Can't get out of a severe flare

Imuran can take quite a while before you would see results. Hopefully it helps you. I am on 6mp and I think it has helped me get stable. It took a very long time for me to see results. I was on it for about 5 months with no results because I wasn't able to increase the dose due to the fact that I had a lot of toxicity to my liver but I was able to add a drug called allopurinol and the results changed drastically. I went from having no theraputic benefits to being way above the theraputic zone. At that point, I started noticing improvement in my flare. Don't lose hope, there is a good possibility that you will have luck with Imuran, you just have to give it time. :(

Unfortunately if you're anythng like me, you won't see much improvement from diet. Food just made me sicker when I was flared up. it's worth a try...

I just read your second post and to be honest, I would drop all the supplements except probiotics. I stopped taking everything OTC and I am not any worse off, in fact, I am doing better. I would stick to the restricted diet but I wouldn't go crazy tryin to remain SCD. For some people, self included, not eating any carbs makes me sicker because I can't put on any weight at all. I lost a ton of weight trying to do SCD while in a severe flare. I was sicker than ever and under 100 pounds at that point. I don't think I would have lost all that weight if it weren't for the SCD. I ate a lot of peanut butter and jelly sandwiches when I was flared up badly. You can use almond butter if you can't handle peanut butter. Avoid jelly with syrups, trader joes has a lot of this type of stuff.

I hope you can find something that works for you until you see results from imuran.

I had UC for 20 years, last 5-10 of which were terrible. I had two kids during this time, and was told by my GI doc that this was "a really, really bad idea." I ended up in the hospital four months into my second pregnancy, and went from 120 to 85 pounds. I recovered somehow (just sulfasalizine and immodium) and then 8 years later, when a colonoscopy showed precancerous cells throughout my entire colon, I had j pouch surgery. This was a very difficult surgery, and I had unexpected complications, but my life is outstanding. I "poop" whenever I pee (no pain, and it takes no linger than it takes me to pee), and almost never have to go to the bathroom because I have to poop. Best yet, I do not have any problems waiting for hours even when I think I need to go.

I just had my first bout of "pouchitis" this year (2011 -- 13 years after initial pouch surgery) but once I realized what was wrong with me - about two weeks after I started feeling poorly - I gave my surgeon a call, and a few days into an antibiotic I was 100% again.

This is no fun - but for years I have actually been very happy I did have a "curable" disease.
Marsha

anyone heard of dr. j john cohen in denver colorado, and immunologist who says hookworms cure UC?

Nat

What foods are you currently eating?
Can you go to your "Profile" and write the meds you are currently taking? this allows people to comment without telling you something you're already doing.

Are you using mesalamine enemas?

If I added rice into the regimen again, I would have some major problems.  Have you made the SCD compliant yogurt?  You need to bring the good bacteria back into your digestive tract.  This may help with some of your problems.  My approach to weight gain at this point are the smoothies I'm making.  I make them with 3 tablespoons of yogurt, a ripe banana, some frozen fruit, half an avocado, 1 cup coconut milk, a teaspoon of honey, and a half a cup of orange juice. We're talking about 700 calories per smoothie, along with other calories from meats and stuff.  I'm at 124 lbs now, and trying to get back to 140-145 lbs.  It will take time, but I'm confident I will get there barring no flares in the near future.   I'm packing on pounds as we speak, along with doing some muscle training.  It took 5 weeks to get to a decent point with this diet.  The yogurt really jump started my progress.  I'm not at 100% but better than I was 5 weeks ago, and the cramping is starting to subside.  I still see some blood from time to time, but I'm only going about 3 times a day now. 

Suebear, the info that you have is outdated. There are lots of UC people that don't have CD and get pouchitis or have high morbidity. Prometheus serology 7 also attempts to predict the likelihood of pouchitis in UC patient only.

This is a recent article with stats:

"Coloproctectomy with ileo-anal anastomosis (CP-IAA) has been in use for 30 years. This intervention is the standard technique when surgery is indicated for familial adenomatous polyposis (FAP) and for ulcerative colitis (UC). Although the surgery is safe with mortality of less than 1%, it is associated with a morbidity of 18-70%. We thought a literature review about long-term complications would be enlightening. Pouchitis is the most common complication; it occurs in 70% of patients over 20 years follow-up; small bowel obstruction affects 25% of patients and pelvic sepsis occurs in 20-30% within 10 years. CP-IAA can impact the patient's sexual life due to erectile and ejaculatory dysfunction, dyspareunia, and incontinence of stool during sexual intercourse. Nevertheless, patients with long-standing UC describe an overall improvement in their sexual function after surgery. The failure rate varies from 3.5 to 15%; major causes of failure are sepsis, unrecognized Crohn's disease, and poor functional results. Cases of dysplasia and cancer have been reported in the reservoir, but more particularly when there is retained colonic glandular mucosa. The transitional zone should be monitored whenever there are risk factors for colon neoplasia. The relatively high morbidity of CP-IAA should not overshadow the good functional results of this technique."

If one believes that UC has a bacterial cause, removing the colon will do nothing:

"PURPOSE: The beneficial effect of antibiotics in pouchitis suggests that an unidentified fecal bacterial product causes this condition. A candidate compound is hydrogen sulfide, a highly toxic gas produced by certain fecal bacteria, which causes tissue injury in experimental models. We investigated hydrogen sulfide release and sulfate-reducing bacterial counts in pouch contents to determine whether hydrogen sulfide production correlates with pouchitis.
METHODS: During incubation at 37 degrees C, the production of hydrogen sulfide, methylmercaptan, carbon dioxide, and hydrogen were studied using fresh fecal specimens obtained from 50 patients with ileoanal pouches constructed after total proctocolectomy for ulcerative colitis (n = 45) or for familial adenomatous polyposis (n = 5). Patients with ulcerative colitis were divided into five groups: a) no history of pouchitis (pouch for at least 2 years; n = 8); b) past episode(s) of pouchitis but no active disease for the previous year (n = 9); c) pouchitis in the past year but presently inactive (n = 9); d) ongoing antibiotic treatment (metronidazole or ciprofloxacin) for pouchitis (n = 11); e) currently suffering from pouchitis (n = 8).
RESULTS: Release of hydrogen sulfide when pouchitis was active (6.06 +/- 1.03 micromol g(-1) 4 h(-1)) or had occurred in the past year (4.71 +/- 0.41 pmol g(-1) 4 h(-1)) was significantly higher (P < 0.05) than when pouchitis had never occurred (1.71 +/- 0.43 micromol g(-1) 4 h(-1)) or had been inactive in the past year (2.62 +/- 0.49 micromol g(-1) 4 h(-1)). Antibiotic therapy was associated with very low hydrogen sulfide release (0.68 +/- 0.29 micromol g(-1) 4 h(-1)). Pouch contents from familial adenomatous polyposis patients produced significantly less hydrogen sulfide (0.75 +/- 0.09 micromol g(-1) 4 h(-1)) than did any group of nonantibiotic-treated ulcerative colitis patients. Sulfate-reducing bacterial counts in active pouchitis (9.5 +/- 0.5 log10/g) were significantly higher than in those who never experienced pouchitis (7.38 +/- 0.32 log10/g), and these counts fell dramatically with antibiotic treatment. No statistically significant differences in carbon dioxide and hydrogen were observed among the groups not receiving antibiotics.
CONCLUSIONS: Pouch contents of patients with ongoing pouchitis or an episode within the previous year released significantly more hydrogen sulfide than did the contents of patients who never had an attack of pouchitis and those with longstanding inactive disease. The response to therapy with metronidazole or ciprofloxacin was associated with marked reductions in hydrogen sulfide release and sulfate-reducing bacteria. These results provide a rationale for additional studies to determine whether the high sulfide production is a cause or effect of pouchitis. The lower hydrogen sulfide production by pouch contents of familial adenomatous polyposis vs. patients with ulcerative colitis suggests a fundamental difference in gut sulfide metabolism that could have implications for the etiology of ulcerative colitis as well as the pouchitis of patients with ulcerative colitis."

And for the record, it was recently published that the right antibiotic combo induces remission in UC as much as steroids, with the RR of no remission = 0.65 for steroids and RR of UC not in remission = 0.64 for antibiotics (RR is the relative risk), so the bacterial theory is becoming stronger.