Jump to content
ACN Latitudes Forums

wisdom_seeker

Premium
  • Posts

    116
  • Joined

  • Last visited

  • Days Won

    10

Everything posted by wisdom_seeker

  1. Thank you both for the good thoughts. He made it into school, and participated for 2 hours. But it took his mentor teacher coming out to chat with him and thus get him out of the car. I hate to ask for that, but he had been curled up into a ball on the front seat, and wasn't going to get out on his own. This morning I used the Klonpin and ... then also adding 30 mg prednisone as he felt he was getting a flare. He made it into school, is exhausted, and I hope proud of himself. I'll cross my fingers that he'll make it tomorrow, first day of academic classes, and the goal is 2-4 days / week. As far as the other suggestions, I agree with all. And we are trying all that seem sensible, even if we don't have clear evidence that they're helping. We already use: NSAIDs Neurontin Mirtazapine (Remeron), a quadricyclic antidepressant Trazodone 25mg every night (a very low dose, helps with onset insomnia) antibiotics Omega3s colostrum / NK support But yesterday as I added melatonin - used when needed. Last night I gave 0.5 mg Klonopin - to try to get him to take a shower. No go. Any other suggestions? I do agree with ERP, but last year I definitely pushed too hard and he was overwhelmed. The trouble is the "manageable steps" part. There's very little between (a) sitting in the car, cringing, outside the school and ( going in with a teacher's support.... except © chatting with teacher for 5-15 min, but not going in. Which we have done sometimes when his anxiety was just too high. The school is amazing. Our CBT therapist was away last week, visiting an ill parent. What I think I need to find is someone in the SF Bay Area who would get him over his anxiety about meditation and build his skills there. He gets intrusive thoughts when his brain is not focussed on distractions, but I think it would hep him to learn to focus.
  2. There is an interesting page on the Pandas Physician Network website analyzing the results of the study, explaining the (unfortunate) protocol choices that likely led to the unexpected set of results: improvement in both the randomized arms ( abx vs. abx +IVIG), and the lower-than-expected improvement during the blinded phase, while a >50% improvement during the open IVIG phase. (parents were only offered 2nd IVIG if their child had < 30% improvement on the 1st IVIG, so there was an unintended strong incentive to minimize (under-report) a positive response during the blinded part of the study). During the open phase (non-blinded) IVIG there was no incentive to under-report, so the 50% improvement is likely the true level.
  3. Hi Wombat, I've heard mixed reviews on Dr. Harris, but generally only very positive comments about Amy Smith. She has been knowledgeable, positive, and cost-conscious -- that last one may come from having a PANS kid of her own, and seeing their life savings eaten up by medical treatments. and they work hard to do IVIG as cheaply as possible without the insane mark-up you can get in a hospital. In fact they now set up many IVIGs as in-home procedures, to minimize the cost and max the convenience. I certainly can't imagine her yelling at a patient! I've not seen anyone else but her, so I can't comment on that, but I am very picky about my kids' health care professionals, and we're keeping her as part of DS16s team. I have been able to say that he can't tolerate the taste of throat spray X, or doing Y, and she finds an alternative, which I appreciate. And when his CAMKII activation came back very high, she was unequivocal that he'll be a great candidate for IVIG, same as I'd later heard from Dr. T. I don't know why you're not getting any response to your phonecall. Mike, the nurse / admin / jack-of-all-trades may not always be available to pick up the phone, but I do get timely responses. I just don't remember if those are to phonecalls or emails. Have you tried contacting Amy through her website? I have to contact them this week as well, so I'll try to send an update with what I find.
  4. My son also tested negative on Igenex, for Lyme and all co-infections. One band on Western blot; that's it. So they don't all come out positive!
  5. Hi all, My DS16 has symptoms that are much worse in crowds, and he has definite cognitive deficits due to PANS, so he has been absolutely panicking about tomorrow's start of school. Last year he missed most of the school year, dropped down to one class and still did most on-line. Now that school is about to start, he's been out of it for so long he is catastrophizing.... Ativan and Klonopin -- not sure if they help at all: I gave him 1.0 mg Ativan today and it helped very little. Tried Klonopin yesterday and it *maybe* helped a bit. Not much though. So I'm rather worried about getting him out of the car and onto campus tomorrow. In addition to worrying about school itself, Kiddo is now also having intrusive thoughts that this stress itself will trigger a PANS flare. Which it has in the past -- possibly along with an illness -- but intense school-related stress has definitely been associated with flares last year. We just finished a prednisone burst last week, after an illness-triggered PANS flare, so I know that prednisone helps him. What do you think -- should I give a few days of 30-?? mg prednisone preventively, to forestall the release of cytokines or whatever happens when he spends a few days in fight-or-flight?
  6. We also add melatonin (0.5 - 1 mg) when DS16 has a rough time with PANS anxiety. Perhaps because we use the melatonin infrequently, he still responds well to a very small dose of melatonin, sublingual: 0.5 -- or even 0.25mg, but I would not hesitate to use 1-3 mg if my kiddo was still not sleeping after a smaller dose. Just beware that getting up the next day may be hard. But -- as you know -- sleep is what your kid needs, so he'll need to catch up FWIW, DS16 has also been on a small stable dose of trazodone ( 1/2 of a 50mg tablet) each evening, for at least 4 years. This helps him fall asleep and stay asleep. Trazodone is an old medicine, a quadricyclic antidepressant that is frequently used as a sleep aid for kids -- and it's been a life-saver for my kid with obstructive sleep apnea, who used to wake every few minutes from phase I/II sleep. Before the trazodone he felt like he never really got into good sleep. With trazodone he still had sleep apnea, but he got to deeper sleep, was less likely to wake completely from each episode of hypopnea (mostly closed off airway, but not completely stopped). And as a result he didn't feel like he spent most of the night awake. It's made a big difference in his quality of life. I bring this up because I think that the small dose of trazodone also keeps PANS from wreaking havoc on DS's sleep, so he doesn't need the melatonin as often. Find a helpful doctor, and don't hesitate to use multiple meds together if one doesn't quite do it for your son. Sleep is so important, for your kiddo and yourself as well. Tapering: The body tries to compensate for any meds that cause sleepiness, increasing the internal drive to stay awake. How do we handle that? we do melatonin for > 3 days, we then taper the dose slowly over a few more days, which prevents a night or two of rebound wakefulness.
  7. Does anyone have access to these studies? I'm posting it in the PANDAS forum because you -- like I -- are the folks with strong motivation to find and analyze all IVIG studies related to PANDAS. Hoeekstra's is presented as a negative study of IVIG for to treat Tourette's. If it's a sophisticated review, such as the Eur Child Adolescent Psych guidelines on treatment of Tourette's, they describe it a study of lack of benefit in unselected patients with a tic disorder. But it was only 30 patients, I believe almost all adults, so likely quite chronic, randomized to IVIG vs. Placebo. In contrast, I find exciting Zykov et. al.'s series of IVIG in pediatric Tourette's patients selected for elevated ganglia autoimmune markers, for whom IVIG seems to have had impressive benefit: Neurosci Behav Physiol. 2009 Sep;39(7):635-8. Neuroimmune aspects of the pathogenesis of Tourette's syndrome and experience in the use of immunoglobulins in children. Zykov VP1, Shcherbina AY, Novikova EB, Shvabrina TV. Abstract A total of 60 patients aged 6-16 years with tics and Tourette's syndrome were studied. Antibodies to caudate nucleus proteins were assayed by western blot hybridization. Ten patients with Tourette's syndrome were found to have antibodies to caudate nucleus protein. Seven patients with neuroleptic-resistant types of Tourette's syndrome received single transfusions of immunoglobulin preparations, which produced regression of vocal and motor hyperkinesias and improvement in behavior (remission for more than six months). The observation of antibodies to caudate nucleus proteins and the positive effects seen on administration of immunoglobulins to patients with Tourette's syndrome support previous data on the possibility of using immunoglobulin therapy in the treatment of tic-type hyperkinesias and provide evidence of the involvement of autoimmune mechanisms inducing damage to the dopaminergic system of the striatum. In Zykov's study, I'm delighted to see a large starting group of patients, so we have more trust in the 1/6 ratio of autoimmune. Still, I need specifics on the distribution of outcomes -- did each of the 7 remit completely, and how sustained were the benefits for each? I'd like to know which autoantibody they tested too :-). T'would be nice if they also compared the outcomes for the untreated patients, showing that the IVIG benefit was strikingly different. As far as Hoekstra's trial (below), it had only 30 patients, randomized 15 to IVIG and 15 to placebo. Not bad, but Zykov found autoimmune basis in only 1/6 of a group of 60. 1/6 would mean only ~5 autoimmune based ... easily as few as 2, perhaps up to 7, randomly assigned to treatment or placebo. No wonder there was no response on tics. But what about the OCD and global improvement? I'm puzzled by the "Then" in Hoekstra's abstract (see the purple "Then" below). My read is that even in this population, not selected by CAMKII levels or other measures of autoantibodies, IVIG had a clinicially important benefit their overall wellbeing score lasting to the end of the study, and of benefit on OCD, but with subclinical OCD the study was way underpowered for that. But that's just an abstract. I'd love to see both full studies, especially any graphs of tics, OCD, wellbeing over time. Ideally graphs of individual patients' scores, so that we could see if Hoekstra perhaps had a stand-out subpopulation of 2-3 whom it was beneficial. J Clin Psychiatry. 2004 Apr;65(4):537-42. Lack of effect of intravenous immunoglobulins on tics: a double-blind placebo-controlled study. Hoekstra PJ1, Minderaa RB, Kallenberg CG. BACKGROUND: Case studies and a placebo-controlled study previously suggested the effectiveness of immunomodulatory therapy in patients with tic or related disorders whose symptoms show a relationship with streptococcal infections. No data are available on the effectiveness of intravenous immunoglobulins (IVIG) on tic severity in unselected tic disorder patients. METHOD: Thirty patients with a DSM-IV tic disorder were randomly assigned to IVIG (1 g/kg on 2 consecutive days; mean age = 28.71 years; range, 14-53 years) or placebo (mean age = 30.73 years; range, 14-63 years). Symptoms were rated with the Yale Global Tic Severity Scale, the Yale-Brown Obsessive Compulsive Scale, and the Clinical Global Impressions scale of symptom change with regard to tic severity. These were used at baseline and on weeks 2, 4, 6, 10, and 14 posttreatment, after which blinding was broken. The study was conducted from March through August 2002. RESULTS: We observed no significant differences between both treatment groups regarding posttreatment changes in tic severity. Severity of obsessions and compulsions, which was in the subclinical range, decreased significantly in the IVIG group compared with the placebo group at week 6 (p =.02). Then, there was a 32.3% improvement in the IVIG group compared with baseline. Though this improvement was maintained over the following 8 weeks, no statistically significant differences between the IVIG and the placebo group with regard to improvements in obsessions and compulsions were detected at subsequent assessments. IVIG treatment was associated with significantly more side effects than placebo, most notably headache. CONCLUSION: Based on the present results, IVIG cannot be recommended in tic disorders.
  8. For my PANS kids, a completely different cause was chronic sinusitis. + sleep apnea. Neither snored, but neither could quite shake their sinus infections... it's like they were always smoldering, ready for a fresh cold to wake them up. It turns out that the deep sleep (stage III, IV) are needed for growth hormones as well as all sorts of memory consolidation, immune system modulation. My kids had apnea/hypopnea episodes 11-27 x / hr, some wheezing, and restless legs from low serum ferritin (<50 is enough to raise the risk of sleep apnea). Together the result was that he kept bopping between brief periods of awakeness and stage I and II sleep. Not a refreshing night's sleep. Once treated, their emotional resilience, motivation, attention, and growth all improved. Especially my 2nd one, who at 13 was nowhere near puberty, at ~2nd percentile, and waking 19x/hr. He had had 0% stage III sleep. And kept getting ill. In 8th grade he was mistaken for a 5th grader. Once he began using a CPAP his social/emotional growth blossomed, and colds no longer all became bouts of sinusitis. They say it takes months to catch up on the chronic sleep deprivation, but eventually he also entered puberty (in 10th grade), and in 10th and 11th caught up in height. He's now around the 50th or 60th percentile. I think it took being on the CPAP (now he wakes ~2/hr), and also getting antibiotics so he wasn't in a constant state of fighting a smoldering sinus infection. Your mileage may vary, but it's worth looking at things like the serum ferritin and sleep apnea as well. Especially if you're also seeing ADHD, with yawning or paradoxical hyperactivity (if your kid is small).
  9. I thought I'd post an update: I got kiddo to the dentist, who upon hearing his updated Dx, including IgA and IgG subclass deficiency, decided that he'd rather the extraction be done by an oral surgeon. Not because it's technically complex, but to reduce the risk of either infection or an immune flare: that an oral surgeon will give a mouth rinse to seriously reduce the oral bacterial load beforehand, can pack the wound with antibiotics, and add a few stitches to close the wound. And perhaps also do the extraction more quickly, with less tissue trauma, which also reduces inflammation.... He said "I'm a parent too, and this is what I'd feel better about". I love our dentist.
  10. Jan251, thanks for the reply, and the clarification about the strep mutans. I'll certainly do mouth rinses, look into the flavescent sophora root. How does it taste? And how long has your DS had braces? Mine's had a flare since pretty much when he got braces on, which I've assumed is a coincidence, but.... Well I'm trying, though I had promised I won't force him. (Not that I could, really; he's taller than I am and weighs 30# more). Anyway, knowing that he has a choice helps reduce his panic to a dull roar. Gotta go -- he's still not dressed.
  11. Have you had experiences with valium? DS's NP suggested that to manage DS's anxiety before a procedure. .... and as he's about to have dental work, I am wondering, but definitely don't want to deal with a paradoxical reaction on the way to the dentist! Klonopin and Ativan didn't do anything for kiddo though I tried hard for at least a placebo effect. I think I'd given 1-2 Klonopin, at 130#. Anxiety possibly even worse, but I'd always given it before trying to get him to go to school, so it's hard to tell what was Klonopin and what was school panic.
  12. Hi all, DS16 needs a baby canine extracted (yes, at 16!) later today. His PANS is mostly stable but he is in a mini-flare (high anxiety, pessimistic, bit paranoid, OCD). DS is already on NSAIDs, zithromax antibiotic, probiotics, anti-anxiety meds. The flare is despite that. This morning I'm worried, really worried about a further setback from the dental extraction scheduled for this afternoon. Either from bacteria having access to his blood, or just the stress of it. We're to fly across the pond in a couple of weeks, and I need him in the best shape he can be. Next week our insurance will decide our appeal for IVIG. So he's possibly/hopefully having IVIG before our flight. Should I delay the extraction (again) till after the IVIG, and/or after our travel? Or what else can I do to prevent a flare from dental work? WS PS. His PANS began a couple of weeks after he'd first gotten braces, and all adjustments cause a setback of at least a week. His permanent upper canine is sitting next to a retained baby canine, it came into the gap where his upper lateral should be. The ortho says "out with it!" and the DDS says "I can get it out easily". But they don't have a kid with PANS. PPS. Some folks on previous threads talk about strep on teeth, but he's already on zithro, and never had strep, so hopefully that's a non-issue?
  13. Hi Mom23boys, I do like the idea of having the MD ask for HD IVIG on the basis of the autoimmune condition that would contraindicate LD IVIG ... as long as it didn't make insurance deny IVIG altogether. Do you think there's much risk of that? DS16 does fit the strict criteria for the subclass deficiency, as long as one looks for the 2/4x increase in titres, or evaluate the lack of persistence of protection when tested a bit beyond the 12-month threshold. MD and Dose - If insurance approves IVIG based on a request by one MD, would they allow IVIG when treated by another MD? Say a closer one, or an in-network one? Some MDs I know are willing to take an approval for LD and just bill extra and administer the HD, but I don't know if this immunologist would be willing to, if we only get approved for LD. wisdom_seeker PS. Unfortunately we are dealing with the correct policy; (supposedly updated in 2015). I say unfortunately for it mentions not a single type of autoimmune encephalitis. Not even the NMDAR!
  14. We're in a similar situation, with the additional quirk that this 16yo doesn't show any strep antibodies at all. Aren't all adolescents already supposed to be immune to strep -- that's why PANDAS was defined to be only a childhood-onset illness, right? In contrast the Cunningham panel shows: DRD1 = 500 [mean 1,056; 500 - 2,000] DRD2L = 4000 [mean 6,000; 2,000-8,000] LYSO = 80 [ 147; 80- 320] Tubulin = 1000 [ 609; 250 -1,000] CAMKII = 184 [ 95; 53 - 130] So DS was below the mean on all tests except for borderline-high Tubulin .... and yet a Cam-KII almost in the range they see with Sydenham's Choera. My uneducated guess is that his PANS is NOT strep triggered and the Cam-KII is picking up the effect of other anti-neuronal antibodies.
  15. Bump. I wish we could pin this, for there's so much wisdom in this thread. I love Dasu's rant (I can so relate!), ibcdbwc's detailed, heart-breaking (and oh so accurate) description of what a flare is like. Missionmamma's wish that her kid would just go to school, and confusion about why he's not. (Describes our house! DS is brilliant, can crack jokes, play certain videogames, and yet most any schoolwork fills him with terror. I think you two put your finger on why.) the discussion of when/how to suspect and test for Lyme, and, last but not least, Albymom's thoughtful description of why she's gone to IVIG + rituximab + cellcept.Interestingly, my son's neurologist just requested rituximab along with IVIG for his first infusion. On recommendation from the PANS clinic, I believe. Of course, Insurance denied both. IVIG is "not medically necessary for encephalitis/PANS". Rituxan is investigational for this condition. The clinical notes the MD sent along as documentation included mention of his PANS diagnosis, as well as her diagnosis of autoimmune encephalitis, and that's what insurance is now latched onto . Dunno if we can recover from that. About the rituximab... I was surprised by the rituximab, so I started reading about it in encephalitides, and the literature I found on anti-NMDA receptor encephalitis also shows better results when rituxan is added early, with suggestions that doctors consider giving the combo as first line treatment. So even though I'm apprehensive, I'd go for it. Both in autoimmune encpehalitis and cancer treatments, I believe that aggressive treatment early has the best outcomes. Which is why I keep wondering if we should just stop waiting, pay for the Tx ourselves, and hope to get reimbursement if/when he has a great response. As far as this topic, I'll add as well. *I* want to know why (or how come) ICD-10 still has no diagnostic code for autoimmune encephaitis? MDs treating anti-NMDA R encephalitis or other encephalitides are able to order IVIG and/or PEX and rituximab, since most insurance plans don't cover those? it appears that MDs for lots of kids on this forum have gotten HD IVIG paid by insurance, even though immune deficiencies are generally only treated with LD IVIG. How do they justify that? And, my newest frustration: How come a phone call to insurance is able to trigger an appeal without the patient or MD realizing it! My MD's office insisted she was working on an appeal, yet Anthem heard a verbal request and ... upheld their previous decision. How come insurance service reps aren't required to get a positive confirmation, such as "are you requesting an appeal?" "Do you want to add any information, or include any specific questions for us to answer?" I believe what happened is that Anthem's provider line took our MD's request for peer-to-peer review, in which our MD asked that "another MD review this" and took it as a request for a 1st line appeal. So now it looks like we've blown that -- with no additional information given to the insurance, and of course, no additional rationale given by the insurance. This wouldn't be terrible if 1st appeal only looks at the plan language anyway, and only the 2nd appeal can rule on "exceptional / extenuating circumstances (like diagnoses w/o an ICD-10 code). In that case blowing the 1st appeal may not matter, but I still would have wanted to at least pose Qs like "what is it that you claim will be more effective than rituximab for his condition?". i'm tired, pissed. Did I say discouraged? Hopefully I'll feel better in the morning, but I've been having a ton of trouble falling asleep. Maybe my kid isn't the only one with intense anxiety and dark intrusive thoughts! So this was both a rant and a real set of questions. Empathy and real answers are both welcome!
  16. We also use and like propranolol. For social and general anxiety -- what I've been told is that it may reduce the negative feedback loop of high anxiety -> blood pressure / racing heart -> noticing the physical response -> more anxiety.
  17. Yes, upon further conversation with DS16, it was pretty clearly a visual processing delay of some sort. And fortunately is gone again. Interesting what you said about Lyme. He's been on Zithromax, and we're planning to go off soon and re-do the Lyme panel from IgeneX. (Not looking forward to persuading him to do another blood draw, but.... And I certainly am thinking about self-paying the IVIG. This is taking soo long. If we pay up front what are the odds that they'd reimburse afterwards, given that IVIG requires precertification? We could pay the drug for one, though I don't know how much the couple of days' hospitalization would cost on top of that. And, I worry that he'll need a few cycles, and I certainly don't want insurance to get the idea that we can continue to self-pay.
  18. Does anyone have experience with how much the Rogers or Rothman programs help prevent or cope with the neuropsychiatric symptoms from subsequent infectious flares? Do they * keep the kids from developing OCD/anxiety... as bad * give them tools to get back to previous baseline after Abx or IVIG? Do Rogers or Rothman discuss this issue explicitly? Also, what is their model of WHEN it is appropriate to do their program? My naive model is that the ERP/CBT programs are best for kids whose brains aren't under autoimmune attack any more -- kids with residual OCD/anxiety after sufficient antibiotic or IVIG treatment -- maybe severe residual symptoms, but that autoimmune markers, like the Cunningham panel, are normal. While if the brain is under autoimmune attack we need treatment first for the brain to heal from the autoimmune inflammation and encephalopathy. The reason I ask is that my son gets URIs every 4-6 weeks with an anxiety spike and symptom flare with each. Before he's recovered from one he gets another infection and new flare. Also, instead of classic OCD he gets overwhelming anxiety, reactive rages, sensory intolerances and (?) delusional symptoms. He often can't even identify what he's anxious about -- so how does one talk oneself out of it? And one neurological thing that he's anxious about DOES always happen -- which suggests to me his brain needs IVIG before we even think about Rogers. Does that make sense? But again, what have you experienced with subsequent flares? And what does Rogers / Rothman say happens after subsequent exacerbations?
  19. Is this a hallucination? How bad would it have to be to justify fast-tracking IVIG? Context: Anthem just denied IVIG though DS16 is pretty disabled (see @ bottom) and deteriorating. Each exacerbation seems to set a new worse "baseline". If this is a hallucination, perhaps it would make it easier for the MG to argue for the IVIG. (Is it possible I am hoping my kid is hallucinating??? Is that crazy? I figure you guys would understand, if nobody else!) And I'm wondering if we should just give him IVIG now, bill Anthem, and continue the appeal process. Here's the frame-by-frame delayed vision symptom: When DS16 quickly moves his eyes or head, it's like his visual system can't keep up, either it's really blurry or he sees things jerkily, frame-by-frame, with a delay, so when he's moving his eyes/head quickly, what he sees is not not what is in front of him. He says that when he stops it takes a second or two till he sees what he is facing and looking at. He already gets dizzy after nodding his head up/down, but this new 'feature' of his brain seems dangerous. The closest I've found is "frame vision" described by those VERY high on pot. So is this a hallucination, or how would you describe it? More importantly, Would MDs (and insurance!) treat it as an urgent symptom to treat? thanks, Wisdom_seeker PS. His other symptoms are Intense anxiety, with dark, aggressive intrusive thoughts, OCD, dizziness if he moves his head up/down, sensory intolerances, can't go to school, deal with water. This is despite NSAIDs, antibiotics, steroid bursts. Every 4-6 weeks he gets a new cold, and each time gets a new flare. .... and then another infection and new flare before he has time to get back to baseline. I sometimes worry this means we're running out of time and he'll be chronic... but I don't know.
  20. We had the MRI. No obvious signs of inflammation. One point bright spot of unknown significance. I'd love to do the SPECT too, because I know there are some really weird things in his brain. And we are near an Amen clinic. However a brain CT sure is a high X-ray dose, and I think the SPECT even higher. And, as importantly, I don't know that any MD, or insurance company, would find a SPECT clinically useful. Or could it show inflammation?
  21. Could you please link the evidence you use for LD IVIG being contraindicated for PANDAS? I've been wondering whether to try with LD, since that's so much easier to get approved for. And, what did you mean ".....nearly a year behind us and his levels are not rising quickly we need to do IVIG? So, did you wind up doing the HD IVIG and get better results? Was Dr. L able to get it preauthorized? For what indication? Hoping to learn from your example!! WS
  22. Thanks. What you say make sense. I was very glad they wrote that "to help boost your body defenses" phrasing, since I can counter that. So no mention of IgG subclass deficiency in the appeal. I guess the remaining question is whether to try to start IVIG faster by having his immunologist apply for IVIG w/ the IgG deficiency, while waiting for the appeal wheels to slowly grind through for the encephalitis indication. He meets all the criteria (recurring infections requiring abx, subclass deficiency, and inadequate response to polysaccharide vaccine). Gpookie's experience makes me think I should consider it -- perhaps start a separate thread to poll folks about LD IVIG for PANS. I sure wish we had a registry already!
  23. I'm not sure how to ask "what would be approved?", and get any info beyond what is listed in their IG clinical guideline document. That doesn't even list anti-NDMAR encephalitis -- so it's so out of date. But you're right; if it were a change in rationale, it wouldn't sound forthright. If I were to pursue the deficiency angle, I think I'd want to expand the argument and state what is the truth, i.e., that we're dealing with two problems. However ....The low dose and high dose seem to have opposite effects -- the low dose is immune-stimulatory, and the high dose immune-regulatory. So I'd be wary of making things worse by giving DS the immune-stimulatory dose. But... what if insurance were to approve say 500mg/kg IVIG product for the IgG deficiency, and my doctor prescribed 1.5 g/kg, would insurance pay for the administration and 1/3 of the Ig product, or nothing? I think I've read of someone on this site whose kid had had LD 2x, which didn't help, then the third time the MD prescribed HD and it did help a lot. So i hope the answer is the former.
  24. Hi all, We've just received the first insurance denial of our request for high dose (HD) IVIG for DS16's autoimmune encephalitis (PANS). Would it add to or undercut our case to simultaneously apply for IVIG based on DS's IgG3 subclass deficiency? Either as a separate application or as part of the appeal? He has low IgA and IgG3 and a long history of chronic sinusitis. I know it all depends on the wording of the denial. Here are ours, for two different diagnoses -- neither of which is a medically necessary indication in our health plan's "clinical guideline". Dx: "the PANS syndrome" I intend to argue that we do not want IVIG to "boost [the] body's defenses", but to modulate the immune system, which high-dose IVIG does, so as to stop his production of the pathogenic auto-antibodies and his elevated CamKII. And that IVIG is the only effective, standard treatment for various autoimmune encephalitides. On the other hand, IgG subclass deficiency IS an approved indication for IVIG, so that makes it tempting to also include his low IgG3 & history in the appeal. But then I worry the could (erroneously) conclude that we do want the IVIG in order to boost the body's defenses. So the way I see it is that the HD IVIG will reduce the production of auto-antibodes, starting the healing process, AND as a side benefit, the IVIG will help keep him healthy for a few months while his BBB and brain heal. But that seems too subtle a distinction. So what do you say? Stick to the reason for HD IVIG, i.e. AE / PANS, or also include the low IgG3? Thanks, WS PS. To complicate things, the clinical plan guideline for IG lists a set of approved conditions, and states that IG therapy "is considered NOT medically necessary for all other indications not listed above as medically necessary." Of course the guidelines don't mention any encephalitis, so they look like they've not been updated in years.... but still that is worriesome (as intended, I'm sure).
×
×
  • Create New...