Laproscopic Proctocolectomy/ Ileal anal anastomosis/ loop ileostomy

[Guest guest]

So I have met with my primary care, my gi dr, transplant surgeon, colorectal

surgeon, hep dr etc and everyone has told me to have this wonderfully fun

surgery done. My colorectal surgeon told me after a transplant my uc (severe

pancolitis) will " blow up " and take away from the healing process of my liver.

He actually said BLOW UP. So I scheduled my surgery for April 17 with a lot of

thinking, this is probably the best thing to do. I know with PSC my risk of

pouchitis will be much higher etc. My PSC is between stage 2 and 3. They told me

prob about 10 years for transplant if my ERCP's are not suspicious (they have

been) and FISH tests remain negative.

Have other people been told this? I remember some have a jpouch. I just want

some reinforcement I guess. I won't be changing my mind, I just want to be

reassured.

Thanks guys!

Holly

[Guest guest]

I had already had PSC dx when my gastro told me it was time to remove my colon

due to dysplasia and severe UC. I then talked with a surgeon who validated that

need. Family and friends said I made the decision with haste because I was

still on the table from my final colonoscopy when I told the doctor I would have

the surgery. I never doubted my decision, but I did defend my decision with

family and friends. I did not make that decision in haste.....I had suffered

from UC for 16 years, and had quarterly scopes done so that if dysplasia/cancer

developed, it would be caught very early on. After explaining this to my

husband, he realized what I said was true and supported me fully. Other friends

never did seem to realize it was not a hasty decision.

I was told that PSC would make the UC worse...but I have no idea how it is

going to affect the jpouch, other than I worry about being hooked up to all

those tubes etc. after transplant and will not be able to use the bathroom.

Jpoucher's don't go days without having to go, so it is probably going to be

bedpan alley.....and I dreadfully hate that option. For those of you with

jpouches....does the term butt-burn mean anything?

[Guest guest]

Hi Lori;

As far as I recall, the associated between colectomy and reduced risk of

recurrence of PSC has only been reported from the group in England. If it is

true, then it would support the hypothesis that: " PSC may be triggered in

genetically susceptible individuals by toxic or infectious agents gaining access

to the liver via a diseased and permeable colon. "

(not my words, but those of: Cullen S, Chapman R 2001 Aetiopathogenesis of

primary sclerosing cholangitis. Best Pract. Res. Clin. Gastroenterol. 15:

577-589.)

But this is still open to debate; others (also from England) argue that the

course of PSC can be totally independent of inflammation in the bowel, and argue

that PSC (and other extra-intestinal manifestations) might be due to long-lived

T cells that express the wrong " address codes " that tell them where to migrate

to in the body. The T cells should normally migrate to the gut, but in PSC they

incorrectly migrate to the liver. According to and Eksteen, these

" long-lived " T cells would persist for a long time after colectomy.

_______________________

Nat. Rev. Immunol. 6: 244-251 (2006)

Aberrant homing of mucosal T cells and extra-intestinal manifestations of

inflammatory bowel disease.

DH, Eksteen B

Liver Research Laboratories, MRC Centre for Immune Regulation, 5th Floor,

Institute for Biomedical Research, Medical School, University of Birmingham,

Edgbaston, Birmingham B15 2TT, UK. d.h.adams@...

Active inflammatory bowel disease (IBD) is often associated with simultaneous

inflammation in the skin, eyes and joints. Inflammatory disease in the liver can

also occur in patients with IBD but seems to be independent of inflammation in

the bowel. In this Opinion article, we propose that the hepatic complications of

IBD are mediated by long-lived mucosal T cells that are recruited to the liver

in response to aberrantly expressed endothelial-cell adhesion molecules and

chemokines that are normally restricted to the gut. Similar mechanisms might

explain why certain diseases are associated with site-specific tissue

distributions and might point to new therapeutic strategies that are based on

modulating tissue-specific lymphocyte homing. PMID: 16498453.

_______________________

I honestly don't know which hypothesis is correct. Perhaps both mechanisms come

into play?

The T-cell idea is very interesting, especially since IBD is now being shown to

involve an imbalance between inflammatory T cells (Th17 cells), and

anti-inflammatory T cells (regulatory T cells or Tregs) (see my recent posts).

and Eksteen have recently shown that retinoic acid (a derivative of

vitamin A) plays an important role in imprinting normal gut-homing T cells with

their proper address codes. Retinoic acid is also involved in switching between

Tregs and Th17 cells. Moreover, retinoic acid regulates gut permeability.

Retinoic acid also regulates the secretion of IgA in the gut; IgA plays an

important role in keeping gut bacterial populations in check. Finally, retinoic

acid plays an important role in regulating bile transporters and metabolism in

the liver. Therefore, I am suscpicious that retinoic acid might be very much

involved in PSC.

One unifying idea would be that an unusual bacterium in the gut somehow

interferes with gut retinoic acid metabolism, throwing Th17 cells versus Tregs

out of balance, causing aberrant homing of T cells, inhibiting secretion of IgA,

increasing the permeability of the colon, and disrupting bile acid transport and

metabolism. If I were a PSC researcher I'd look to see if a bug like this one

(cytophaga-flavobacter-bacteroidetes (CFB)reported by Ivanov) was responsible

for this mess:

___________________________

Cell Host Microbe. 2008 Oct 16;4(4):337-49.

Specific microbiota direct the differentiation of IL-17-producing T-helper cells

in the mucosa of the small intestine.

Ivanov II, Frutos Rde L, Manel N, Yoshinaga K, Rifkin DB, Sartor RB, Finlay BB,

Littman DR

Kimmel Center for Biology and Medicine of the Skirball Institute, Department of

Microbiology, New York University School of Medicine, New York, NY 10016, USA.

The requirements for in vivo steady state differentiation of IL-17-producing

T-helper (Th17) cells, which are potent inflammation effectors, remain obscure.

We report that Th17 cell differentiation in the lamina propria (LP) of the small

intestine requires specific commensal microbiota and is inhibited by treating

mice with selective antibiotics. Mice from different sources had marked

differences in their Th17 cell numbers and animals lacking Th17 cells acquired

them after introduction of bacteria from Th17 cell-sufficient mice.

Differentiation of Th17 cells correlated with the presence of

cytophaga-flavobacter-bacteroidetes (CFB) bacteria in the intestine and was

independent of toll-like receptor, IL-21 or IL-23 signaling, but required

appropriate TGF-beta activation. Absence of Th17 cell-inducing bacteria was

accompanied by increase in Foxp3+ regulatory T cells (Treg) in the LP. Our

results suggest that composition of intestinal microbiota regulates the

Th17:Treg balance in the LP and may thus influence intestinal immunity,

tolerance, and susceptibility to inflammatory bowel diseases. PMID: 18854238.

___________________

If such an unusual bacterium was the cause, then this would also fit with the

recent vancomycin studies (i.e. treatment with an antibiotic should restore the

balance).

Best regards,

Dave

(father of (23); PSC 07/03; UC 08/03)

>

> I assume that this confirms that cholangitis plays a significant role in

causing PSC if removing a colon helps prevent problems with the liver, PSC???

>  

[Guest guest]

Hi Holly, I had surgey back in 95. For me it was the best thing i did dealing with uc. I have a j pouch and maybe about four times a year I get pouchitis. I felt great after the surgey. I wish I would've had it down years earlier. I hope you have the same luck I did with the surgey and recovery. Take care CASEY UC 90, Jpouch 95, PSC 06

[Guest guest]

Hi Holly, I had surgey back in 95. For me it was the best thing i did dealing with uc. I have a j pouch and maybe about four times a year I get pouchitis. I felt great after the surgey. I wish I would've had it down years earlier. I hope you have the same luck I did with the surgey and recovery. Take care CASEY UC 90, Jpouch 95, PSC 06