and protect them in your love

Hope, I am so happy that your Dr. was willing to do this. Did he hastle you about it at all? Will your insurance cover the titers test? I hope you'll post your daughter's results. Sure will be praying that she shows "protective" levels, althou several people are reporting that their Dr.s are recommending females have rubella titers tested prior to starting a family as many are showing no immunity even when having had 2 MMR's. My SIL was one and she didn't show immunity. I hope your daughter handled the draw Ok!

Caryn, Yes, I do think we are thinking along the same lines. From what I understand of the celiac genes, you can have gluten sensitivity without full blown celiac depending on which gene is involved? I think I need to explain something about the bony tumor (I should be saying "overgrowth of cartiledge" tumor). From reading everything that I can get my hands on it appears that these tumors are rare and the theories that I am aware of, in regards to their development are something called LOH or loss of heterozygocity which basically means that you had one bum copy of a gene or allele and something happens to knock out the other working gene or allele and #2. something referred to as "gene dose. " My point, it sure seems like you could have a mutation in one of these genes, and express NO tumor. As I have said before, my youngest son does not have any tumor either, yet I would think it unlikely that these same genes are not involved. The other thing that may be important to others is the fact that a mutation in these genes results in a lack of N acetylglucosamine. This substance has recently been reported to have astounding (I think that was the word that they used) results in protecting cells from autoimmune reactions. Look at this study http://www.ncbi.nlm.nih.gov/pubmed/2394351 Mannan and oligomers of N-acetylglucosamine protect intestinal mucosa of celiac patients with active disease from in vitro toxicity of gliadin peptides.Auricchio S, De Ritis G, De Vincenzi M, Magazzù G, Maiuri L, Mancini E, Minetti M, Sapora O, Silano V. Department of Pediatrics, II Faculty of Medicine, University of Naples, Italy. Wheat flour and other cereals toxic for celiac patients contain an alcohol-soluble protein fraction that, under experimental conditions simulating in vivo protein digestion, yields peptides that agglutinate undifferentiated K 562(S) cells. In contrast, cereals well tolerated in celiac disease (i.e., rice and maize) do not. Furthermore, purified A-gliadin peptides that damage in vitro-cultured flat celiac mucosa are powerful agglutinins for K 562(S) cells, whereas A-gliadin peptides that do not show any adverse in vitro effect on celiac intestine lack agglutinating activity. Mannan, acetylglucosamine, and its oligomers (N,N'-diacetylchitobiose and N,N',N"-triacetylchitotriose) were able to prevent and reverse cell agglutination induced by peptides from all the toxic cereals. Moreover, mannan and N,N',N"-triacetylchitotriose exhibited a protective effect on intestinal mucosa specimens of patients with active celiac disease cultured with wheat protein-derived peptides. These data are consistent with the hypothesis that the agglutinating and toxic peptides are bound by carbohydrates. http://today.uci.edu/news/release_detail.asp?key=1612 http://www.newscientist.com/article.ns?id=mg19426074.500 and . I hope when you get done with your study on HCl, you will take a look at NAG! Would like your take on it.

edit double post ,

Caryn, I found this back when you posted your response but didn't know if there was any significance, still don't but it is kind of interesting. These are the genes that suspected to be involved in my son's osterochondroma http://www.ncbi.nlm.nih.gov/pubmed/9037597 8q24.1 (EXT1),11p11-13 (EXT2), and 19p (EXT-3). The EXT1 and EXT2 genes were isolated recently and show extensive sequence homology to each other. This is an abstract on celiac's http://www.biomedcentral.com/1471-2350/2/12 Linkage analysis of HLA and candidate genes for celiac disease in a North American family-based study Genomic searches for CD have been conducted in several European populations. In 1996, Zhong et al. [29] studied 40 affected sib pairs from 11 families, and reported significant linkage at 6p23 and weak evidence at 11p11, 7q31.3, 22cen, 15q26, 5q33.3, 19p13.1 and 19q13.2. Houlston et al I have never been able to find anything more specific on the location of the 19p gene, so I did a search for " EXT gene at 19p" and this popped up. Do you think there is anything to this? Since 8q24 is in the area of one of the EXT genes and 19p13 is metioned in the celiac abstract , I'm wondering if the position of the EXT 19 is going to be found to be in the p13 area? Results: Several potentially important genomic regions were identified, such as 8q24 for hip bone size (logarithm of the ratio of the odds that two loci are linked (LOD) 3.27) and 2p24 (LOD 2.04) for spine bone size. 8q24 may also interact with 19p13 to affect hip bone size. Several sex-specific QTL were also detected, such as 14q21 (LOD 2.94) for wrist bone size in women and 16q12 (LOD 2.19) for hip bone size in men. EXT 2) to the short arm of chromosome 19 by linkage to a microsatellite DNA marker at the D19S221 locus,

I removed an article that I had posted in the above response. I realized that the article could be taken in a different way than I originally interpreted it, and found where it could be hurtful or offensive to some members. That was not the way I took it, but when I checked the link, I reread the article and it struck me a different way. To anyone who read, and felt what I did the 2nd time, my apologies!

Michele, I just wanted to add that had I have known back when my oldest son was 3 or 4 (thru about the age of 9 to 11?) about all of these spectrum disorders, I would have had a nervous break down. I could tell you some stories! He is soon to turn 16 and I have to tell you that this is one of the most polite, outgoing, sensitive, wonderful young men. I'm not saying that he isn't short tempered with his brother at times, doesn't use some language or phrases that drive me crazy etc. (he's a normal teenager, believe me) but in hind site, I really feel that a lot of the "behaviors" were because he just didn't feel well a lot of the time. I hope that you take away just a bit of peace from this. I know you will continue to fight for any and all accomodations that you think may be helpful to him, but I wanted you to know that some of these issues may well take care of themselves. You take care of yourself too. You are a wonderful Mom!

Hope, The best advice that I can give you is to do nothing until you are perfectly comfortable with your decision, either way. I know this means that your daughter may miss some school and I know that is probably the last thing that you want with a child just starting kindergarden because it is a huge adjustment for most kids, but if your gut is sending you panic signals, personally, I would listen. You may feel much better after you have fully researched. You may end up feeling that the benefits of the vaccine outweigh the risk in your daughters case. If you are comfortable that you have done evereything that you can to inform yourself, I think it makes it much easier. Our best, is all we can ever really ask of ourselves. Did your daughter have the first MMR at one year? Are you aware that the 2nd MMR is NOT A BOOSTER? It's given to catch the 3 to 5% (approx) of children who did not achieve what is considered an adequate level of response to the first vaccine? If your daughter did have the first MMR, did you know that you can have titers tested to see if she is considered immune? I think you may be thinking of the tic and thimerosal connection? Or the suspected autism/MMR connection? Peglem is right, the MMR has never contained thimerosal for the reason that she stated. The individual vaccines for MMR do not contain thimerosal either. Here is a page with info exclusive to NY exemptions. Not sure if this was posted already or not http://www.vaclib.org/exempt/newyork.htm Here is a pkg insert so you can look at the ingredients in one of the combo MMR vaxes http://www.merck.com/product/usa/pi_circul...i/mmr_ii_pi.pdf This is a table with the vaccines which still contain thimerosal......there are some marked with** that contain trace amts according to the manufacturer but no one seems to be able to answer the question of who is monitoring "trace" amts. Apparently the vaccines are still being manufactured with thimerosal, but then it's removed. Some parents are leary of how much "trace" really means. http://safershots.wordpress.com/2008/09/12...sed-his-autism/ Hope, are you positive that the only vaccine that your daughter is missing is the MMR? I'm afraid that you are going to get blind sided tomorrow. It seems that 5 yr old appt. is time for more than that one vaccine? I'm going to check the recommended schedule. Edit Ok here is an easy read chart. Is there a reason that your daughter is not being required to get any others? Maybe some of these are recommended but not mandatory in NYS? I'm thinking of chicken pox, which I'm not sure if it's mandatory for school entry or just recommended at this point? http://www.chop.edu/consumer/jsp/division/...ic.jsp?id=75700

Momto2pandas, You are probably my best shot of having someone answer something (without going outside of this forum) that I have been wondering about. I would really appreciate any thoughts you might have on this. Do you think glucuronic acid, or a lack of, could play a part in the way some people react to different medications? My oldest son has a condition that seems to require glucuronic acid and N acetylglucosamine to form "normal" heparan sulfate chains (GAGS). From recent research, it seems he may have altered gene expression that catalyses these substances. It is just being looked at in regards to neuro conditions. I also saved a site that said that 17 out of 17 autistic children tested low in glucuronic acid. I can't find the part on the site that talks about it right now, but I thought it was interesting. Here is something for anyone else reading that tells a little about glucuronic acid with an explanation of "xenobiotics" first. I think it's an intermediate in the processing of vit. C too? This same son was jaundiced with a wicked case of cradle cap too (also developed quite a case of infant acne at about 1 month). http://en.wikipedia.org/wiki/Xenobiotic_metabolism Xenobiotic metabolism is the set of metabolic pathways that modify the chemical structure of xenobiotics, which are compounds foreign to an organism's normal biochemistry, such as drugs and poisons. http://en.wikipedia.org/wiki/Glucuronidation#Glucuronidation Glucuronidation Glucuronic acid is highly soluble in water. In the animal body, glucuronic acid is often linked to the xenobiotic metabolism of substances such as drugs, pollutants, bilirubin, androgens, estrogens, mineralocorticoids, glucocorticoids, fatty acid derivatives, retinoids, and bile acids. These linkages involve O-glycosidic bonds, and this linkage process is known as glucuronidation.[1] Glucuronidation occurs mainly in the liver, although the enzyme responsible for its catalysis, UDP-glucuronyltransferase, has been found in all major body organs, e.g., heart, kidneys, adrenal gland, spleen, and thymus.[2] UDP-glucuronic acid (glucuronic acid linked via a glycosidic bond to uridine diphosphate) is an intermediate in the process and is formed in the liver. The substances resulting from glucuronidation are known as glucuronides (or glucuronosides) and are typically much more water-soluble than the non-glucuronic acid-containing substance from which they were originally synthesised. The human body uses glucuronidation to make a large variety of substances more water-soluble, and, in this way, allow for their subsequent elimination from the body upon urination. Hormones may also be glucuronidated to allow for easier transport around the body. Pharmacists also commonly link drugs to glucuronic acid to allow for easier drug delivery.

Patty, I'm so sorry you/your little guy are going through this scare. I have often wished I would have found this forum when the kids were younger so I would have been aware of some of the things that I am now, but on the other hand, I know I would have worried and obsessed more too. Both boys were given albuterol treatments in Peds office and rx for home use. Oldest, a lot more than his younger brother. I know it would wind him up. He would say that his heart would pound. After discovering this forum, I resisted whenever they recommended it. It was always for a respiratory illness, neither were ever diagnosed with asthma altho Dr. would always comment on "illness induced asthma." I don't ever remember any explosion in tics with it's use. I can't say if it truly increased tics as both boys were always "ticcier" at the onset of an illness anyway. When they were flat out sick, they would never tic. It seemed to be at onset or after. Try not to worry too badly. If your son has had albuterol before, even if he does have a mild increase, I'm hopeful it will pass quickly. Patty, you have done sooo much to help your son gain good health, have faith! There is only so much we can do, the rest lies in the hands of someone with a whole lot more control than we have. Prayers are with you and your family. Please keep us updated on how he's doing. Hugs Kim

NT= without looking up a definition I guess I would say "no noticable signs of neurological problems" or "neurologically normal/typical" Juls, There have been a lot of articles shared on different forums about Bisphenol A. You may want to search it+Precocious Puberty and see if you can find a specific correlation. I wonder if it's another example of a subset of people, just not handling toxins as well as others? Here's one article http://foodconsumer.org/7777/8888/C_ooking...ne_system.shtml Sunday Sept. 7, 2008 (foodconsumer.org) -- A new review suggests that adult exposure to bisphenol A, a common plastic ingredient may affect the brain, reproductive system and immune system in men and probably also in women.

P Mom, I believe a poster who hasn't been around lately (Laurensmom) said that her daughter had never been immunized. I think we have one or two other poster's that I'm aware of, who's kids didn't have any or minimal. Personally, I believe there are multiple causes of movement disorders. In our case, I feel we probably had a genetic predisposition, but vaccines/vax ingredient may very well have triggered a problem which may have never manifested otherwise. My boys were both immunized on schedule in the 1990's. They received different vaccines with different amts of thimerosal at different ages tho (almost 4 yrs apart in age). They have very different symptoms. You may find a few of these article interesting. I have read a few studies that sure make it appear that kids/people may be more susceptable to illness after vaccination. I'm thinking of Michelle's comment here. Vaccines and Immune Suppression citations http://www.whale.to/vaccines/immune.html Also, In the study that is being referred to below, remember, they didn't test AUTISTIC children for harmful associations from thimerosal exposure....they may have discounted the very population that was AT INCREASED RISK. This "tic" association has come up at least twice, and I think there is a 3rd study that showed this too. WHY AREN"T THEY GETTING SOME ANSWERS TO THAT QUESTION? Tics are hardly even referred to in vax/injury discussions. They will list asthma, diabetes, ADD, ADHD, autism, etc. but hardly ever mention TICS, yet this is one area with the most ammo according to their "engineered to sell the public that vaccines are safe" studies. It just burns me. I have to wonder what may be learned, even for people who have never recieved a mercury containing vaccine. What about amalgams, rhoGAM injections, other metals? For anyone who may have missed this before http://www.huffingtonpost.com/david-kirby/...s-_b_66007.html CDC: Mercury in Vaccines Damaged Your Child. Or Not. http://content.nejm.org/cgi/content/full/357/13/1281 Check this statement out. If "millions" are affected and "more thimerosal/more tics" (or possibly just more immunizations/more tics) have been shown/acknowledged, why isn't it being immediately investigated? Sorry, I guess I got a little "off topic" here, so I'll end my rant! http://www.medicalnewstoday.com/articles/120537.php Article Date: 06 Sep 2008 Millions of children across the United States suffer from disorders such as Tourette's Syndrome and anxiety disorders, including Obsessive-Compulsive Disorder - conditions which often affect their performance in school on both social and academic levels

I believe the vaccine being discussed here is Menactra and yes that would be the same vaccine that used to be pushed for college students. http://articles.mercola.com/sites/articles...-reactions.aspx http://www.cbc.ca/health/story/2007/10/30/...s-menactra.html http://www.fda.gov/bbs/topics/NEWS/2007/NEW01729.html Info from FDA You can read the package insert with ingredient here http://www.fda.gov/CbER/products/menactra.htm

Buster, Sorry for the delay in a huge "thank you" for that response. It would have taken me hours and hours to come up with anything close to that. I'm hoping you will put some of your info on PANDAS on one thread, so we can ask Cheri to pin or sticky it at the top of the forum. In light of this discussion, I want to bring up something that I have touched on here before. http://www.newscientist.com/article.ns?id=mg19426074.500 This article is is talking about N-acetylglucosamine (GlcNAc). This substance, in my mind, is almost certainly involved (an inability to synthesize properly) in my boys condition, which is not primarily PANDAS although we have had many problems involving strep and staph. Would love to discuss it in more detail, if anyone has the time or inclination. I should probably update some of what I'm talking about on a different thread here. It involves research relating to a bony tumor that my oldest son has and I've recently come across an article connecting GlcNac deficiency and hyperpigmentation which my oldest son also developed in an area on his back where he had a mole removed and developed staph. I'm hoping that someone (with an awesome Dr.) will ask about this article in possible treatment for PANDAS kids. Interesting that they specifically talk about TH1 and T cells. I believe Crohn's is primarily thought to have problems in overactivation involving the TH1 arm also? EAMom This is something I ran across (saved) as I was looking for the glucosamine article. Since you mention your daughter not eating and anorexia was brought up recently by another poster, this just looks interesting. http://lib.bioinfo.pl/pmid:17823502 Neuroendocrinology. 2007 Sep 7; : 17823502 (P,S,E, Regulation of Food Intake by Inflammatory Cytokines in the Brain. Jessica B Buchanan, Rodney W Johnson A number of inflammatory cytokines are synthesized and released after activation of the immune system. In addition to other biological effects, these cytokines can potently inhibit food intake. Cytokine-mediated inhibition of food intake is of particular importance because excessive production of peripheral inflammatory cytokines is often associated with the cachexia-anorexia syndrome seen in some chronic diseases. The weight loss in cachexia is associated with an increase in morbidity and mortality. Understanding how cytokines regulate food intake may be crucial in enhancing quality of life and facilitating recovery in patients exhibiting cachexia. This review describes the main inflammatory cytokines that influence food intake and explores how peripheral cytokines communicate with hypothalamic nuclei to influence feeding. Copyright © 2007 S. Karger AG, Basel.

angelictwins, I have a son with an extremly limited diet and he is also a sugar craver and a gagger. He seems drawn to wheat..... Townhouse crackers, freezer pretzels, Pepperidge Farms fish crackers, recently pizza crust which he would never touch before, etc. His diet is a bigger concern than tics as his have always been on the mild side too. I know first hand how hard it is to do anything with food changes in a child like that. Anyway, just wanted to say welcome. I'm sure as you read thru the threads here, you'll see you/your children are not alone and start forming many ideas as to ways to improve things.

I almost missed this. Thanks a lot for the info on spectracell/zinc. BTW, thanks too for the vote of confidence about my lack of confusion. I also wanted to tell you PC, I couldn't be happier to read about your son's improvement with Amox and his staph infection

Michelle, if you look at the Actos study it doesn't look like they really know the mechanism by which it may help. I haven't read it again since Peglem first posted it, but I think they were hoping that it would tamp down TH2. Then it says one small study appeared to boost it? Maybe it was having the wrong effect with your son. Something else I'm wondering about (maybe peg or buster have a thought here) Look at this study regarding strep and RA, which I thought you would be interested in. Does this mean that it will only be certain strep bacteria that express these M proteins that will cause the autoimmune reaction? Could you "have strep," but not see any increase in problems, if the strep doesn't have the M protein that an individual has a problem with? http://www.jimmunol.org/cgi/content/abstract/146/9/3132 Epitopes of group A streptococcal M protein shared with antigens of articular cartilage and synovium RW Baird, MS Bronze, W Kraus, HR Hill, LG Veasey and JB Dale Department of Veterans Affairs Medical Center, Memphis, TN 38104. Rabbit antisera evoked by purified pepsin-extracted group A streptococcal M proteins were screened for the presence of joint cross- reactive antibodies by indirect immunofluorescence using thin sections of mouse knee joints. Pep M1, M5, and M18 antisera contained antibodies that cross-reacted with chondrocytes, cartilage, and synovium. Immunofluorescence inhibition assays showed that some of the joint cross-reactive epitopes were shared among the three heterologous serotypes of M protein. The pep M5 joint cross-reactive epitopes were localized to three different synthetic peptides of the C-terminal region of pep M5. Immunoblot analyses showed that the M5 joint cross- reactive antibodies recognized two proteins of human synovium and cartilage of molecular mass 56 and 58 kDa. The cross-reactive antibodies binding to the 56-kDa protein were inhibited by purified vimentin in immunoblot inhibition experiments. M protein-specific antibodies from patients with acute rheumatic fever were also shown to cross-react with joint tissue in a pattern similar to the rabbit antisera. Rabbit and human M protein-specific antibodies that were bound to articular cartilage activated significant levels of complement when compared to control serum, suggesting that M protein joint cross- reactive antibodies could potentially be involved in the pathogenesis of ARF and arthritis. I haven't been abe to get my mind around the fact that they found nothing in these 12 children, but IF it's only a certain strep for a certain child that causes a problem, would they catch it using only 12 kids over 2 years? I wonder how many confirmed strep infections each child had during the 2 year period. I'm also wondering about this statement. How did they determine this without a specimen of the brain tissue, which would be pretty hard to obtain from living subjects. I know there must be a logical answer to that question. I wonder if the actual study is available yet? http://www.hopkinschildrens.org/newsDetail.aspx?id=4914 June 04, 2008 A small but revealing study from Johns Hopkins Children’s Center challenges a controversial theory that strep infections cause a neuropsychiatric disorder in children marked by tics, jerking movements and obsessive-compulsive behaviors. The findings appear in the June issue of Pediatrics. Working from the hypothesis that an overactive immune system in the wake of a strep infection mistakenly attacks a child’s brain and causes neuropsychiatric symptoms, researchers followed for two years 12 children diagnosed with PANDAS, (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections), but found no changes in the levels of immune proteins, the classic markers of autoimmune inflammation, during symptom exacerbation. Moreover, researchers found no evidence of strep antibodies – the antibodies produced by the immune system against the streptococcus bacterium – binding to or interacting with brain tissue, a finding that makes an immune origin of PANDAS unlikely, investigators say.

CP, If you get a minute could you see what your son's level of zinc was? I'm concerned about all of the white spots reappearing on my youngest sons fingernails again, school starting and the strep goo and other bugs that he will soon be exposed to again. I was wondering what the normal range shows on the spectracell test. kim

CP, I want to say, "You should expect to see improvement!" I would just be very optimistic right now and carefully observe. Has your son be tested for and had negative cultures in the past? Also, I'm not clear if your son was showing symptoms of being ill, or if the Ped visit was prompted by the vocal?

Peglem/Michelle, So glad you guys are able to discuss this. Michelle, you said "tics were worse while on Actos." Did you see improvement in any other area? Can you say how long Andrew was on it? Peg, Your very welcome. This is just the way I'm interputing this and I'm sure no expert here, but it looks like a direct attack by a form of T cell has been suspected in past studies. Yes, something in the strep bacteria is causing an autoimmune attack, but not by antibodies. Here is one talking about rheumatic fever, but makes this point (I think). This study is dated 1995, so I'm sure there is more current research but I was looking for something to sort of confirm that a TH1 response could be responsible for a reaction. The first part talks about the normal antibody attack, then it goes into this.... bolding mine http://www.circ.ahajournals.org/cgi/content/full/92/3/281 AND Also, the challenge with the vaccine was interesting. I'm wondering if that vax contained aluminum (which is notorious for prompting a TH2 response). I found a study where children with nephrotic syndrome were given a 23-valent pneumococcal polysaccharide vaccine. At 4 weeks, if there was a twofold increase in the antibody titers, the children were considered "antibody responders." I'm wondering, in light of your daughters non response to the first vaccine, if the immunologist had any thoughts. The idea that he "fixed" a problem with the immune system with a double dose of an aluminum spiked vaccine (if indeed it contained alum) seems a bit bizarre to me. So he was able to achieve what is considered an acceptable antibody response using 13 weakened strains of pneumonnia and an adjuvant, twice. Why didn't he focus more on her response that was outside of the norm to the first injection and see what knowledge could be gleened from that? If vaccines were going to fix a genetic preexisting deficit in the TH2 arm of the immune system, I'm sure they would have accomplished that with her childhood vaccines (assuming she had all of them). Sorry for the negative undertone, it's just frustration. Maybe you have some other thoughts on the results. This is the study I was referring to http://www.advmolmed.com/issue/20074/fulltext/txt_03.asp

Peglem, In the absence of elevated titers, your thinking makes sense to me. I'm understanding it the same way you are. This article looked interesting. This would suggest more of a TH1 involvement, I would think. In this scenario, could the TH2 response be suppressed (hence antibody production)? From the last sentence, I wonder what epitope that refers to? http://neuro.psychiatryonline.org/cgi/content/full/16/3/252 Most recently, a prospective study provided convincing evidence establishing a temporal relationship between GABHS infections and PANDAS. In this study, authors proposed the role of GABHS-associated toxins in the development of pathophysiology of PANDAS instead of the role of traditional antibodies. GABHS-associated toxins act as superantigens within the host. By binding both the Class II major histocompatibility complex molecules on antigen presenting cells (HLA Class II) and specific Variable-ß regions on the T cell receptor, superantigens can undermine immune function. Allelic changes within the HLA Class II can lead to proliferation of specific T cell clones at a far higher orders of magnitude than what would be expected in the absence of superantigens. These expanded T cells interact not only with the M protein epitope but also cross-react with the epitope within the host tissues. In regards to IgE, from the looks of this it appears both arms would be involved if you look at these statements. I'm assuming that your daughter doesn't appear to have inhaled type allergies? TH1 Cellular Immunity A branch of the immune system which involves direct attack by immune cells often called "T" cells. Antibodies play less of a role. TH2 Humoral Immunity This refers to immunity to infection created by proteins termed antibodies, often referred to as "B" cells. http://www.gene.com/gene/products/educatio...nology/ige.html IgE and the Allergic Cascade In some people, allergen exposure can cause a reaction known as the allergic response. This occurs when allergens are inhaled into the respiratory tract (nose, throat and lungs) and attach to the mucous membranes. These allergens are seen by the immune system as foreign invaders and an immune response is produced as the body prepares to fight them off. During this response, T-cells (a cell type of the immune system) send a signal to B-cells (B-lymphocytes) and stimulate production of IgE antibodies — a key protein involved in the allergic cascade

Peglem, I have read the study a couple of times and could probably read it 5 more and get more questions each time! I'm thinking that the ahh haa was the part about the body sort of burning out, with producing antibodies, hence low titers? I thought Dnase detected something that the strep put off itself. I didn't look at ASO (used to know this stuff but I think I have forgotten more than I've retained!) then I found these two statements, so I'm wondering which it is? I'm thinking the it's the "antibodies against." That was something that always confused me. I guess the first statement just leaves out the antibody part. http://www.healthatoz.com/healthatoz/Atoz/...ibody_tests.jsp Antideoxyribonuclease-B titer (anti-DNase B, or ADB) Anti-DNase-B, or ADB, also detects antigens produced by group A strep, and is elevated in most patients with rheumatic fever and poststreptococcal glomerulonephritis. http://cancerweb.ncl.ac.uk/cgi-bin/omd?anti-DNAse+B anti-DNAse B This is a serologic blood test used to detect antibodies against antideoxyribonuclease B (anti-DNAse , an antigen that is produced by group A streptococci I also wanted to share an article written by Hilary Butler. I was fortunate enough to be reading a forum where she was actively posting a while back. It was a vaccine forum. I learned so much from her. Not only in relationship to vaccines, but nutrition, functioning of the immune system etc. This article has some really good discussion on the Th1 TH2 stuff that you might be interested in, not necessarily related to vaccination, just functioning. http://www.whale.to/vaccines/butler.html This is just an excerpt of a pretty long discussion: I think Michelle was either using Actos for her son for a short period, or it was recommended and she declined. Maybe she will pop in with her experience. I know how frustrating it is to find/read info and not have anyone to discuss it with, but any part of this that you want to have a go at, I'm with ya!

Matt, I was wondering if you would mind sharing why you had the rods placed? Was it a bone problem, injury, scoliosis? I am particularly interested in anything to do with tics and bone, cartilage problems or any form of clotting disorders or autoimmune issues . Seems we have some genes in our family that may be susceptible to problems in this area. Also, could I ask if you have any unusual reactions to any types of medications? Since you don't mention your eyes even feeling dry and you have had many tests (I'm assuming that there was nothing suggesting autoimmune problems) I doubt that anything here will apply, but I have wondered about the occasional eye rolls and my youngest son saying that his eyes felt dry at different times. This was something that I ran across and wondered if there was anything here that rang any bells for you? Sjogren's Syndrome http://www.medicinenet.com/sjogrens_syndrome/article.htm

Lyn, I have to ask, was your friends son immunized anytime within the past year? Do you know if he had any viral or bacterial illness prior to onset? Any injuries? The only thing that I can add is that I had a very special friend who recently passed away unexpectedly, who developed extreme anxiety and tics after a case of naturally occuring chicken pox at around the same age. We have other parents here who have reported onset at a later age too. If you can provide any other info about his circumstances, it may be helpful. Any high fevers lately? Mono? Caryn, Is celiac considered autoimmune? I didn't think it was, but in looking at the site that you linked, it almost looked like an autoimmune component is suspected? This study looked interesting. There's the anti-ganglioside thingies again (PANDAS?). I'll post below what wiki says about ganglioside. This was the definition that I found for haptenization that is referred to in the study below The combination of an antigenic compound with a carrier protein molecule, intended to achieve a high enough molecular weight to stimulate an immune response. http://www.ncbi.nlm.nih.gov/pubmed/16766047 Transglutaminase-independent binding of gliadin to intestinal brush border membrane and GM1 ganglioside.Alaedini A, Latov N. Department of Neurology and Neuroscience, 1300 York Ave, Weill Medical College of Cornell University, New York, NY 10021, USA. ara2004@med.cornell.edu Anti-ganglioside antibodies have been described in celiac disease or gluten sensitivity, in conjunction with the presence of central and peripheral nervous system deficits. The observed antibody reactivity to gangliosides is postulated to be related to the anti-gliadin immune response, either through antigenic mimicry, or by formation of gliadin-ganglioside complexes and haptenization. We examined the possibility of the presence of ganglioside-like epitopes in gliadin, as well as the potential for complex formation between gliadin and GM1 ganglioside. Low levels of glycosylation were present in gliadin, but ganglioside-like carbohydrate epitopes were not detected. However, gliadin was found to bind to GM1 ganglioside and to the GM1-rich intestinal brush border membrane. The described complex formation and possible haptenization of GM1 by gliadin may be responsible for driving the anti-ganglioside antibody response in some patients with gluten sensitivity. Furthermore, binding of gliadin to GM1 on the intestinal epithelium might have a role in the anti-gliadin immune response and contribute to the intestinal inflammatory reaction in celiac disease. http://en.wikipedia.org/wiki/GM1 GM1 (monosialotetrahexosylganglioside) the "prototype" ganglioside, is a member of the ganglio series of gangliosides which contain one sialic acid residue. GM1 has important physiological properties and impacts neuronal plasticity and repair mechanisms, and the release of neurotrophins in the brain. Besides its function in the physiology of the brain, GM1 acts as the site of binding for both Cholera toxin and E. coli heat-labile enterotoxin (Traveller's diarrhea).[1] Antibodies to GM1 are increased in Guillain-Barré syndrome, dementia and lupus but their function is not clear.[2] There is some evidence to suggest these antibodies are associated with diarrhoea in Guillain-Barré syndrome.[3] http://en.wikipedia.org/wiki/Ganglioside Ganglioside is a compound composed of a glycosphingolipid (ceramide and oligosaccharide) with one or more sialic acids (AKA n-acetylneuraminic acid) linked on the sugar chain. The 40+ known gangliosides differ mainly in the position and number of NANA residues. It is a component of the cell plasma membrane which modulates cell signal transduction events. It appears they concentrate in lipid rafts. They have recently been found to be highly important in immunology. Natural and semisynthetic gangliosides are considered possible therapeutics for neurodegenerative disorders