wisdom_seeker

Update: BCBS initial determination: Denied -- with the following rationales: "We cannot approve your request for a blood product to help boost your body's defenses (IVIG). Your request tells us that you have the PANS syndrome. Medical studies have not shown that IVIG improves health for this problem. For this reason we believe that IVIG is not medically necessary for you." The same paragraph except substituting for "...PANS syndrome." "...a problem with your brain (encephalitis and encephalomyelitis)." Our goal is not "to boost the body's defenses", so their premise is wrong. Still our policy's BCBS clinical health plan guideline for IG has a set of approved indications, ending with the following blanket exclusion. Amazingly, this BCBS policy doesn't approve IVIG for any autoimmune encephalitis, not even the often-deadly NDMAR autoimmune encephalitis, discovered in 2007, for which IVIG is an absolutely standard, life-saving treatment. So I'm guessing that this is a pretty old clinical guideline, developed before antineuronal antibody tests were used in encephalitis dx. But I can't even point to a specific elevated auto-antibody level, just the downstream CAM-KII over-activation. And because that test is so new and expensive, there isn't any published data demonstrating that IVIG will reduce CAM-KII in proportion to decrease in symptoms.Does anyone know what journal article says / proves that abnormal CAM-KII activation is the result of antineuronal antibodies attaching to nerve cells? (as opposed to say a fever, NSAID use, or some other irrelevant cause)? Maybe I should ask that as a separate post?

To Philamom, I thought that if we apply under IgG subclass deficiency & chronic sinusitis as well as the autoimmune encephalitis Dx, they're more likely to just approve low-dose IVIG, which isn't immunomodulatory, unlike the HD one. I've read some posts saying that their kids got worse after LD IVIG, but improved when they finally got HD. What I've read is that HD IVIG induces the production of T-regs and helps turn off the production of the aberrant antibodies. But maybe the LD is enough for some? @Gpookie, Did your kids' PANS improve after the LD IVIG? And if they did, on what grounds did insurance just approve HD IVIG? wisdom_seeker

Yay!! I think you will see a much improved son after he finishes recovering from surgery and the residual strep. That might take 6+ weeks, since he's been ill so long. Please do send an update though -- it'll be useful to others who have a kid who's on antibiotics for a long time w/o obvious tonsillitis, and w/o success. WS PS. As I'd just said to someone else, I strongly suggest probiotics during and especially at the end of antibiotic treatment, so you don't wind up with GI inflammation from a messed up microbiome. We tend to rotate a few different types of probiotics so he'd have a broad set of the good bacteria. Someone had written here which types aren't killed by typical antibiotics, but I forget -- I think the Lactobacilli.

Also, have your son carefully checked for residual infections. Sometimes an infection is resistant to one antibiotic yet sensitive to another, maybe simpler abx. My older PANS son in 11th grade had continued having chronic sinusitis symptoms -- overwhelming fatigue, irritability, some post-nasal drip -- even after many months of abx + steroids, even after (needed) sinus and sleep apnea surgeries. Anxiety was super high also, focus down the drain, we were both discouraged. They were not obvious sinus symptoms, and likely not ones that would have been cultured with a simple throat or nose swab. I took him to a sinus specialist (not just regular ENT) who put an endoscope up his nostrils, found an area of infection, cultured it, did antibiotic sensitivity testing, and showed us that the bacterium was resistant to tons of abx even floxacins, quinolones, .... but sensitive to the old standby amoxicillin! 10 days on amoxicilin (+ saline sinus irrigations, allergy nose sprays) and he was 90+% better. ... and continued improving. I had been discouraged then as well, because we'd had him on so much, so long, and the surgeries were supposed to have taken care of the issues. Well, they were necessary but not sufficient, and a change to the simple, old-fashioned amoxicillin cured him..... Oh, per our MD's recommendations, we also stuffed him with probiotics during and after abx. For us the key is to really carefully search for any possible sources of residual infections. And for other things that could affect the immune system -- like the sleep apnea (he had never snored, but still woke 15x/hr, had almost no stage III/IV restorative sleep) After he finished HS, had an easier initial college schedule (starting at noon, not 8 am!), he was able to get enough quality sleep to finally be (almost) done with PANS. He's now got a full load in a rigorous school, is social again, and thriving. If your kid has tonsils, an infection could easily be hiding in the crypts in the back, and the zithro just suppressing it somewhat. Maybe it's partially sensitive to zithro, but not enough to cure him.

I agree with what's been posted -- our son's flares are from any infection and, I've come to realize lately, also from severe emotional stress overload. Turns out that the sympathetic nervous system and immune system are intimately linked, and -- just as infections have effects on mood, the fight-flight response can trigger an increased inflammatory response. It's not a simple effect (see this nice review) and I don't know enough yet to know which inflammations also cause a break in the blood-brain barrier, but just as @MomwithOCDson discovered, keeping the anxiety lower helps avoid the negative feedback loop. So definitely follow up on the possible infections described above, but also pay attention to whether things like allergies, GI inflammation, or extended emotional overload might contribute to triggering a flare of his Colitis symptoms -- either along with or before the PANS symptoms-- or simply making an exacerbation worse. That feedback loop between anxiety and inflammation (and thus also autoimmunity) just stinks, IMHO. We all have to stress the kid with ordinary life, and stretch the boundaries of "can't" in order to minimize the impact of each flare. For my son the worst triggers are being criticized, blamed, not believed, being pushed to go into school when he had school panic, or interrupted and told by DH that he needs to switch from something he's in the middle of (OCD worry that he'll forget). So if that's an issue for you, what's helped me is to work really hard to understand him, accept, and thus develop a healing partnership so that we can ration the stresses, try to have fun, and I can help repair the damage from painful/overwhelming events (whether caused by me, DH, or a blood draw.) @Rowingmom, thanks for having such a detailed signature. It gives me ideas for things to try, and hope for the future. That your DD no longer flares with infections is so comforting to read!!! I'll look for some of your other posts to see how/why you decided to add the gf/cf diet to the herbs, as well as to minimize EMF exposure .... plus the other things that helped you get to 90%.

Thanks to everyone. I will certainly post an update once we have a determination. @Gpookie and @Tj21 -- which specific subclass deficiencies did your kids have, and did they have low total IgG and low response to pneumococcal vaccine challenge as well as clinical symptoms? Tj21, thanks for the link to your other thread. Very helpful! I skimmed it and will read in detail tonight.... but I think I'm asking for info you didn't give there. And since you have BCBS as well, and got high dose IVIG approved, this info is especially relevant. @Gpookie, how well (if at all) do your kids' PANS symptoms respond to the high dose and the monthly low dose IVIG? My DS only has IgG3 (and partial IgA) deficiencies, with borderline normal response so does not fit CVID despite tons of sinusitis illnesses. I need to review the pneumovax rsponses to see if they really could fit, unfortunately the MD didn't order tests for all the 23 subtypes, and the pre and post weren't even the same sets (different lab), so it's a bit confusing. My update: Until this week I've been waiting for the MD who's willing to take on our case to have the blocks of time she needs time to review all of our son's records and write the letter of medical necessity. ... I just heard from her that she will start this week. Frustrating, but I know she is thorough, kind, and overworked, and that this is a thankless task for any MD. So I'm really trying to focus on the positive.

Hi folks, My son has PANS with very high Cam-KII, but no anti-strep antibodies. It's now been over 7 months now since his symptom onset, and he's no better; a brilliant HS Junior unable to attend school. We've exhausted non-IVIG medical management, so we've been recommended high-dose IVIG+prednisone. How does a doctor (or I) persuade an insurance company that this is a rational, effective treatment, when all the (few) studies are on PANDAS, which he does not have? I'd love any advice on how to file a successful application and/or appeal! And, clarification on what is my optimal role? The MDs aren't jumping up to apply to the insurance, perhaps having been refused before. How can I help the MDs write a successful letter, given that it's not easy/pleasant for MDs either. Given DS16's high Cam-KII activation levels, autoimmune encephalitis seems a completely rational Dx, though his brain MRI was essentially negative, and (a) I don't even know if the Cunningham Panel test is accepted as evidence for autoimmune encephalitis, much less if it would be sufficient for Anthem BCBS to accept the Dx, ( we don't know the specific anti-neuronal antibody that causes his Cam-KII activation, and © there's still the matter of showing that IVIG is a necessary and rational treatment, even as a 3rd line Tx. I can easily search PubMed, read the journal articles, but so far I haven't found any trials or even case series of IVIG for PANS or (nonspecific) autoimmune encephalitis. Have I missed even prospective or retrospective case series of IVIG / plasmaphresis for (nonspecific) autoimmune encephalitis. (The only studies I've found were for the potentially fatal NMDAR-encephalitis, or things like Guillain-Barre syndrome.) Still, many of you seem to have persuaded the insurance companies effectively. How? Thanks! wisdom_seeker

Hi Mike, I take it from your message that you have a sinus infection -- and maybe have had for a long time. PANDAS stinks. Sinus infections hurt, they are exhausting, and if they drag on discouraging. You want to do whatever you can to get rid of it. I get it -- I'm not an MD, but someone who used to have chronic sinus infections, and with two kids who used to have chronic sinusitis (and eventually had FESS, but they're oddballs in many ways). We go see two MDs who focus on nothing but complex sinus disease, and we've gotten much better. So what have I gleaned from my years of experience: First, don't give up on antibiotics -- make sure you've got the right one! Just because your "reliable" antibiotic isn't treating the infection this time doesn't mean that the current bacteria aren't sensitive to another one -- you just need to know which. Otherwise it would be like saying that you're giving up on foreign-language dictionaries because your German-English and Russian-English dictionaries haven't helped you translate some French text. You first need to see what language you're dealing with! So you need to figure out what is the right antibiotic -- for that you need to go to an ENT who will do an endoscopically-guided culture, where they suction up some mucus, and culture it to see what specific bacteria (and or fungi) you have, and what antibiotics those bacteria are sensitive to. In addition, a good sinus doctor should also recommend practical things to help your body rinse out the mucus that is a breeding ground for bacteria, namely guaifenesin w/ decongestant (Mucinex-D) along with a ton of liquid to help you drain, perhaps followed by a steaming shower. Second, we always do saline sinus irrigations to actively rinse out the mucus and moisturize with bacteria-unfriendly liquid -my kids and I do these irrigations a few times a day when sick, with a mild mucus-thinner (e.g. a few drops of listerine, or baby shampoo -- it sounds much worse than it is). We use Dr. Grossan's salt for irrigation, for it includes Xylitol, which is anti-viral and antibacterial. Hopefully you've also been tested for allergies, to see if those are helping you make more mucus, keep your nose more easily colonized by bad bacteria. Perhaps you've done all these, along with the right antibiotic? If so then.... Next, steroids. A few times it has helped to add a few days of steroids to the antibiotics; the key benefit is that they really help decongest and drain them, with a short-term anti-inflammatory benefit. However, if you can open up your sinuses with decongestants and mucolytics, and then use a steroid nasal spray, you may not need them. If you do need steroids, then I bet you can prevent the panic side effect: The Xanax itself might well be enough to prevent that. What does your doctor say? If you want secondary insurance, I've seen a few case reports of treating even severe steroid-induced panic attacks with SSRIs, e.g. this, so you could ask about pre-treating with a few weeks of SSRIs to be sure to prevent the panic. Lastly, FESS. I know nothing about your condition -- for all I know you've been recommended FESS for years. Also I'm not an MD; I only speak as a veteran of FESS, with two kids who've had chronic sinus infections and FESS. FESS in the right hands, for sinuses that need it, can be very effective -- but it is invasive, and the recovery is not easy, even though it is surgery on a small part of the body. How do you know if it's a good idea for you? If the right antibiotic, irrigations, decongestants, and a course of steroids have not helped and you continue to have infections, then an MRI will show if there's a structural reason why, and/or if there are thick diseased mucus membranes. The thing is that FESS doesn't just remove bacteria -- it is used to increase the size of sinus drainage openings (the osteomeatal complex) and then to scrape away diseased tissue, scar tissue or to remove thin bones that prevent drainage. ( If there is a lot of fungus, then FESS is the right thing - but that's uncommon, and would be visible on culture or MRI too.) My kids had deviated septums with a concha bullosa that prevented drainage, and my 2nd grader had had a year of pansinusitis -- infection in most of his sinuses. FESS did help a lot. Still, If you can make the mucus membranes on your sinuses healthy with the other measures, you'll be better off.

We finally have DS16's Cunningham Panel, IgeneX, and other lab results. Given the elevated CaMKII, there is definitely an autoimmune reaction, but it's not clear to me how intense, and whether any of the pathogens he tests positive to are likely to be the culprits, or if we need to look further. Cunningham panel: test = value (normal range; mean) DRD1 IgG = 500 (500-2,000; 1,056) DRD2L IgG = 4,000 (2,000-8,000; 6,000) LYSO-GM1 = 80 ( 80-320; 147) anti-Tubulin = 1,000 ( 250-1,000; 609) CaMKII = 184 ( 53-130; 95) The Ca++/Calmoudin-dependent protein kinase (CAM KII) activation seems high. But how high is it? Moleculera Lab writes that they now have a database of over 1000 patients, but their attached 2006 paper by Kirvan, Swedo, Snider, Cunningham only shows data on their first 16 PANDAS patients. DS's levels are higher than all but two of those reference kids with acute PANDAS, and almost as high as that in kids with Sydenham's chorea, but is that high enough to impress someone like Swedo or Dr. K? And more importantly, insurance companies to approve IVIG? I'm also fuzzy on how CAMKII activation would acount for the extreme anxiety, multisensory integration, choreiform movements, pessimistic thinking and other symptoms. Causative agents: MDL / IgeneX, stool pathology, etc: The good news is that there's no sign of Lyme or coinfections by ELISA or Western blot. He does have elevated antibodies to some pathogens (EBV, HHV-6, west nile virus, Mycoplasma) but PCR is negative. Does that mean those area all past infections, or simply dormant at the moment? For example, here's Epstein-Barr virus, tested in 11/2011 and 2016 Also tested now through MDL, which give unit-less index values, plus they test for virus fragments by PCR. MDL index 2011 2016 normal (neg <= 0.89, pos >=1.10) EBV EA IgM 0.52 EBV EA IgG 39 41 <100 u/mL 0.48 EBV VCA IgM 4 18 <100 0.09 EBV VCA IgG 1030 H 971 H <100 4.88 EBV EBNA IgM 0.21 EBV EBNA IgG 444 H 510 H < 100 1.83 EBV RT PCR negative OK, how to interpret this? I thought IgM disappears after a few months, not that there are low residual levels. And that IgG ought to drop with increasing years since an infection unless there are reactivations. So: Does a +15% in EBNA and quadrupling in IgM simply show uncertainty in lab results, or that there have been some reactivations since? Since EBV RT PCR is negative, does that mean we need not worry about EBV as a causative agent for his PANS, or simply that there's not been a reactivation the last month? How can there be such a difference between the two labs? I'd assumed the index is simply an absolute value / normal level, which fits the EA IgG, but not the VCA or EBNA values. Similarly, Mycoplasma pneumoniae: 2016 normal MDL index: IgM EIA 78 <770 0.38 IgG EIA 1.21 <0.90 1.43 PCR negative Does this indicate a distant infection? I read that IgM can last up to a few months, so I'm surprised to see any level of IgM. Unless it too can establish a latent intracellular infection, as theorized. Still, there are no smoking guns here. Ditto for HHV-6, West Nile Virus. The only other things that fournd were MARCONS in Dec, and 4+Mucoid Escnarchia coli and 3+ Citrobacter freundi complex in stool parastiology. Where do we go from here?

Since the antibiotics made the bad thoughts go away and made her feel normal, but symptoms returned after the azythromycin got out of her system (about 10- days after she began, for it has a very long half-life), then you know the antibiotics were the right thing, but she did not get them for long enough to really get rid of the infection, merely to suppress it for a while. My kids used to get frequent sinusitis, and the MD's rule was to stay on until all symptoms were gone + four days, and if the symptoms returned within a week, to IMMEDIATELY call and he'll put DS back on the antibiotic. My suggestion (as a non-MD) is that you ask to re-start her on Augmentin, even while you wait for the results of the mycoplasma test. The reason for doing it quickly is that the bacterial load is likely lower now, and you don't want it to have the time to rebuild to the previous level. And this may also reduce the damage to her blood-brain-barrier. Good luck. Please let us know how it goes.

Finally have repeat Ammonia results, and they are completely normal!! So this was likely a false positive due to inadequately rapid chilling / delayed processing of the blood sample. This is a reminder to myself and everyone that the more tests that are run, the more likely that at least one one will be a false positive (false abnormal) or false negative (false normal). Despite that knowledge, until I find what chronic infections are driving DS16's PANS, I want to leave no stone unturned. (But even that isn't clear .... I am about to create another post w/ questions regarding his infection tests' IgM/IgG results).

@llm, as usual, an informative, helpful response. Thanks! that gave me some structure, and focus, including a valuable item: your description of some genes relevant to DS that interact. I am glad you don't think it's an unusually large number of mutations -- I don't know enough yet. Simply on LiveWello I saw that the two categories in which he had the largest proportion of mutations were IgA and methylation. And I already know that IgA is an issue, and this had a lot more homogeneous mutations. Yes, DS is definitely a warrior/worrier, and takes a lot longer to come down than DH or my other son, so I'll definitely look at MAO-B and COMT. I'll post again once we have the results of his next ammonia test. In the meanwhile I am guessing it was a false positive, so I don't want to make changes to his diet/supplements till then, since if it was a false positive, I don't want to conclude erroneously "oh, it's better: he needs to continue with this or that supplement". And, lastly, I love the style of the Neurological Research Institute's educational handout on methylation. It is likely to be much easier to grasp and remember! I only wish that it differentiated between statements based on Yakso's theory and those elements that are well-established in medicine. So that, for things that aren't well-established, that if they seem relevant to DS's situation, that I'd try to find reputable sources to substantiate those. Related to that, so that I wouldn't unknowingly claim something, or request something, of an MD that would reduce my credibility... w/o being ready to support the item with good quality evidence. I do think Yasko does some interesting work -- but she does recommend so many supplements, and makes money off the tests and the many supplements she sells, so I want to be cautious. Still, I will look up Yasko's and the other videos you recommended, and read that handout. I do want to be able to wrap my head around methylation.

Parasites reproduce around the full moon? Can someone get me a scientific citation for that? I found references that plankton, and reef fish have a lunar-phase dependent spawning cycle, but nothing about parasites of any sort. I'm typically pretty good at finding things, so I searched within PubMed by terms such as Parasite & Moon -- got lots of things written by a Moon :-) Parasite & "Lunar cycle" Parasite reproduction cycle parasite reproduction light but got nothing. There are a half dozen websites that assert that parasites are most active, reproduce or are most susceptible around the full moon, but no references to any scientific observations in veterinary or human parasites.

DS's doctor is great -- and he was also puzzled, but not concerned, because DS's liver enzymes are all fine. Yesterday I discovered that it's relatively easy to have false positives on the Ammonia test, because the ammonia levels rise rapidly if whole blood is not immediately iced and processed w/in 15-30 minutes. So DS has another ammonia test on order, and I will confirm with the lab how they're going to process it.

Wow!! I just came across a recent post from @LLM mentioning that she is prone to high sulphur / ammonia because of a mutation in her CBS gene, part of the transsulfuration pathway. He does not have any mutations in CBS (according to 23andme, as interpreted by LiveWello). DS does have many mutations in other methylation-related genes, but I don't know which of those are relevant to ammonia production / metabolism. He is taking anti-inflammatory supplements, including turmeric and ginger, as well as a passel of meds to try to manage the symptoms, and underlying allergies (mirtazapine, trazodone, meloxicam, gabapentin, propranolol, fexofenadine) No NAC, though I've considered it as a mucolytic. I am hoping that @llm or someone else could comment whether any of these methylation genes w/ mutations DS has are also part of the same pathway. Homozygous: ACE BHMT-02, -04 COMT H62H COMT V158M MAOB MTHFD1L (rs6922269, rs 803422) MTRR A664A TCN2 Heterozygous: AGT FUT2 GAD1 (heterozygous in 9/11 SNPs reported) NOS2 NOS3 SOD3 VDR Bsm It's a lot, isn't it? Unfortunately, so far it's mostly an alphabet soup to me; I used to be reasonably smart, and (over 30 years ago) had absolutely loved intro biology, but I just can't wrap my head around the methylation pathways. In the last week I've printed out a couple of diagrams of the methylation pathways, but they don't show most of these genes. Even more importantly, I am fuzzy on what the purpose of various products of the pathways are, and what they're for, and w/o that it's hard to build a meaningful mental model. Perhaps if I could find a good Youtube video, rather than a wall of text?

llm, I don't want to hijack, but I was struck by your reference to high ammonia. Given what you know about the transsulfuration pathsways, could you please respond to the thread I started earlier today about my son's high ammonia levels? Thanks

With IVIG you get the pooled antibodies from hundreds (a thousand?) donors, right? A key benefit is that you get their resistance to invading germs. So it would make sense to me that she'd gain more antibodies against Strep from the IVIG, showing up as higher anti-Strep antibody levels.

High IgE levels come from allergies (or parasites), but if he has a congested nose, it sets him up for a bacterial infection. The first thing I'd suggest is to use a mucolytic (like Mucinex), saline sinus irrigations (neti pot or Neil Med nasal squirt bottle -- not as bad as it sounds). And/or a nasal steroid to reduce the inflammation (like Nasonex, which is now over the counter). The steroids are absorbed very very little, need a few days to show an effect, but they and the irrigations are the main medical prevention for sinus infections. (Speaking of which, I need to get my DS on the topical steroids again! With the BEG spray we've stopped, for ideally you're supposed to wait for an hour after the BEG... and then I forget) If you suspect there's already an infection, due to the PANS flare, you can do a nasal culture. Either a regular one, by any internist or ENT (with like a speculum to hold the nostril open so you don't just get surface contamination), or an endoscopic culture by an ENT, in which they numb the nose, put in a thin rigid rod with a fiberoptic light and suction tip, and then they can suction up and culture any mucus. Or a test for MarCoNS, as we've discussed in another post. My kids and I used to get that the endoscopic sinus cultures with many sinus infections, since they had chronic sinusitis, and the sinus specialist ENT we go to likes to know what he's treating and what it's sensitive to, i.e., to do culture-guided antibiotics rather than "empirical" trial-and-error. It's the gold standard culture, and it can visually show where there's an infection, and/or whether the membranes look pale and allergic. The trouble is that it's more expensive, of course. But if you have this association with a flare, and you have insurance, it's certainly worth doing with a couple of flares, and see if you find something worth treating. But, if there are high IgEs, I suspect allergies set up the congestion that leads to an infection. In the future, ideally you'd try to prevent a flare by regular use of the topical steroid nose sprays. They are the treatment of choice against nasal allergies. Really make a big difference -- it's just that people forget, and /or you have to find one that your kid doesn't mind (too much) taking. Cause the key thing is to take them.

Any MD can request a MarCONS collection kit and follow the instructions. However you need a doctor who will be careful to keep the swab from contacting the mucus membranes at the front, and pay attention to how deep to go and how much to brush the membrane. We had it done by a Lyme/PANS doctor. I have never had a general ENT or internist suggest these. It's not a term used generally, and no consensus that this is important, so 3-week nasal cultures are not standard. But it's not completely crazy. Here's more information on MarCoNS, the theory, and a few references that gave it (to me) enough plausibility, though they don't at all prove that MarCoNS are the culprits in PANS. MarCoNS is a name used by Dr. Shoemaker to describe slow-growing multi-drug-resistant COag-Negative Staph found deep in the nasal cavity, which he believes cause chronic illness. A prominent member is S. Epidermis, which is found everywhere on our skin, outer part of the nostrils, esp. armpits -- and is considered to be benign except when it colonizes an indwelling "foreign" object, such as a catheter, mesh, implant. Since everyone has S. epidermis and other such "benign" Staph, most regular MDs will likely dismiss this, and treat this as normal flora from the front of the nose or skin. And that since 20%+ of people harbor MRSA, finding multi-drug-resistant Staph is no big deal. The trouble with S.epidermis and other coag-neg staph on mucus membranes that most of these can form a biofilm, and may cause low-grade inflammation, secrete toxins, and trade resistance genes with other species of Staph (such as S. Aureus). Dr. Shoemaker is a fringe doctor, not an utter crackpot, but .... he has interesting theories and protocols, but NOT not rigorous studies, no pathology/immunology collaborators, no clinical trials. He is revered in some circles, and reviled by many. Years ago he found mold in buildings as a source of chronic illness. Now he's got a complex protocol for chronic disease that starts with eradicating mold, and includes a bunch of other steps to get at these persistent infections, methylation issues, etc. (I may have it a bit wrong; it's been a few months since I looked him up). (Note: There was a lawsuit against him, which he lost, and was forced to retire from active practice so now he has a company instead. The problem is that there have been no clinical trials of his protocols, nor even carefully done case series to substantiate his theories, e.g., that that nasal MarCONS are associated with marks of inflammation, BBB break-down (even in rats), etc.... I take his pronouncements with a mound of salt. I don't dismiss all he said. But I try to find well-done studies that back what he writes. What convinced me that MarCONS are worth treating were two studies. First, a 2010 publication showing that S. epidermis (normally considered to not produce toxins, unlike S Aureus), actually does produce a potent toxin against leukocytes, just not in as large an amount. And, second, a more damming article: A study of 30 tissue samples removed during surgery for chronic sinusitis, in which 97% had bacteria, and 23 of 30 had biofilms. 37% of different strains found were those of Coag-neg S. epidermis.(The next biggest variety was of, E. Coli with 10% of the 62 strains. Of the 62, 58 strains were cultured, and "only" 29% strains were biofilm forming strains. However, 23 of 30 of the deep nasal mucosal samples showed biofilm formation, with destruction of the epithelium, ranging from disarrayed to absent cilia. (Scanning electron microscopes were needed to identify biofilms, which is why that's not a normal test ). So, if the MarCoNS are only found on a 3-week culture, they must be slow-growing, and slow-growing staph are often ones enveloped within biofilms, hidden from the body's immune system or antibiotics, but able to release toxins to make their homes more hospitable. That is the logic. Lastly, for anyone who wants to go deeper into the effects on local immunity and activation/inflammation, and on the complexity of "what causes" chronic sinusitis, PLoS One. 2015 Aug 14;10(8):e0136068. doi: 10.1371/journal.pone.0136068. eCollection 2015. Association of Mucosal Organisms with Patterns of Inflammation in Chronic Rhinosinusitis. Chalermwatanachai T1, Zhang N2, Holtappels G2, Bachert C3. Their conclusion is that it is not any particular set of bacteria, but likely "dysbiosis", an imbalance of the normal set of bacteria that results in an overgrowth of one or a few types, [and thi density is what allows there to be enough to initiate a biofilm]. Which suggests that even a powerful spray like BEG may only be a part of the solution; that one also needs to re-establish a good broad microbiome. But how?? I don't know. Am J Rhinol Allergy. 2012 Mar-Apr;26(2):104-9. doi: 10.2500/ajra.2012.26.3718. Epub 2011 Dec 16. Biofilm formation and Toll-like receptor 2, Toll-like receptor 4, and NF-kappaB expression in sinus tissues of patients with chronic rhinosinusitis. Laryngoscope. 2013 Oct;123(10):2347-59. doi: 10.1002/lary.24066. Epub 2013 Apr 1. Use of topical nasal therapies in the management of chronic rhinosinusitis. Wei CC1, Adappa ND, Cohen NA.

Hi all, The good news is that I've finally gotten DS 16 to do blood work. The chemistry and basic IgX results are now released, but annoyingly while his MD is out, so I can't ask about the item(s) that concern me. Here are the key abnormal items so far. I'm especially puzzled about the Ammonia. Ammonia 94 (11-32 umol/L) H IgA 42 (68- 259 mg/dL) L IgG 851 (522-1703 mg/dL) IgM 53 (28- 179 mg/dL) The IgA can explain why he comes down with any and all colds, though it's not super low. However.... WTF is with the Ammonia!? I know how much Ammonia burns, so at almost 3x max normal, I am concerned. Here's where I wish I was an MD/RN. Now I read how neurotoxic it is -- could cause a lot of the behavioral symptoms we associate with PANS -- and that it should be turned into urea in the liver. He's certainly on enough meds that there can be interactions w liver, kidneys. (but BUN, creatinine are just fine). Anyone experienced this? What is the differential diagnosis? Could it be a false positive, because of a meal he ate, or his stress, or how the sample was handled? Here's the basics I've found so far: Ammonia is produced from the deamination of amino acids in the muscle and the kidneys, and by the action of bacteria in the colon and small intestine. Ammonia is neurotoxic and is detoxified in the body by conversion to urea via the urea cycle in the liver, thus maintaining a low concentration of ammonia in the circulation. It can also be incorporated into glutamate to form glutamine, an important metabolic fuel for some tissues, and a source of amino groups in purines and pyrimidines.

Agreed, and why not. Metals have to act as intercellular antenna for concentrating signals. Both DD and myself have noticed a big decrease in electrosensitivity by detoxing metals with cilantro/diatomaceous earth daily. I can actually go into a mall or coffee shop without developing palpitations now, and we are much more successful at sleeping in wireless areas (ie hotels with free wifi) than we used to be. DD used to be very electrosensitive, with significant symptoms of fatigue, headache, bone pain and ticcing. She used to hate going shopping because it always meant suffering. Now she's good to go! Are your kids still electrosensitive, @Rowingmom and @Sf_mom? A couple of questions: What EMF radiation levels do you find healthy? Assuming you tested. And, how low did your kids need to go to not have symptoms when they were electrosensitive? And, what heavy metals did you test your kids for, and what was the indication used by the MD (or non-md)? We'd done mercury a couple of years back, and his levels were low. My iphone's Magnetometer app reads 30-55 micro-Teslas right now, ~45 by our headboards. But I just haven't done the research to find out what's "typical" in an urban/suburban environment w/ and w/o wifi or what's induced by nearby cell towers. Nor what was typical a century ago, before all this. Nor even whether it is the lowest levels that are most bio-active, like with some estrogen-mimics. I do know that we are in a soup of EMF waves. We have our wifi on all the time, and bunches of phones and laptops with wifi turned on, and even wireless electrical switches. Beyond which, outside the house there are all the competing cell companies' towers, (not to mention high-voltage transmission lines -- for us maybe a mile away). But I know that power falls away w/ the cube of distance, so those may not be relevant. So not that I want to add another thing to worry about, but if it's relevant, I will. (And DH, the EE, would certainly give his $0.02, so I'd love some data.) Thanks, wisdom_seeker (still a novice)

I've also read the reference on biofilms, thanks. Most of it make sense, fits with other things I've read. And our family allergist's recommendation of sinus irrigations with a couple of drops of baby shampoo or other surfactant as a way to break up the biofilms. Wisdom_seeker PS. For full disclosure, though the biofilms article was well-done, I disagree with the Tx, the Marshall Protocol. This aside is not relevant to what you said, but more for anyone else who goes to that website. Vit D is so important to immunity, restricting it in other illnesses could be disastrous. Marshall, PhD, may be brilliant, but he's not an MD, and needs published clinical data to support his claim. Even I, a non-MD, was able to collaborate with MDs to get a pilot grant and conduct a clinical trial (in breast cancer Tx & decision-making, not PANS). In contrast, Dr. Marshall founded an institute, and is associated with a fine med school -- if he can't be persuasive enough with the science to get a pilot approved by the IRB, or to have an MD collaborator, I'm very suspicious. At a minimum he should be able to get a prospective observational, correlational study that follows folks with autoimmune illnesses and prospectively tracks symptoms and the two Vit D levels. Hopefully also find a direct way to see if the Vit D receptor is blocked, like he says. Despite his institute and med school association, Marshall hasn't done this foundational work, nor what's really needed -- a solid prospective clinical trial of the two Vit D levels and their association with symptoms on his protocol, (done in illnesses other than the sarcoidosis). Sarcoidosis includes a bad VitD metabolism feedback loop, as he describes. But he's generalizing to other illnesses).

Thanks so much LLM! I talked over with DS16 what you wrote, and why the irrigations and sprays are important, and the last few days he's been doing them religiously. With only token complaints, despite how much the BEG spray and throat spray burn. He's a good kid. And perhaps also more able to deal with stuff now that the prednisone burst reduced some of his anxiety and other symptoms. I'll definitely talk that over with Amy. Also I read that pre-treating with a Xylitol spray for a week can reduce the stinging, so we'll try that as well. Might be that the Xylitol helps by reducing the bacterial/viral load already, and so reduces the inflammation, but maybe there's another effect.

Thanks! I will talk to Amy about the C4a and C3a, and Lyme etc. I understand about the possibility of multiple hurdles co-conspiring against his health. And talk to her about the nebulizer. What are the ingredients you had compounded for it, and for what indications? DS might be OK with it, esp if it does not burn like the BEG spray, and esp. if he can watch TV or play on the computer while he uses it. Since it's a holiday, so far I've only I talked to DS16, and apparently mold and water damage had been an issue in multiple of their portable classrooms last year. Of course he's not been in classes enough this year to find out, but he was pleasantly surprised and impressed when I told him that that isn't acceptable, and that I would talk to the principal. That IF there was a musty smell in one of the classrooms, AND either he tests positive for mold or, like your daughter, has a worsening of symptoms with exposure, I will go to his principal and say that he just cannot be in those classrooms. Perhaps it should simply be enough if there's a musty smell, independent of other proof of damage to him? I think the school will understand, though I don't know what they can do, and how quickly. It's a health hazard, but it's a small charter HS, so they only have one 1th grade Chem classroom, one AP Lit classroom, for example. They have been impressive so far -- and they are spending significant money for his school psychologist, behaviorist and other IEP support; I'd be happy for them to redirect some of that to mold remediation instead. If only it were that simple. And now I'll get off the computer and investigate our basement.

Just as a f/u, last month we saw Dr. Brown in Pleasant Hill, CA, a pediatric neurologist who is also associated with the PANS clinic at Stanford. Completely different reception. She wasn't bothered that the presentation isn't classical, especially given he had responded to prednisone, and there was a positive family history (DS21 and my brother both had sudden onset OCD/anxiety, DS21 was Abx responsive, and my brother's (long ago and far away) had been associated with many strep infections. Dr. Brown agreed with the PANS Dx. Given that, her main goal was not to explain what's happening in his brain (oh well), but to get DS's PANS treated -- to get him into the Stanford multidisciplinary PANS clinic, and probably on IVIG. I'm OK with that, though concerned about how booked out they seem to be, .... and how many more tests they'd require before doing an IVIG. I'm waiting for them to review my intake questionnaire and Dr. Brown's referral, and don't yet know how far out they book. And I wonder if/how I might get most of the tests done before I see them. We have a brain MRI scheduled at Stanf for 2/9 (with sedation), and hope to lots of testing for infectious triggers done beforehand as well.