Desensitization and coronary artery disease

January 5, 2008

Article by Scripps Clinic (available free on JAMA) :

http://jama.ama-assn.org/cgi/content/full/292/24/3017

--------

Abstract

--------

JAMA. 2004 Dec 22;292(24):3017-23. Links

Aspirin sensitivity: implications for patients with coronary artery disease.

Gollapudi RR, Teirstein PS, son DD, Simon RA.

Divison of Cardiovascular Diseases, Scripps Clinic and the Scripps Research

Institute, La

Jolla, Calif 92037, USA.

CONTEXT: Although acetylsalicylic acid (aspirin) is commonly used for patients

with

chronic cardiovascular disease, a minority of patients have a sensitivity to

acetylsalicylic

acid and other nonsteroidal anti-inflammatory drugs. OBJECTIVE: To provide a

diagnostic

strategy for evaluating and treating patients with aspirin sensitivity, with

additional

consideration for issues specific to patients with coronary artery disease

(CAD). EVIDENCE

ACQUISITION: Published articles were identified through a search of MEDLINE and

the

Cochrane databases using the dates 1966 to June 2004 and the search terms

aspirin

allergy, coronary artery disease, aspirin desensitization, and aspirin

sensitivity. References

of retrieved articles were also reviewed for pertinent studies. Articles were

included in this

review if they were controlled studies, published in the English language, and

appeared in

a peer-reviewed journal.

EVIDENCE SYNTHESIS: The prevalence of aspirin-exacerbated respiratory tract

disease is

approximately 10% and for aspirin-induced urticaria the prevalence varies from

0.07% to

0.2% of the general population. Aspirin sensitivity is most often manifested as

rhinitis and

asthma or urticaria/angioedema induced by cross-reacting nonsteroidal

anti-inflammatory

drugs that inhibit cyclooxygenase 1. The primary mechanism of sensitivity is

less often

related to drug-specific IgE antibody production leading to urticaria/angioedema

and

rarely to anaphylaxis. Most patients with acetylsalicylic acid sensitivity are

able to undergo

desensitization therapy safely and successfully except in cases of chronic

idiopathic

urticaria. However, there have not been any randomized trials that specifically

focus on the

efficacy of aspirin desensitization. Furthermore, experience with

acetylsalicylic acid

desensitization in patients with CAD is very limited. After successful

desensitization,

acetylsalicylic acid therapy must be indefinitely continued to prevent

resensitization.

CONCLUSIONS: Acetylsalicylic acid sensitivity is common and desensitization can

be

performed safely in many patients. Large-scale trials are warranted to determine

the

safety and efficacy of acetylsalicylic acid desensitization therapy in patients

with

concomitant CAD because data are currently limited to small case series.

January 5, 2008

Lori

I think the 10% number refers to the percentage of asthmatics who are also aspirin sensitive ,not the general population as a whole. At least thats the context in which I have heard it used in the past.

Marcus

January 5, 2008

This is interesting to me, but mainly because I still don't get what

they are talking about at Scripps in terms of the prevalence. I have

been bothered by this for YEARS.

What are they talking about, ten percent of the general population?

Are they JUST talking here about those who are sensitive to aspirin

in general, and not Samter's syndrome?

I honestly think they completely inflate thier numbers to get more

money for funding, and I would love to know where they get this

information. One in ten people? I think they are not talking about

Samter's here but rather just about people who have reactions to

Samter's and can't take it.

But I still think son claimed at an earlier date that it might

have been something like one percent of people in this country who

have Samters, and I still find that preposterous. How many of you

know even one other person outside of this group that has Samters?

More than two people including yourself?

Anyway the reason it made me so angry was because I was trying to get

funding and help through a listing in the rare diseases database and

he completely thwarted my efforts to do this in a very rude way,

besides which I just think the prevalence data about this is very

questionable. I think the information is on my old computer so I'd

have to find it. I just wish there were a way to know how to get

this prevalance data.

Lori

>

> Article by Scripps Clinic (available free on JAMA) :

>

> http://jama.ama-assn.org/cgi/content/full/292/24/3017

>

> --------

> Abstract

> --------

> JAMA. 2004 Dec 22;292(24):3017-23. Links

> Aspirin sensitivity: implications for patients with coronary artery

disease.

>

> Gollapudi RR, Teirstein PS, son DD, Simon RA.

> Divison of Cardiovascular Diseases, Scripps Clinic and the Scripps

Research Institute, La

> Jolla, Calif 92037, USA.

>

> CONTEXT: Although acetylsalicylic acid (aspirin) is commonly used

for patients with

> chronic cardiovascular disease, a minority of patients have a

sensitivity to acetylsalicylic

> acid and other nonsteroidal anti-inflammatory drugs. OBJECTIVE: To

provide a diagnostic

> strategy for evaluating and treating patients with aspirin

sensitivity, with additional

> consideration for issues specific to patients with coronary artery

disease (CAD). EVIDENCE

>

> ACQUISITION: Published articles were identified through a search of

MEDLINE and the

> Cochrane databases using the dates 1966 to June 2004 and the search

terms aspirin

> allergy, coronary artery disease, aspirin desensitization, and

aspirin sensitivity. References

> of retrieved articles were also reviewed for pertinent studies.

Articles were included in this

> review if they were controlled studies, published in the English

language, and appeared in

> a peer-reviewed journal.

>

> EVIDENCE SYNTHESIS: The prevalence of aspirin-exacerbated

respiratory tract disease is

> approximately 10% and for aspirin-induced urticaria the prevalence

varies from 0.07% to

> 0.2% of the general population. Aspirin sensitivity is most often

manifested as rhinitis and

> asthma or urticaria/angioedema induced by cross-reacting

nonsteroidal anti-inflammatory

> drugs that inhibit cyclooxygenase 1. The primary mechanism of

sensitivity is less often

> related to drug-specific IgE antibody production leading to

urticaria/angioedema and

> rarely to anaphylaxis. Most patients with acetylsalicylic acid

sensitivity are able to undergo

> desensitization therapy safely and successfully except in cases of

chronic idiopathic

> urticaria. However, there have not been any randomized trials that

specifically focus on the

> efficacy of aspirin desensitization. Furthermore, experience with

acetylsalicylic acid

> desensitization in patients with CAD is very limited. After

successful desensitization,

> acetylsalicylic acid therapy must be indefinitely continued to

prevent resensitization.

>

> CONCLUSIONS: Acetylsalicylic acid sensitivity is common and

desensitization can be

> performed safely in many patients. Large-scale trials are warranted

to determine the

> safety and efficacy of acetylsalicylic acid desensitization therapy

in patients with

> concomitant CAD because data are currently limited to small case

series.

>

January 6, 2008

Well last night I took another daily dosage of 100mg and has no reaction at all except my finger joints being a little sore. It's fairly obvious that it's best taking with food, later today I will up to 150mg. Also read recently we should not eat many bananas and oranges due to mucus accumulation, can anyone comment on this? Re: Re: Desensitization and coronary artery

disease

Lori

I think the 10% number refers to the percentage of asthmatics who are also aspirin sensitive ,not the general population as a whole. At least thats the context in which I have heard it used in the past.

Marcus

Sent from - a smarter inbox.

January 6, 2008

I agree and had the same thought about funding - 10% of the general population

would be

an aberrantly high figure, and anywhere between 0,01%-0,05% and 2%-3% would be

an

order of magnitude much closer to our empirical observations.

Anyway, it's hard to bring up a good estimation, because AERDs are of genetic

origin, but

not everyone has the same gene(s) and not everyone expresses the gene(s)

involved. Also,

the expression requires " triggers " (viruses, pollutants, others). Above that,

not all genes

and triggers have the same effects, not everyone has the same medical history,

etc.

So, many people who could develop the disease under the wrong set of conditions

actually

do not, because these wrong conditions are precisely not fulfilled - which is

great for our

kin, who share part of our genes.

The pool of potential (genetically predisposed) AERD patients may therefore be

quite

" large " compared to the number of known patients today. Furthermore, one can

conjecture

that increasing globalization and pollution will create more opportunities for

" triggers " and

consequently bring about a higher prevalence of AERDs.

Also, under-diagnosis is common. One ENT said I was the first case he saw in his

entire

40-year career (thousands of patients?), but that was because he rarely referred

chronic

sinusitis patients to the scan, and never asked anyone if they were sensitive to

aspirin -

and this is why he failed to diagnose me in the beginning.

But that still does not give us any precise idea of the potential and actual

number of

patients.

Regarding the future, one strategy is indeed to try to qualify as a rare

disease, because no

one can deny that prevalence is objectively low, even if AERDs are

under-diagnosed by

ignorance ; another strategy, perhaps underlying inflated numbers - if they

really were

voluntarily inflated in the first place, which is not certain at all - is to

attract industrial

interest, which will never come if no economies of scale can be achieved.

My opinion is that there is in fact no real economic dilemma here in the long

run :

- if prevalence is high, or potentially very high because many more people could

express

the gene(s), and even more so because of increased allergens, pollution, etc,

the

perspectives will naturally attract industrial interest and funding ;

- if prevalence is low, even rare, I still believe that the industry will

ultimately get

interested, because there are excellent economic reasons for that. AERDs are at

the

confluent of widespread or extremely widespread diseases (asthma, chronic

inflammations

of all sorts, sensitivities, allergies, chronic rhinosinusitis, etc). The

Arachidonic Acid

mechanism (and all that goes along with it), mucosal function, lung function,

etc are the

key to innumerable pathologies, and unlocking their workings and links to these

pathologies is more than certain to be extremely profitable.

Just think about how much money pharmaceutical companies would have saved if

they had

invested more in inflammation research, and avoided the COX-2-inhibitor scandals

? We

are potentially talking about not only avoiding billions of dollars of future

losses because

of who knows what new mistake, but also of designing solutions that may lead to

breakthroughs for millions, if not tens of millions, of people.

In perphaps cynic and shocking terms, AERD patients can be considered extremely

profitable to study in the long run, whatever the prevalence, because so much

can be

discovered researching only one disease that combines and links many pathologies

that

used to be thought of as distinct in a not too remote past.

So, if there are any pharmaceutical companies out there reading our posts,

please take

notice, do some scientific and financial analysis to get convinced of that, and

start

investing.

(...)

> I honestly think they completely inflate thier numbers to get more

> money for funding, and I would love to know where they get this

> information. One in ten people? I think they are not talking about

> Samter's here but rather just about people who have reactions to

> Samter's and can't take it.

January 11, 2008

I will have to find the information, it's from several years ago.

But basically I wrote to the NORD organization for rare diseases, to

get some assistance. They asked me for experts to contact to verify

that this may be a rare disease. One of the names I provided them

with was that of Dr. son. Dr. son wrote back to them and

told them that Samters is far from rare, he said it's very common.

I want to separate out two things, though -- there is aspirin-

sensitive asthma, and there is Samter's. Some people (including

those at Scripps, I believe, but I'm not sure) use the names

interchangeably. But I have members of my family who have aspirin-

sensitize asthma but no other signs of Samters. For example, if they

take an aspirin, they get an asthma attack. Otherwise they do not

have any asthma symptoms EVER and no sinus symptoms. Samters in a

way is almost the opposite of that, that even if we avoid aspirin we

still have symptoms as if we are taking aspirin and reacting to it.

But anyway, what Dr. son said AT THAT TIME and what he told

NORD unfortunately was that 10 to 15 percent of asthmatics in the US

have Samter's. At the time we figured out there were about 15

million asthmatics in the United States, which meant that there were

supposedly over one to two million people with Samter's IN THE US.

And I'm sorry, but I just do not believe it. Yes, it is

underdiagnosed. Yes, not everyone has it as severe. But that would

also mean that it would be like one in every 150 people that have

it. Those percentages just don't add up for me in terms of the

number of people I know (outside of this group) who have Samters --

which is only one. How many of you know people outside of the group

with it?

Anyway, Asfyso, I don't remember your name right now, but there is a

group called the Samters Foundation on . We have not been

active but the more people we can get the better, and you seem like

someone who might be interested in this. You are welcome to look it

up and go there and then we can invite you to join. Really anyone is

welcome to join if you have interest in starting an organization to

help with patient support, education, research, etc.

Lori

> (...)

> > I honestly think they completely inflate thier numbers to get

more

> > money for funding, and I would love to know where they get this

> > information. One in ten people? I think they are not talking

about

> > Samter's here but rather just about people who have reactions to

> > Samter's and can't take it.

>

January 11, 2008

My personal belief based upon my experience is that aspirin

absolutely always 100 percent should not only be taken with food but

with a meal.

I took aspirin for seven years while desensitized and I never had any

stomach problems related to it, and I honestly never ever took it

without a full meal.

No idea about bananas. I don't eat oranges.

Lori

>

> Well last night I took another daily dosage of 100mg and has no

reaction at all except my finger joints being a little sore. It's

fairly obvious that it's best taking with food, later today I will up

to 150mg. Also read recently we should not eat many bananas and

oranges due to mucus accumulation, can anyone comment on this?

>

> Re: Re: Desensitization and coronary artery

disease

>

> Lori

>

> I think the 10% number refers to the percentage of asthmatics who

are also aspirin sensitive ,not the general population as a whole. At

least thats the context in which I have heard it used in the past.

>

> Marcus

>

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January 11, 2008

To be honest, even though I know people with sinus problems and people with asthma. I don't know anyone with the aspirin sensitivity. I have never met anyone with Samters. I have had eight sinus surgeries. Last one the frontal obliteration. No one I talk to even knows what Samters is. Many doctors and a lot of nurses have given me blank looks when I was trying to tell them what I have. I truly don't believe it is so common.

Evie

-- Re: Desensitization and coronary artery disease

I will have to find the information, it's from several years ago. But basically I wrote to the NORD organization for rare diseases, to get some assistance. They asked me for experts to contact to verify that this may be a rare disease. One of the names I provided them with was that of Dr. son. Dr. son wrote back to them and told them that Samters is far from rare, he said it's very common. I want to separate out two things, though -- there is aspirin-sensitive asthma, and there is Samter's. Some people (including those at Scripps, I believe, but I'm not sure) use the names interchangeably. But I have members of my family who have aspirin-sensitize asthma but no other signs of Samters. For example, if they take an aspirin, they get an asthma attack. Otherwise they do not have any asthma symptoms EVER and no sinus symptoms. Samters in a way is almost the opposite of that, that even if we avoid aspirin we still have symptoms as if we are taking aspirin and reacting to it.But anyway, what Dr. son said AT THAT TIME and what he told NORD unfortunately was that 10 to 15 percent of asthmatics in the US have Samter's. At the time we figured out there were about 15 million asthmatics in the United States, which meant that there were supposedly over one to two million people with Samter's IN THE US.And I'm sorry, but I just do not believe it. Yes, it is underdiagnosed. Yes, not everyone has it as severe. But that would also mean that it would be like one in every 150 people that have it. Those percentages just don't add up for me in terms of the number of people I know (outside of this group) who have Samters -- which is only one. How many of you know people outside of the group with it?Anyway, Asfyso, I don't remember your name right now, but there is a group called the Samters Foundation on . We have not been active but the more people we can get the better, and you seem like someone who might be interested in this. You are welcome to look it up and go there and then we can invite you to join. Really anyone is welcome to join if you have interest in starting an organization to help with patient support, education, research, etc.Lori> (...) > > I honestly think they completely inflate thier numbers to get more > > money for funding, and I would love to know where they get this > > information. One in ten people? I think they are not talking about > > Samter's here but rather just about people who have reactions to > > Samter's and can't take it.>

"Snow Bunny"

Made by Ada

's Doodles

font is Comic Sans

January 11, 2008

My ENT told me to eat at least one banana

a day because of my asthma. I don’t eat oranges though because when I was

pregnant I craved them and ate so many it turned me off them after my daughter

was born.

From: samters [mailto:samters ] On Behalf Of truelori

Sent: Saturday, 12 January 2008

6:48 AM

samters

Subject: Re:

Desensitization and coronary artery disease

My personal belief based upon my experience is that

aspirin

absolutely always 100 percent should not only be taken with food but

with a meal.

I took aspirin for seven years while desensitized and I never had any

stomach problems related to it, and I honestly never ever took it

without a full meal.

No idea about bananas. I don't eat oranges.

Lori

>

> Well last night I took another daily dosage of 100mg and has no

reaction at all except my finger joints being a little sore. It's

fairly obvious that it's best taking with food, later today I will up

to 150mg. Also read recently we should not eat many bananas and

oranges due to mucus accumulation, can anyone comment on this?

>

> Re: Re: Desensitization and coronary artery

disease

>

> Lori

>

> I think the 10% number refers to the percentage of asthmatics who

are also aspirin sensitive ,not the general population as a whole. At

least thats the context in which I have heard it used in the past.

>

> Marcus

>

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January 14, 2008

Lori,

The case you mention in your family of aspirin-sensitive asthma is very

interesting,

because it is already known that a subset of Samter's patients do not have

asthma, and

theferore have only upper airways symptoms (polyps), but it is the first time I

hear about a

case of lower airways symptoms without any upper airways symptoms. Have these

members of your family been scanned for polyps ? Does their skin or anything

else apart

from the lower airways react to aspirin ?

I had a theory of asthma development in Samter's - I believed the leukotrienes

or their

products falling down from the upper airways started inflaming the lower airways

from the

top down. This inflammation would be progressive, over months or years, but

would

nevertheless eventually lead to an overexpression of inflammatory molecules in

the lower

airways, and therefore to asthma.

I had two small pieces of support for this theory, one being that I read the

same thing in a

research article - I cannot remember where exactly on the spot - and another

being that I

have the clear feeling the longer one stays without irrigating, the more one

starts to

cough, and the more the cough seems to come from an inflamed lower point (I am

aware

this is more empirical than scientific, but I still believe it makes sense).

This case of yours

clearly shows that there may be other pathways for the genesis of

aspirin-induced asthma,

and they may be linked to mucosal differentiation (ie what makes the lung mucosa

and all

that is behind it different from the sinonasal mucosa).

Regarding the definition of Samter's, we know it has been observed first by

Fernand Widal,

then later on and more precisely defined by Samter, as a combination of aspirin

sensitivity,

polyps in the nose and/or sinuses, and asthma. We also know that a subset of

members

do not exhibit asthma - at least measurable asthma. If subjected to an asthma

provocation test, it is possible they might show very low asthma. Also, they may

exhibit

asthma later on in their lives.

Then, as we also know, the research community realized there were some other

variants in

the symptoms, and proceeded to define the larger set of Aspirin Exacerbated

Respiratory

Diseases (AERDs) as encompassing - the name says it all - any airways pathology

worsened by aspirin - whether lower or upper. Aspirin-exacerbated diseases can

fall into

two categories : those directly linked to aspirin in itself (ie aspirin

hypersensitivity), and

those where aspirin only serves as an exacerbating/revealing agent but does not

create

the pathology. As currently discussed by the specialists, AERDs fall into the

second

category - aspirin is only a revealing/worsening agent. AERDs have been clearly

linked to

deficiencies/abnormal functioning of the Arachidonic Acid inflammatory pathway,

also

known as the Omega-6 inflammatory pathway. The gold-standard method for

diagnosis

used to be oral provocation (progressive aspirin intake under hospital care),

but may

evolve because of the risks (or has already begun to evolve) to nasal

provocation (lysin-

aspirin spray) or urinary leukotriene dosage.

In my opinion, the " point of view " of AERDs is a good one, because I think we

will learn

more or faster by focusing on the common characteristics of Samter's,

Aspirin-induced-

asthma, etc. than by focusing exclusively on disease subsets. Of course,

identifying and

improving on disease subsets is very important, first because of patient focus

(all patients

belong to a subset), second because it is necessary to validate hypotheses on

common

characteristics by tests on specific subsets, and third because, beyond the only

well

established common fact that all AERDs are related to AA pathway defects, each

subset

may derive from a different defect, or from the same defect in a different

localization, or

whatever else.

In the case of your family members, several interesting hypotheses can be

imagined :

- (more probable, and very interesting) it may be that they have an AA pathway

defect in

the lower airways only, and that their upper airways are in perfect shape.

- or (less probable) that they have an AA pathway defect in the upper airways

but, for

some reason (also very interesting), the upper airways resist quite well to the

defect.

In both cases, this means something. I do believe that research has many things

to learn

by following the path of mucosal differentiation.

Regarding numbers, I do know of three persons outside this group who would

qualify as

AERDs (two certain from my family, one less certain outside of family but still

very likely,

and two other family members with AERD genes - acute rhinonasal sensitivity -

but no

clear expression). The reason they are not on this group is that they either do

not use the

internet, don't have time to invest in disease knowledge, or have a disease

management

level that is satisfactory from their point of view (in particular, all have no

asthma, but do

suffer either from allergy or more or less chronic rhinosinusitis). Moreover,

none was ever

diagnosed as AERDs and I was the first one to make the suggestion that their

symptoms

(airways, aspirin sensitivity) could be linked. This being said, a cluster does

not make a

trend, especially because almost all cases are in the family, which is a

statistical biais. I will

have a look at the Samter's foundation site, but if you want to continue the

discussion

specifically on numbers, do you have a mail address ?

> > (...)

> > > I honestly think they completely inflate thier numbers to get

> more

> > > money for funding, and I would love to know where they get this

> > > information. One in ten people? I think they are not talking

> about

> > > Samter's here but rather just about people who have reactions to

> > > Samter's and can't take it.

> >

>

January 14, 2008

How very interesting and informative. Actually facinating as I think of my family. I am one of 10 children. 3 siblings suffer from chronic asthma but have never had the first polyp. My father died at age 64 from complications from chronic asthma/lung disease. He had never had any asthma until his early forties. I had asthma until I was 14 but no longer do. I started "growing" polyps around age 30 and have had 9 sinus surgeries. I know there is a family link here and I have believed strongly for years that my father had Samters. Janeasfyso <asfyso@...> wrote: Lori,The case you mention in your family of aspirin-sensitive asthma is very interesting, because it is already known that a subset of Samter's patients do not have asthma, and theferore have only upper airways symptoms (polyps), but it is the first time I hear about a case of lower airways symptoms without any upper airways symptoms. Have these members of your family been scanned for polyps ? Does their skin or anything else apart from the lower airways react to aspirin ?I had a theory of asthma development in Samter's - I believed the leukotrienes or their products falling down from the upper airways started inflaming the lower airways from the top down. This inflammation would be progressive, over months or years, but would nevertheless eventually lead to an overexpression of inflammatory molecules in the lower airways, and therefore

to asthma.I had two small pieces of support for this theory, one being that I read the same thing in a research article - I cannot remember where exactly on the spot - and another being that I have the clear feeling the longer one stays without irrigating, the more one starts to cough, and the more the cough seems to come from an inflamed lower point (I am aware this is more empirical than scientific, but I still believe it makes sense). This case of yours clearly shows that there may be other pathways for the genesis of aspirin-induced asthma, and they may be linked to mucosal differentiation (ie what makes the lung mucosa and all that is behind it different from the sinonasal mucosa).Regarding the definition of Samter's, we know it has been observed first by Fernand Widal, then later on and more precisely defined by Samter, as a combination of aspirin sensitivity, polyps in the nose and/or sinuses, and asthma. We also

know that a subset of members do not exhibit asthma - at least measurable asthma. If subjected to an asthma provocation test, it is possible they might show very low asthma. Also, they may exhibit asthma later on in their lives.Then, as we also know, the research community realized there were some other variants in the symptoms, and proceeded to define the larger set of Aspirin Exacerbated Respiratory Diseases (AERDs) as encompassing - the name says it all - any airways pathology worsened by aspirin - whether lower or upper. Aspirin-exacerbated diseases can fall into two categories : those directly linked to aspirin in itself (ie aspirin hypersensitivity), and those where aspirin only serves as an exacerbating/revealing agent but does not create the pathology. As currently discussed by the specialists, AERDs fall into the second category - aspirin is only a revealing/worsening agent. AERDs have been clearly linked

to deficiencies/abnormal functioning of the Arachidonic Acid inflammatory pathway, also known as the Omega-6 inflammatory pathway. The gold-standard method for diagnosis used to be oral provocation (progressive aspirin intake under hospital care), but may evolve because of the risks (or has already begun to evolve) to nasal provocation (lysin-aspirin spray) or urinary leukotriene dosage. In my opinion, the "point of view" of AERDs is a good one, because I think we will learn more or faster by focusing on the common characteristics of Samter's, Aspirin-induced-asthma, etc. than by focusing exclusively on disease subsets. Of course, identifying and improving on disease subsets is very important, first because of patient focus (all patients belong to a subset), second because it is necessary to validate hypotheses on common characteristics by tests on specific subsets, and third because, beyond the only well established

common fact that all AERDs are related to AA pathway defects, each subset may derive from a different defect, or from the same defect in a different localization, or whatever else. In the case of your family members, several interesting hypotheses can be imagined :- (more probable, and very interesting) it may be that they have an AA pathway defect in the lower airways only, and that their upper airways are in perfect shape.- or (less probable) that they have an AA pathway defect in the upper airways but, for some reason (also very interesting), the upper airways resist quite well to the defect.In both cases, this means something. I do believe that research has many things to learn by following the path of mucosal differentiation.Regarding numbers, I do know of three persons outside this group who would qualify as AERDs (two certain from my family, one less certain outside of family but still very likely, and two

other family members with AERD genes - acute rhinonasal sensitivity - but no clear expression). The reason they are not on this group is that they either do not use the internet, don't have time to invest in disease knowledge, or have a disease management level that is satisfactory from their point of view (in particular, all have no asthma, but do suffer either from allergy or more or less chronic rhinosinusitis). Moreover, none was ever diagnosed as AERDs and I was the first one to make the suggestion that their symptoms (airways, aspirin sensitivity) could be linked. This being said, a cluster does not make a trend, especially because almost all cases are in the family, which is a statistical biais. I will have a look at the Samter's foundation site, but if you want to continue the discussion specifically on numbers, do you have a mail address ?> > (...) > > > I honestly think they completely inflate thier numbers to get > more > > > money for funding, and I would love to know where they get this > > > information. One in ten people? I think they are not talking > about > > > Samter's here but rather just about people who have reactions to > > > Samter's and can't take it.> >>

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January 14, 2008

First of all, I want to say I appreciate the discussion and critical

thinking around this, so anything I say must be put in that context.

Obviously no one knows everything about this.

I don't know who says that a subset of Samter's patients do not have

asthma. I have never agreed with this idea. I think the full-blown

Samter's syndrome with all three components can take a while to

develop, but I think all three are part of the diagnosis. If not, I

would like to see where it says so. I have heard people here say

they have Samter's without one of the three areas, but I have never

seen it written anywhere in any definition of the syndrome. That's

why it's called a triad. I suspect people who only have two parts of

the triad probably do have the third and it's just very mild or it

has not developed yet. I could be wrong, but I still believe that it

is and must be a triad.

Besides, for some of us, our aspirin sensitivity in Samter's is not

always just aspirin-sensitive asthma. It is a whole syndrome. When

I take aspirin I have many systems involved, not just my lower

respiratory tract. It is my sinuses, my stomach, my skin, my

cardiovascular system. AND the asthma in Samter's is not only from

aspirin (neither are the polyps).

So there are three components, and without the three components I

have always held that it is a little bit short of a diagnosis of this

syndrome. I actually do NOT think AERD is meant to be a broader

diagnosis. I think it is meant to be a more narrow diagnosis.

I don't think people have to be scanned for polyps. If they have no

symptoms at all, they likely have no polyps. Surely someone with any

degree of nasal polyps would have some symptoms.

There are multiple members in multiple generations of my family who

have asthma that is caused only from aspirin and NSAIDs and they have

no other symptoms related to aspirin, allergies, sinuses or

otherwise. They do not have Samter's syndrome. They have aspirin-

sensitive asthma, or aspirin-induced asthma, if you will, and there

are many, many, many people who have this, not just in my family. It

is much more common than Samter's. Also, I thought this was maybe

what son was referring to in that cardiology article anyway.

My father had nasal polyps, but he is not sensitive to aspirin and

does not have asthma, and he had the polyps removed many decades ago

and they never came back.

I don't think your theory about the development of Samter's is true

because the symptoms come in a different order for everyone. My

order was asthma first (very sudden onset in college), then aspirin

sensitivity two and a half years later, then about a year later sinus

problems (about three and a half years after the asthma symptoms

started) and eventually a diagnosis of the polyps. It was several

years before I got a diagnosis of Samter's when I came to New York

and found someone who knew about it.

I did not have ANY sinus symptoms ever in my life before the asthma

or until three years after development of the asthma. I had had a

CAT scan for something else in the interim and there were no polyps

on the scan.

Anyway I am having surgery soon (unrelated to Samter's) so I will be

off the computer for a while, but I'm sure we can continue the

discussion at some point!

Cheers

Lori

January 14, 2008

I would be very interested to hear how others with this Triad disease have had skin issues. Can anyone describe their skin issues? I have had some drastic skin changes in the last ten years and would really be curious to hear if others have had similar issues. Janetruelori <lori@...> wrote: First of all, I want to say I appreciate the discussion and critical thinking around this, so anything I say must be put in that context. Obviously no one knows everything about this. I don't know who says

that a subset of Samter's patients do not have asthma. I have never agreed with this idea. I think the full-blown Samter's syndrome with all three components can take a while to develop, but I think all three are part of the diagnosis. If not, I would like to see where it says so. I have heard people here say they have Samter's without one of the three areas, but I have never seen it written anywhere in any definition of the syndrome. That's why it's called a triad. I suspect people who only have two parts of the triad probably do have the third and it's just very mild or it has not developed yet. I could be wrong, but I still believe that it is and must be a triad. Besides, for some of us, our aspirin sensitivity in Samter's is not always just aspirin-sensitive asthma. It is a whole syndrome. When I take aspirin I have many systems involved, not just my lower respiratory tract. It is my sinuses, my stomach, my

skin, my cardiovascular system. AND the asthma in Samter's is not only from aspirin (neither are the polyps). So there are three components, and without the three components I have always held that it is a little bit short of a diagnosis of this syndrome. I actually do NOT think AERD is meant to be a broader diagnosis. I think it is meant to be a more narrow diagnosis. I don't think people have to be scanned for polyps. If they have no symptoms at all, they likely have no polyps. Surely someone with any degree of nasal polyps would have some symptoms. There are multiple members in multiple generations of my family who have asthma that is caused only from aspirin and NSAIDs and they have no other symptoms related to aspirin, allergies, sinuses or otherwise. They do not have Samter's syndrome. They have aspirin-sensitive asthma, or aspirin-induced asthma, if you will, and there are many, many, many

people who have this, not just in my family. It is much more common than Samter's. Also, I thought this was maybe what son was referring to in that cardiology article anyway.My father had nasal polyps, but he is not sensitive to aspirin and does not have asthma, and he had the polyps removed many decades ago and they never came back.I don't think your theory about the development of Samter's is true because the symptoms come in a different order for everyone. My order was asthma first (very sudden onset in college), then aspirin sensitivity two and a half years later, then about a year later sinus problems (about three and a half years after the asthma symptoms started) and eventually a diagnosis of the polyps. It was several years before I got a diagnosis of Samter's when I came to New York and found someone who knew about it.I did not have ANY sinus symptoms ever in my life before the asthma or

until three years after development of the asthma. I had had a CAT scan for something else in the interim and there were no polyps on the scan.Anyway I am having surgery soon (unrelated to Samter's) so I will be off the computer for a while, but I'm sure we can continue the discussion at some point! :)CheersLori

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January 14, 2008

I have developed very dry skin which I never had before. Don't know if it is the samters. hypothyroid or menopause that has caused this as they all started around the same time. Unfortunately my skin is just drying up like a prune. Any suggestions to lessen this would be helpful. I do moisturise which helps a bit but the underlying condition remains.Maggiesamters From: janesmarino@...Date: Mon, 14 Jan 2008 18:02:49 -0800Subject: Re: Re: Desensitization and coronary artery disease

I would be very interested to hear how others with this Triad disease have had skin issues. Can anyone describe their skin issues? I have had some drastic skin changes in the last ten years and would really be curious to hear if others have had similar issues. Janetruelori <loritruelori> wrote: First of all, I want to say I appreciate the discussion and critical thinking around this, so anything I say must be put in that context. Obviously no one knows everything about this. I don't know who says

that a subset of Samter's patients do not have asthma. I have never agreed with this idea. I think the full-blown Samter's syndrome with all three components can take a while to develop, but I think all three are part of the diagnosis. If not, I would like to see where it says so. I have heard people here say they have Samter's without one of the three areas, but I have never seen it written anywhere in any definition of the syndrome. That's why it's called a triad. I suspect people who only have two parts of the triad probably do have the third and it's just very mild or it has not developed yet. I could be wrong, but I still believe that it is and must be a triad. Besides, for some of us, our aspirin sensitivity in Samter's is not always just aspirin-sensitive asthma. It is a whole syndrome. When I take aspirin I have many systems involved, not just my lower respiratory tract. It is my sinuses, my stomach, my

skin, my cardiovascular system. AND the asthma in Samter's is not only from aspirin (neither are the polyps). So there are three components, and without the three components I have always held that it is a little bit short of a diagnosis of this syndrome. I actually do NOT think AERD is meant to be a broader diagnosis. I think it is meant to be a more narrow diagnosis. I don't think people have to be scanned for polyps. If they have no symptoms at all, they likely have no polyps. Surely someone with any degree of nasal polyps would have some symptoms. There are multiple members in multiple generations of my family who have asthma that is caused only from aspirin and NSAIDs and they have no other symptoms related to aspirin, allergies, sinuses or otherwise. They do not have Samter's syndrome. They have aspirin-sensitive asthma, or aspirin-induced asthma, if you will, and there are many, many, many

people who have this, not just in my family. It is much more common than Samter's. Also, I thought this was maybe what son was referring to in that cardiology article anyway.My father had nasal polyps, but he is not sensitive to aspirin and does not have asthma, and he had the polyps removed many decades ago and they never came back.I don't think your theory about the development of Samter's is true because the symptoms come in a different order for everyone. My order was asthma first (very sudden onset in college), then aspirin sensitivity two and a half years later, then about a year later sinus problems (about three and a half years after the asthma symptoms started) and eventually a diagnosis of the polyps. It was several years before I got a diagnosis of Samter's when I came to New York and found someone who knew about it.I did not have ANY sinus symptoms ever in my life before the asthma or

until three years after development of the asthma. I had had a CAT scan for something else in the interim and there were no polyps on the scan.Anyway I am having surgery soon (unrelated to Samter's) so I will be off the computer for a while, but I'm sure we can continue the discussion at some point! :)CheersLori Never miss a thing. Make your homepage.

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January 14, 2008

I’m going through menopause but not

sure if this is the problem or not but I suffer from dry skin also.

From: samters [mailto:samters ] On Behalf Of Margaret

Sent: Tuesday, 15 January 2008

2:02 PM

samters

Subject: RE: Re:

Desensitization and coronary artery disease

I have developed very dry skin which I never had before. Don't know if

it is the samters. hypothyroid or menopause that has caused this as they all

started around the same time. Unfortunately my skin is just drying up like a

prune.

Any suggestions to lessen this would be helpful. I do moisturise which helps a

bit but the underlying condition remains.

Maggie

samters

From: janesmarino

Date: Mon, 14 Jan 2008 18:02:49 -0800

Subject: Re: Re: Desensitization and coronary artery disease

I would be very interested to hear how others with this Triad disease

have had skin issues. Can anyone describe their skin issues? I have

had some drastic skin changes in the last ten years and would really be curious

to hear if others have had similar issues.

Jane

truelori

<loritruelori> wrote:

First of all, I want to

say I appreciate the discussion and critical