Has anyone had IVIG and gotten better?

Discussion in 'Fibromyalgia Main Forum' started by ulala, Aug 30, 2008.

  1. ulala

    ulala New Member

    I've read about some getting better and relapsing after stopping the IVIG and others getting better and continuing to feel well.

    I wonder if IVIG would mask tests for enterovirus or parvoov virus after the IVIG treatment?

    Any experiences with IVIG would be appreciated! Thanks.
  2. joanierav

    joanierav Member

    and it hasnt done a thing for my cfs or fibro. i get the infusions for a condition called gammaglobulinemia once a month. before the infusions i was getting many respiratory infections, that landed me in the hospital for days. i dont get the infections anymore. but the gammaglobulin (ivig) gives me baaaddddd side effects afterwards. and the treatment takes 7 hrs. and im told i will need them for the rest of my life. ulala, i dont know if it would mask any tests, sorry cant help you there. hope this helps a little. you can ask me any questions if i didnt make myself clear, or if you want to know anything else. happy to help. joanierav
  3. acer2000

    acer2000 New Member

    My Dr. has suggested this as an option for me. I too am looking for info on it. I recently ran across a mention of Dr. Tae Park in Korea who had a poster paper at the most recent CFS conference in Fla who supposedly has good results with it. But I can't find the paper in pubmed, so I suppose its just him reporting his own results at the conference,and not a real study. Does anyone know? There have been other studies that have shown no benefit, or benefit for children only. The other thing I don't know is what markers or labs (if any) would make a Dr. choose this treatment over say antibiotics, or Valcyte, etc...
  4. joanierav

    joanierav Member

    hi again. the doctor explained to me that the ivig was not going to help the cfs fatigue, or the pain of fibro. ivig is gamma globulin, and gamma g. are antibodies, that is part of the white blood cell that fights infections. when we are low on the antibodies, we get the serious infections. ie: pneumonia, sinus infections, bronchial. when my doctor tested my sub classes, i was very very low on the antibodies., also my white blood cell was very low. so he sent me to a hemotologist and he put me right on the ivig infusions. and like i said they have helped the infections 100%. if im not on the ivig , i would be very sick with infections and living on antibiotics, which incidentally dont always kick in when your low on antibodies. thanks for listening, hope this was a little clearer. joanierav
  5. TXFMmom

    TXFMmom New Member

    I have been diagnosed with CFS and FM for over twelve years.

    I was finally diagnosed with primary immunodeficiency just six months ago and I am taking IV IG's for that. It does seem to have helped with my infections.

    I wonder how many of your physicians have tested you guys for primary immunodeficiency, or the B lymphocyte subclasses and given you stimulation tests to see if you are even capable of responding.

    If not, then you have primary immunodeficiency with the fatigue and the infections and all the other things.

    The IV IG's can be difficult to tolerate, I have hives and itching with them, we think from the preservative in them, and have to take benadryl.
  6. joanierav

    joanierav Member

    because the hemotologist told me i most likely had this from infancy. looking back over the yrs. i always got very bad flu illneses , even two or more a yr. so i kinda believe him. i had been checked for subclasses over the yrs. but nobody did anything about them. so they just labeled me cfs. when in reality it was immunodeficiency all along. i made the doctor write it out for me. it said hypogammaglobulinemia. a real mouthful. the doctor said without the ivig , if i got a really bad infection like mrsa, or ecoli etc it would kill me , cause i just dont make the antibodies to fight it. so i suffer every month with the awful side effects, because i think it is the lesser of two evils. very distressing. joanierav
  7. ulala

    ulala New Member

    Thankis for all the replies!

    joanierav- I was hoping that some had gotten better from the IVIG. I'm sorry that you have to have this for the rest of your life! Did your tests show any abnormal subclasses? I have low IgG2 and IgG3 and high IgE. And high CD(B cells). I'm not sure what this all means but I'm scheduled to have my first infusion on Wednesday. What kind of side effects do you get? Did they give you benadryl before the infusions? Can they tell what caused your hypogammaglobulinemia? So you don't know if you have CFS or not? I hope they can find what caused the hypogamma...!

    arosenb10-I posted a draft of a study about a child who benefitted from IVIG, an allergy diet and anti-oxidants. See my post on 1/24/08 to lichu. I'm going to post it in the next post because I think it ties in to the enteroviruses that are showing up in people's stomach biopsies. I think the docs have to check to see if you have any abnormal IgG Subclasses.

    meringue- did you have abnormal subclasses? What made them decide to give you the IVIG. In the article that I referenced to arosenb10 it references enterobacteria and oxidative and nitrosative stress. They were all addressed along with the IVIG to get the patient better.

    TXfmmom-do the IVIG's help with your fatigue? Did you get your first one in the hospital? They have me staying in the hospital for 23 hours for the first infusion to watch for any reactions. I'm going to be sure to take benadryl!

    [This Message was Edited on 08/31/2008]
  8. ulala

    ulala New Member

    and nitrosative stress.

    Normalization of the increased translocationof endotoxin from gram negativeenterobacteria (leaky gut) is accompanied bya remission of chronic fatigue syndromeMichael Maes1, Francis Coucke2, Jean-Claude Ategis3MCare4U Outpatient Clinics, BelgiumDepartment of Internal Medicine Jan Portaels Hospital, Vilvoorde, BelgiumLaboratory Ategis, Waver, BelgiumCorrespondence to:Michael Maes, MD., PhD.Director: M-Care4U Outpatient Clinics, Olmenlaan 9, 2610 Antwerp, BelgiumPHONE:+32-3-4809282FAX:+32-3-2889185EMAIL: crc.mh@telenet.be; www.michaelmaes.comSubmitted: November 5, 2007 Accepted: November 21, 2007Key words:chronic fatigue syndrome; intestinal mucosal dysfunction; leaky gut; leaky gut diet; oxidative stress; immunoglobins intravenously; antioxidantsNeuroendocrinol Lett 2007;28(6):101–000 PMID: XXXXXXXX NEL280607AXX © 2007

    Neuroendocrinology Letters • www.nel.eduAbstractThere is now evidence that chronic fatigue syndrome (CFS) is accompanied by anincreased translocation of endotoxins from gram-negative enterobacteria through the gut wall, as demonstrated by increased prevalences and median values forserum IgM and IgA against the endotoxins of gram-negative enterobacteria.

    This condition can also be described as increased gut permeability or leaky gut andindicates intestinal mucosal dysfunction (IMD). Here we report a case of a 13 year old girl with CFS who showed very high values for serum IgM against the LPSof some enterobacteria and signs of oxidative and nitrosative stress, activation ofthe inflammatory response system, and IgG3 subclass deficiency.

    Upon treatment with specific antioxidants and a “leaky gut diet”, which both aim to treat increased gut permeability, and immunoglobins intravenously, the increased translocation of the LPS of gram negative enterobacteria normalized and this normalization wasaccompanied by a complete remission of the CFS symptoms.1.2.3.Recently, we have shown that gram-negativeenterobacteria may play a role in the etiology ofchronic fatigue syndrome (CFS) [1]. We detected anincreased IgM and IgA response to the lipopolysac-charide (LPS) of different enterobacteria in CFS.

    These results were interpreted to indicate an in-creased gut-intestinal permeability in CFS which in turn allows an increased translocation of LPS from gram-negative enterobacteria through the gut wall. The latter, in turn, causes an immune response di-rected against the translocated LPS.

    This condition is also described as leaky gut and indicates intestinal mucosal dysfunction [1]. Accordingly, we suggested that CFS patients should be treated for leaky gut byspecific antioxidants such as glutamine, N-acetylcysteine and zinc [1].

    Here we report a case of a 13 years old girl. No-vember 10, 2006, she entered our consultation roomsitting in a wheel chair because she was unable towalk or stand due to muscle pain and weakness.The symptoms had begun in January 2005 aftera common pharyngitis. The symptoms did notUncorrected Proof
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    102Copyright © 2007 Neuroendocrinology Letters ISSN 0172–780X • www.nel.eduMichael Maes, Francis Coucke and Jean-Claude Ategisreside and she developed progressive muscle weakness, muscle hypotonia, abdominal bloating, headache, andconcentration and sleep disorders. There was a weightloss of 10 kg in a few months (from 57 kg to 47 kg). Since a Belgian University Department of internal medicinedetected a mycoplasma infection, she was treated withBiclar.

    But, at the same time the internal specialistssuspected a strong “psychogenic component” and senther to the Department of Psychiatry. Fortunately, theparents did not follow this advice and went to another University Department specialized in CFS.

    There, theyfound a number of inflammatory markers, such as:increased serum IgM and increased leukocyte elastaseactivity, increased PKR activity, and RNAse activity and lowered natural killer cell activity, which was as low as 8.4%.

    These are well-known biomarkers for CFS [2]. Inaddition, very low serum IgG3 levels (14 mg/dL) and a lactose intolerance could be detected, as well as increased serum IgM levels to the LPS of gram negative bacteria (Table 1, 04-06-2005). Consequently, the correct diag-nosis of CFS due to gut dysbiosis was made.

    She thenwas treated with Ciproxine 500 mg tid, for 10 days amonth, to be repeated during several months. However,due to further symptoms of muscle weakness, “paralysis” and a further weight loss of 4 kg she was admitted intoanother hospital for nutritional treatment by the second co-author of this study. The latter, found also a stomach paresis, another biomarker for CFS. When the nutritional parameters were more or less normalized she was send tothe Department of Neurology for further examination.

    The latter showed: normal EMG and MRI of the brain, and an aspecific type II muscle fiber atrophia (musclebiopsy of the M. quadriceps femoris). Therefore, theneurologists posited that a mild axonal type of Guilain-Barré syndrome might be present.

    Their main diagnosis, however, was “conversion hysteria”. The latter was based on the symptom “la belle indifference”, established by the senior neurologist. In their referral letter they stated that “the previous CFS specialist of course made the diagnosis of CFS”, but in no way, they could even consider CFS as a possible diagnosis.We could register the following symptoms: fatigue,muscle weakness, impossibility to walk or to stand,muscle contractions, sore throat, tender lymph nodes,abdominal complaints (bloating), malaise, nausea, verti-go, concentration difficulties and failing recent memory, sleep disorders and unrefreshing sleep, headache, andrepeated subjective experiences of infection.

    Thus, thepatient fulfilled the diagnosis of CFS according to theCenters for Disease Control and Prevention (CDC)criteria [3]. The first author of this paper, a psychiatrist, could not detect anything as “la belle indifference”.

    What we saw was a young lady who was very ill and suffered from her illness and not being able to go to school and meet with her friends.Blood analyses revealed a number of immune disor-ders, i.e. with reference to the normal limits as established for these analytes in accredited laboratories: low serum IgG3 (11 mg/dL), increased serum immune complexes(C1Q=25 µg Eq/mL), increased serum IgM (392 mg/dL), complement C3 (148 mg/dL), and antibody levels against gangliosides (GT1b-IgM), and somewhat increased mi-crosomial TPO antibodies (68 IU/mL).

    There were signs of increased oxidative and nitrosative stress (O&NS) and damage caused by O&NS to fatty acids, DNA and pro-teins, i.e. high oxydized LDL-antibodies (>1 200 µU/mL), increased excretion of 8-OH-desoxyguanosine (32.1 µg/g creatinin), and increased serum IgM levels directedagainst phosphatidyl inositol, nitro-cysteinyl, andserum bovine albumin [4].

    A number of anti-oxidantswere significantly decreased, i.e. plasma free carnitine(14.5 µmol/L), total carnitine (20.3 µmol/L), acylcarnitine (5.8 µmol/L) and coenzyme Q10 (CoQ10; 42.3 µg/L).Finally, we found also decreased levels of the T3-poly-unsaturated fatty acids, eicosapentanoiac acid (EPA) and docosahexaeenic acid (DHA), which constitute otherbiomarkers for CFS [5].

    A repeated measurement of the IgM responses directed against the LPS of gram-negative enterobacteria showed very high IgM responses (Table 1; 08-06-2005).

    These results show a very severe transloca-tionofthe LPS ofgram-negativeenterobacteria and,thus, suggest a very severe IMD, which was more pronounced than some months earlier. Our diagnosis was: chronicfatigue syndrome (as far as this label is adequate: see fur-ther) caused by IMD, damage due to O&NS, a lowered antioxidant status, and activation of the inflammatoryresponse system (IRS) with an autoimmune response.

    We started our treatment (10-11-2005) which consist-ed of: antioxidants, i.e. a mixture of L-carnitine, CoQ10, lipoic acid, and taurine; and another supplement consist-ing of substances that are known to treat gut permeability, consisting of L-glutamine, gamma oryzanol, zinc, etc.

    In addition, we started a specific “leaky gut diet” (Maes, Van Nunen and Heynssens, unpublished data; the diet canbe requested from the corresponding author). We alsostarted a treatment with intravenous immunoglobulins(IVIg), i.e. sandoglobuline 6 g/day during 1 month, and thereafter 6 g each two weeks for the following months [6].

    During the next few moths, i.e. from December 2005 to May 2006, no change in the clinical picture could bedetected. The IgM values against LPS remained very high but were already significantly lower than before startingthe treatment (Table 1; 13-01-2006 and 22-03-2006).However, August 18, 2006 the patient walked in intoour consultation room. She told us that she regainedstrength, that her concentration was much better andcould read books again, and that her sleep disorders were much better.

    She had restarted her swimming classes. She still suffered from a non-refreshing sleep and abdominal complaints. The IgM response against LPS again wasimproved (Table 1, 18-08-2006).The next consultation, December 8, 2006, learned thather clinical condition was again much better: she could study and could concentrate just as before her illness. Her sleep became refreshing and the abd0ominal complaints including bloating were better although sometimes she Uncorrected Proof
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    103Neuroendocrinology Letters Vol. 28 No. 6 2007 • Article available online: http://node.nel.eduNormalization of the increased translocation of endotoxin from gram negative enterobacteriahad diarrhea and nausea.

    During one week she hadsuffered from sore throat and tender lymph nodes.The IgM responses to LPS were considerably attenu-ated (Table 1; 15-11-2006), indicating less severe IMD. Blood analyses showed that the immune complexes and serum IgM levels and other inflammatory markers had normalized.

    Also, plasma L-carnitine and CoQ10 levels and the urinary excretion of 8-OH-desoxyguanosine had normalized, although plasma oxidized LDL antibodies were still increased.February 1, 2007 she told us that in January she had returned to school and took part in swimming and fit-ness classes.

    She ascertained that all her symptoms had disappeared and that she felt just as good as before herillness. We then stopped IVIg but continued the antioxi-dants and the leaky gut diet, although we had to motivate the patient to continue with it.July 13, 2007 she was very proud to tell us that shefinished the school year with a very good score (>80%). Table 1 (26-06-2007) shows that the IgM responses werenormalized.

    By now – November, 2007 – all CFS symp-toms are still in remission.DISCUSSIONThis patient fulfilled the diagnostic symptomaticcriteria for CFS [3], i.e. the patient had a severe chronic fatigue of longer than six months; and suffered frommore than four symptoms, i.e. substantial impairmentin short-term memory or concentration, sore throat,tender lymph nodes, muscle pain, headache of a newtype, pattern or severity, unrefreshing sleep, and post-exertional malaise lasting more than 24 hours.

    Althoughthese diagnostic criteria are now well established, manyspecialists – neurology and internal medicine in thiscase report – still miss and dismiss this diagnosis. Theyrather conclude that patients with this medical disor-der suffer – in accordance with Freud’s non-scientifictheories – from “conversion symptoms with a strongpsychogenic component”, a symptom complex whichcould not be detected by the first author, a skilled psy-chiatrist.

    It is common practice in our Benelux countries that those patients then are referred to a psychiatrist toundergo the mainstream treatment for that condition,i.e. psychodynamic therapies.

    This means that patients with severe medical disorders are being treated as hav-ing a mental illness with “a nonsense treatment” thatdoes not treat anything. Even worse, in Belgium, some doctors who treat CFS are prosecuted by the nationalhealth care insurances, e.g. by the Christian Mutualiteit (CM).

    In another Benelux country, the Netherlands,scientists and professors who work on psychoneuroim-mune disorders in CFS are called quacks by an anti-quack organization, which is officially supported by the Ministery of Health – since previous ministers or their deputies directly took part in this organization. Phrased differently, the Dutch Ministery of Health supports anti-quacks to blame academicians of being quacks because they consider CFS (and other medical illnesses such as postnatal depression) as a medical disorder.

    The above are indeed organized attempts of the political world totry to eliminate the scientific view that CFS is a medical disorder.

    The official acceptance of the latter obviously would mean that the national health care systems areobliged to financially support those patients who noware considered hypochondriacs and, therefore, may eas-ily be suspended from the national health care systems.One of the above diagnostic criteria implies that the patient has to have a severe chronic fatigue of longerthan six months while no other known medical condi-tion could explain the CFS. However, using specific bio-markers, which we described above, a specific organicdisorder may be observed, characterized by intracellular inflammation, O&NS and damage due to O&NS, andan increased translocation of the LPS of gram-negative bacteria and sometimes auto-immunity. This meansTable 1. Measurement of serum IgM against the LPS of 6 different gram negative bacteria during treatment with antioxidants, leaky gut dietand intravenous immunoglobulins.

    The treatment was started 11-10-2005.Variables06-04-200508-06-200513-01-200622-03-200618-08-200615-11-200626-06-2007Hafnia Alvei3.912. Aeruginosa0. Morganii5. Putida5.511.410. Koseri3. Pneumoniae1.816. sum20.963.64238.132.826.612.

    2The measurements are shown as standard deviations. The analyses are performed by means of an indirect ELISA method according to themethods outlined in [1]. Each serum sample was measured in duplicate and tested simultaneously with three standard solutions. Resultsare considered normal when <3.0 SD.

    The total sum gives an indication of the total “LPS translocation load”, i.e. the mounted IgM-relatedresponse to the translocated LPS from the 6 different bacteria [1].Uncorrected Proof
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    104Copyright © 2007 Neuroendocrinology Letters ISSN 0172–780X • www.nel.eduMichael Maes, Francis Coucke and Jean-Claude Ategisthat the diagnosis CFS according to the CDC criteriacannot be used when the known biomarkers describedabove are measured.

    Therefore, the diagnostic criteriashould be adapted to meet the new findings that CFShas a specific organic pathophysiology.There is now some evidence that CFS is accompanied by an activation of the IRS, including signs of poor cel-lular immunity; and by increased O&NS [review: 4,7,8].

    Also, this patient showed signs of activation of the IRS, such as: increased serum IgM; immune complexes;complement C3; microsomial TPO antibodies; anti gan-glioside GT1b IgM antibodies; leukocyte elastase activ-ity,PKR activity, and RNAse activity and lowered natural killer cell activity. She also showed signs of O&NS and a lowered antioxidant status, such as increased oxydizedLDL-antibodies; 8-OH-desoxyguanosine; and serumIgM levels directed against phosphatidyl inositol, nitro-cysteinyl, and serum bovine albumin; and decreasedplasma free L-carnitine; total carnitine; acylcarnitineand CoQ10.

    As previously discussed by us, the different immune findings in CFS, e.g. activation of the IRS, intracellular inflammation, O&NS, autoimmunity, etc. may be related to the increased translocation of LPS of gram-negativebacteria [1].

    Thus, the trigger factors of CFS, e.g. infec-tions – in this case report a mycoplasma infection –,psychological stress, and physical exhaustion may haveinduced IRS activation and O&NS [1]. Inflammationmay – through an increased production of interferon-gamma (IFN?) and interleukin-6 (IL-6) - cause a loss ofthe epithelial barrier function [9–11].

    This in turn may cause normally poorly invasive enterobacteria to exploit lipid raft-mediated transcytotic pathways to cross theintestinal epithelium, and these effects may precedecytokine-induced disruption of tight junctions [9–11].

    This increased translocation of the LPS of enterobacteria may then mount an immune response against the LPSof gram-negative enterobacteria thereby aggravatingpreexisting inflammation and O&NS in CFS or – when primary – induce inflammation and consequently CFS.

    We have discussed previously, that different triggerfactors, such as psychological stress, viral and bacte-rial infections, physical exhaustion and leaky gut, maycause induction of nuclear factor kappa beta (NF?ß),the major upstream, intracellular mechanism whichregulates inflammatory and O&NS mediators [12], suchas cyclo-oxygenase (COX-2) and inducible NO synthase (iNOS).

    Indeed, we found that the production of NF?ß, COX-2 and iNOS is significantly higher in patients withCFS than in normal controls [12,13]. The translocated LPS of the gram-negative enterobacteria may induce a) NF?ß, COX-2 and iNOS, and consequently, the IRS and O&NS; and b) TOLL-like receptors, which may activatethe PKR pathway [14]. These mechanisms could explain the occurrence of IRS activation and the increased PKR activity in this patient. It is also known that systemic LPS causes chronic central neuroinflammation.

    Thus, sys-temic LPS results in rapid brain tumor necrosis factor-a (TNFa) increases, which remain elevated for 10 months, and activate brain microglia to produce chronically el-evated pro-inflammatory factors [15]. It is well-known that a central neuroinflammation with increased pro-duction of pro-inflammatory cytokines, such as TNFa,is accompanied by the sickness behaviour complex [15].

    This mechanism could also explain the sleep disorders, cognitive disorders, anorexia and frank weight loss inthis patient. Moreover, increased gut permeability may also explain the occurrence of autoimmunity in CFS,such as against gangliosides, as found in this case report[1,17,18]. Enterobacteria may act as superantigens forT lymphocytes or may induce autoimmunity through a mechanism called molecular mimicry [19,20].

    Indeed,these enterobacteria have antigenic sites very similarto those of neuronal tissue and its lipid structures.These antigens will go into various tissues and triggerinflammation and once autoantibodies are formed theinflammation may become more chronic. Similar causal mechanisms have been presented to occur in Guillain-Barré syndrome [17], a diagnosis which was considered by the neurologist in this case report, although he didnot measure ganglioside antibodies.

    Thus, systemic LPS caused by an increased translocation not only inducesperipheral inflammation and O&NS, but may also in-duce a longstanding central neuroinflammation and anautoimmune responses directed against neurons.

    This patient also had an IgG3 subclass deficiency, acondition which is over-represented in patients with CFS (Maes et al. in preparation) and is related to recurrentinfections, environmental allergies, and autoimmuneresponses [21,22].

    Therefore, it may be hypothesizedthat the IgG3 subclass deficiency had increased the risk to develop CFS since it induces an increased propensity towards infections, IRS activation and autoimmune re-sponses.During the combined treatment with antioxidants,the “leaky gut diet”, and IVIg, the translocation of LPS from gram negative bacteria decreased and normalized which was accompanied by an attenuation of most of the IRS and O&NS variables measured by us.

    There is now some evidence that specific antioxidants, e.g. glutamine [23], N-acetyl-cysteine [24], and zinc [25,26], show asignificant efficacity in the treatment of increased gutpermeability. Since our patient showed signs of O&NSand damage due to O&NS, such as lipid peroxidation,damagetoDNA and proteins, and decreased antioxidant defences, we administered a specific antioxidant mixture based on L-carnitine, CoQ10, lipoic acid and taurine.These substances are known to: inhibit oxygen radicalformation; help protect tissues from O&NS damage;protect mitochondria from oxidative damage; improvemitochondrial function; increase energy levels in themitochondria through ß-oxidation and, thus, functionas mitochondrial nutrients; modulate immune function; and have cyto- and neuroprotective activities [27–30].It is our expertise that – in order to restore IMD – theabove antioxidants should be combined with a “leakyUncorrected Proof
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    105Neuroendocrinology Letters Vol. 28 No. 6 2007 • Article available online: http://node.nel.eduNormalization of the increased translocation of endotoxin from gram negative enterobacteriagut diet” consisting of milk allergic, gluten-free andlow-carb diet.

    The latter sometimes should be combined with an exclusion diet, based on the elimination ofdietary allergens. This is comparable with rheumatoidarthritis patients who sometimes show leaky gut andmay develop aggravation of the symptoms as a resultof allergens in their diet [31]. In this respect, we should also point toward the finding of a lactose-intolerance in our patient.

    Since our patient had also lowered IgG3 serum levels and signs of inflammatory and autoimmune reactions, we also started a treatment with IVIg. Indeed, IVIg haveusually been administered for replacement therapy ofhumoral immunodeficiencies, including commonvariable hypogammaglobulinemia and IgG subclassdeficiencies [32]. IVIg shows a significant efficacy inpreventing respiratory symptoms and in treating recur-rent bronchitis and asthma in hypogammaglobulinemic patients [32].

    Moreover, IVIg are now also widely used as immunomodulators because of their efficacy intreating inflammatory and autoimmune disorders.

    The exact mechanism of action by which IVIg are of benefit in these immune disorders is only partly understood.There is now some evidence that IVIg may attenuatecytokine-induced NF?ß production; inflammation and the production of IFN? and IL-6; may exhibit immuno-modulatory effects on T-cell activation; modulate andpromote the immune response; neutralize infectious agents; favour phagocytosis; and inhibit LPS-stimulated cytokine production [33–37].

    Secondly, IVIg containantiidiotypic antibodies against human autoantibodies, which may explain its efficacy in treating autoimmune disorders [38]. Last but not least, IVIgmay decrease bac-terial translocation beyond the mesenteric lymph nodes, i.e. IVIg protects the intestinal ecological equilibriumby decreasing bacteria overgrowth in the intestinal mi-croflora; decreases the number of translocated bacteria; and prevents bacterial translocation spread [39].

    Thus, IVIg may be useful to treat IMD because IVIg decreasebacterial translocation beyond the mesenteric lymphnodes; have anti-inflammatory effects; and attenuatethe production of pro-inflammatory cytokines that mayinduce IMD, i.e. IFN? and IL-6; neutralize microorgan-isms; favour phagocytosis; and inhibit LPS-stimulatedcytokine production.

    The above working mechanismsmay explain why our treatment with antioxidants, the“leaky gut diet” and IVIg is able to attenuate IRS activa-tion, reverse O&NS and damage due to O&NS, and may decrease LPS translocation, which all together have lead to a normalization of the IMD after some months oftreatment.

    In conclusion, in this case report, we show that thenormalization of the increased translocation of gram-negative enterobacteria – obtained with a specific diet, specific antioxidants and IVIg – is accompanied byan attenuation or normalization of IRS activation andO&NS and by a clinical remission.REFERENCESMaes M, Mihaylova I, Leunis JC.

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  9. acer2000

    acer2000 New Member

    yeah I have seen this article before... its very interesting... It follows along the lines of K. DeMeirlier's current theory from what I understand. I think RedLabs belgium does the aforementioned IGM test against intestinal bacteria as well as the LPS test. Its interesting to note however that according to the article, taking cipro and re-populating the gut didn't seem to be enough.. I wonder what the "leaky gut diet" they refer to consists of?
  10. joanierav

    joanierav Member

    hi ulala, my ivig subclasses showed igg 2 and 4 low. and iga serum also low. they are all normal now, but it took about 5 infusions for them to become normal. yes they give me benedryl, reglan, and prednisone for the side effects all iv. also tylenol by mouth. the only thing that i dont get anymore is the nausea and vomiting, i guess the reglan took care of that. now i just get the fever and severe acheyness. the stress to my body from the infusions puts my cfs into a relapse. i also have very low t cells , in the low 300's. they call that condition lymphocytopenia, and for that i must be tested every 6 mos. they watch that very closely so it doesnt go any lower. its all white cell problems. the hemotologist did say i had cfs. i was dx with cfs way before the ivig problems. when i looked it all up on the net, it did say it comes from infancy, the hypogammaglobulinemia i mean. hey i get my infusion on wed. too. we will send warm thoughts to each other. good luck dear. joanierav
  11. TXFMmom

    TXFMmom New Member

    More and more, I am beginning to see individuals who have been diagnosed with FM and CFS, as was I, discovering that they are really suffering from various forms of primary immunodeficiency, but were not diagnosed in infancy, childhood, or adolescence. They are genetic, but in some cases, individuals manage to cope with it until something overwhelms them. The problem is, that many doctors don't listen and tie the infections, rashes, etc. to the pain, etc. and DON'T TEST FOR THE CORRECT THINGS. Then, they say you are a crock.

    Everyone diagnosed with these diseases, FM and CFS, should be tested for the immunodeficiency diseases, of which there are around one hundred different ones, and they are serious disorders. Once one gets a diagnosis of that, the doctors suddenly are very sympathetic, say you are SICK, and insurance companies CANNOT GIVE YOU A PROBLEM, AS IN DISABILITY, AND SSDI CANNOT, AS WELL.

    As I said, they do come in different forms, but my primary immunodeficiency is with the B lymphocytes and one is treated with IV IG's. I have had itching, hives, headache, and a little HXing-like symptoms, but I think I am beginning to feel better, I do have to take Benadryl, and it is likely it is the preservative in the IV IG that is the problem, and my fatigue is improving.

    I encourage everyone to be tested, as the cost is low, compared to a lot of the stuff we have to be tested for, and a diagnosis can relieve a lot of your problems by getting treated, having fewer infections, a little less fatigue, and GETTING A WHOLE LOT MORE RESPECT FROM THE MEDICAL COMMUNITY AND YOU CAN STOP THE HARASSMENT FROM DISABILITY THINGS DEAD IN THEIR TRACKS.

    Anyone with a primary immunity problem has to be very cautious, get a lot of rest, cannot tolerate heat, infection, stress, and must be very, very careful and THEY CAN'T SAY IT IS MENTAL, AND IT IS RECOGNIZED AS A DISABLING PERMANENT CONDITION.

    One does not want to be ill, but it is better to know what it is, get the appropriate treatment, and be able to get financial assistance, as well.
  12. ulala

    ulala New Member

    leaky gut diet was that they used. That was also my first question. I tracked down the author of the article and e-mailed that questions. Unfortunately they never answered. Barrowinnovations has a lot of info about a leaky gut diet because she has gut dybosis. I think the bacteria that some people here (swedeboy for one) have been tested for in the stomach is enteroviruses or bacteria. The treatment may be beta interferon for that.

    jonierav-We both have two abnormal Sub class results. Interesting that your IgG is low and mine is high, I'll have to look up why that is. My IgG is 203. Normal is less than 100. Thanks for letting me know what meds they give. I don't want to take prednisone. I take a low dose of methotrexate, hopefully that will suffice.

    How long do The fever and severe acheyness last? Could you have primary immunodeficiency that TXfmmom posted about? I'm not sure which lab results show white blood cell counts. I have high CD19 which is B cells. I'm not sure if that's what TXfmmom mentioned in her post. I'll have to also check that.

    I hope that you continue to feel better and that your side effects continue to decrease. I'm getting nervous about this first infusion! Best wishes and warm hugs to you and thank you for your kind words. We'll compare notes after tomorrow. Thank you for all The info about The IVIG experience. At least I’ll know what to expect. The doctors and nurses seem to forget to tell The patients what to expect!

    TXfmmom-Thank you for your great post! I've heard about primary immunodeficiency but didn't pay much attention to it and will have to start reading about it. I did read just a little and one of The symptoms is autoimmune disease, which I have. My body has ferociously attacked my eyes which caused me to have over 25 eye surgeries..

    You mentioned that your P.I is with B lymphocytes. How did they diagnosis that? My B cells are high. I'm not sure what that means. Are your B cells high or low? I guess that P.I. can't be cured only controlled?

    Thank you for posting this. It sounds like many of us should get tested as we all have so many infections that most people just breeze through.

    Best wishes for a full recovery!
  13. joanierav

    joanierav Member

    hi ulala. the side effects start as soon as i come home. the fever last month lasted about 24 hrs maybe a little more, with the acheyness. please dont worry, we are all so different. there are a lot of people that dont suffer any side effects. pray god that you may be one of them. warm hugs to you , please keep us posted. joanierav
  14. acer2000

    acer2000 New Member

    By Dr. Tae H. Park
    CFS/ME Clinic of Seoul, South Korea
    Dr Tae Park M.D.
    Dr.Park runs his own CFS clinic in
    Seoul, Korea. Dr. Park attended the
    Invest in ME International ME/CFS
    Conference in London in May 2007
    and has subsequently supplied this
    and the following articles.


    To see the effectiveness of low dose gammaglobuline
    treatment in CFS/ME patients with strict control of diet,
    activities and sleep.

    As is commonly known the research into CFS/MEpatients is progressing rapidly, but treatments of CFS/ME patients in the clinical frontline is very limited, and most of the treatments are aimed toward the symptomatic relief of CFS/ME. Here (in South Korea), we have 10 years experience of treating CFS/ME with IVIG, strict diet control, ample hydration and activity or exercise control.

    Overall the response rate is 90% with these regimens. Those who responded had returned to work and resumed normal activities.

    Contrary to the CDC report that initial symptoms are important for the prognosis of CFS/ME, our study showed that the severity and duration of sx of CFS/ME are not major determinants of prognosis (J.Reeves CDC).

    There have been several reports about IV gammaglobuline therapy (K.S.Row, Lloyd) but the cost and adverse effect of IVIG treatments prevent CFS/ME patients to have IVIG tx.

    Further more, the results of IVIG tx are not significant enough to recommend for general use for CFS/ME patients Except Dr.Row’s report that 75-80% of children return to normal school activities and 5-6 yr follow-up also showed the significant improvements.

    Selection of patients

    Among our clinic’s 5378 patients, we selected 50 patients
    who met the 1994 Fukuda criteria in random fashion.

    Duration of illness: from 2 years to 15 years

    Ages of patients: 18 to 50

    Gender: male: 28

    Method of treatments

    Sleep control:
    Sleep before midnight and at least 7 hours sleep. If there is DIMS (difficulties in initiating and maintaining sleep), used klonopine and (or) prozac (10-20mg) at night.

    Diet control
    Organic foods: rice and vegetables
    Avoidance of certain foods: bread, canned food,
    coffee, chocolate, monosodium glutamate, aspartame
    and hot peppers, orange juice, carbonated beverages.
    A high protein diet (but avoidance of pork).

    Ample hydration
    2-3 litres of water with 2 tsp of salt.

    Strict control of exercise and activities.
    No heavy lifting (anything using upper extremities – such
    as house cleaning) is prohibited.
    Walking is allowed if patient improves.
    If the patient feels any post-exertional malaise, then
    reduce the exercise.

    IV Gammaglobuline
    One gram per week in 500cc of 0.9% normal saline
    infused over one hour.
    Avoid NSAID (non-steroidal anti-inflammatory drugs)
    medication, and avoid tests using contrast media (like
    CT-scan, or IVP)

    How to have rest
    Rest (like monks meditate),
    No loud music and no reading books.
    In acute stages, absolutely no exercise.
    If anyone does exercise they may develop
    cardiomyopathy or severe cardiac arrhythmia - even

    Results of treatment
    90% of patients who were treated with the above regimens recovered and returned to work, or returned to school. Showed KS score from 40 to 90. The fatigue impact scale improved from 120 to 20-40. Especially, we found improvements in the cognitive functions. We found improvements in concentration and comprehension, but short-term memory is the last to recover.

    Most of our CFS/ME patients showed impaired renal functions. They showed reduced GFR (glomerular filtration rate) and when compared with normal controls (Park, presented at Japan CFS/ME conference 2007). Diet control Organic foods: rice and vegetables
    Avoidance of certain foods: bread, canned food,
    coffee, chocolate, monosodium glutamate, aspartame
    and hot peppers, orange juice, carbonated beverages.
    A high protein diet (but avoidance of pork).

    Ample hydration
    2-3 litres of water with 2 tsp of salt.

    Strict control of exercise and activities.
    No heavy lifting (anything using upper extremities – such
    as house cleaning) is prohibited.
    Walking is allowed if patient improves.
    If the patient feels any post-exertional malaise, then
    reduce the exercise.

    IV Gammaglobuline

    One gram per week in 500cc of 0.9% normal saline infused over one hour.

    Avoid NSAID (non-steroidal anti-inflammatory drugs) medication, and avoid tests using contrast media (like CT-scan, or IVP)

    In CFS/ME patients, 88% of patients showed GFR below 80ml/min (compared with non-diabetic general populations: 39%), 46% of CFS/ME patients showed GFR below 60ml/min (compared with 19% of general non-diabetic population). Due to the low GFR nearly all of CFS/ME patients we need to be careful to monitor their renal function on a regular basis (every 3 months to check s-creatinine).

    Method of follow up of patients

    1. Check quality of sleep: dreams, DIMS, snoring with apnea, refreshing sleep.
    2. Check BP: each time of visit, manually checking BP and record correctly. If BP is rising from low BP, then patient’s fatigue sx is getting better. If BP is still low with hydration of 2 litres of water with 2 tsp of salts, then add florinef.
    3. Nocturia: check how frequently patients experience nocturia. If nocturia reduces, then patient’s sx of CFS/ME improves.
    5. DIMS (difficulties in initiating and maintaining sleep). If DIMS diminishes then the patient’s sx improves.
    6. Strict control of exercise and activity. No heavy lifting (anything using upper extremities such as house cleaning is prohibited). Walking is allowed if patient improves. If patient feels post-exertional malaise then reduce the amount of exercise.
    7. Check GFR in all CFS/ME patients (nearly 50% of CFS/ME patient’s GFR is close to chronic kidney disease range (near GFR of 60 ml/min).
    8. Avoid the use of NSAID and contrast media using tests such as CT or IVP.
    8. Hunger discomfort (such as sudden weakness, sweating) indicates the patient’s liver is enlarged. That means that the patient’s activity level is too high or the patient’s level of exercise is too great.
    10. Check liver and spleen at each consultation. If the liver and (or) spleen became smaller then the patient sx improves. If a patient’s liver and (or) spleen are enlarged that means patient’s activity level is too high or patient’s diet control is poor.


    To prove that CFS/ME is a major cause of chronic kidney
    disease (CKD) in the general population.

    Cross-sectional study

    Participants are 20 years of age and older
    400 CFS/ME patients
    There is a sudden increase in occurrence of non-diabetic,
    chronic kidney disease patients in the last 3-4 years.
    In one report (Class et al), 39% of the non-diabetic
    population showed GFR below 80ml/min.
    Among them 14% showed GFR below 60ml/min.

    We collected data from our 400 CFS/ME patients who
    meet the Fukuda criteria of 1994 and calculated the GFR
    using the Cockcroft-Gauld formula.
    The results which we found in our study are striking.

    Among our 400 CFS/ME patients we found 88% of the
    patients showed GFR below 80ml/in and 46% GFR below
    If we subdivided stage 3 CKD patients (GFR below
    I60ml/min) then 38.4% showed GFR between 55-60, 33.6%
    showed GFR 50-54, 29% showed GFR 45-49.

    In stage 2 CKD classification (GFR below 90) our study
    showed 84.7% of CFS/ME patient met stage 2 criteria.
    Among stage 2 patients we further subdivided patients.
    The result is as follows - GFR 60-65 is 43%, 65-70 is 45%.
    Even in stage 2 classification we found 88% of CFS/ME
    patients were close to CKD.
    What this means is that these CFS/ME patients will be
    CKD patients in the near future without any diabetes or
    A recent report showed 80% of CFS/ME patients are not
    diagnosed yet, with only 20% being diagnosed.
    If we bear these facts in mind, and if many of CFS/ME
    patients are misdiagnosed as having a psychiatric
    disease or as having HIV, then these non-diagnosed
    CFS/ME patients would contribute to a major risk factor
    of CKD in general populations.

    We suggest that every CFS/ME patient is checked for
    s-creatinine based GFR and that this is recorded.
    Furthermore, one should avoid medication like Non-
    steroidal anti-inflammatory drugs (NSAIDs) to control
    pain and most importantly to avoid many tests using
    contrast media - CT scan, intravenous pyelogram (IVP)
    especially coronary angiography, even if they have
    non-specific chest pains.

  15. acer2000

    acer2000 New Member

    I found that article on an ME site that spoke about Dr. Park's studies. I have not been able to find his work on PubMed, but perhaps I am searching wrong. I'll try to find a the link. Anyone ever spoken to this Dr.? Anyone who has been to any of the conferences?


    Edit: here is the link:


    Its from an "Invest in ME" newsletter. I am not familiar with this org. It appears to be in the UK.[This Message was Edited on 09/02/2008]
  16. consuegra

    consuegra New Member

    Dr. Park had a poster paper at the conference in January 2007 in FL. He and his wife were talking to anyone who would listen, as is to be expected. I spoke to him briefly and he emphasized quite strongly that his treatment involves dietary and lifestyle restrictions as well as pacing. According to him, it is a total package and in this way differs from previous attempts with IVIG.

    I saw him again in London in May 2008. This was a one day conference and he did not make a presentation but he was included on the summary panel. I don't remember if he made a contribution but it would be on the DVD on the conference.

    I asked him if this concept of treatment was available in the U.S. and he said no.

  17. jenbooks13

    jenbooks13 New Member

    When I was able to get 2.5 gram bottles I used them weekly after my IV vitamin/mineral and glutathione.

    Now that I can only get 5 gram bottles, I do them about every 2-3 weeks.

    I prefer the smaller amount more often.

    This is not standard practice. I don't want bigger amounts. It has its side effects for me, and I know it increases blood viscosity.

    But it is really helpful.
  18. ulala

    ulala New Member

    I just saw it and quickly skimmed it because I'm on my way out. I'll post about it later. Thanks again for posting it!!!

    Best wishes!!
  19. deliarose

    deliarose New Member

    You use what?
  20. jenbooks13

    jenbooks13 New Member

    IVIG. That's what this thread was about. I use small amounts. It helps.

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