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Old 12-09-2007, 02:23 PM #11
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You know, inhalation is an interesting topic. How many of us use spray bottles and cans of products. I have limited my use quite a bit, as I overtly react now to most cleaning products sprayed out of anything....you gotta think...of course we inhale droplets!!! I just can not imagine aerosolizing pig neural tissue!!!
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Old 12-09-2007, 04:09 PM #12
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Default I bet that

we will not find out the whole 'processing' procedures at that plant until we are far more older and 'grayer'! That plant will probably close down and be demolished before an appropriate investigation is done. That's the way it is in this world. It really could be something else entirely, it depends on what CDC preliminary investigations reveal about plant safety, hygiene and where/how all the affected folks lived. Could be other 'common' factors and the plant is just a 'co-incidence'. I would be tho, whatever the results? We won't know about them until some nasty law suit about 5-10 years from now in some kind of Erin Brockovich way.
More important is clear analytic diagnosis and environmental assesments, for those affected. IF they truly have CIDP, We know their employer is NOT gonna cover IVIG treatments, no way no how, not for that number of folks! Then they are left disabled and to fend for themselves. Right now, IG is only covered adequately under medicare/medicaid disabilities with one heck of a hefty copay each infusion[that only pays for inherited conditions, not acquired]...often at a fee more than my own insurance pays for each treatment. There are lots of strange things going on in this world and the ripple effects for those families are going to be horrid. Many of us know the repercussions of the CIDP neuropathies on our lives...Essentially turned inside out and upside down? I, for one, wish I knew how to help and support them, while not financially at least information-wise.
Good thoughts to all otherwise? - j
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Old 12-09-2007, 04:59 PM #13
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Red face I have a shred of optimism...

I am hoping this horrible incident paves the way to explain autoimmune
PN for others. This is unfortunately how medicine works. Some pay a price
to point the way to knowledge that ends up helping others.
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Old 12-09-2007, 07:05 PM #14
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I get a bit confused on some of this CIDP. I assume that if you have Idiopathic Small Fiber Neuropathy, they have ruled out CIDP. I wonder how the distinction comes in as small fibers are c fibers and alpha delta (thinly myelinated fibers)....so myelinated fibers are affected in small fiber neuropathy. It must be based on lymphocytic infiltration, and if your epidermal nerve fiber biopsy does not show lymphocytic infiltration and/or you have no other inflammatory markers, it must be dubbed 'idiopathic SNF'. Is this a correct deduction?

The below quote is from

http://www.emedicine.com/neuro/topic467.htm

"The term chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) has been used to identify patients with a chronically progressive or relapsing symmetric sensorimotor disorder with cytoalbuminologic dissociation and interstitial and perivascular endoneurial infiltration by lymphocytes and macrophages. In many ways, CIDP can be considered the chronic equivalent of acute inflammatory demyelinating polyradiculoneuropathy (AIDP), the most common form of Guillain-Barré syndrome (GBS).

A number of variants of CIDP have been described that have immune or inflammatory aspects and electrophysiologic and/or pathologic evidence of demyelination in common. No consensus exists on the best approach to the nomenclature of these disorders. CIDP is a major subset of chronic acquired demyelinating polyneuropathies (CADP). In this context, CIDP is considered when patients have a symmetric proximal and distal motor predominant disorder.

CIDP variants include patients with predominantly sensory symptoms, those with a distal symmetric disorder (DADS), those with multifocal sensorimotor neuropathy or sensorimotor mononeuropathy multiplex with prominent conduction block (also known as Lewis-Sumner neuropathy), and those with CIDP with associated CNS demyelination or with other systemic disorders.

The following disorders are considered distinct from CIDP because they have specific pathophysiologic features and respond to treatments differently than do patients with CIDP: Demyelinating neuropathies associated with immunoglobulin M (IgM) paraproteins, including those with anti–myelin-associated glycoprotein (MAG) antibodies; polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes (POEMS) syndrome; and multifocal motor neuropathy."
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Old 12-09-2007, 08:13 PM #15
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Default I've read a lot fo the literature in this area--

--and my understanding as to the distinctions and nomenclature is pretty much along the lines of that emedicine.com summary.

But--and this is an important caveat, gleaned not only from looking at a lot of the small-fiber skin biopsy material (especially the early work from the Johns Hopkins researchers) but from talking this over with Drs. Latov, Chin, et. al.--inflammation is likely a component of almost any of these immune-mediated neuropathies. Without getting into heavy biochemistry, the distinction is basically between those neuropathies that, like CIDP, have more classic "cellular" (macrophage/lymphocyte) infiltration, and those, such as the ones associated with M-proteins, in which the attack is protein/antibody mediated. The processes are biochemically dissimilar--you get "key in the lcok" receptor site cross-reactivity in the latter--but the result is still inflammatory, although it may be harder for measures such as C-reactive protein to pick up the latter. One of the most common findings on skin biopsy, for those who have small-fiber neuropathy, is swelling of the axons, and that's an inflammatory antecedent.

The example of small-fiber gluten neuropathy is instructive--in those with gangliosides along their C-fibers that are structurally similar to the gliadin molecule, antibodies formed to gliadin cross-react with those gangliosides, with the resultant small-fiber axonal dysfunction. There is generally a period of swelling and excessive branching before the fibers discorporate.

Last edited by glenntaj; 12-10-2007 at 07:00 AM.
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Old 12-09-2007, 10:22 PM #16
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Default mel

Did you get the answer to your question?? Look how many years before you walked into a Dr. office before you heard have you ever been asked have
have you ever had Black Lung Diease?? People did and still do
worked in those mines,why now good money.. And in the past it was a way
to buy food...It was years befor men or women wore masks on
asseembly lines,for years they couldn't be force..They claimed they were hot.
But they supported there family's...I would imageine the same for these Mn.
workers..Oh I know this is a simple way of answering the question,you
would think things would have changed but unless some lawsuits are invoved,
it's sad because even in the health field patients and heath care workers
lives are shortened why years of not wearning gloves are washing there hands.

Aerosol spray cans,we have known about for years ,but so many still use
them..Oil rigs next to Holleywood Highschool. Oh in Mo. for years shoe factories,which are now being converted into homes for seniors..Money
and when it effects your heath in some way you do it to feed your family..
Unless we demand better health care and working conditions,thease boards
will contiue..Not to mention weathy neighborhoods who charge home owners
to burn there garabage..Why you President will tell you it's gives people
jobs until they get sick,that we figure out..I doubt if this will be printed,
just wanted to make sure your question,was answered...To all the above you are brillant ,thank you. Keep up the battle.. Sincerely Sue
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Old 12-10-2007, 12:53 PM #17
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Default Thank you for your explanation

Glenntaj:

Thanks for your info. I appreciate it.

I checked my biopsy report. No mention is made of swelling axons, only a length dependent pattern, sweat gland density being low...calf area down to 2 fibers per mm and a -3 in sweat glands....one normal hair follicle was in the sample...one Langerhans cell was located in the thigh sample stained positive with PGP.

Nothing about onion bulbs, or axonal swelling.

I have some horizontal pattern of innervation in the calf.

Nothing seems conclusive........my biopsy was done by a very respected research physician who trained and worked at Mayo....he set up the autonomic testing facility where I go, likely based on his experience at Mayo, so next to Mayo itself, I think it is pretty reliable.

I have never been there, but, I don't hear much mention of Vanderbilt's Autonomic Center, but I read it is quite good and developed from testing astronauts autonomic reaction in space. Of course, not all small fiber neuropathy results in autonomic neuropathy.

Like I said before, I think I have just reached the end of the internet, for now.

I don't think that I can scientifically substantiate a case for molecular mimicry based on B. Burgdorferi, even tho I have the specific bands for Lyme and the clinical diagnosis from EM, and a rising titer, established at that time. Lyme testing is extremely controversial. I did have one lab that tested bands that most labs do not test, (ironically the very same proteins they used for that Lymerix vaccine.) I am positive on all bands for Bb. I am negative on the tests that test IgG, positive on tests of IgM. (Women have different immune systems then men or the fetus would not survive-I have read women have more IgM response) Early antibiotic therapy aborts the immune response to Bb....and all further testing depends on that immune response. I have had negative PCR of spinal fluid, so I do not think there is any active infection. They took 20cc of spinal fluid, so that is a lot to test for Bb proteins.

If axonal degeneration is an outcome of Bb, thru molecular mimicry, it would cost the 'system' quite a bit of money for IVIG. I do not see research proceeding in the direction of proving molecular mimicry causing axonal or neuronal degeneration. The cost of IVIG would bankrupt insurers, and drive up the cost of IVIG due to shortages.

All inflammatory markers, thus far, are negative....which is why I pushed genetic, just to see. Chances of a hereditary cause are likely low, but due to disease progression and my own work on pedigree, my doc agreed.

If I could make a case, I would likely be on IVIG...but my case would be based on Lyme, and Lyme gets a bad rap. Insurers won't buy it.

This biopsy is getting pretty old now, almost 4 years old and symptoms are much worse now then when it was done.

I think confusion comes in with abreviations....CIAP=Chronic Idiopathic Axonal Polyneuropathy, versus, CIDP=Chronic Inflammatory Demyelinating Polyneuropathy....two very distinct types of PN. Even with a medical background, I have to really double check things. I think it would be worth a posting showing all these abreviations and explaining these diseases and how many different types of PN there are.

With idiopathic cases, showing no inflammation, showing disease progression, with negative finds for any of the known disease entities responsible for axonal degeneration, (except for Lyme) I do not think it unreasonable to explore heredity.
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Old 12-11-2007, 02:05 PM #18
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Default OK the 'science' begins?

Or not, call me a sceptic about these issues, but here's the latest on what all is being done about this all: http://www.medicalnewstoday.com/articles/90789.php

I'd say, watch the business news for that plant's closure due to 'financial reasons'. - j

Sand but true, it is the reality of the times we live in.
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Old 12-12-2007, 09:55 AM #19
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Default Good find

It only takes an inquiring mind and good investigative work to locate these clues. Why can't they see the picture? We can. And hey,...I'm no Einstein.

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