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Unfortunately, no. Someone correct me if I'm wrong, but there is no evidence that removal of the colon prevents PSC. PSC is thought to be an autoimmune disease, like UC is. The " trigger " is still there, whether the colon is or not.

Arne

55 - UC 1977, PSC 2000

Alive and (mostly) well in Minnesota

________________________________

From: [mailto: ] On Behalf Of keithrschmidt

....If I get my colon removed are my chances less that I will get PSC in

the future? I am thinking about surgery for my UC and if it would

help prevent PSC that would be great too. I'm getting fed up with the

whole medicine thing and when will I flare again worries.

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Unfortunately, no. Someone correct me if I'm wrong, but there is no evidence that removal of the colon prevents PSC. PSC is thought to be an autoimmune disease, like UC is. The " trigger " is still there, whether the colon is or not.

Arne

55 - UC 1977, PSC 2000

Alive and (mostly) well in Minnesota

________________________________

From: [mailto: ] On Behalf Of keithrschmidt

....If I get my colon removed are my chances less that I will get PSC in

the future? I am thinking about surgery for my UC and if it would

help prevent PSC that would be great too. I'm getting fed up with the

whole medicine thing and when will I flare again worries.

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Guest guest

I understand that there will always be a chance of PSC but I was wondering if it was more likely if I still had UC. Plus I take 6-mp and my flares are severe; can severe flares attack your Liver since it is so close to your colon?

I was hoping that eliminating the 6-mp and the flares would lower my chances of getting PSC, or am I just wishing?

With UC don't you have a 5% chance of getting PSC? I was figuring if you didn't have UC anymore then the chances would be less for PSC.

Thanks

Unfortunately, no. Someone correct me if I'm wrong, but there is no evidence that removal of the colon prevents PSC. PSC is thought to be an autoimmune disease, like UC is. The " trigger " is still there, whether the colon is or not.

Arne 55 - UC 1977, PSC 2000 Alive and (mostly) well in Minnesota

________________________________

From: [

mailto: ] On Behalf Of keithrschmidt

....If I get my colon removed are my chances less that I will get PSC in

the future? I am thinking about surgery for my UC and if it would help prevent PSC that would be great too. I'm getting fed up with the

whole medicine thing and when will I flare again worries.

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Guest guest

I understand that there will always be a chance of PSC but I was wondering if it was more likely if I still had UC. Plus I take 6-mp and my flares are severe; can severe flares attack your Liver since it is so close to your colon?

I was hoping that eliminating the 6-mp and the flares would lower my chances of getting PSC, or am I just wishing?

With UC don't you have a 5% chance of getting PSC? I was figuring if you didn't have UC anymore then the chances would be less for PSC.

Thanks

Unfortunately, no. Someone correct me if I'm wrong, but there is no evidence that removal of the colon prevents PSC. PSC is thought to be an autoimmune disease, like UC is. The " trigger " is still there, whether the colon is or not.

Arne 55 - UC 1977, PSC 2000 Alive and (mostly) well in Minnesota

________________________________

From: [

mailto: ] On Behalf Of keithrschmidt

....If I get my colon removed are my chances less that I will get PSC in

the future? I am thinking about surgery for my UC and if it would help prevent PSC that would be great too. I'm getting fed up with the

whole medicine thing and when will I flare again worries.

Link to comment
Share on other sites

Guest guest

I understand that there will always be a chance of PSC but I was wondering if it was more likely if I still had UC. Plus I take 6-mp and my flares are severe; can severe flares attack your Liver since it is so close to your colon?

I was hoping that eliminating the 6-mp and the flares would lower my chances of getting PSC, or am I just wishing?

With UC don't you have a 5% chance of getting PSC? I was figuring if you didn't have UC anymore then the chances would be less for PSC.

Thanks

Unfortunately, no. Someone correct me if I'm wrong, but there is no evidence that removal of the colon prevents PSC. PSC is thought to be an autoimmune disease, like UC is. The " trigger " is still there, whether the colon is or not.

Arne 55 - UC 1977, PSC 2000 Alive and (mostly) well in Minnesota

________________________________

From: [

mailto: ] On Behalf Of keithrschmidt

....If I get my colon removed are my chances less that I will get PSC in

the future? I am thinking about surgery for my UC and if it would help prevent PSC that would be great too. I'm getting fed up with the

whole medicine thing and when will I flare again worries.

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Hi ;

These are tough questions. I've read that PSC can occur before

development of inflammatory bowel disease (IBD), at the same time, or

many years after development of IBD, and even after the colon is

removed. But you would think that keeping the IBD under control

should be helpful in reducing risk of PSC, and/or its rate of

progression? Dr. has developed a theory that there are

long-lived mucosal memory T-cells (lymphocytes) that originate in the

inflamed gut, and that drive the hepatic inflammation of PSC. These

memory T-cells may hang around, and remain capable of being

activated, for years after the bowel is removed.

________________________

Clin Med. 2004 Mar-Apr;4(2):173-80.

Lymphocyte homing in the pathogenesis of extra-intestinal

manifestations of inflammatory bowel disease.

Eksteen B, Miles AE, Grant AJ, DH.

Liver Research Laboratories, MRC Centre for Immune Regulation,

University of Birmingham, Queen Hospital, Birmingham.

Inflammatory bowel disease is associated with extra-intestinal

manifestations which occur either at the same time as flares of bowel

inflammation (skin and eye disease) or run a course that is

independent to inflammation in the bowel (liver and some joint

syndromes). It has been suggested that the skin and eye complications

occur as a consequence of the recruitment of activated effector cells

released from the gut into the circulation to extra-intestinal site

where they cause acute damage. However, this does not explain how

patients can develop primary sclerosing cholangitis many years after

having their colon removed for colitis. We propose that long-lived

populations of memory lymphocytes arise as a consequence of bowel

inflammation and that these cells express homing receptors that

direct their subsequent migration not only to the gut but also to the

liver. These long-lived cells may recirculate to the liver for many

years and, in the absence of a local activating stimulus, will not

cause damage. However, if they are subsequently activated in the

liver this will lead to the development of inflammation and tissue

damage which promotes the recruitment of more mucosal lymphocytes

resulting in persistent inflammation and disease. The recent findings

that MAdCAM-1 and CCL25, previously thought to be restricted to the

gut, are up-regulated in the liver during inflammatory liver diseases

that complicate IBD support the concept that common mechanisms

control lymphocyte recruitment to the inflamed liver and gut.

Publication Types:

Review

PMID: 15139741

________________________

(father of (21); PSC 07/03; UC 08/03)

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Guest guest

Hi ;

These are tough questions. I've read that PSC can occur before

development of inflammatory bowel disease (IBD), at the same time, or

many years after development of IBD, and even after the colon is

removed. But you would think that keeping the IBD under control

should be helpful in reducing risk of PSC, and/or its rate of

progression? Dr. has developed a theory that there are

long-lived mucosal memory T-cells (lymphocytes) that originate in the

inflamed gut, and that drive the hepatic inflammation of PSC. These

memory T-cells may hang around, and remain capable of being

activated, for years after the bowel is removed.

________________________

Clin Med. 2004 Mar-Apr;4(2):173-80.

Lymphocyte homing in the pathogenesis of extra-intestinal

manifestations of inflammatory bowel disease.

Eksteen B, Miles AE, Grant AJ, DH.

Liver Research Laboratories, MRC Centre for Immune Regulation,

University of Birmingham, Queen Hospital, Birmingham.

Inflammatory bowel disease is associated with extra-intestinal

manifestations which occur either at the same time as flares of bowel

inflammation (skin and eye disease) or run a course that is

independent to inflammation in the bowel (liver and some joint

syndromes). It has been suggested that the skin and eye complications

occur as a consequence of the recruitment of activated effector cells

released from the gut into the circulation to extra-intestinal site

where they cause acute damage. However, this does not explain how

patients can develop primary sclerosing cholangitis many years after

having their colon removed for colitis. We propose that long-lived

populations of memory lymphocytes arise as a consequence of bowel

inflammation and that these cells express homing receptors that

direct their subsequent migration not only to the gut but also to the

liver. These long-lived cells may recirculate to the liver for many

years and, in the absence of a local activating stimulus, will not

cause damage. However, if they are subsequently activated in the

liver this will lead to the development of inflammation and tissue

damage which promotes the recruitment of more mucosal lymphocytes

resulting in persistent inflammation and disease. The recent findings

that MAdCAM-1 and CCL25, previously thought to be restricted to the

gut, are up-regulated in the liver during inflammatory liver diseases

that complicate IBD support the concept that common mechanisms

control lymphocyte recruitment to the inflamed liver and gut.

Publication Types:

Review

PMID: 15139741

________________________

(father of (21); PSC 07/03; UC 08/03)

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Thanks for the replies... I am just wondering if the general consensus among the medical community is that the chances of getting PSC is NOT lowered if someone with UC has their colon removed. I know that there are always doctors out there that don't agree with the accepted medical theories.

I am also concerned with my medicine (6-mp), does that increase my chances of PSC? Or is PSC just an auto-immune disease and I won't be able to lower or raise my likely-hood of PSC no matter what I do?

I really do appreciate the forums' help...I had a scare with PSC last summer when I was in the hospital; I had all sorts of liver doctors visiting me and wanting to do tests on me (which I refused). I have learned a lot over the past year about UC and now I want to know as much about it as possible about PSC.

Thanks again!!!

Hi ;These are tough questions. I've read that PSC can occur before development of inflammatory bowel disease (IBD), at the same time, or many years after development of IBD, and even after the colon is removed. But you would think that keeping the IBD under control should be helpful in reducing risk of PSC, and/or its rate of progression? Dr. has developed a theory that there are long-lived mucosal memory T-cells (lymphocytes) that originate in the inflamed gut, and that drive the hepatic inflammation of PSC. These memory T-cells may hang around, and remain capable of being activated, for years after the bowel is removed.________________________

Clin Med. 2004 Mar-Apr;4(2):173-80. Lymphocyte homing in the pathogenesis of extra-intestinal manifestations of inflammatory bowel disease.Eksteen B, Miles AE, Grant AJ, DH.Liver Research Laboratories, MRC Centre for Immune Regulation, University of Birmingham, Queen Hospital, Birmingham.Inflammatory bowel disease is associated with extra-intestinal manifestations which occur either at the same time as flares of bowel inflammation (skin and eye disease) or run a course that is independent to inflammation in the bowel (liver and some joint syndromes). It has been suggested that the skin and eye complications occur as a consequence of the recruitment of activated effector cells released from the gut into the circulation to extra-intestinal site where they cause acute damage. However, this does not explain how patients can develop primary sclerosing cholangitis many years after having their colon removed for colitis. We propose that long-lived populations of memory lymphocytes arise as a consequence of bowel inflammation and that these cells express homing receptors that direct their subsequent migration not only to the gut but also to the liver. These long-lived cells may recirculate to the liver for many years and, in the absence of a local activating stimulus, will not cause damage. However, if they are subsequently activated in the liver this will lead to the development of inflammation and tissue damage which promotes the recruitment of more mucosal lymphocytes resulting in persistent inflammation and disease. The recent findings that MAdCAM-1 and CCL25, previously thought to be restricted to the gut, are up-regulated in the liver during inflammatory liver diseases that complicate IBD support the concept that common mechanisms control lymphocyte recruitment to the inflamed liver and gut.

Publication Types: ReviewPMID: 15139741________________________ (father of (21); PSC 07/03; UC 08/03)

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Thanks for the replies... I am just wondering if the general consensus among the medical community is that the chances of getting PSC is NOT lowered if someone with UC has their colon removed. I know that there are always doctors out there that don't agree with the accepted medical theories.

I am also concerned with my medicine (6-mp), does that increase my chances of PSC? Or is PSC just an auto-immune disease and I won't be able to lower or raise my likely-hood of PSC no matter what I do?

I really do appreciate the forums' help...I had a scare with PSC last summer when I was in the hospital; I had all sorts of liver doctors visiting me and wanting to do tests on me (which I refused). I have learned a lot over the past year about UC and now I want to know as much about it as possible about PSC.

Thanks again!!!

Hi ;These are tough questions. I've read that PSC can occur before development of inflammatory bowel disease (IBD), at the same time, or many years after development of IBD, and even after the colon is removed. But you would think that keeping the IBD under control should be helpful in reducing risk of PSC, and/or its rate of progression? Dr. has developed a theory that there are long-lived mucosal memory T-cells (lymphocytes) that originate in the inflamed gut, and that drive the hepatic inflammation of PSC. These memory T-cells may hang around, and remain capable of being activated, for years after the bowel is removed.________________________

Clin Med. 2004 Mar-Apr;4(2):173-80. Lymphocyte homing in the pathogenesis of extra-intestinal manifestations of inflammatory bowel disease.Eksteen B, Miles AE, Grant AJ, DH.Liver Research Laboratories, MRC Centre for Immune Regulation, University of Birmingham, Queen Hospital, Birmingham.Inflammatory bowel disease is associated with extra-intestinal manifestations which occur either at the same time as flares of bowel inflammation (skin and eye disease) or run a course that is independent to inflammation in the bowel (liver and some joint syndromes). It has been suggested that the skin and eye complications occur as a consequence of the recruitment of activated effector cells released from the gut into the circulation to extra-intestinal site where they cause acute damage. However, this does not explain how patients can develop primary sclerosing cholangitis many years after having their colon removed for colitis. We propose that long-lived populations of memory lymphocytes arise as a consequence of bowel inflammation and that these cells express homing receptors that direct their subsequent migration not only to the gut but also to the liver. These long-lived cells may recirculate to the liver for many years and, in the absence of a local activating stimulus, will not cause damage. However, if they are subsequently activated in the liver this will lead to the development of inflammation and tissue damage which promotes the recruitment of more mucosal lymphocytes resulting in persistent inflammation and disease. The recent findings that MAdCAM-1 and CCL25, previously thought to be restricted to the gut, are up-regulated in the liver during inflammatory liver diseases that complicate IBD support the concept that common mechanisms control lymphocyte recruitment to the inflamed liver and gut.

Publication Types: ReviewPMID: 15139741________________________ (father of (21); PSC 07/03; UC 08/03)

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Thanks for the replies... I am just wondering if the general consensus among the medical community is that the chances of getting PSC is NOT lowered if someone with UC has their colon removed. I know that there are always doctors out there that don't agree with the accepted medical theories.

I am also concerned with my medicine (6-mp), does that increase my chances of PSC? Or is PSC just an auto-immune disease and I won't be able to lower or raise my likely-hood of PSC no matter what I do?

I really do appreciate the forums' help...I had a scare with PSC last summer when I was in the hospital; I had all sorts of liver doctors visiting me and wanting to do tests on me (which I refused). I have learned a lot over the past year about UC and now I want to know as much about it as possible about PSC.

Thanks again!!!

Hi ;These are tough questions. I've read that PSC can occur before development of inflammatory bowel disease (IBD), at the same time, or many years after development of IBD, and even after the colon is removed. But you would think that keeping the IBD under control should be helpful in reducing risk of PSC, and/or its rate of progression? Dr. has developed a theory that there are long-lived mucosal memory T-cells (lymphocytes) that originate in the inflamed gut, and that drive the hepatic inflammation of PSC. These memory T-cells may hang around, and remain capable of being activated, for years after the bowel is removed.________________________

Clin Med. 2004 Mar-Apr;4(2):173-80. Lymphocyte homing in the pathogenesis of extra-intestinal manifestations of inflammatory bowel disease.Eksteen B, Miles AE, Grant AJ, DH.Liver Research Laboratories, MRC Centre for Immune Regulation, University of Birmingham, Queen Hospital, Birmingham.Inflammatory bowel disease is associated with extra-intestinal manifestations which occur either at the same time as flares of bowel inflammation (skin and eye disease) or run a course that is independent to inflammation in the bowel (liver and some joint syndromes). It has been suggested that the skin and eye complications occur as a consequence of the recruitment of activated effector cells released from the gut into the circulation to extra-intestinal site where they cause acute damage. However, this does not explain how patients can develop primary sclerosing cholangitis many years after having their colon removed for colitis. We propose that long-lived populations of memory lymphocytes arise as a consequence of bowel inflammation and that these cells express homing receptors that direct their subsequent migration not only to the gut but also to the liver. These long-lived cells may recirculate to the liver for many years and, in the absence of a local activating stimulus, will not cause damage. However, if they are subsequently activated in the liver this will lead to the development of inflammation and tissue damage which promotes the recruitment of more mucosal lymphocytes resulting in persistent inflammation and disease. The recent findings that MAdCAM-1 and CCL25, previously thought to be restricted to the gut, are up-regulated in the liver during inflammatory liver diseases that complicate IBD support the concept that common mechanisms control lymphocyte recruitment to the inflamed liver and gut.

Publication Types: ReviewPMID: 15139741________________________ (father of (21); PSC 07/03; UC 08/03)

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Hi ;

It's difficult to find good research on the question of the chance

of getting PSC if the colon is removed for UC. But this paper

suggests that it may have a beneficial effect:

_________________________

Hepatogastroenterology. 1995 Feb;42(1):68-72.

Liver involvement and its course in patients operated on for

ulcerative colitis.

Mikkola K, Kiviluoto T, Riihela M, Taavitsainen M, Jarvinen HJ.

Second Department of Surgery, Helsinki University Central Hospital,

Finland.

The prevalence of associated liver involvement in 214 patients with

ulcerative colitis undergoing definitive surgery was evaluated, with

special emphasis on the subsequent course of liver changes. At the

time of colectomy or proctocolectomy 45 patients (21%) had more than

transient liver involvement, and 13 (6.1%) fulfilled the criteria of

primary sclerosing cholangitis (PSC). Of the other 32 patients with

minor liver involvement four had steatosis, one chronic active

hepatitis, one viral A hepatitis, and 14 possibly early sclerosing

cholangitis or unspecific reactive hepatitis. During a mean follow-

up of nine years, four patients with PSC (31%) showed clinical

progression, but none of those with minor histological changes or

those with no liver disease at surgery did so. Alkaline phosphatase

levels showed a decreasing tendency, and minor histological changes

improved after surgery, while repeated cholangiography mostly

demonstrated progression or a static state. The results indicate

that asymptomatic sclerosing cholangitis in association with

ulcerative colitis is not always a progressive disease, and

proctocolectomy may have a beneficial effect on the long-term course

of sclerosing cholangitis in its early phase.

PMID: 7782040

________________________

I don't think that there is any evidence to indicated that 6-MP will

increase risk of developing PSC, but if others in the group have

evidence to the contrary I'd be interested in seeing it.

Best regards,

Dave

(father of (21); PSC 07/03; UC 08/03)

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Guest guest

Hi ;

It's difficult to find good research on the question of the chance

of getting PSC if the colon is removed for UC. But this paper

suggests that it may have a beneficial effect:

_________________________

Hepatogastroenterology. 1995 Feb;42(1):68-72.

Liver involvement and its course in patients operated on for

ulcerative colitis.

Mikkola K, Kiviluoto T, Riihela M, Taavitsainen M, Jarvinen HJ.

Second Department of Surgery, Helsinki University Central Hospital,

Finland.

The prevalence of associated liver involvement in 214 patients with

ulcerative colitis undergoing definitive surgery was evaluated, with

special emphasis on the subsequent course of liver changes. At the

time of colectomy or proctocolectomy 45 patients (21%) had more than

transient liver involvement, and 13 (6.1%) fulfilled the criteria of

primary sclerosing cholangitis (PSC). Of the other 32 patients with

minor liver involvement four had steatosis, one chronic active

hepatitis, one viral A hepatitis, and 14 possibly early sclerosing

cholangitis or unspecific reactive hepatitis. During a mean follow-

up of nine years, four patients with PSC (31%) showed clinical

progression, but none of those with minor histological changes or

those with no liver disease at surgery did so. Alkaline phosphatase

levels showed a decreasing tendency, and minor histological changes

improved after surgery, while repeated cholangiography mostly

demonstrated progression or a static state. The results indicate

that asymptomatic sclerosing cholangitis in association with

ulcerative colitis is not always a progressive disease, and

proctocolectomy may have a beneficial effect on the long-term course

of sclerosing cholangitis in its early phase.

PMID: 7782040

________________________

I don't think that there is any evidence to indicated that 6-MP will

increase risk of developing PSC, but if others in the group have

evidence to the contrary I'd be interested in seeing it.

Best regards,

Dave

(father of (21); PSC 07/03; UC 08/03)

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Guest guest

>

> Hi ;

>

> It's difficult to find good research on the question of the chance

> of getting PSC if the colon is removed for UC. But this paper

> suggests that it may have a beneficial effect:

>> ________________________

>

>

> I don't think that there is any evidence to indicated that 6-MP

will

> increase risk of developing PSC, but if others in the group have

> evidence to the contrary I'd be interested in seeing it.

>

> Best regards,

>

> Dave

> (father of (21); PSC 07/03; UC 08/03)

In spite of the study posted by my experience has been that

current consensus of doctors do not link removal of the colon as a

preventative measure of developing PSC. When asking this specific

question to the doctors I have dealt with the asnwer has always been

no, removal of the colon will not affect the outcome or development

of PSC.

I suppose it is a personal decision but if it were me I would not

remove my colon in the hopes of preventing or slowing PSC. Removal

of the colon can of course lead to other issues such as pounchitis as

well.

What is definitely agreed is that those with UC are at a higher risk

of colon cancer and those with both PSC and UC at an even higher

risk. Removal of the colon would certainly address that issue but

again, for me personally, since I get a colonoscopy yearly I am not

too worried since I could have my colon removed at a very early stage.

I also agree with that there has been no evidence that 6MP

causes or increases the risk of developing PSC.

in Seattle

UC 1991, PSC 2001

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Guest guest

>

> Hi ;

>

> It's difficult to find good research on the question of the chance

> of getting PSC if the colon is removed for UC. But this paper

> suggests that it may have a beneficial effect:

>> ________________________

>

>

> I don't think that there is any evidence to indicated that 6-MP

will

> increase risk of developing PSC, but if others in the group have

> evidence to the contrary I'd be interested in seeing it.

>

> Best regards,

>

> Dave

> (father of (21); PSC 07/03; UC 08/03)

In spite of the study posted by my experience has been that

current consensus of doctors do not link removal of the colon as a

preventative measure of developing PSC. When asking this specific

question to the doctors I have dealt with the asnwer has always been

no, removal of the colon will not affect the outcome or development

of PSC.

I suppose it is a personal decision but if it were me I would not

remove my colon in the hopes of preventing or slowing PSC. Removal

of the colon can of course lead to other issues such as pounchitis as

well.

What is definitely agreed is that those with UC are at a higher risk

of colon cancer and those with both PSC and UC at an even higher

risk. Removal of the colon would certainly address that issue but

again, for me personally, since I get a colonoscopy yearly I am not

too worried since I could have my colon removed at a very early stage.

I also agree with that there has been no evidence that 6MP

causes or increases the risk of developing PSC.

in Seattle

UC 1991, PSC 2001

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Guest guest

>

> Hi ;

>

> It's difficult to find good research on the question of the chance

> of getting PSC if the colon is removed for UC. But this paper

> suggests that it may have a beneficial effect:

>> ________________________

>

>

> I don't think that there is any evidence to indicated that 6-MP

will

> increase risk of developing PSC, but if others in the group have

> evidence to the contrary I'd be interested in seeing it.

>

> Best regards,

>

> Dave

> (father of (21); PSC 07/03; UC 08/03)

In spite of the study posted by my experience has been that

current consensus of doctors do not link removal of the colon as a

preventative measure of developing PSC. When asking this specific

question to the doctors I have dealt with the asnwer has always been

no, removal of the colon will not affect the outcome or development

of PSC.

I suppose it is a personal decision but if it were me I would not

remove my colon in the hopes of preventing or slowing PSC. Removal

of the colon can of course lead to other issues such as pounchitis as

well.

What is definitely agreed is that those with UC are at a higher risk

of colon cancer and those with both PSC and UC at an even higher

risk. Removal of the colon would certainly address that issue but

again, for me personally, since I get a colonoscopy yearly I am not

too worried since I could have my colon removed at a very early stage.

I also agree with that there has been no evidence that 6MP

causes or increases the risk of developing PSC.

in Seattle

UC 1991, PSC 2001

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Guest guest

Hi ;

Thanks for this important clarification. I thought it was

interesting that the one paper that I cited hinted at a possible

beneficial effect of colon removal .. but I have not been able to

find much additional research to back this up! You are perfectly

correct that the current consensus of doctors seems to be that colon

removal does not affect the clinical course of PSC. This is in fact

stated in Worthington and Chapman's recent review (p. 2):

www.orpha.net/data/patho/GB/uk-PrimarySclerosingCholangitis.pdf

Best regards,

Dave

(father of (21); PSC 07/03; UC 08/03)

> In spite of the study posted by my experience has been that

current consensus of doctors do not link removal of the colon as a

preventative measure of developing PSC. When asking this specific

question to the doctors I have dealt with the asnwer has always

been no, removal of the colon will not affect the outcome or

development of PSC.

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Guest guest

Hi ;

Thanks for this important clarification. I thought it was

interesting that the one paper that I cited hinted at a possible

beneficial effect of colon removal .. but I have not been able to

find much additional research to back this up! You are perfectly

correct that the current consensus of doctors seems to be that colon

removal does not affect the clinical course of PSC. This is in fact

stated in Worthington and Chapman's recent review (p. 2):

www.orpha.net/data/patho/GB/uk-PrimarySclerosingCholangitis.pdf

Best regards,

Dave

(father of (21); PSC 07/03; UC 08/03)

> In spite of the study posted by my experience has been that

current consensus of doctors do not link removal of the colon as a

preventative measure of developing PSC. When asking this specific

question to the doctors I have dealt with the asnwer has always

been no, removal of the colon will not affect the outcome or

development of PSC.

Link to comment
Share on other sites

Guest guest

Hi ;

Thanks for this important clarification. I thought it was

interesting that the one paper that I cited hinted at a possible

beneficial effect of colon removal .. but I have not been able to

find much additional research to back this up! You are perfectly

correct that the current consensus of doctors seems to be that colon

removal does not affect the clinical course of PSC. This is in fact

stated in Worthington and Chapman's recent review (p. 2):

www.orpha.net/data/patho/GB/uk-PrimarySclerosingCholangitis.pdf

Best regards,

Dave

(father of (21); PSC 07/03; UC 08/03)

> In spite of the study posted by my experience has been that

current consensus of doctors do not link removal of the colon as a

preventative measure of developing PSC. When asking this specific

question to the doctors I have dealt with the asnwer has always

been no, removal of the colon will not affect the outcome or

development of PSC.

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Guest guest

That pretty much sums it up. Just about every medicine out there has

some disclaimer in regards to impact on the liver since most

medications are metabolized in the liver. As long as you monitor

LFT's every once in awhile you should be fine.

In the absence of diagnosis of liver disease reasonable alcohol

consumption should be fine but if your LFT's are elevated I would

encourage you to cut your consumption to a minimum. No sense makinbg

things worse.

in Seattle

>

> Thanks for all of your replies....so from what everyone wrote I can

assume

> that there is nothing that I can do to *lower or raise* my chances

of

> getting PSC....it's an auto-immune disease and because I have UC I

have a 5%

> chance of getting PSC.

>

> I was concerned about taking 6-mp and liver damage but my GI even

said that

> I could drink while taking 6-mp.

>

> --

>

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