Re: Variant angina and Samter's

[Guest guest]

Afyso,If aspirin sensitivity is genetic then I will shoot myself (joke). I have four children and it would kill me to think that this is the inheritance that we have provided for them. What amazes me is that there is absolutely no one in Toms family who suffers from nasal polyps. Asthma yes, but then ever second cough is diagnosed as asthma these days. The only thing is that Tom is an only son with 3 sisters - so maybe this plays a part. Then as is the case with Cystic Fibrosis maybe genes have to come from both parents to trigger defect. His parents are both still alive - his father will be 89 next week and his mother 88 in August - so much for family

genes.Breda Variant angina and Samter'sI found by chance this abstract, which says that some people have genetic thromboxane receptor defects, and that they are more likely to have aspirin-intolerant asthma. It does not say anything about any causality whatever behind the relationship, but it does mention the existence of thromboxane receptor antagonists and thromboxane synthase

inhibitors, which may therefore be of some use against variant angina.------------ --------- --------Clin Exp Allergy. 2005 May;35(5):585- 90. LinksAssociation of thromboxane A2 receptor gene polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma.Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon, Korea.BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a receptor for a potent bronchoconstrictor, TBXA2 which is known to be related to bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been found to be effective in the management of asthmatic patients. This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA). METHODS: TBXA2R

gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were determined using a single-base extension method in 93 AIA patients compared with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs) recruited from the Korean population. HLA DPB1*0301 genotype was performed using a direct sequencing method. RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly higher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C polymorphism was also associated with extent of percent fall in forced expiratory volume in 1 s (FEV1) after the inhalation of lysine-acetyl salicylic acid in AIA patients (P=0.009); AIA patients homozygous for the +795 C allele had a greater percent fall of FEV1 compared with individuals with TBXA2R+795 CT or TT genotypes. The frequency of patients carrying both the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was significantly higher in AIA patients (29.4%) than in ATA patients (7.3%)

(P=0.008, odds ratio=5.3). CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C may increase bronchoconstrictive response to ASA, which could contribute to the development of the AIA phenotype.

[Guest guest]

So, an update on my angina...

I decreased my aspirin to 325 mg/day on June 4th. Prior to that

date, I was experiencing chest pain almost everyday, if not multiple

times a day. Since the decrease in aspirin, I have only had pain

twice.

Whether or not my doctors believe it, this seems like a pretty

straight forward conclusion to me. Nothing else has changed... not

medication, not lifestyle, not food, nothing. Aspirin is the only

variable.

Between the abstracts that you've found, the research that I have

done, and my own experience, I think this is enough information to

hopefully convince my ENT that some further studies need to be done.

We'll see.

Kate

P.S. Luckily I've found another support group for variant angina. I

also asked them if anyone there suffered from " allergies " and whether

they thought it was related. I didn't want to bring up Samter's

since there are probably a lot of undiagnosed people out there that

just think they have allergies/asthma. Anyway, no one there seemed

to think there was any relationship either. For everyone's sake, I

hope there isn't. But maybe I'm living proof that there is.

>

> I found by chance this abstract, which says that some people have

> genetic thromboxane receptor defects, and that they are more likely

to

> have aspirin-intolerant asthma. It does not say anything about any

> causality whatever behind the relationship, but it does mention the

> existence of thromboxane receptor antagonists and thromboxane

synthase

> inhibitors, which may therefore be of some use against variant

angina.

>

> -----------------------------

>

> Clin Exp Allergy. 2005 May;35(5):585-90. Links

> Association of thromboxane A2 receptor gene polymorphism with the

> phenotype of acetyl salicylic acid-intolerant asthma.

> Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.

> Department of Allergy and Rheumatology, Ajou University School of

> Medicine, Suwon, Korea.

>

> BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a

> receptor for a potent bronchoconstrictor, TBXA2 which is known to be

> related to bronchial asthma and myocardial infarction. TBXA2R

antagonist

> and TBX synthase inhibitors have been found to be effective in the

> management of asthmatic patients. This study was aimed to evaluate

> whether genetic variants of TBXA2R may be related with development

of

> acetyl salicylic acid (ASA)-intolerant asthma (AIA).

>

> METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C)

were

> determined using a single-base extension method in 93 AIA patients

> compared with 172 patients with ASA-tolerant asthma (ATA) and 118

normal

> controls (NCs) recruited from the Korean population. HLA DPB1*0301

> genotype was performed using a direct sequencing method.

>

> RESULTS: The rare C allele frequency of TBXA2R+795T>C was

significantly

> higher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C

polymorphism

> was also associated with extent of percent fall in forced expiratory

> volume in 1 s (FEV1) after the inhalation of lysine-acetyl salicylic

> acid in AIA patients (P=0.009); AIA patients homozygous for the

+795 C

> allele had a greater percent fall of FEV1 compared with individuals

with

> TBXA2R+795 CT or TT genotypes. The frequency of patients carrying

both

> the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was significantly

> higher in AIA patients (29.4%) than in ATA patients (7.3%) (P=0.008,

> odds ratio=5.3).

>

> CONCLUSION: These results suggest that the polymorphism of

TBXA2R+795T>C

> may increase bronchoconstrictive response to ASA, which could

contribute

> to the development of the AIA phenotype.

>

[Guest guest]

No one in my family has polyps, aspirin sensitivity, ear problems, or asthma but me. My father is 87 - my mother died at 72 following a heart valve replacement surgery but her death was due to human error in the hospital.

I pray my two kids don't get this -- I was about 45 when it hit me and my kids are now 29 and 33. (My 29 has major problems with Type 1 diabetes.) This hit me when I moved from Kansas to Phoenix following a very stressful divorce - I wonder if stress played a big part. I also wonder if any of you have Irritable Bowel Syndrom -- I really suffer from this and don't know if some of these meds contribute to this.

From: Breda OBrien <zippyelle@...>Subject: Re: Variant angina and Samter'ssamters Date: Sunday, June 15, 2008, 4:38 PM

Afyso,If aspirin sensitivity is genetic then I will shoot myself (joke). I have four children and it would kill me to think that this is the inheritance that we have provided for them. What amazes me is that there is absolutely no one in Toms family who suffers from nasal polyps. Asthma yes, but then ever second cough is diagnosed as asthma these days. The only thing is that Tom is an only son with 3 sisters - so maybe this plays a part. Then as is the case with Cystic Fibrosis maybe genes have to come from both parents to trigger defect. His parents are both still alive - his father will be 89 next week and his mother 88 in August - so much for family genes.Breda

Variant angina and Samter's

I found by chance this abstract, which says that some people have genetic thromboxane receptor defects, and that they are more likely to have aspirin-intolerant asthma. It does not say anything about any causality whatever behind the relationship, but it does mention the existence of thromboxane receptor antagonists and thromboxane synthase inhibitors, which may therefore be of some use against variant angina.------------ --------- --------Clin Exp Allergy. 2005 May;35(5):585- 90. LinksAssociation of thromboxane A2 receptor gene polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma.Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon, Korea.BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a receptor for a potent bronchoconstrictor, TBXA2 which is known to be related to bronchial

asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been found to be effective in the management of asthmatic patients. This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA). METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were determined using a single-base extension method in 93 AIA patients compared with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs) recruited from the Korean population. HLA DPB1*0301 genotype was performed using a direct sequencing method. RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly higher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C polymorphism was also associated with extent of percent fall in forced expiratory volume in 1 s (FEV1) after the inhalation of lysine-acetyl salicylic

acid in AIA patients (P=0.009); AIA patients homozygous for the +795 C allele had a greater percent fall of FEV1 compared with individuals with TBXA2R+795 CT or TT genotypes. The frequency of patients carrying both the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was significantly higher in AIA patients (29.4%) than in ATA patients (7.3%) (P=0.008, odds ratio=5.3). CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C may increase bronchoconstrictive response to ASA, which could contribute to the development of the AIA phenotype.

[Guest guest]

Just regarding your IBS - I developed this and wondered if meds played a part. I varied my diet and found that wheat caused my IBS so now I avoid wheat. Before Samters I was fine eating wheat. I have had tests and am not a Coeliac. Just a thought. Beckywkapikorn <wkapikorn@...> wrote: No one in my family has polyps, aspirin sensitivity, ear problems, or asthma but me. My father is 87 - my mother died at 72

following a heart valve replacement surgery but her death was due to human error in the hospital. I pray my two kids don't get this -- I was about 45 when it hit me and my kids are now 29 and 33. (My 29 has major problems with Type 1 diabetes.) This hit me when I moved from Kansas to Phoenix following a very stressful divorce - I wonder if stress played a big part. I also wonder if any of you have Irritable Bowel Syndrom -- I really suffer from this and don't know if some of these meds contribute to this. From: Breda OBrien <zippyelle >Subject: Re: Variant angina and Samter'ssamters Date: Sunday, June 15, 2008, 4:38 PM Afyso,If aspirin sensitivity is genetic then I will shoot myself (joke). I have four children and it would kill me to think that this is the inheritance that we have provided for them. What amazes me is that there is absolutely no one in Toms family who suffers from nasal polyps. Asthma yes, but then ever second cough is diagnosed as asthma these days. The only thing is that Tom is an only son with 3 sisters - so maybe this plays a part. Then as is the case with Cystic Fibrosis maybe genes have to come from both parents to trigger defect. His parents are both still alive - his father will be 89 next week and his mother 88 in August - so much for family genes.Breda Variant angina and Samter's I found by chance this abstract, which says that some people have genetic thromboxane receptor defects, and that they are more likely to have aspirin-intolerant asthma. It does not say anything about any causality whatever behind the relationship, but it does mention the existence of thromboxane receptor antagonists and thromboxane synthase inhibitors, which may therefore be of some use against variant angina.------------ --------- --------Clin Exp Allergy. 2005 May;35(5):585- 90. LinksAssociation of thromboxane A2 receptor gene polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma.Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.Department of

Allergy and Rheumatology, Ajou University School of Medicine, Suwon, Korea.BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a receptor for a potent bronchoconstrictor, TBXA2 which is known to be related to bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been found to be effective in the management of asthmatic patients. This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA). METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were determined using a single-base extension method in 93 AIA patients compared with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs) recruited from the Korean population. HLA DPB1*0301 genotype was performed using a direct sequencing method. RESULTS: The rare C allele frequency of TBXA2R+795T>C was

significantly higher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C polymorphism was also associated with extent of percent fall in forced expiratory volume in 1 s (FEV1) after the inhalation of lysine-acetyl salicylic acid in AIA patients (P=0.009); AIA patients homozygous for the +795 C allele had a greater percent fall of FEV1 compared with individuals with TBXA2R+795 CT or TT genotypes. The frequency of patients carrying both the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was significantly higher in AIA patients (29.4%) than in ATA patients (7.3%) (P=0.008, odds ratio=5.3). CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C may increase bronchoconstrictive response to ASA, which could contribute to the development of the AIA phenotype.

Sent from .

A Smarter Email.

[Guest guest]

I developed my asthma when I was 27 after

a bout of very bad bronchitis and the rest as they say is history. I have

a daughter just turned 23 and she doesn’t have any allergies, asthma or

anything and I’m praying that she’s going to stay that way. I’m

not sure if I have IBS or not but I certainly have some of the symptoms. As to

stress, yes that does play a huge part, I went through a very upsetting divorce

five years ago and had shocking asthma at that stage and about six months later

had to undergo polyp surgery.

Maybe we could get a poll going with some

of the symptoms we have?

From:

Bannister [mailto:beckyb256@...]

Sent: Monday, 16 June 2008 6:38 PM

samters

Subject: Re: Variant

angina and Samter's

Just regarding your IBS - I developed this and wondered if meds played

a part. I varied my diet and found that wheat caused my IBS so now I avoid

wheat. Before Samters I was fine eating wheat. I have had tests and am not a

Coeliac.

Just a thought.

Becky

wkapikorn <wkapikorn > wrote:

No one in my family has polyps, aspirin sensitivity,

ear problems, or asthma but me. My father is 87 - my mother died at 72

following a heart valve replacement surgery but her death was due to human

error in the hospital.

I pray my two kids don't get this -- I was about 45

when it hit me and my kids are now 29 and 33. (My 29 has major problems

with Type 1 diabetes.) This hit me when I moved from Kansas

to Phoenix

following a very stressful divorce - I wonder if stress played a big

part. I also wonder if any of you have Irritable Bowel Syndrom -- I

really suffer from this and don't know if some of these meds contribute to

this.

From: Breda OBrien

<zippyelle >

Subject: Re: Variant angina and Samter's

samters

Date: Sunday, June 15, 2008, 4:38 PM

Afyso,

If aspirin sensitivity is genetic then I will shoot myself (joke). I have

four children and it would kill me to think that this is the inheritance that

we have provided for them.

What amazes me is that there is absolutely no one in Toms family who suffers

from nasal polyps. Asthma yes, but then ever second cough is diagnosed

as asthma these days. The only thing is that Tom is an only son with 3

sisters - so maybe this plays a part. Then as is the case with Cystic

Fibrosis maybe genes have to come from both parents to trigger defect. His

parents are both still alive - his father will be 89 next week and his mother

88 in August - so much for family genes.

Breda

Variant angina and Samter's

I found by chance this

abstract, which says that some people have genetic thromboxane receptor

defects, and that they are more likely to have aspirin-intolerant asthma. It

does not say anything about any causality whatever behind the relationship,

but it does mention the existence of thromboxane receptor antagonists and

thromboxane synthase inhibitors, which may therefore be of some use against

variant angina.

------------ --------- --------

Clin Exp Allergy. 2005 May;35(5):585- 90. Links

Association of thromboxane A2 receptor gene

polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma.

Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.

Department of Allergy and Rheumatology, Ajou

University School

of Medicine, Suwon, Korea.

BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a receptor

for a potent bronchoconstrictor, TBXA2 which is known to be related to

bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been

found to be effective in the management of asthmatic patients. This study was

aimed to evaluate whether genetic variants of TBXA2R may be related with

development of acetyl salicylic acid (ASA)-intolerant asthma (AIA).

METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were

determined using a single-base extension method in 93 AIA patients compared

with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls

(NCs) recruited from the Korean population. HLA DPB1*0301 genotype was

performed using a direct sequencing method.

RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly

higher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C polymorphism was

also associated with extent of percent fall in forced expiratory volume in 1

s (FEV1) after the inhalation of lysine-acetyl salicylic acid in AIA patients

(P=0.009); AIA patients homozygous for the +795 C allele had a greater

percent fall of FEV1 compared with individuals with TBXA2R+795 CT or TT

genotypes. The frequency of patients carrying both the TBXA2R+795T>C rare

allele and HLA DPB1(*)0301 was significantly higher in AIA patients (29.4%)

than in ATA patients (7.3%) (P=0.008, odds ratio=5.3).

CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C

may increase bronchoconstrictive response to ASA, which could contribute to

the development of the AIA phenotype.

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[Guest guest]

Hi Breda, I am the only daughter and have 3 brothers - I am the only one with Samters...so far. My grandpa had Samters and diesd young of a heart attack. So far none of his children or other grandchildren have Samters...only me. BeckyBreda OBrien <zippyelle@...> wrote: Afyso,If aspirin

sensitivity is genetic then I will shoot myself (joke). I have four children and it would kill me to think that this is the inheritance that we have provided for them. What amazes me is that there is absolutely no one in Toms family who suffers from nasal polyps. Asthma yes, but then ever second cough is diagnosed as asthma these days. The only thing is that Tom is an only son with 3 sisters - so maybe this plays a part. Then as is the case with Cystic Fibrosis maybe genes have to come from both parents to trigger defect. His parents are both still alive - his father will be 89 next week and his mother 88 in August - so much for family genes.Breda

Variant angina and Samter's I found by chance this abstract, which says that some people have genetic thromboxane receptor defects, and that they are more likely to have aspirin-intolerant asthma. It does not say anything about any causality whatever behind the relationship, but it does mention the existence of thromboxane receptor antagonists and thromboxane synthase inhibitors, which may therefore be of some use against variant angina.------------ --------- --------Clin Exp Allergy. 2005 May;35(5):585- 90. LinksAssociation of thromboxane A2 receptor gene polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma.Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon, Korea.BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a receptor for a potent bronchoconstrictor,

TBXA2 which is known to be related to bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been found to be effective in the management of asthmatic patients. This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA). METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were determined using a single-base extension method in 93 AIA patients compared with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs) recruited from the Korean population. HLA DPB1*0301 genotype was performed using a direct sequencing method. RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly higher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C polymorphism was also associated with extent of percent fall in forced expiratory volume in 1 s (FEV1) after the inhalation

of lysine-acetyl salicylic acid in AIA patients (P=0.009); AIA patients homozygous for the +795 C allele had a greater percent fall of FEV1 compared with individuals with TBXA2R+795 CT or TT genotypes. The frequency of patients carrying both the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was significantly higher in AIA patients (29.4%) than in ATA patients (7.3%) (P=0.008, odds ratio=5.3). CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C may increase bronchoconstrictive response to ASA, which could contribute to the development of the AIA phenotype.

Sent from .

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[Guest guest]

I too think that stress is a factor in triggering Samters. I come from an asthmatic family - my father and two sisters and a brother all had it. My sibblings had it in childhood and have largely grown out of it. I escaped for most of my life and had only hayfever to contend with. For me Samters symptons all came along soon after a very messy divorce. It took me over 2 years to get my ex to agree to a settlement - she engaged a solicitor who was intent upon draining our resources rather than reaching a deal, but unfortunately my ex believed everything he said. She had to eventually settle on less than I had offered 18 months earlier as he had messed up big time. However there are no victors in such things and perhaps I escaped financially better than might have been the case without the fight but health wise I now pay a very high price.

There is always a silver lining and I developed a much closer bond with my three children during that stressful time and the words in the three fathers day cards I had hand delivered yesterday lifted my spirits after a rotten Samters week. Two of my children had chronic childhood asthma but one, like me, escaped. They are all fine young adults now, making their way in the world. Suffice to say I'm a proud dad!

Regards to all

UK Mike

samters From: soniarobins@...Date: Mon, 16 Jun 2008 18:56:08 +1000Subject: RE: Variant angina and Samter's

I developed my asthma when I was 27 after a bout of very bad bronchitis and the rest as they say is history. I have a daughter just turned 23 and she doesn’t have any allergies, asthma or anything and I’m praying that she’s going to stay that way. I’m not sure if I have IBS or not but I certainly have some of the symptoms. As to stress, yes that does play a huge part, I went through a very upsetting divorce five years ago and had shocking asthma at that stage and about six months later had to undergo polyp surgery.

Maybe we could get a poll going with some of the symptoms we have?

From: Bannister [mailto:beckyb256 (DOT) co.uk] Sent: Monday, 16 June 2008 6:38 PMsamters Subject: Re: Variant angina and Samter's

Just regarding your IBS - I developed this and wondered if meds played a part. I varied my diet and found that wheat caused my IBS so now I avoid wheat. Before Samters I was fine eating wheat. I have had tests and am not a Coeliac.

Just a thought.

Beckywkapikorn <wkapikorn > wrote:

No one in my family has polyps, aspirin sensitivity, ear problems, or asthma but me. My father is 87 - my mother died at 72 following a heart valve replacement surgery but her death was due to human error in the hospital.

I pray my two kids don't get this -- I was about 45 when it hit me and my kids are now 29 and 33. (My 29 has major problems with Type 1 diabetes.) This hit me when I moved from Kansas to Phoenix following a very stressful divorce - I wonder if stress played a big part. I also wonder if any of you have Irritable Bowel Syndrom -- I really suffer from this and don't know if some of these meds contribute to this.

From: Breda OBrien <zippyelle >Subject: Re: Variant angina and Samter'ssamters Date: Sunday, June 15, 2008, 4:38 PM

Afyso,If aspirin sensitivity is genetic then I will shoot myself (joke). I have four children and it would kill me to think that this is the inheritance that we have provided for them. What amazes me is that there is absolutely no one in Toms family who suffers from nasal polyps. Asthma yes, but then ever second cough is diagnosed as asthma these days. The only thing is that Tom is an only son with 3 sisters - so maybe this plays a part. Then as is the case with Cystic Fibrosis maybe genes have to come from both parents to trigger defect. His parents are both still alive - his father will be 89 next week and his mother 88 in August - so much for family genes.Breda

Variant angina and Samter's

I found by chance this abstract, which says that some people have genetic thromboxane receptor defects, and that they are more likely to have aspirin-intolerant asthma. It does not say anything about any causality whatever behind the relationship, but it does mention the existence of thromboxane receptor antagonists and thromboxane synthase inhibitors, which may therefore be of some use against variant angina.------------ --------- --------Clin Exp Allergy. 2005 May;35(5):585- 90. LinksAssociation of thromboxane A2 receptor gene polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma.Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon, Korea.BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a receptor for a potent bronchoconstrictor, TBXA2 which is known to be related to bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been found to be effective in the management of asthmatic patients. This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA). METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were determined using a single-base extension method in 93 AIA patients compared with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs) recruited from the Korean population. HLA DPB1*0301 genotype was performed using a direct sequencing method. RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly higher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C polymorphism was also associated with extent of percent fall in forced expiratory volume in 1 s (FEV1) after the inhalation of lysine-acetyl salicylic acid in AIA patients (P=0.009); AIA patients homozygous for the +795 C allele had a greater percent fall of FEV1 compared with individuals with TBXA2R+795 CT or TT genotypes. The frequency of patients carrying both the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was significantly higher in AIA patients (29.4%) than in ATA patients (7.3%) (P=0.008, odds ratio=5.3). CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C may increase bronchoconstrictive response to ASA, which could contribute to the development of the AIA phenotype.

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Messenger's gone Mobile! Get it now!

[Guest guest]

Mike your settlement and divorce is a

mirror of mine and you’re right, no winners accept maybe for the lawyers. As

with youm my daughter and I are very close as a result and fortunately so far she’s

in the clear health wise.

From: Mike Hammond

[mailto:rovenmike@...]

Sent: Monday, 16 June 2008 10:52

PM

samters

Subject: RE: Variant

angina and Samter's

I too

think that stress is a factor in triggering Samters. I come from an

asthmatic family - my father and two sisters and a brother all had it. My

sibblings had it in childhood and have largely grown out of it. I escaped

for most of my life and had only hayfever to contend with. For me Samters

symptons all came along soon after a very messy divorce. It took me over

2 years to get my ex to agree to a settlement - she engaged a solicitor who was

intent upon draining our resources rather than reaching a deal, but

unfortunately my ex believed everything he said. She had to eventually

settle on less than I had offered 18 months earlier as he had messed up big

time. However there are no victors in such things and perhaps I escaped

financially better than might have been the case without the fight but

health wise I now pay a very high price.

There is always a silver lining and I developed a much closer bond with my

three children during that stressful time and the words in the three

fathers day cards I had hand delivered yesterday lifted my spirits after a

rotten Samters week. Two of my children had chronic childhood asthma but

one, like me, escaped. They are all fine young adults now, making

their way in the world. Suffice to say I'm a proud dad!

Regards to all

UK

Mike

samters

From: soniarobinstsn (DOT) cc

Date: Mon, 16 Jun 2008 18:56:08 +1000

Subject: RE: Variant angina and Samter's

I developed my asthma when I was 27 after

a bout of very bad bronchitis and the rest as they say is history. I have

a daughter just turned 23 and she doesn’t have any allergies, asthma or

anything and I’m praying that she’s going to stay that way. I’m not sure if I

have IBS or not but I certainly have some of the symptoms. As to stress, yes

that does play a huge part, I went through a very upsetting divorce five years

ago and had shocking asthma at that stage and about six months later had to

undergo polyp surgery.

Maybe we could get a poll going with some

of the symptoms we have?

From:

Bannister [mailto:beckyb256 (DOT) co.uk]

Sent: Monday, 16 June 2008 6:38 PM

samters

Subject: Re: Variant

angina and Samter's

Just regarding your IBS - I developed this and

wondered if meds played a part. I varied my diet and found that wheat caused my

IBS so now I avoid wheat. Before Samters I was fine eating wheat. I have had

tests and am not a Coeliac.

Just a thought.

Becky

wkapikorn <wkapikorn > wrote:

No one in my family has polyps, aspirin sensitivity,

ear problems, or asthma but me. My father is 87 - my mother died at 72

following a heart valve replacement surgery but her death was due to human

error in the hospital.

I pray my two kids don't get this -- I was about 45

when it hit me and my kids are now 29 and 33. (My 29 has major problems

with Type 1 diabetes.) This hit me when I moved from Kansas

to Phoenix

following a very stressful divorce - I wonder if stress played a big

part. I also wonder if any of you have Irritable Bowel Syndrom -- I

really suffer from this and don't know if some of these meds contribute to

this.

From: Breda OBrien <zippyelle >

Subject: Re: Variant angina and Samter's

samters

Date: Sunday, June 15, 2008, 4:38 PM

Afyso,

If aspirin sensitivity is genetic then I will shoot myself (joke). I have

four children and it would kill me to think that this is the inheritance that

we have provided for them.

What amazes me is that there is absolutely no one in Toms family who suffers

from nasal polyps. Asthma yes, but then ever second cough is diagnosed

as asthma these days. The only thing is that Tom is an only son with 3

sisters - so maybe this plays a part. Then as is the case with Cystic

Fibrosis maybe genes have to come from both parents to trigger defect. His

parents are both still alive - his father will be 89 next week and his mother

88 in August - so much for family genes.

Breda

Variant angina and Samter's

I found by chance this abstract, which says that

some people have genetic thromboxane receptor defects, and that they are more

likely to have aspirin-intolerant asthma. It does not say anything about any

causality whatever behind the relationship, but it does mention the existence

of thromboxane receptor antagonists and thromboxane synthase inhibitors,

which may therefore be of some use against variant angina.

------------ --------- --------

Clin Exp Allergy. 2005 May;35(5):585- 90. Links

Association of thromboxane A2 receptor gene

polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma.

Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.

Department of Allergy and Rheumatology, Ajou

University School

of Medicine, Suwon, Korea.

BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a receptor

for a potent bronchoconstrictor, TBXA2 which is known to be related to

bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been

found to be effective in the management of asthmatic patients. This study was

aimed to evaluate whether genetic variants of TBXA2R may be related with

development of acetyl salicylic acid (ASA)-intolerant asthma (AIA).

METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were

determined using a single-base extension method in 93 AIA patients compared

with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls

(NCs) recruited from the Korean population. HLA DPB1*0301 genotype was

performed using a direct sequencing method.

RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly

higher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C polymorphism was

also associated with extent of percent fall in forced expiratory volume in 1

s (FEV1) after the inhalation of lysine-acetyl salicylic acid in AIA patients

(P=0.009); AIA patients homozygous for the +795 C allele had a greater

percent fall of FEV1 compared with individuals with TBXA2R+795 CT or TT

genotypes. The frequency of patients carrying both the TBXA2R+795T>C rare

allele and HLA DPB1(*)0301 was significantly higher in AIA patients (29.4%)

than in ATA patients (7.3%) (P=0.008, odds ratio=5.3).

CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C

may increase bronchoconstrictive response to ASA, which could contribute to

the development of the AIA phenotype.

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[Guest guest]

Certainly seems like divorce has played havoc on a lot of our lives. Could samter's be triggered by stress?

From: Breda OBrien <zippyelle (DOT) com>Subject: Re: Variant angina and Samter'ssamters@groups .comDate: Sunday, June 15, 2008, 4:38 PM

Afyso,If aspirin sensitivity is genetic then I will shoot myself (joke). I have four children and it would kill me to think that this is the inheritance that we have provided for them. What amazes me is that there is absolutely no one in Toms family who suffers from nasal polyps. Asthma yes, but then ever second cough is diagnosed as asthma these days. The only thing is that Tom is an only son with 3 sisters - so maybe this plays a part. Then as is the case with Cystic Fibrosis maybe genes have to come from both parents to trigger defect. His parents are both still alive - his father will be 89 next week and his mother 88 in August - so much for family genes.Breda

Variant angina and Samter's

I found by chance this abstract, which says that some people have genetic thromboxane receptor defects, and that they are more likely to have aspirin-intolerant asthma. It does not say anything about any causality whatever behind the relationship, but it does mention the existence of thromboxane receptor antagonists and thromboxane synthase inhibitors, which may therefore be of some use against variant angina.------------ --------- --------Clin Exp Allergy. 2005 May;35(5):585- 90. LinksAssociation of thromboxane A2 receptor gene polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma.Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon , Korea .BACKGROUND AND OBJECTIVE: The

thromboxane A2 receptor (TBXA2R) is a receptor for a potent bronchoconstrictor, TBXA2 which is known to be related to bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been found to be effective in the management of asthmatic patients. This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA). METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were determined using a single-base extension method in 93 AIA patients compared with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs) recruited from the Korean population. HLA DPB1*0301 genotype was performed using a direct sequencing method. RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly higher in AIA than in ATA (P=0.03) and the

TBXA2R+795T>C polymorphism was also associated with extent of percent fall in forced expiratory volume in 1 s (FEV1) after the inhalation of lysine-acetyl salicylic acid in AIA patients (P=0.009); AIA patients homozygous for the +795 C allele had a greater percent fall of FEV1 compared with individuals with TBXA2R+795 CT or TT genotypes. The frequency of patients carrying both the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was significantly higher in AIA patients (29.4%) than in ATA patients (7.3%) (P=0.008, odds ratio=5.3). CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C may increase bronchoconstrictive response to ASA, which could contribute to the development of the AIA phenotype.

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[Guest guest]

It could. Mine came after a very stressful period. I've been very happy for the past two weeks, and my polyps are shrinking. Although, I'm also taking vitamin C, drinking more water, eating oranges and exercising pursuant to helpful posts about the same time, so I can't say that stress is the only factor. Variant angina and Samter's

I found by chance this abstract, which says that some people have genetic thromboxane receptor defects, and that they are more likely to have aspirin-intolerant asthma. It does not say anything about any causality whatever behind the relationship, but it does mention the existence of thromboxane receptor antagonists and thromboxane synthase inhibitors, which may therefore be of some use against variant angina.------------ --------- --------Clin Exp Allergy. 2005 May;35(5):585- 90. LinksAssociation of thromboxane A2 receptor gene polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma.Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon , Korea .BACKGROUND AND OBJECTIVE: The

thromboxane A2 receptor (TBXA2R) is a receptor for a potent bronchoconstrictor, TBXA2 which is known to be related to bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been found to be effective in the management of asthmatic patients. This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA). METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were determined using a single-base extension method in 93 AIA patients compared with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs) recruited from the Korean population. HLA DPB1*0301 genotype was performed using a direct sequencing method. RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly higher in AIA than in ATA (P=0.03) and the

TBXA2R+795T>C polymorphism was also associated with extent of percent fall in forced expiratory volume in 1 s (FEV1) after the inhalation of lysine-acetyl salicylic acid in AIA patients (P=0.009); AIA patients homozygous for the +795 C allele had a greater percent fall of FEV1 compared with individuals with TBXA2R+795 CT or TT genotypes. The frequency of patients carrying both the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was significantly higher in AIA patients (29.4%) than in ATA patients (7.3%) (P=0.008, odds ratio=5.3). CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C may increase bronchoconstrictive response to ASA, which could contribute to the development of the AIA phenotype.

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Mine came after a very stressful period too - we were redecorating our bedroom and had time-limit of a weekend to complete painting before a new carpet was to be fitted. Also, our toddler and baby came down with chicken pox and both were covered and our baby boy hasd such a high temp he went into hospital for a while. I was so stressed with it all and didn't sleep for 3 days, then started what I thought was a cold, but it didn't stop, it just carried on for weeks and weeks getting worse - it was the samters developing, first the polyps and sinusitis then the asthma. But that difficult weekend was the start of it all.I know it's not as stressful as divorce, but I still remember how very stressed I felt - it was an acute stress on top of longer-term stress. Also, my symptoms are always worse now when I'm stressed...that makes sense really! BeckyBob <rthomp0215@...> wrote: It could. Mine came after a very stressful period. I've been very happy for the past two weeks, and my polyps are shrinking. Although, I'm also taking vitamin C, drinking more water, eating oranges and exercising pursuant to helpful posts about the same time, so I can't say that stress is the only factor. ----- Original

Message ----From: wkapikorn <wkapikorn >samters Sent: Monday, June 16, 2008 11:18:31 AMSubject: RE: Variant angina and Samter's Certainly seems like divorce has played havoc on a lot of our lives. Could samter's be triggered by stress? From: Breda OBrien <zippyelle (DOT) com>Subject: Re:

Variant angina and Samter'ssamters@groups .comDate: Sunday, June 15, 2008, 4:38 PM Afyso,If aspirin sensitivity is genetic then I will shoot myself (joke). I have four children and it would kill me to think that this is the inheritance that we have provided for them. What amazes me is that there is absolutely no one in Toms family who suffers from nasal polyps. Asthma yes, but then ever second cough is diagnosed as asthma these days. The only thing is that Tom is an only son with 3 sisters - so maybe this plays a part. Then as is the case with Cystic Fibrosis maybe genes have to come from both parents to trigger defect. His parents are both still alive - his father will be 89 next week and his mother 88 in August - so much for family

genes.Breda Variant angina and Samter's I found by chance this abstract, which says that some people have genetic thromboxane receptor defects, and that they are more likely to have aspirin-intolerant asthma. It does not say anything about any causality whatever behind the relationship, but it does mention the existence of thromboxane receptor antagonists and thromboxane synthase inhibitors, which may therefore be of some use against variant angina.------------ --------- --------Clin Exp

Allergy. 2005 May;35(5):585- 90. LinksAssociation of thromboxane A2 receptor gene polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma.Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon , Korea .BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a receptor for a potent bronchoconstrictor, TBXA2 which is known to be related to bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been found to be effective in the management of asthmatic patients. This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA). METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were

determined using a single-base extension method in 93 AIA patients compared with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs) recruited from the Korean population. HLA DPB1*0301 genotype was performed using a direct sequencing method. RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly higher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C polymorphism was also associated with extent of percent fall in forced expiratory volume in 1 s (FEV1) after the inhalation of lysine-acetyl salicylic acid in AIA patients (P=0.009); AIA patients homozygous for the +795 C allele had a greater percent fall of FEV1 compared with individuals with TBXA2R+795 CT or TT genotypes. The frequency of patients carrying both the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was significantly higher in AIA patients (29.4%) than in ATA patients (7.3%) (P=0.008, odds ratio=5.3). CONCLUSION: These results suggest that the

polymorphism of TBXA2R+795T>C may increase bronchoconstrictive response to ASA, which could contribute to the development of the AIA phenotype. Sent from . A Smarter Email. No virus found in this incoming message.Checked by AVG.Version: 8.0.100 / Virus Database: 270.3.0/1504 - Release Date: 6/15/2008 5:52 PM Messenger's gone Mobile ! Get it now! No virus found in this incoming message.Checked by AVG.Version: 8.0.100 / Virus Database: 270.3.0/1504 - Release Date: 6/15/2008 5:52 PM

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[Guest guest]

Yes I too suffer from ibs and am now suspecting it may have to do with additives

in food and salicytes in various food and drinks

Sent from my Verizon Wireless BlackBerry

Re: Variant angina and Samter's

samters

Date: Sunday, June 15, 2008, 4:38 PM

Afyso,

If aspirin sensitivity is genetic then I will shoot myself (joke). I have four

children and it would kill me to think that this is the inheritance that we have

provided for them. 

What amazes me is that there is absolutely no one in Toms family who suffers

from nasal polyps.  Asthma yes, but then ever second cough is diagnosed as

asthma these days.  The only thing is that Tom is an only son with 3 sisters -

so maybe this plays a part. Then as is the case with Cystic Fibrosis maybe genes

have to come from both parents to trigger defect. His parents are both still

alive - his father will be 89 next week and his mother 88 in August - so much

for family genes.

Breda

Variant angina and Samter's

I found by chance this abstract, which says that some people have genetic

thromboxane receptor defects, and that they are more likely to have

aspirin-intolerant asthma. It does not say anything about any causality whatever

behind the relationship, but it does mention the existence of thromboxane

receptor antagonists and thromboxane synthase inhibitors, which may therefore be

of some use against variant angina.

------------ --------- --------

Clin Exp Allergy. 2005 May;35(5):585- 90. Links

Association of thromboxane A2 receptor gene polymorphism with the phenotype of

acetyl salicylic acid-intolerant asthma.

Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.

Department of Allergy and Rheumatology, Ajou University School of Medicine,

Suwon, Korea.

BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a receptor for

a potent bronchoconstrictor, TBXA2 which is known to be related to bronchial

asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors

have been found to be effective in the management of asthmatic patients. This

study was aimed to evaluate whether genetic variants of TBXA2R may be related

with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA).

METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were

determined using a single-base extension method in 93 AIA patients compared with

172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs)

recruited from the Korean population. HLA DPB1*0301 genotype was performed using

a direct sequencing method.

RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly higher

in AIA than in ATA (P=0.03) and the TBXA2R+795T>C polymorphism was also

associated with extent of percent fall in forced expiratory volume in 1 s (FEV1)

after the inhalation of lysine-acetyl salicylic acid in AIA patients (P=0.009);

AIA patients homozygous for the +795 C allele had a greater percent fall of FEV1

compared with individuals with TBXA2R+795 CT or TT genotypes. The frequency of

patients carrying both the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was

significantly higher in AIA patients (29.4%) than in ATA patients (7.3%)

(P=0.008, odds ratio=5.3).

CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C may

increase bronchoconstrictive response to ASA, which could contribute to the

development of the AIA phenotype.

[Guest guest]

Could someone remind me who sent the original e-mail describing how they were eating a number of oranges a day, etc. and having relief? There have been so many e-mails over the last week and I really had meant to write down what this individual was taking along with a certain number of oranges a day. Maybe it was also the onion irrigation. Anyway, I am ready to start anything at this point. If anyone knows where I might find that e-mail, I would sure appreciate it.

Thanks,

Jane

From: Breda OBrien <zippyelle (DOT) com>Subject: Re: Variant angina and Samter'ssamters@groups .comDate: Sunday, June 15, 2008, 4:38 PM

Afyso,If aspirin sensitivity is genetic then I will shoot myself (joke). I have four children and it would kill me to think that this is the inheritance that we have provided for them. What amazes me is that there is absolutely no one in Toms family who suffers from nasal polyps. Asthma yes, but then ever second cough is diagnosed as asthma these days. The only thing is that Tom is an only son with 3 sisters - so maybe this plays a part. Then as is the case with Cystic Fibrosis maybe genes have to come from both parents to trigger defect. His parents are both still alive - his father will be 89 next week and his mother 88 in August - so much for family genes.Breda

Variant angina and Samter's

I found by chance this abstract, which says that some people have genetic thromboxane receptor defects, and that they are more likely to have aspirin-intolerant asthma. It does not say anything about any causality whatever behind the relationship, but it does mention the existence of thromboxane receptor antagonists and thromboxane synthase inhibitors, which may therefore be of some use against variant angina.------------ --------- --------Clin Exp Allergy. 2005 May;35(5):585- 90. LinksAssociation of thromboxane A2 receptor gene polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma.Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon , Korea .BACKGROUND AND OBJECTIVE: The

thromboxane A2 receptor (TBXA2R) is a receptor for a potent bronchoconstrictor, TBXA2 which is known to be related to bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been found to be effective in the management of asthmatic patients. This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA). METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were determined using a single-base extension method in 93 AIA patients compared with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs) recruited from the Korean population. HLA DPB1*0301 genotype was performed using a direct sequencing method. RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly higher in AIA than in ATA (P=0.03) and the

TBXA2R+795T>C polymorphism was also associated with extent of percent fall in forced expiratory volume in 1 s (FEV1) after the inhalation of lysine-acetyl salicylic acid in AIA patients (P=0.009); AIA patients homozygous for the +795 C allele had a greater percent fall of FEV1 compared with individuals with TBXA2R+795 CT or TT genotypes. The frequency of patients carrying both the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was significantly higher in AIA patients (29.4%) than in ATA patients (7.3%) (P=0.008, odds ratio=5.3). CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C may increase bronchoconstrictive response to ASA, which could contribute to the development of the AIA phenotype.

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[Guest guest]

I suffered with IBS for most of my young life through about my early 30s. I found, and research supports, that if you take at least, 250mg of magnesium a day, the symptoms go away. Many believe that IBS is directly related to a magnesium deficiency. I find that when I start skipping it, I run into trouble again. I take 500 mg. daily at bedtime.

Jane

From: Breda OBrien <zippyelle@...>

Subject: Re: Variant angina and Samter's

samters

Date: Sunday, June 15, 2008, 4:38 PM

Afyso,

If aspirin sensitivity is genetic then I will shoot myself (joke). I have four

children and it would kill me to think that this is the inheritance that we

have provided for them. What amazes me is that there is absolutely no one in Toms family who suffers

from nasal polyps. Asthma yes, but then ever second cough is diagnosed as

asthma these days. The only thing is that Tom is an only son with 3 sisters -

so maybe this plays a part. Then as is the case with Cystic Fibrosis maybe genes

have to come from both parents to trigger defect. His parents are both still

alive - his father will be 89 next week and his mother 88 in August - so much

for family genes.

Breda

Variant angina and Samter's

I found by chance this abstract, which says that some people have genetic

thromboxane receptor defects, and that they are more likely to have

aspirin-intolerant asthma. It does not say anything about any causality

whatever behind the relationship, but it does mention the existence of

thromboxane receptor antagonists and thromboxane synthase inhibitors, which may

therefore be of some use against variant angina.

------------ --------- --------

Clin Exp Allergy. 2005 May;35(5):585- 90. Links

Association of thromboxane A2 receptor gene polymorphism with the phenotype of

acetyl salicylic acid-intolerant asthma.

Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.

Department of Allergy and Rheumatology, Ajou University School of Medicine,

Suwon, Korea.

BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a receptor

for a potent bronchoconstrictor, TBXA2 which is known to be related to

bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase

inhibitors have been found to be effective in the management of asthmatic

patients. This study was aimed to evaluate whether genetic variants of TBXA2R

may be related with development of acetyl salicylic acid (ASA)-intolerant

asthma (AIA). METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were

determined using a single-base extension method in 93 AIA patients compared

with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs)

recruited from the Korean population. HLA DPB1*0301 genotype was performed

using a direct sequencing method. RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly

higher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C polymorphism was

also associated with extent of percent fall in forced expiratory volume in 1 s

(FEV1) after the inhalation of lysine-acetyl salicylic acid in AIA patients

(P=0.009); AIA patients homozygous for the +795 C allele had a greater percent

fall of FEV1 compared with individuals with TBXA2R+795 CT or TT genotypes. The

frequency of patients carrying both the TBXA2R+795T>C rare allele and HLA

DPB1(*)0301 was significantly higher in AIA patients (29.4%) than in ATA

patients (7.3%) (P=0.008, odds ratio=5.3). CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C may

increase bronchoconstrictive response to ASA, which could contribute to the

development of the AIA phenotype.

------------------------------------

[Guest guest]

I have been diagnosed with Samters almost as long as I have been married! That's 28 years! I often tell my hubby that he is the number one Polyp in my life. Actually, our life has been anything but stress-free and I can most definitely note times in my life when flare ups occurred at very stressful times. In fact, most of my 13 polyp surgeries seemed to always happen at the worst times, when we had no money or some other significant issue was happening at the same time. I definitely feel there is a relationship between stress and flare-ups.

Jane

From: Breda OBrien <zippyelle (DOT) com>Subject: Re: Variant angina and Samter'ssamters@groups .comDate: Sunday, June 15, 2008, 4:38 PM

Afyso,If aspirin sensitivity is genetic then I will shoot myself (joke). I have four children and it would kill me to think that this is the inheritance that we have provided for them. What amazes me is that there is absolutely no one in Toms family who suffers from nasal polyps. Asthma yes, but then ever second cough is diagnosed as asthma these days. The only thing is that Tom is an only son with 3 sisters - so maybe this plays a part. Then as is the case with Cystic Fibrosis maybe genes have to come from both parents to trigger defect. His parents are both still alive - his father will be 89 next week and his mother 88 in August - so much for family genes.Breda

Variant angina and Samter's

I found by chance this abstract, which says that some people have genetic thromboxane receptor defects, and that they are more likely to have aspirin-intolerant asthma. It does not say anything about any causality whatever behind the relationship, but it does mention the existence of thromboxane receptor antagonists and thromboxane synthase inhibitors, which may therefore be of some use against variant angina.------------ --------- --------Clin Exp Allergy. 2005 May;35(5):585- 90. LinksAssociation of thromboxane A2 receptor gene polymorphism with the phenotype of acetyl salicylic acid-intolerant asthma.Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon , Korea .BACKGROUND AND OBJECTIVE: The

thromboxane A2 receptor (TBXA2R) is a receptor for a potent bronchoconstrictor, TBXA2 which is known to be related to bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been found to be effective in the management of asthmatic patients. This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA). METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were determined using a single-base extension method in 93 AIA patients compared with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs) recruited from the Korean population. HLA DPB1*0301 genotype was performed using a direct sequencing method. RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly higher in AIA than in ATA (P=0.03) and the

TBXA2R+795T>C polymorphism was also associated with extent of percent fall in forced expiratory volume in 1 s (FEV1) after the inhalation of lysine-acetyl salicylic acid in AIA patients (P=0.009); AIA patients homozygous for the +795 C allele had a greater percent fall of FEV1 compared with individuals with TBXA2R+795 CT or TT genotypes. The frequency of patients carrying both the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was significantly higher in AIA patients (29.4%) than in ATA patients (7.3%) (P=0.008, odds ratio=5.3). CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C may increase bronchoconstrictive response to ASA, which could contribute to the development of the AIA phenotype.

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[Guest guest]

I took 5-htp tablets in the UK which had magnesium and found

improvements in both polyp control and my nervousness not to mention my sleeping.

I agree with the stress comments, I endured a huge amount of

stress I my life and used to break out in a rash years ago but now affects me

in different ways. I struggle character wise to find contentment and relax, if

you place me in a cardboard box I will still be jumping finding things to talk,

do and organise.

From: samters

[mailto:samters ] On Behalf Of Jane Marino

Sent: 16 June, 2008 18:50

samters

Subject: Re: Variant angina and Samter's

I

suffered with IBS for most of my young life through about my early 30s.

I found, and research supports, that if you take at least, 250mg of magnesium

a day, the symptoms go away. Many believe that IBS is directly related

to a magnesium deficiency. I find that when I start skipping it, I run

into trouble again. I take 500 mg. daily at bedtime.

Jane

From: Breda OBrien <zippyelle@...>Subject: Re: Variant angina and Samter'ssamters Date: Sunday, June 15, 2008, 4:38 PM Afyso, If aspirin sensitivity is genetic then I will shoot myself (joke). I have fourchildren and it would kill me to think that this is the inheritance that wehave provided for them. What amazes me is that there is absolutely no one in Toms family who suffersfrom nasal polyps. Asthma yes, but then ever second cough is diagnosed asasthma these days. The only thing is that Tom is an only son with 3 sisters -so maybe this plays a part. Then as is the case with Cystic Fibrosis maybe geneshave to come from both parents to trigger defect. His parents are both stillalive - his father will be 89 next week and his mother 88 in August - so muchfor family genes. Breda Variant angina and Samter's I found by chance this abstract, which says that some people have geneticthromboxane receptor defects, and that they are more likely to haveaspirin-intolerant asthma. It does not say anything about any causalitywhatever behind the relationship, but it does mention the existence ofthromboxane receptor antagonists and thromboxane synthase inhibitors, which maytherefore be of some use against variant angina. ------------ --------- -------- Clin Exp Allergy. 2005 May;35(5):585- 90. LinksAssociation of thromboxane A2 receptor gene polymorphism with the phenotype ofacetyl salicylic acid-intolerant asthma.Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.Department of Allergy and Rheumatology, Ajou University School of Medicine,Suwon, Korea. BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a receptorfor a potent bronchoconstrictor, TBXA2 which is known to be related tobronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthaseinhibitors have been found to be effective in the management of asthmaticpatients. This study was aimed to evaluate whether genetic variants of TBXA2Rmay be related with development of acetyl salicylic acid (ASA)-intolerantasthma (AIA). METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) weredetermined using a single-base extension method in 93 AIA patients comparedwith 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs)recruited from the Korean population. HLA DPB1*0301 genotype was performedusing a direct sequencing method. RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantlyhigher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C polymorphism wasalso associated with extent of percent fall in forced expiratory volume in 1 s(FEV1) after the inhalation of lysine-acetyl salicylic acid in AIA patients(P=0.009); AIA patients homozygous for the +795 C allele had a greater percentfall of FEV1 compared with individuals with TBXA2R+795 CT or TT genotypes. Thefrequency of patients carrying both the TBXA2R+795T>C rare allele and HLADPB1(*)0301 was significantly higher in AIA patients (29.4%) than in ATApatients (7.3%) (P=0.008, odds ratio=5.3). CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C mayincrease bronchoconstrictive response to ASA, which could contribute to thedevelopment of the AIA phenotype. ------------------------------------

[Guest guest]

Samter's is indeed genetic in origin, ie patients have what is called a

gene polymorphism (or maybe several, this is not really that well

established), meaning a genetic variation, that affects what is known as

the arachidonic acid metabolism, a chemical cascade of reactions, and

this pathway does not function exactly the way it ought to.

But empirical observations show that this does not mean at all that all

descendants of a patient will develop the disease, and even if it

develops in some children, the form it takes may vary from one

generation to the other as well as from one sibling to another. Like all

genes, there is no certainty that the gene will be inherited in the same

form, and even then, there is no certainty that the gene will express

itself. Many genes stay quiet for the better !

To express itself, it has been hypothesized that this gene (like others,

this is not really specific behaviour) needs triggers that can be

internal or environmental. Some articles speak of viruses, smoke,

diesel particles or similar things as potential triggers. Maybe taking

aspirin or NSAIDS can be counted as triggers, meaning that they may

" wake up " the gene, but I don't remember if it has been demonstrated or

not.

So, whatever, the sensible attitude should be that, since we do not know

whether or not our children have inherited any gene, they should be as

reasonably as possible spared excessive exposure to potential triggers.

For instance, smoking would be a risk ; working in a heavily polluted

environment might be another ; same thing for taking aspirin or NSAIDS.

>

> Afyso,

>

> If aspirin sensitivity is genetic then I will shoot myself (joke). I

have four children and it would kill me to think that this is the

inheritance that we have provided for them.

>

> What amazes me is that there is absolutely no one in Toms family who

suffers from nasal polyps. Asthma yes, but then ever second cough is

diagnosed as asthma these days. The only thing is that Tom is an only

son with 3 sisters - so maybe this plays a part. Then as is the case

with Cystic Fibrosis maybe genes have to come from both parents to

trigger defect. His parents are both still alive - his father will be 89

next week and his mother 88 in August - so much for family genes.

>

> Breda

>

>

>

> Variant angina and Samter's

>

>

> I found by chance this abstract, which says that some people have

genetic thromboxane receptor defects, and that they are more likely to

have aspirin-intolerant asthma. It does not say anything about any

causality whatever behind the relationship, but it does mention the

existence of thromboxane receptor antagonists and thromboxane synthase

inhibitors, which may therefore be of some use against variant angina.

>

> ------------ --------- --------

>

> Clin Exp Allergy. 2005 May;35(5):585- 90. Links

> Association of thromboxane A2 receptor gene polymorphism with the

phenotype of acetyl salicylic acid-intolerant asthma.

> Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.

> Department of Allergy and Rheumatology, Ajou University School of

Medicine, Suwon, Korea.

>

> BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a

receptor for a potent bronchoconstrictor, TBXA2 which is known to be

related to bronchial asthma and myocardial infarction. TBXA2R antagonist

and TBX synthase inhibitors have been found to be effective in the

management of asthmatic patients. This study was aimed to evaluate

whether genetic variants of TBXA2R may be related with development of

acetyl salicylic acid (ASA)-intolerant asthma (AIA).

>

> METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were

determined using a single-base extension method in 93 AIA patients

compared with 172 patients with ASA-tolerant asthma (ATA) and 118 normal

controls (NCs) recruited from the Korean population. HLA DPB1*0301

genotype was performed using a direct sequencing method.

>

> RESULTS: The rare C allele frequency of TBXA2R+795T>C was

significantly higher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C

polymorphism was also associated with extent of percent fall in forced

expiratory volume in 1 s (FEV1) after the inhalation of lysine-acetyl

salicylic acid in AIA patients (P=0.009); AIA patients homozygous for

the +795 C allele had a greater percent fall of FEV1 compared with

individuals with TBXA2R+795 CT or TT genotypes. The frequency of

patients carrying both the TBXA2R+795T>C rare allele and HLA DPB1(*)0301

was significantly higher in AIA patients (29.4%) than in ATA patients

(7.3%) (P=0.008, odds ratio=5.3).

>

> CONCLUSION: These results suggest that the polymorphism of

TBXA2R+795T>C may increase bronchoconstrictive response to ASA, which

could contribute to the development of the AIA phenotype.

>

[Guest guest]

This is real-time experimentation ! More seriously, it shows some

medical research can really help.

This also looks like good news for you, and thanks for the info.

> >

> > I found by chance this abstract, which says that some people have

> > genetic thromboxane receptor defects, and that they are more likely

> to

> > have aspirin-intolerant asthma. It does not say anything about any

> > causality whatever behind the relationship, but it does mention the

> > existence of thromboxane receptor antagonists and thromboxane

> synthase

> > inhibitors, which may therefore be of some use against variant

> angina.

> >

> > -----------------------------

> >

> > Clin Exp Allergy. 2005 May;35(5):585-90. Links

> > Association of thromboxane A2 receptor gene polymorphism with the

> > phenotype of acetyl salicylic acid-intolerant asthma.

> > Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.

> > Department of Allergy and Rheumatology, Ajou University School of

> > Medicine, Suwon, Korea.

> >

> > BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a

> > receptor for a potent bronchoconstrictor, TBXA2 which is known to be

> > related to bronchial asthma and myocardial infarction. TBXA2R

> antagonist

> > and TBX synthase inhibitors have been found to be effective in the

> > management of asthmatic patients. This study was aimed to evaluate

> > whether genetic variants of TBXA2R may be related with development

> of

> > acetyl salicylic acid (ASA)-intolerant asthma (AIA).

> >

> > METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C)

> were

> > determined using a single-base extension method in 93 AIA patients

> > compared with 172 patients with ASA-tolerant asthma (ATA) and 118

> normal

> > controls (NCs) recruited from the Korean population. HLA DPB1*0301

> > genotype was performed using a direct sequencing method.

> >

> > RESULTS: The rare C allele frequency of TBXA2R+795T>C was

> significantly

> > higher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C

> polymorphism

> > was also associated with extent of percent fall in forced expiratory

> > volume in 1 s (FEV1) after the inhalation of lysine-acetyl salicylic

> > acid in AIA patients (P=0.009); AIA patients homozygous for the

> +795 C

> > allele had a greater percent fall of FEV1 compared with individuals

> with

> > TBXA2R+795 CT or TT genotypes. The frequency of patients carrying

> both

> > the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was significantly

> > higher in AIA patients (29.4%) than in ATA patients (7.3%) (P=0.008,

> > odds ratio=5.3).

> >

> > CONCLUSION: These results suggest that the polymorphism of

> TBXA2R+795T>C

> > may increase bronchoconstrictive response to ASA, which could

> contribute

> > to the development of the AIA phenotype.

> >

>

[Guest guest]

I took 5-htp tablets in the

UK which had magnesium and found improvements in both polyp control and my

nervousness not to mention my sleeping.

I agree with the stress

comments, I endured a huge amount of stress I my life and used to break out in

a rash years ago but now affects me in different ways. I struggle character

wise to find contentment and relax, if you place me in a cardboard box I will

still be jumping finding things to talk, do and organise.

From: samters

[mailto:samters ]

On Behalf Of Jane Marino

Sent: 16 June, 2008 18:50

samters

Subject: Re: Variant

angina and Samter's

I suffered with IBS for most

of my young life through about my early 30s. I found, and research

supports, that if you take at least, 250mg of magnesium a day, the symptoms go

away. Many believe that IBS is directly related to a magnesium

deficiency. I find that when I start skipping it, I run into trouble

again. I take 500 mg. daily at bedtime.

Jane

From: Breda OBrien <zippyelle@...>

Subject:

Re: Variant angina and Samter's

To:

samters

Date:

Sunday, June 15, 2008, 4:38 PM

Afyso,

If

aspirin sensitivity is genetic then I will shoot myself (joke). I have four

children

and it would kill me to think that this is the inheritance that we

have

provided for them.

What

amazes me is that there is absolutely no one in Toms family who suffers

from

nasal polyps. Asthma yes, but then ever second cough is diagnosed as

asthma

these days. The only thing is that Tom is an only son with 3 sisters -

so

maybe this plays a part. Then as is the case with Cystic Fibrosis maybe genes

have

to come from both parents to trigger defect. His parents are both still

alive

- his father will be 89 next week and his mother 88 in August - so much

for

family genes.

Breda

-----

Original Message ----

From:

asfyso <asfyso (DOT) fr>

To:

samters@groups .com

Sent:

Sunday, June 15, 2008 5:35:06 PM

Subject:

Variant angina and Samter's

I

found by chance this abstract, which says that some people have genetic

thromboxane

receptor defects, and that they are more likely to have

aspirin-intolerant

asthma. It does not say anything about any causality

whatever

behind the relationship, but it does mention the existence of

thromboxane

receptor antagonists and thromboxane synthase inhibitors, which may

therefore

be of some use against variant angina.

------------

--------- --------

Clin

Exp Allergy. 2005 May;35(5):585- 90. Links

Association

of thromboxane A2 receptor gene polymorphism with the phenotype of

acetyl

salicylic acid-intolerant asthma.

Kim

SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD.

Department

of Allergy and Rheumatology, Ajou University School of Medicine,

Suwon,

Korea.

BACKGROUND

AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a receptor

for

a potent bronchoconstrictor, TBXA2 which is known to be related to

bronchial

asthma and myocardial infarction. TBXA2R antagonist and TBX synthase

inhibitors

have been found to be effective in the management of asthmatic

patients.

This study was aimed to evaluate whether genetic variants of TBXA2R

may

be related with development of acetyl salicylic acid (ASA)-intolerant

asthma

(AIA).

METHODS:

TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were

determined

using a single-base extension method in 93 AIA patients compared

with

172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs)

recruited

from the Korean population. HLA DPB1*0301 genotype was performed

using

a direct sequencing method.

RESULTS:

The rare C allele frequency of TBXA2R+795T>C was significantly

higher

in AIA than in ATA (P=0.03) and the TBXA2R+795T>C polymorphism was

also

associated with extent of percent fall in forced expiratory volume in 1 s

(FEV1)

after the inhalation of lysine-acetyl salicylic acid in AIA patients

(P=0.009);

AIA patients homozygous for the +795 C allele had a greater percent

fall

of FEV1 compared with individuals with TBXA2R+795 CT or TT genotypes. The

frequency

of patients carrying both the TBXA2R+795T>C rare allele and HLA

DPB1(*)0301

was significantly higher in AIA patients (29.4%) than in ATA

patients

(7.3%) (P=0.008, odds ratio=5.3).

CONCLUSION:

These results suggest that the polymorphism of TBXA2R+795T>C may

increase

bronchoconstrictive response to ASA, which could contribute to the

development

of the AIA phenotype.

------------------------------------

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[Guest guest]

GOD BLESS YOU! THANK YOU! I will go buy the magnesium Tomorrow! I really am thankful for all the "group wisdom" . . . not to mention the understanding from all of you. You have really improved my life. From: Breda OBrien <zippyelle (DOT) com> Subject: Re: Variant angina and Samter's samters@groups .com Date: Sunday, June 15, 2008, 4:38 PM

Afyso, If aspirin sensitivity is genetic then I will shoot myself (joke). I have four children and it would kill me to think that this is the inheritance that we have provided for them. What amazes me is that there is absolutely no one in Toms family who suffers from nasal polyps. Asthma yes, but then ever second cough is diagnosed as

asthma these days. The only thing is that Tom is an only son with 3 sisters - so maybe this plays a part. Then as is the case with Cystic Fibrosis maybe genes have to come from both parents to trigger defect. His parents are both still alive - his father will be 89 next week and his mother 88 in August - so much for family genes. Breda

Variant angina and Samter's I found by chance this abstract, which says that some people have genetic thromboxane receptor defects, and that they are more likely to have aspirin-intolerant

asthma. It does not say anything about any causality whatever behind the relationship, but it does mention the existence of thromboxane receptor antagonists and thromboxane synthase inhibitors, which may therefore be of some use against variant angina. ------------ --------- -------- Clin Exp Allergy. 2005 May;35(5):585- 90. Links Association of thromboxane A2 receptor gene polymorphism with the phenotype of

acetyl salicylic acid-intolerant asthma. Kim SH, Choi JH, Park HS, Holloway JW, Lee SK, Park CS, Shin HD. Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon, Korea. BACKGROUND AND OBJECTIVE: The thromboxane A2 receptor (TBXA2R) is a receptor for a potent bronchoconstrictor, TBXA2 which is known to be related to bronchial asthma and myocardial infarction. TBXA2R antagonist and TBX synthase inhibitors have been found to be effective in the

management of asthmatic patients. This study was aimed to evaluate whether genetic variants of TBXA2R may be related with development of acetyl salicylic acid (ASA)-intolerant asthma (AIA). METHODS: TBXA2R gene polymorphisms (TBXA2R+795T>C, TBXA2R+924T>C) were determined using a single-base extension method in 93 AIA patients compared with 172 patients with ASA-tolerant asthma (ATA) and 118 normal controls (NCs) recruited from the Korean population. HLA DPB1*0301

genotype was performed using a direct sequencing method. RESULTS: The rare C allele frequency of TBXA2R+795T>C was significantly higher in AIA than in ATA (P=0.03) and the TBXA2R+795T>C polymorphism was also associated with extent of percent fall in forced expiratory volume in 1 s (FEV1) after the inhalation of lysine-acetyl salicylic acid in AIA patients (P=0.009); AIA patients homozygous for the +795 C allele had a greater percent fall of FEV1 compared with individuals

with TBXA2R+795 CT or TT genotypes. The frequency of patients carrying both the TBXA2R+795T>C rare allele and HLA DPB1(*)0301 was significantly higher in AIA patients (29.4%) than in ATA patients (7.3%) (P=0.008, odds ratio=5.3). CONCLUSION: These results suggest that the polymorphism of TBXA2R+795T>C may increase bronchoconstrictive response to ASA, which could contribute to the development of the AIA phenotype.

------------ --------- --------- ------

[Guest guest]

Steve, you described me to a 'T': a real stress bunny, always looking for something to do, happiest when I'm busy or around others who are busy (although I do love sitting and talking for hours on end!), and yes, since I started taking magnesium supplements my life is a lot more balanced and my symptoms lessened. For a while there I though I was bipolar 2, such was the see-sawing mood swings caused by samters.

wishing you good health, peace and prosperity, Beverley Paine

[Guest guest]

Excellent,

I think taking all the med’s affect our nervous systems as

I am jumpy and have palpatations for no reason, I have cut back to 2 coffee’s

max a day and sometimes none and taking some supplements make me feel a little

more relaxed. I aim to cut my coffee/caffeine intake further and I never ever

drink soft drinks like , fanta, sprite, coke etc these are a definite no no for

samters sufferers. It took me years to completely stop as I loved coke, Irn

Bru, lemonade but it’s makes a huge difference. Also without getting any

deeper into this subject I love my wine and have now found some great Organic

brands which I stock up on, cheap wine generally means more acid and more

problems with sneezing etc with sulphites but this is an area most samters suffers

should look at sorting out, and also I do not drink beer/lager it gives me an

instant sore head and the hangover is terrible.

Any beer/lager drinkers out there to comment on this, I just can’t

handle beers/lagers not sure if it’s the chemicals , wheat whatever,

yeast……

Cheers

Steve

From: samters

[mailto:samters ] On Behalf Of Beverley Paine

Sent: 16 July, 2008 20:06

samters

Subject: Re: Variant angina and Samter's

Steve, you described me to a 'T': a

real stress bunny, always looking for something to do, happiest when I'm busy

or around others who are busy (although I do love sitting and talking for hours

on end!), and yes, since I started taking magnesium supplements my life is a

lot more balanced and my symptoms lessened. For a while there I though I was

bipolar 2, such was the see-sawing mood swings caused by samters.

wishing you good health, peace and prosperity,

Beverley Paine

[Guest guest]

Actually, I think it more boils down to what affects different people and how. I live on caffeine. I drink a 16 oz travel mug of coffee in the morning and at least 3 12 oz diet coke's every day during the week. There was a period a couple years ago I had to go completely off caffeine for several months due to unexplained tachycardia. I did not notice any improvement in my sinus health during that time. And the tachycardia was never explained but ultimately blamed on stress and less-than-fully-controlled asthma (and it did go away and I am back to drinking my normal amount of caffeine!). I drink beer and wine. Yes, they stuff me up and usually after 1 beer or 1-2 glasses of wine I am stuffy and can't smell anything but by morning I am fine, so I refuse to give them up. Sometimes I drink these things and don't have problems, sometimes the problems are worse. No idea what it is, but I suspect alcohol in general as mixed drinks will also make me stuffy. Go figure. But I think it boils down to no, I can't explain what it is in beer that affects you. For me I suspect it is my strong grass allergies affecting me. But who knows?

K.

On Fri, Jul 18, 2008 at 12:23 PM, Steve <skunkburner@...> wrote:

Excellent,

I think taking all the med's affect our nervous systems as I am jumpy and have palpatations for no reason, I have cut back to 2 coffee's max a day and sometimes none and taking some supplements make me feel a little more relaxed. I aim to cut my coffee/caffeine intake further and I never ever drink soft drinks like , fanta, sprite, coke etc these are a definite no no for samters sufferers. It took me years to completely stop as I loved coke, Irn Bru, lemonade but it's makes a huge difference. Also without getting any deeper into this subject I love my wine and have now found some great Organic brands which I stock up on, cheap wine generally means more acid and more problems with sneezing etc with sulphites but this is an area most samters suffers should look at sorting out, and also I do not drink beer/lager it gives me an instant sore head and the hangover is terrible.

Any beer/lager drinkers out there to comment on this, I just can't handle beers/lagers not sure if it's the chemicals , wheat whatever, yeast……

Cheers

Steve

From: samters [mailto:samters ] On Behalf Of Beverley Paine

Sent: 16 July, 2008 20:06samters Subject: Re: Variant angina and Samter's

Steve, you described me to a 'T': a real stress bunny, always looking for something to do, happiest when I'm busy or around others who are busy (although I do love sitting and talking for hours on end!), and yes, since I started taking magnesium supplements my life is a lot more balanced and my symptoms lessened. For a while there I though I was bipolar 2, such was the see-sawing mood swings caused by samters.

wishing you good health, peace and prosperity, Beverley Paine

[Guest guest]

I’m sure the medications have to affect

the nervous system. I was put on anti depressants because of anxiety attacks

and still get jumpy or agitated, more so if I have too much coffee or fizzy

drinks. In Australia

there’s organic wines and I’ve found them to be excellent as I love the odd

glass. I would have around two beers a year if that and only if it’s very hot

and I’m extremely thirsty, but they’re ‘lite’ so no problems.

I’m going to try the magnesium supplements

though after reading your comment Beverley

From: Steve

[mailto:skunkburner@...]

Sent: Saturday, 19 July 2008 2:24

AM

samters

Subject: RE: Re: Variant

angina and Samter's

Importance: High

Excellent,

I think taking all the med’s affect our nervous systems as I am

jumpy and have palpatations for no reason, I have cut back to 2 coffee’s max a

day and sometimes none and taking some supplements make me feel a little more

relaxed. I aim to cut my coffee/caffeine intake further and I never ever drink

soft drinks like , fanta, sprite, coke etc these are a definite no no for

samters sufferers. It took me years to completely stop as I loved coke, Irn

Bru, lemonade but it’s makes a huge difference. Also without getting any deeper

into this subject I love my wine and have now found some great Organic brands

which I stock up on, cheap wine generally means more acid and more problems

with sneezing etc with sulphites but this is an area most samters suffers

should look at sorting out, and also I do not drink beer/lager it gives me an

instant sore head and the hangover is terrible.

Any beer/lager drinkers out there to comment on this, I just

can’t handle beers/lagers not sure if it’s the chemicals , wheat whatever,

yeast……

Cheers

Steve

From: samters

[mailto:samters ]

On Behalf Of Beverley Paine

Sent: 16 July, 2008 20:06

samters

Subject: Re: Variant

angina and Samter's

Steve, you described me to a 'T': a real stress bunny, always

looking for something to do, happiest when I'm busy or around others who are

busy (although I do love sitting and talking for hours on end!), and yes, since

I started taking magnesium supplements my life is a lot more balanced and my

symptoms lessened. For a while there I though I was bipolar 2, such was the

see-sawing mood swings caused by samters.

wishing you good health, peace and prosperity,

Beverley Paine

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I cannot drink any alcohol, especially wine. My understanding is that it is the yeast used in the fermenting process that is left over especially in wine and beers that is the culprit.

Excellent,

I think taking all the med's affect our nervous systems as I am jumpy and have palpatations for no reason, I have cut back to 2 coffee's max a day and sometimes none and taking some supplements make me feel a little more relaxed. I aim to cut my coffee/caffeine intake further and I never ever drink soft drinks like , fanta, sprite, coke etc these are a definite no no for samters sufferers. It took me years to completely stop as I loved coke, Irn Bru, lemonade but it's makes a huge difference. Also without getting any deeper into this subject I love my wine and have now found some great Organic brands which I stock up on, cheap wine generally means more acid and more problems with sneezing etc with sulphites but this is an area most samters suffers should look at sorting out, and also I do not drink beer/lager it gives me an instant sore head and the hangover is terrible.

Any beer/lager drinkers out there to comment on this, I just can't handle beers/lagers not sure if it's the chemicals , wheat whatever, yeast……

Cheers

Steve

From: samters [mailto:samters ] On Behalf Of Beverley PaineSent: 16 July, 2008 20:06samters Subject: Re: Variant angina and Samter's

Steve, you described me to a 'T': a real stress bunny, always looking for something to do, happiest when I'm busy or around others who are busy (although I do love sitting and talking for hours on end!), and yes, since I started taking magnesium supplements my life is a lot more balanced and my symptoms lessened. For a while there I though I was bipolar 2, such was the see-sawing mood swings caused by samters.

wishing you good health, peace and prosperity, Beverley Paine