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Printer Friendly Page The treatment for all the autoimmune diseases is similar. These
diseases are caused by inflammation, triggered by bacteria or
viruses or chemicals. You
have to reduce inflammation. You can do that with many drugs or non
drugs (herbal, homeopathic or holistic) treatments. The cornerstone for
treatment has in the past has been steroids which are fast going out the door due to
their side effect profile. However if use steroids on alternate days and in
small doses they still can provide adequate treatment.
One should always begin treatment with diet modifications
described in the diet chapter. The next step will be to avoid
toxins. If the disease was caused by exposure to diesel fumes then
the patient should avoid them. Avoid pesticides if you are a
farmer in New Zealand spraying your field and you can smell
the toxin. A farmer in Bangladesh and Northern India is exposed to
high Arsenic exposure in the ground water. The high arsenic is
brought about by excessive pesticide usage. This will cause and trigger many autoimmune diseases.
The farmers in Vietnam are exposed to the deadly agent orange used
in the Vietnam Era wars. After denying benefits to the poor US
veterans who were suffering from agent orange associated CIDP, skin
and lung disorders the VA administration finally agreed to pay them
restitution as a service connected disability. That was a great
victory for the VA administration doctors who had been trying to
help these veterans.
The
next step in medications is supplements like vitamin B-12, Folate,
B-6 they are usually available in a sublingual tablet. If you
read our e-book you see we recommend foods as alternative to these
vitamins.
For specific therapy of autoimmune diseases please read our
E-BOOK. This will also help us and support this foundation and your
personnel health. If you can afford then please donate through one
of the buttons on the services page.
Please read the miracle treatments in the
Lahore page. CIDPUSA has published the
autoimmune diseases E-BOOK which we have named ,"The Flame
Within". The Book contains treatment of alzheimers,
CIDP, neuropathies, Pemphigus, acne, alopecia , every type of
arthritis and many more by simple antibiotics. Save your money and
purchase this book online today 24 hour delivery to your email.
Check this offer on our home page. Hundreds of
satisfied patients worldwide. Remember this is true research by
university doctors and not the research that you see in the news
supported by Big Pharma. We figured out that bugs cause autoimmune
diseases and eliminating these bugs will stop the progression of
autoimmune diseases.
Intravenous immune globulin (IVIG) has also been found to be
beneficial. in CIDP treatment. IVIG is usually given in divided doses over 4 or 5
consecutive days at a total dose of 2g/kg. Dr. Dalakas has
shown that if the total infusion can be given in two large doses it
works better for the patient. He also recommends that for all the
neurological disorders the dose of IVIg should be 2gm/kg.
Maintenance doses are often needed at monthly
intervals to maintain clinical response. Serious side effects of
IVIG treatment incude, (fatal anaphylaxis in IgA-deficient
patients seen in {In patients who have anti IgA antibodies}.
We recommend that before the infusion the total IgA level be
measured. If the level is below 58 then anti IgA ANTIBODIES NEED TO
BE MEASURED. However a case has been reported with IgA LEVEL of 58
who later developed IgA reaction. So a careful history should be
taken of all patients first starting IVIg. If the lab reports IgA
<20 IT MAY BE SAFE TO ASSUME THAT IT IS ZERO. Not Always. Check
the patients history! ( Who is your IVIg PROVIDER)? Learn to give
IVIg safely, learn the secret!
Potential nephrotoxicity (renal failure) risk from IVIg
exists, especially in patients with
pre-existing renal disease. FDA issued this advisory when lots of
patients developed nephrotoxicity. FDA also issued recalls after
Hepatitis was induced after the use of IVIg. This led to a
nationwide IVIg shortage. A nurse from a prominent IVIg company
contacted us and informed us that when she was administering IVIg
she noticed a yellowish discoloration , she said that she did not
want to infuse the product however she did. The patient spent 6 days
in the hospital with a terrible headache. Then her physical
condition was weak. The risk is there and there are simpler ways to
treat Multiple Sclerosis so please read our e-book and follow the
treatment protocols.
For those patients that are resistant to IVIg therapy one needs to check
if the dose being given is correct. If the dose has been 2g/kg then
one can consider adding steroids to the IVIg. If that does not work
then Cyclophosphamide, Rituxan, Cyclosporin can be considered.
IVIg is used as a rescue therapy or first line agent and then a
second line agent is started like cyclosporin. In time this becomes
the agent of choice for chronic maintenance.
For very simple treatment of your autoimmmune disorder which can
be done with a oral course of medication available any part of
planet earth please purchase our
E-BOOK
.
Do not forget about supplements we recommend in our
E-BOOK
.
Have any questions or need help then
please contact us.
| Neurology. 1998 Dec;51(6 Suppl 5):S16-21. |
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Treatment of chronic inflammatory
demyelinating polyneuropathy with intravenous immunoglobulin.
Hahn AF.
Department of Clinical Neurological Sciences, University of Western
Ontario, London Health Sciences Centre, Canada.
Chronic inflammatory demyelinating polyneuropathy (CIDP) is a defined
clinical entity with a chronic progressive or chronic relapsing
course, lasting months to years. It causes variable but often severe
chronic disability. CIDP is considered an autoimmune disorder caused
by both cellular and humoral immune processes. Various
immunomodulatory therapies, i.e., IVIg, therapeutic plasma exchange
(PE), and prednisone, are of proven benefit. Comparative studies
indicate that IVIg and PE confer equal short-term benefit. Efficacy of
IVIg is maintained; regularly timed pulse treatments may stabilize
relapsing CIDP. The combination of IVIg and prednisone may be
advantageous in long-term management. Despite the high cost, IVIg is
considered the preferred first treatment. The safety profile is
similar to that reported for other conditions; close monitoring during
the infusion is recommended. The precise mechanisms of IVIg action in
CIDP are not known. Anti-idiotypic neutralization of autoantibodies,
binding of complement, and blockade of macrophages may prevent the
ongoing inflammatory demyelination.
| Neurology. 2002 Dec 24;59(12 Suppl 6):S33-40. |
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Intravenous gammaglobulin (IVIg) for treatment of
CIDP and related immune-mediated neuropathies.
Brannagan TH 3rd.
Peripheral Neuropathy Center, Department of Neurology and
Neuroscience, Weill Medical College of Cornell University, New York,
NY 10021, USA.
Intravenous immune globulin (IVIg) is considered an effective and safe
treatment for autoimmune neuropathies, especially in comparison to the
alternative treatments such as corticosteroids, chemotherapy, and
plasmapheresis. Patients are frequently given a standard induction
dose of 2 g/kg, which may be followed by maintenance therapy as
needed. Mild infusion-related reactions are frequent but these can
often be controlled by slowing the infusion rate or by symptomatic
medications. Serious adverse effects are rare and can include
thromboembolic events, renal failure, anaphylaxis, or septic
meningitis. Patients with IgA deficiency are at risk for anaphylaxis.
Immobility, increased serum viscosity, and preexisting vascular
disease can increase the risk for thromboembolic events. Preexisting
renal insufficiency or the use of sucrose-containing IVIg preparations
can increase the risk for renal failure, and patients with migraine
are at risk for development of aseptic meningitis. Screening patients
for risk factors that predispose to development of adverse events may
reduce the incidence of complications.
For those with multi-focal neuropathy with conduction block the
rules for treatment are different. Those patients get worse with
steroids and do not do very well with plasma exchange, but do respond
well to IVIg.
Some patients with CIDP have a para-protein in the blood, which is
an abnormal protein produced by the bone marrow. These patients may
respond to CIDP treatments, but may also require treatment for the
excess para-protein.
To conclude, CIDP is a very variable condition. It is auto-immune and is treatable. It is exceptional for CIDP not
to respond to at least one of the available drugs. The first choice of
treatment is either prednisolone or IVIg. The diagnosis is difficult,
much less so than GBS, depending critically on the nerve conduction
studies and neuro-physiologies. Trials for immuno-suppression have
shown promise. ..........
-
| Brain. 1996 Aug;119 ( Pt 4):1067-77. |
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Intravenous immunoglobulin treatment in chronic
inflammatory demyelinating polyneuropathy. A double-blind,
placebo-controlled, cross-over study.
Hahn AF, Bolton CF, Zochodne D, Feasby TE.
University of Western Ontario, London, Canada.
Thirty patients with definite or probable chronic inflammatory
demyelinating polyradiculoneuropathy (CIDP) of chronic progressive
(16 patients) or relapsing (14 patients) course were randomly
assigned to receive intravenous immunoglobulin (IvIg) 0.4 g per kg
body weight or a placebo treatment on 5 consecutive days in a
double-blind, cross-over trial. Neurological function was
monitored by serial quantitative assessments [neurological
disability score (NDS); clinical grade (CG) and grip strength (GS)
measurements] and by electrophysiological studies before and after
each treatment period. Twenty-five patients completed both
treatment periods. A comparison of the observed changes in
clinical outcome measures revealed statistically significant
differences in favour of IvIg, with (mean +/- SD) improvements in
NDS by 24.4 +/- 5.4 points (P < 0.002) in CG by 1 +/- 0.3 points
(P < 0.001) in GS by +6.3 +/- 1.7 kg (P < 0.005), whereas scores
were unchanged or worse with placebo. A secondary two-groups
analysis of the first trial period included all 30 patients; 16
patients had been randomly assigned to IvIg and 14 to placebo
treatments. Again significant differences in favour of IvIg were
observed in all the clinical end-points: improvement in NDS was
35.6 +/- 25 points (P < 0.0001), in CG it was 1.3 +/- 1.9 points
(P < 0.002) and in GS +9.8 +/- 7.7 kg (P < 0.001), whereas all
scores worsened with placebo. Of the 30 patients, 19 (63%)
improved with IvIg treatments; nine out of 16 patients (56%) with
chronic progressive CIDP, and 10 out of 14 patients (71%) with
relapsing CIDP (differences were not statistically significant). A
placebo response was seen in five patients. Comparison of paired
electrophysiological measurements before and 4 weeks after IvIg
treatments revealed statistically significant improvements in the
summed motor conduction velocities (sigma MCV; P < -0.0001) and in
the summed compound muscle action potentials (CMAP) evoked with
proximal stimulation (sigma proximal CMAP, P < 0.03) of median,
ulnar, peroneal and tibial nerves. Eight of nine IvIg responders
with chronic progressive CIDP improved gradually to normal
function with a single 5 day course of IvIg; in five of these,
small doses of prednisone were prescribed during follow-up. In 10
IvIg responders with relapsing CIDP, improvements lasted a median
6 weeks (range 3-22 weeks) and was reproducible with open label
treatments. All 10 patients have been maintained and stabilized
with IvIg pulse therapy of 1 g per kg body weight or less, given
as a single infusion prior to the expected relapse. A beneficial
response to IvIg was found to be most likely in patients with
acute relapse or with disease of one year or less. Patients with
predominantly sensory signs did not improve.-
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