I was in Ohio last month visiting my family and got really sick. I am pretty sure it was a supplement I was trying. Unfortunately for me I don't react within hours or days but only after a few weeks and then it takes me forever to recover...am still having problems a month after stopping supplement.
I went to see a GI and he sent me to get a CT scan. The only reason I agreed was because a few years ago at the Mayo they found cysts on my pancreas that a repeat endoscopic ultrasound could not find. It is always in the back of my mind and with the actor dying recently from pancreatic cancer I decided to go ahead with the CT scan and drink all that awful stuff. So, the results have confused me and I wonder if anyone has any thoughts.
It found nothing on the pancreas which was great. It did find abnormal mucosal enhancement in the large bowel with loss of the normal haustral pattern seen in the transverse colon and the descending colon which extends to the sigmoid colon and rectum. There is mild pericolic congestion with prominent pericolic vascularity noted in the transverse colon. The rectum is collapsed. Prominent pericolic vascularity adjacent to the colonic loops.
These findings appear concerning for an inflammatory bowel disease. Ulcerative colitis is most likely given the distribution and extent of involvement.
The GI walked into the exam room and handed me these findings and before I could read them said my history of LC is what the problem is and to take entocort and walked out of the room. He was literally there less than a minute.
So, I am not bleeding nor have I ever bleed. As you may remember I have a DX of LC and went to Dr. Pardi at the Mayo who said I did not have it after looking at the biopsies. From my enterolab results I know I have food intolerences and do get D when I eat those foods although I have never had watery D.
I am confused because I thought it was called microscopic colitis because you couldn't see it unless it was under a microscope. It seems to me that if my colon is so inflamed it is apparent on a CT scan then it must be something other than or in addition to LC. I am also wondering what impact a collapsed rectum has on symptoms. It is an internal problem as nothing is extending outside of my body.
So I am back on entocort again and again it is doing nothing for me. I continue on as I have for 4 years with a very restrictive diet and while it is important to keep up with the diet as I am worse when I don't, it is not the whole answer for me.
Any insights or thoughts would be greatly appreciated.
Love,Cristi
I Need Some Help
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Hi Cristi,
It's always something, isn't it?
Their remark, suggesting the likelihood of UC, is simply based on the fact that MC is normally completely off the radar for anyone who is part of the medical community, combined with the fact that UC begins in the distal colon, and is normally confined there, unlike Crohn's disease, which is often concentrated in the proximal colon, (if it is not pancolonic). IOW, since the proximal end of your colon appeared normal, but the balance showed abnormal markers, the default choice was UC. If you had UC, it should have been obvious, during your last colonoscopy, (unless that was many years ago).
You're probably thinking about a prolapsed rectum. A collapsed rectum is nothing to get excited about - that's simply the normal resting state. In the resting state, the anus and rectum are typically empty, and the side walls are collapsed, (together). The sigmoid colon, just above them, has relatively high intraluminal pressure, (compared with the rest of the colon), and it functions as a partial sphincter to retain bowel content in the descending colon, (above it). During a colonoscopy, the colon is inflated with air, so the rectum probably won't be collapsed, during that exam. If the rectum is not collapsed, during normal operation, then continence is much more difficult to maintain, obviously.
Anyway, that's the way I see it.
Love,
Tex
It's always something, isn't it?Remember that endoscopy allows a view of the inside of the intestine, while a CT scan allows a view through the walls of the intestines. My CT scans showed some of the same findings. In a CT scan, a colon with an inflammatory bowel disease is typically going to appear stiffer, and thicker, than a normal colon, (because it is inflamed), and that includes MC.Cristi wrote:It did find abnormal mucosal enhancement in the large bowel with loss of the normal haustral pattern seen in the transverse colon and the descending colon which extends to the sigmoid colon and rectum. There is mild pericolic congestion with prominent pericolic vascularity noted in the transverse colon. The rectum is collapsed.
These findings appear concerning for an inflammatory bowel disease. Ulcerative colitis is most likely given the distribution and extent of involvement.
Their remark, suggesting the likelihood of UC, is simply based on the fact that MC is normally completely off the radar for anyone who is part of the medical community, combined with the fact that UC begins in the distal colon, and is normally confined there, unlike Crohn's disease, which is often concentrated in the proximal colon, (if it is not pancolonic). IOW, since the proximal end of your colon appeared normal, but the balance showed abnormal markers, the default choice was UC. If you had UC, it should have been obvious, during your last colonoscopy, (unless that was many years ago).
You're probably thinking about a prolapsed rectum. A collapsed rectum is nothing to get excited about - that's simply the normal resting state. In the resting state, the anus and rectum are typically empty, and the side walls are collapsed, (together). The sigmoid colon, just above them, has relatively high intraluminal pressure, (compared with the rest of the colon), and it functions as a partial sphincter to retain bowel content in the descending colon, (above it). During a colonoscopy, the colon is inflated with air, so the rectum probably won't be collapsed, during that exam. If the rectum is not collapsed, during normal operation, then continence is much more difficult to maintain, obviously.
Anyway, that's the way I see it.
Love,
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Hi Tex,
Thanks so much for the explanation. Makes more sense to me now. I was confusing collapsed with prolapsed. I remember a discussion a while ago about perhaps when entocort doesn't work is because it is not opening in the appropriate area. I never see the capsule exiting intact, but I am guessing if I am not absorbing nutrients well, a possible reason could be lack of stomach acid. Does entocort depend on a certain acid level to break down at the appropriate time? I wonder if I should experiment with HCL pills to see if would help.
In keeping with the stomach acid hypothesis, I was put on amitriptyline 10 mg a couple of years ago for sleeping problems and it was supposed to be good for people with D. I just found a pubmed article that says that amitriptyline in higher doses than I am taking significantly reduces stomach acid production. So, I am going to try to get off the amitriptyline, just in case .....but I wonder if others here have had success with other prescription sleep medications.
Thanks again, Tex.
Love,
Cristi
Thanks so much for the explanation. Makes more sense to me now. I was confusing collapsed with prolapsed. I remember a discussion a while ago about perhaps when entocort doesn't work is because it is not opening in the appropriate area. I never see the capsule exiting intact, but I am guessing if I am not absorbing nutrients well, a possible reason could be lack of stomach acid. Does entocort depend on a certain acid level to break down at the appropriate time? I wonder if I should experiment with HCL pills to see if would help.
In keeping with the stomach acid hypothesis, I was put on amitriptyline 10 mg a couple of years ago for sleeping problems and it was supposed to be good for people with D. I just found a pubmed article that says that amitriptyline in higher doses than I am taking significantly reduces stomach acid production. So, I am going to try to get off the amitriptyline, just in case .....but I wonder if others here have had success with other prescription sleep medications.
Thanks again, Tex.
Love,
Cristi
Cristi,
Yes, the enteric coating on Entocort EC capsules is pH dependent. Unless your stomach is significantly under-producing hydrochloric acid, and/or, your pancreas is significantly over-producing bicarbonate, taking something to enhance gastric acid production probably won't make much difference, because your pancreas is going to to "optimize" the pH of the chime as it enters the duodenum, anyway.
I'm just thinking out loud here, but if that CT scan analysis is reasonably accurate, then the reason why Entocort doesn't provide much benefit, is because most of your inflammation is located in portions of the colon downstream of the optimum target area for Entocort. MC is typically somewhat similar to Crohn's disease, in that it can affect any part of the GI tract, from mouth to anus, but it most commonly is the most concentrated, in the proximal colon, and the distal small intestine, (the ilium), (IOW, in the vicinity of the cecum), which is the optimum target area of Entocort EC. That's why Entocort is not an ideal choice of treatments for UC - it activates too soon.
I wonder if you might have better luck with one of the newer 5-ASA meds, (delayed-release mesalamine), targeted at the treatment of UC. The newest is Apriso, (released last year), but I believe it's mostly designed as a maintence med for UC. Lialda is the strongest of the group of 5-ASA meds available, and if you can tolerate sulfasalazine-based medications, it might be worth a try. UC is usually confined to the rectum, sigmoid colon, and descending colon. If it weren't for the fact that your transverse colon is probably affected by MC, a suppository form, (or even an enema form, such as Rowasa), might be a better bet, but those types of treatment wouldn't effectively reach the transverse colon.
http://www.drugs.com/apriso.html
http://www.drugs.com/lialda.html
As you can see, the ingredients of Lialda avoid the main problem with Asacol, namely the lactose.
Tex
Yes, the enteric coating on Entocort EC capsules is pH dependent. Unless your stomach is significantly under-producing hydrochloric acid, and/or, your pancreas is significantly over-producing bicarbonate, taking something to enhance gastric acid production probably won't make much difference, because your pancreas is going to to "optimize" the pH of the chime as it enters the duodenum, anyway.
I'm just thinking out loud here, but if that CT scan analysis is reasonably accurate, then the reason why Entocort doesn't provide much benefit, is because most of your inflammation is located in portions of the colon downstream of the optimum target area for Entocort. MC is typically somewhat similar to Crohn's disease, in that it can affect any part of the GI tract, from mouth to anus, but it most commonly is the most concentrated, in the proximal colon, and the distal small intestine, (the ilium), (IOW, in the vicinity of the cecum), which is the optimum target area of Entocort EC. That's why Entocort is not an ideal choice of treatments for UC - it activates too soon.
I wonder if you might have better luck with one of the newer 5-ASA meds, (delayed-release mesalamine), targeted at the treatment of UC. The newest is Apriso, (released last year), but I believe it's mostly designed as a maintence med for UC. Lialda is the strongest of the group of 5-ASA meds available, and if you can tolerate sulfasalazine-based medications, it might be worth a try. UC is usually confined to the rectum, sigmoid colon, and descending colon. If it weren't for the fact that your transverse colon is probably affected by MC, a suppository form, (or even an enema form, such as Rowasa), might be a better bet, but those types of treatment wouldn't effectively reach the transverse colon.
http://www.drugs.com/apriso.html
http://www.drugs.com/lialda.html
As you can see, the ingredients of Lialda avoid the main problem with Asacol, namely the lactose.
For Apriso, they're:The inactive ingredients of Lialda tablets are sodium carboxymethylcellulose, carnauba wax, stearic acid, silica (colloidal hydrated), sodium starch glycolate (type A), talc, magnesium stearate, methacrylic acid copolymer types A and B, triethylcitrate, titanium dioxide, red ferric oxide and polyethyleneglycol 6000.
Here are the inactive ingredients in Asacol, for comparison:colloidal silicon dioxide, magnesium stearate, microcrystalline cellulose, simethicone emulsion ethylacrylate/methylmethacrylate copolymer nonoxynol 100 dispersion, hypromellose, methacrylic acid copolymer, talc, titanium dioxide, triethyl citrate, aspartame, anhydrous citric acid, povidone, vanilla flavor, and edible black ink.
Love,colloidal silicon dioxide, dibutyl phthalate, edible black ink, iron oxide red, iron oxide yellow, lactose, magnesium stearate, methacrylic acid copolymer B (Eudragit S), polyethylene glycol, povidone, sodium starch glycolate, and talc.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.