Guest guest Posted June 14, 2006 Report Share Posted June 14, 2006 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. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2006 Report Share Posted June 14, 2006 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. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2006 Report Share Posted June 14, 2006 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. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2006 Report Share Posted June 14, 2006 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. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2006 Report Share Posted June 14, 2006 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. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2006 Report Share Posted June 14, 2006 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) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2006 Report Share Posted June 14, 2006 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) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2006 Report Share Posted June 14, 2006 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) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2006 Report Share Posted June 14, 2006 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) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2006 Report Share Posted June 14, 2006 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) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2006 Report Share Posted June 14, 2006 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) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 14, 2006 Report Share Posted June 14, 2006 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) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 15, 2006 Report Share Posted June 15, 2006 > > 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 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 15, 2006 Report Share Posted June 15, 2006 > > 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 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 15, 2006 Report Share Posted June 15, 2006 > > 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 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 15, 2006 Report Share Posted June 15, 2006 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. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 15, 2006 Report Share Posted June 15, 2006 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. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 15, 2006 Report Share Posted June 15, 2006 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. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 19, 2006 Report Share Posted June 19, 2006 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. > > -- > > Quote Link to comment Share on other sites More sharing options...
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