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Re: Dr. Lerner and Nitric Oxide Experiments

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Last semester I had a teacher who had a fair case of psoriasis, and I

worked up the courage to ask her about the condition without making

myself look like too much of a jackass. She said she has taken

medication that lessens the immune system's response ( forget the

name ) and that her skin is now much improved. Anyone else doing the

same for rosacea? Perhaps if we find enough people that have taken

any of these type medications against the immune system we'll be

closer to drawing a correlation.

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Marjorie, Adam and Group,

This makes incredible sense to me. I suffer from rosacea, but am

also a sufferer of ITP (Immune Thrombocytopenic Purpura) and

Psoriasis (on elbows and knees), all immune mediated disorders,

which tend to appear concomitantly in many individuals. I had

thought of your theory before, but never really developed such a

simple, yet detailed explanation of what seems so obvious now that

you have said it.

> " None of these sound like problems with food or

> problems with stress management -- fair-skinned people don't

> differ from others to account for these difference, for example " .

I agree to a point, but also disagree with the part that food or

stress management don't play much of a role in this condition, since

I know from 15 years of suffering ITP (I was splenectomized 5 years

ago, and am part of the 15% who did not have remision after

splenectomy) that I have had relapses during very stressful

situations (while preparing for the USMLE Step 1) and also have

exacerbations of my psoriasis despite treatement. A recent theroy

has linked ITP to H. pilory infection, maybe due to a mechanisim

similar to the one involved in rheumatic fever (The antibodies to

streptococcal antigens cross-react with host cardiac and

extracardiac antigens, leading to damage to connective tissues in

the heart, joints or other organs. Alternatively it has been

proposed that there is induction of hypersensitivity or autoimmunity

by Streptococcal products) But in the case of ITP, this antibodies

are directed aganist the Glycoproteins IIb/IIIa of immature

platelets. It is theorized that this immune response is usually

suppressed by anti-idiotype antibodies (antibodies aganist our own

antibodies produced by our own cells) but when the immune system

function declines due to stress (this has been established for a

while now) then the autoimmune condition has a surge. I don't know

how clear this is coming out, but if you do a web search on the

recent theories regarding ITP you might be enlightened even more.

About food, I believe the gastrointestinal tract acts as a secretory

organ, and an immune sensing device responsible for immunization

against incoming antigens and tolerance to frequently appearing

antigens. The permeability of the GIT determines how much antigenic

material get inside, and maybe this plays a role as to how food

triggers vary so much amongst rosacea sufferers.

> " But a genetic cause for the inflammation could account for all

> this, some aberrant gene that now codes for a substance that goes

> to the dermis of the central face and stimulates some part of the

> immune sytem " .

It could very well be an aberrant substance, but it can be as simple

as differences between people in the gene coding for GIT

permeability, hence, for some the response is not as harmless as it

is supposed to be. Or maybe a gene coding for the auto-antibody

directed specifically towards, lets say, the vascular bed of the

face (such as in the autoimmune vasculitis. I find it unlikely to

be an immune damage due to substances applied to surface of the skin

of the face mainly because the lysozymes that the skin secrete are

the main substances responsible for antigen protection and not

antibodies. Again, I am just theorizing here.

Could you get some funding to start a research project on this

hypothesis? (I'm kind of kidding, but it would be great if this

became true!)

Eliza

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Marjorie, Adam and Group,

This makes incredible sense to me. I suffer from rosacea, but am

also a sufferer of ITP (Immune Thrombocytopenic Purpura) and

Psoriasis (on elbows and knees), all immune mediated disorders,

which tend to appear concomitantly in many individuals. I had

thought of your theory before, but never really developed such a

simple, yet detailed explanation of what seems so obvious now that

you have said it.

> " None of these sound like problems with food or

> problems with stress management -- fair-skinned people don't

> differ from others to account for these difference, for example " .

I agree to a point, but also disagree with the part that food or

stress management don't play much of a role in this condition, since

I know from 15 years of suffering ITP (I was splenectomized 5 years

ago, and am part of the 15% who did not have remision after

splenectomy) that I have had relapses during very stressful

situations (while preparing for the USMLE Step 1) and also have

exacerbations of my psoriasis despite treatement. A recent theroy

has linked ITP to H. pilory infection, maybe due to a mechanisim

similar to the one involved in rheumatic fever (The antibodies to

streptococcal antigens cross-react with host cardiac and

extracardiac antigens, leading to damage to connective tissues in

the heart, joints or other organs. Alternatively it has been

proposed that there is induction of hypersensitivity or autoimmunity

by Streptococcal products) But in the case of ITP, this antibodies

are directed aganist the Glycoproteins IIb/IIIa of immature

platelets. It is theorized that this immune response is usually

suppressed by anti-idiotype antibodies (antibodies aganist our own

antibodies produced by our own cells) but when the immune system

function declines due to stress (this has been established for a

while now) then the autoimmune condition has a surge. I don't know

how clear this is coming out, but if you do a web search on the

recent theories regarding ITP you might be enlightened even more.

About food, I believe the gastrointestinal tract acts as a secretory

organ, and an immune sensing device responsible for immunization

against incoming antigens and tolerance to frequently appearing

antigens. The permeability of the GIT determines how much antigenic

material get inside, and maybe this plays a role as to how food

triggers vary so much amongst rosacea sufferers.

> " But a genetic cause for the inflammation could account for all

> this, some aberrant gene that now codes for a substance that goes

> to the dermis of the central face and stimulates some part of the

> immune sytem " .

It could very well be an aberrant substance, but it can be as simple

as differences between people in the gene coding for GIT

permeability, hence, for some the response is not as harmless as it

is supposed to be. Or maybe a gene coding for the auto-antibody

directed specifically towards, lets say, the vascular bed of the

face (such as in the autoimmune vasculitis. I find it unlikely to

be an immune damage due to substances applied to surface of the skin

of the face mainly because the lysozymes that the skin secrete are

the main substances responsible for antigen protection and not

antibodies. Again, I am just theorizing here.

Could you get some funding to start a research project on this

hypothesis? (I'm kind of kidding, but it would be great if this

became true!)

Eliza

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