I saw your posts. Hopefully you won't have to wait that long to find a cure or have to find one yourself when you get out of Med School. There have been some very interesting recent developments in this field. The most interesting ones to me relate to intestinal flora. Either an "imbalance" in the intestinal flora or a single microbial species (fusobacterium varium), seem to be the culprit for UC. I was 22 when I got UC, the same age you are now. My unfortunate and intimate knowledge of the disease left me with the impression that the disease was not autoimmune in nature. Like yourself, I thought bacteria were to blame. Searching PubMed at NCBI yielded a few, in my view, noteworthy papers. I will append the refs and abstracts (see below), to this email. You and others may find them interesting.
1) 1: J Clin Gastroenterol. 2003 Jul;37(1):42-7. Related Articles, Links
Treatment of ulcerative colitis using fecal bacteriotherapy.
Borody TJ, Warren EF, Leis S, Surace R, Ashman O.
Centre for Digestive Diseases, 144 Great North Rd, Five Dock NSW 2046, Australia. firstname.lastname@example.org
BACKGROUND: Although the etiology of idiopathic ulcerative colitis (UC) remains poorly understood, the intestinal flora is suspected to play an important role. Specific, consistent abnormalities in flora composition peculiar to UC have not yet been described, however Clostridium difficile colitis has been cured by the infusion of human fecal flora into the colon. This approach may also be applicable to the treatment of UC on the basis of restoration of flora imbalances. GOAL: To observe the clinical, colonoscopic and histologic effects of Human Probiotic Infusion s (HPI) in 6 selected patients with UC. CASE REPORTS: Six patients (3 men and 3 women aged 25-53 years) with UC for less than 5 years were treated with HPI. All patients had suffered severe, recurrent symptoms and UC had been confirmed on colonoscopy and histology. Fecal flora donors were healthy adults who were extensively screened for parasites and bacterial pathogens. Patients were prepared with Antibiotics and oral polyethylene glycol lavage. Fecal suspensions were administered as retention enemas within 10 minutes of preparation and the process repeated daily for 5 days. By 1 week post-HPI some symptoms of UC had improved. Complete reversal of symptoms was achieved in all patients by 4 months post-HPI, by which time all other UC medications had been ceased. At 1 to 13 years post-HPI and without any UC medication, there was no clinical, colonoscopic, or histologic evidence of UC in any patient. CONCLUSIONS: colonic infusion of donor human intestinal flora can reverse UC in selected patients. These anecdotal results support the concept of abnormal bowel flora or even a specific, albeit unidentified, bacterial pathogen causing UC.
PMID: 12811208 [PubMed - in process]
2) 1: Gut. 2003 Jan;52(1):79-83. Related Articles, Links
Induction of experimental ulcerative colitis by Fusobacterium varium isolated from colonic mucosa of patients with ulcerative colitis.
Ohkusa T, Okayasu I, Ogihara T, Morita K, Ogawa M, Sato N.
Department of Gastroenterology, Juntendo University, School of Medicine, Tokyo, Japan.
BACKGROUND: Bacteria are implicated in certain forms of model chronic colitis but the identity and role of bacteria in human ulcerative colitis (UC) are uncertain. AIMS: To isolate pathogenic bacteria from inflamed mucosa of patients with UC, to examine whether the bacteria have a toxin to Vero cells, and to determine whether the toxin induces UC-like lesions in animals. METHODS: Bacteria were isolated from UC patients and supernatants from cultures were filtered and tested for cytotoxicity to Vero cells. Bacterial cells producing the cytotoxic supernatants were examined by polymerase chain reaction for verotoxin genes. Culture supernatants of cytotoxic strains were examined by high performance liquid chromatography for organic acid concentrations. Mice were given enemas containing organic acid at the mean concentration in the supernatants of cytotoxic strains to ascertain whether colonic lesions appear in UC. RESULTS: Only supernatants from cultures of Fusobacterium varium killed Vero cells. Bacterial cells lacked verotoxin genes. Bacterial culture supernatants contained high concentrations of n-butyric acid and the mean concentration (32 mmol/l) was cytotoxic to Vero cells. Twenty four hours after mice were given enemas containing either butyric acid or F varium culture supernatants, colonic ulcers with crypt abscesses, inflammatory cell infiltration, and apoptotic changes were observed. CONCLUSIONS: Butyric acid in culture supernatants from cultures of F varium caused UC-like lesions in mice. This study indicates that F varium may be one of the elusive pathogenic factors in UC.
PMID: 12477765 [PubMed - indexed for MEDLINE]