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Everything posted by Buster

  1. The Dnase in December would indicate a potential infection in September/October. The low ASO is pretty meaningless as it is less than one dilution apart. I'll explain below: First, to compare results you need to use the same laboratory and test procedure. Generally a positive rise is defined as > than a 2 dilution rise. This means that if you measured 1:60 when convalescent and later 1:120 you would be considered to have a positive rise. The dilutions are typically: 1:60, 1:85, 1:120, 1:170, 1:240, 1:340, 1:480, 1:680, 1:960, 1:1,360, 1:1,920, and 1:2,720. Numbers that fall inbetween can be done by individual labs but aren't standardized. Numbers under 60 are outside the sensitivity of the typical measurement system (although you might want to check your particular lab). Basically, I'm saying they can't tell you very much about your ASO because it is below 60 (the first dilution). So for what you posted, the anti-DnaseB would be considered a rise indicating that there was a likely infection in late September. It is not surprising that the ASO would not rise. In terms of what your doctor will say, he/she will likely say both are "normal" despite the rise (because most doctors don't know that rise is more important than absolute value). The CDC back in 1971 set the upper limit of normal http://www.ncbi.nlm.nih.gov/pmc/articles/PMC377331/ for school-age kids of: school age, ASO = 170; ADNB of 170. Kaplan from the world health organization did a broader study in 1998 http://pediatrics.aappublications.org/cgi/content/abstract/101/1/86 and found the ULN for their sample to be 240 for ASO and 640 for AntiDNAseB. Many laboratories (including the Mayo clinic) use an ULN of 400 for ASO. Bottom line is that rise is more important than absolute value. If you don't have a prior reading you are forced to use ULN. To compare for rise, you must use the same laboratory and equipment/test. A rise must be two dilutions apart to avoid experimental error. Regards, Buster
  2. PhillyPA, Call your doctor. Shooting chest pains and shortness of breath are definitely cause for concern. Both are rare side effects attributable to augmentin. Is the shooting chest pain more gastric reflux or heartburn? He may not know what that feels like. Also, did your child have other movement disorder or subcutaneous nodules before the diagnosis of PANDAS? Regards, Buster
  3. Vickie's comment is also correct. There is asymptomatic carriage where there is only colonization, then there is low level invasion ( I.e where there is an immunologic response such as elevated ASO/AntiDNAseB) and then there is all out infection where the bacteria overwhelms the immune system. Only the first one is referred to as asymptomatic carriage because in the second case there is an immunologic response. I asked Dr Kaplan why he think there isn't an immunologic response in the first (i.e., couldn't it just be ineffective IgA clearance of the colonization). He said they don't know. They just know that antibiotics such as penicillin don't work great if the bacteria is growing slowly. So for those with colonization only and slow growth, they need a different type of antibiotic to clear that doesn't rely on rate of growth. Buster
  4. Usually carrier is a shorthand for "asymptomatic carrier". This means that someone is carrying the bacteria and can be cultured positive (colonization) but does not have immunologic signs of an infection (no classic sore throat, no rise in ASO, no rise in AntiDNAseB, etc). Dr. Kaplan (world health organization) refers to carriage as an "enigma" because it isn't exactly known what is happening in those who only get colonization and don't progress to infection. Several theories have been presented that perhaps the GABHS is "starved" by other competing flora in the throat. Others think streptolysin gets neutralized in some people due to differences in pH (or cholesterol levels), and there's lots of other items. There's actually very little study of carriage and while many doctors think it is benign, there really isn't any evidence that this is true. There is some evidence that those with chronic carriage do not progress to acute rheumatic fever, but that might just be that the strain being carried is not a rheumatic strain. Asymptomatic carriers have been harder to clear than symptomatic carriers. One strong reason is that most of the common treatments (Pennicilin and derivatives) only work when the bacteria is growing quickly -- if the bacteria is slowly growing amoxicillin, penicillin, augmentin are less effective. So asymptomatic carriage may merely be an inability of the immune system to really take out the bacteria -- sort of a chronic light colonization. Buster
  5. The fever definitely happens. Our dd9 had the fever after both IVIGs. Headache too. Advil was very effective for our daughter with Tylenol being less so. In our case, fever lasted 1 day, headache lasted 2 days, symptoms worsened for first 2 weeks post IVIG then rapid fall off. Buster
  6. That's my theory -- the antibodies think they are connecting with a true antigen when actually they're just finding host cells. Essentially, I think the BBB is the real culprit here and the critical item is getting the BBB closed. After that you can address the antigens or the antibodies. But that's just a theory -- rather than fact from some study. Regards, Buster
  7. Frankly, I'm not sure. I've heard three good explanations that warrant further investigation: there is a targeted antigen that keeps the B-cells activated there is a superantigen that has incorrectly recruited the B-cell there is inflammation that causes the BBB to open The first one is sort of saying that the T-cells/B-cells are finding a tiny bit of the real antigen (say GABHS) and generating a bunch of antibodies. The second one is saying that GABHS (and other infections) can cause the release of antibodies even though the exact signature of the bacteria wasn't present -- there are a lot of reasons this happens in the immune system. The third one is probably the most likely. There are sort of two types of immune response. Normally, T-cells/Antigen Presenting Cells (APC) come along and find something not quite right and present fragments of that to B-cells. If the key fits, the B-cell "unlocks" and releases/creates a bunch of antibodies. A second type of immune response occurs when there is a super antigen. These can activate a lot of T-cells and a lot of B-cells directly (i.e., sort of exhausting a person's immune response). Lyme seems to work this way. That is actually a theory -- in the case of 24.3.1 it targets GlcNAC which is a pretty common carbohydrate and on the GABHS exterior wall.
  8. This is really good: http://www.schoolnursenews.org/BackIssues/2003/0903/pandas0903.pdf
  9. What is the role of Th17 in GABHS inflammation

    1. Buster


      Very important paper by Wang and Cleary on GABHS colonization inducing Th17 response http://www.pnas.org/content/107/13/5937.short

  10. Hi Priscilla, I think the post you are referring to is : http://www.latitudes.org/forums/index.php?showtopic=6685 The graph is no longer active (too much time since that post) but the paramaters are still good. What I found most helpful was to have a wall calendar or daily log where you wrote down anything really odd that happened on that day. And then plotted the symptoms on a weekly basis (daily was, well, just too much data). You have to use some judgement, but it works pretty well. What you want to catch are REALLY bad times and really good times and get a sense for whether certain symptoms went into remission or were pretty constant. What we found was that the sum of symptoms was more important than looking at any one symptoms. When things were bad, it was really bad. When things were good, all symptoms (but 2) were good. Buster
  11. Sure, I'll do my best.... The antibodies are just "normal" antibodies (meaning they have the typical Y shape pattern of antibodies) and are released by B cells into the blood stream. -- let me know if you'd like an explanation of B cells. The antibodies are called "anti-neuronal" because the antibodies seem to interfere with signalling of neurons. I know they should have called this "neuron interfering antibodies" but for reasons lost to me they call them anti-neuronal. This interference is found through a technique called competitive ELISAs which means they add the antibodies and then add stuff that should bind with the neuronal cells. If the normal stuff doesn't bind like it should when the antibodies aren't there, they assume that the antibodies interfered with the binding. Okay, so are anti-neuronal or neuronal interfering antibodies bad? -- well, actually, not really. There's this part of your brain called the Blood brain barrier. The whole purpose of the BBB is to keep proteins in your blood from interfering with stuff in the brain. Stuff does cross the BBB but it's a pretty good filter. So now we call anti-neuronal antibodies "things that could interfere with neuronal signalling if they ever got across the BBB". A bit long... If the antibodies don't reach the brain they don't do anything... they just hang out in the blood stream for about 2-3 months and then disappear as the blood is cleaned by the liver. So are the antibodies damaging -- so far the evidence is no. They just sort of interfere, but don't cause permanent damage. Do we really know it's these antibodies -- well, sort of. The antibodies (such as this funny one called 24.3.1 was found in Sydenham Chorea kids in the spinal fluid). Whether this antibody is actually causing the symptom or just a byproduct is really not known. On your final question of what sends them to the brain -- that's really a great question. It's not that they go "to the brain" it's more that they are getting distributed throughout the body but have nothing to attach to. The pattern in the Y that makes up monoclonal antibodies has to find a very specific sequence. That sequence seems to be similar to lysogangliosides and similar to a portion of dopamine. Essentially, the antibodies are floating around going sort of everywhere but when they finally get across the BBB, they find some dopamine receptors in the basal ganglia and bind there. Let me know if this was too much detail or not enough (i.e., please ask again). Very best regards, Buster Sorry to veer a bit off topic here, but could you please explain exactly what antineuronal antibodies are, Buster? I know they're the bad antibodies that think they're attacking our strep when they're really just attacking out brain.. But that's about it. What makes them different? Why are they called "antineuronal"? & what sends them to the brain, of all places?
  12. Hi folks, just a comment that I've updated the research papers to include some recent papers by Wang and Cleary in 2010. http://www.latitudes.org/forums/index.php?showtopic=5144&st=0&p=36300entry36300
  13. With respect to your question... Not exactly. It is possible you are seeing a breach of BBB rather than an active infection. Just as a reminder, the antibodies thought to cause PANDAS are not the ASO or Anti-DNAseB, but rather a set of antineuronal antibodies to GABHS (e.g., see Kirvan2006 with antibody 24.3.1). Current thought is that symptoms are due to the combination of three events rise in anti-neuronal antibodies anti-neuronal antibodies hang out in serum for ~3 months breach of the blood brain barrier The breach of the BBB just seems to take inflammation -- that can come from an infection or stress. The rise in anti-neuronal antibodies seems to take about 1-2 weeks to occur -- however, the antibodies have a half-life of around 28 days. This means they hang around a while (i.e., the 3 months). So any disruption to the BBB could in theory cause symptom exacerbation. Yes. However, timing is really tricky. I would strongly urge a throat culture within 3 days of symptom exacerbation. For 53% of people, ASO will rise 1-4 weeks after symptoms of strep throat. No, in Swedo's studies (see http://www.ucdmc.ucdavis.edu/mindinstitute/events/toxicology_recorded_events.html ) for those kids who did have rising titers, their titers rose 1-2 weeks after symptom onset (i.e., correlated with a preceding strep infection). Hope my response is equally clear. Now there are a few complexities here... Nasal carriage might be enough to trigger a breach of the BBB. There are a couple of really nice papers on Th17, GABHS and breach of BBB. Probably the most impressive are Kerbir (2007) "Human Th17 lymphocytes promote blood-brain barrier disruption and central nervous system inflammation" http://www.nature.com/nm/journal/v13/n10/abs/nm1651.html. Here he showing that the BBB can be disrupted by Th17 cells in the blood. Recently (2010), Wang and Cleary publish "Induction of TGF-β1 and TGF-β1-dependent predominant Th17 differentiation by group A streptococcal infection" (see http://www.pnas.org/content/107/13/5937.short). Where they show that Th17 autoimmune and highly inflammatory response can occur with only nasal colonization in mice. Now Mice are not people, but this was a fascinating finding that might explain why colonization may be all that is necessary in PANDAS kids who already have the anti-neuronal antibodies in the serum. What I'm trying to highlight is that ASO and Anti-DNAseB rises will just tell you if strep got into the blood. However you could have symptoms if the antibodies are still in the blood and the BBB is opened due to other causes (such as Th17). I think this circulation of antibodies with breach is what makes this so darn hard to isolate -- two factors rather than just one. Buster
  14. Hi Kerry, The question tried to get after the IVIG information by looking at who had 400mg/kg, 1.5g/kg and 2g/kg and whether those had efficacy > 3 months or there had been recurrance. Only about 50% of the people answered this section of the material, so I've got about 50 children to run stats on. Given the 3:1 boy/girl ratio, the studies are all going to be underpowered for any age variance (which is why I was looking there first). If we have different trends in boys/girls on symptoms (or efficacy), then I have to split on sex for trending. Unfortunately, this means that I'm really looking at something more like 15 girls and 45 boys for this section of the study. Drawing trends on only 15 girls with other random factors will just confound -- but I'll pull what I can. Buster
  15. Here is another cut of the data from the survey. Here we're looking at the answers to the questions regarding symptoms and their presence at onset, at exacerbations pre-treatment and during exacerbations post-treatment (whatever treatment meant to folks). Not everyone answered this question so I only have data on about 55 kids. Also please remember that this should still be treated as anecdotal since this was not a formal research study with a formal control. The way to read the slide is that this is the number of respondents who said their child had these symptoms at the three time windows. What is striking on the slide is that Urinary symptoms, tantrums, vocal tic, social anxiety issues resolved for 54%, 45%, 40% and 35% of the cases (respectively) post treatment. I didn't ask intensity questions so there may be more here than is obvious in the slide, but the overall trend if very interesting. Similarly, the following symptoms seemed to linger post treatment: bedtime rituals, mood issues, obsessions, motor abnormalities, separation anxiety. These moved 13%, 17%, 20% and 22% respectively. This probably means I needed to have asked severity questions rather than whether the sympom existed. Given all the huge numbers of variables here (such as time elapsing, different treatments, different interpretations, ...) I was hesitant to post this graph, but thought it a good summary of what I've heard anecdotally on the forum. Please remember that the survey does not have a control and so the information really should be treated as more things for followup surveys/case studies to study. Buster
  16. Clinically, Dr. K has studied this group and finds that there seem to be 3 classes of anorexia sensory -- restriction due to color, texture, odor, ... obsession -- restriction due to fear of choking dysmorphia -- restriction due to body dysmorphia or fear of weight gain He sees the first 2 in younger kids and the last one in kids post puberty. Our child had the third type at age 7. Dr. Mae Sokol studied these three groups and as far aas I know her work wasn't pursued after her death. Here is one of her early papers: http://www.ncbi.nlm.nih.gov/pubmed/10933123 Buster
  17. This is actually the problem in the survey. I have the data, but even with 100 participants it would be considered underpowered for cutting for factors like age. The mean age of onset for girls (5.7 years) -- median 6 mean age of onset for boys (4.96 years) -- median 4 Many of the symptoms are not distinguishable in the younger set.
  18. CaM Kinase II was not correlated with male/female (that I could determine). Anti-neuronals also did not seem correlated with symptoms or with sex. This surprised me. I wonder if I didn't make the question tight enough to ensure symptoms could be correlated with CaM Kinase II. I think the only way to really get at this would be to run as longitudinal studies. Buster
  19. Some other results from the survey: First, please remember that this is not a controlled research study and is anecdotal -- but I sure would like a followup on this. For 35 girls and 65 boys: Only 15% of girls had elevated ASO or Anti-DNAseB over the course of the illness Whereas 54% of boys had elevated ASO or Anti-DNAseB In addition, 23% of girls did not have a rise in ASO or Anti-DNAseB despite a positive throat culture whereas 14% of boys had this situation. What I'm raising is that boys were ~4x more likely to have a rise in ASO or Anti-DNAseB Whereas girls were ~2x more likely to be labeled as "carriers" If we look over the whole of the illness, people indicate the following symptoms: There are differences between overall symptoms over entire course, symptoms at onset and symptoms pre and post interventions. In this data set, you'll see that boys have more tics/vocal and girls more restrictive eating. Buster P.S. AI: stands for "Age Inappropriate" in the graph
  20. Okay, here's a very interesting result in the data... (I might have to pull this out to its own thread) First, please remember that this is not a controlled research study and is anecdotal -- but I sure would like a followup on this. For 35 girls and 65 boys: Only 15% of girls had elevated ASO or Anti-DNAseB over the course of the illness Whereas 54% of boys had elevated ASO or Anti-DNAseB In addition, 23% of girls did not have a rise in ASO or Anti-DNAseB despite a positive throat culture whereas 14% of boys had this situation. What I'm raising is that boys were ~4x more likely to have a rise in ASO or Anti-DNAseB Whereas girls were ~2x more likely to be labeled as "carriers" I'm doing other scrubbing on data, but these ratios seem to hold true despite filtering on other criteria. Buster
  21. Has anyone else put this map next to a map of reported lyme cases? Check on the second (blue) map at this link. http://www.aldf.com/usmap.shtml It could be due to density of population or some other factor.. but it is very interesting... but I am reading "cure unknown" right now so everything looks like lyme and I am questioning everything I read or hear from the medical establishment... Map of PANDAS is correlated with population density -- almost perfectly. This could be because of a lot of reasons (like people in such populations are more likely to be on this forum :-))
  22. Bloody noses, hallucinations and shouting very loud all stood out in the OTHER responses.
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