September 25, 2017

Treatment of Ulcerative Colitis using Fecal Bacteriotherapy

Ulcerative Colitis sustained remission after fecal transplants without the continued use of medications.

The excerpt below documents six cases of Ulcerative Colitis that were successfully treated using fecal transplants also known as fecal bacteriotherapy.  The article Treatment of Ulcerative Colitis Using Fecal Bacteriotherapy was published in the American Journal of Gastroenterology in 2003 by Dr. Thomas Borody and his team of doctors at the Centre for Digestive Disease in Australia. These are examples of long term remission achieved by using fecal microbiota transplants to treat Ulcerative Colitis.  In the article the doctor refers to fecal transplants / fecal microbiota transplantation as Human Probiotic Infusion (HPI) and fecal bacteriotherapy.

It was my discovery of this article in March 2011 that convinced me to cancel surgery which is irreversible and give the fecal transplant treatments a chance to work. It turns out fecal transplants truly changed my life just like it did for these six patients, as I now live a life free of illness. In fact I now have better digestive health than I can remember at almost any point in my life.

Patient 1

A 25-year-old man presented with a 6-year history of UC. He had experienced frequent blood in stools, diarrhea (6–7 motions per day), abdominal pain, cramping, urgency, nausea, fevers, fatigue,and weight loss of 6 kg over 2 years. He had previously been treated with prednisone 25 mg/d, salazopyrin 3 g/d, codeine phos-phate 30 mg/d, and nightly prednisolone sodium phosphate enemas,(see Table 1), but he refused azathioprine. A number of attempts to reduce steroid dosage resulted in recurrence of diarrhea and bleeding. Colonoscopy confirmed pancolitis with granular mucosa,contact bleeding, microulceration and histologically active chronic colitis. The patient had low serum iron and elevated alanine aminotransferase (ALT) levels, at times up to 10-fold above normal, together with elevated alkaline phosphatase (ALP) and g-glutamyl transpeptidase (GGT), presumed (no liver biopsy performed) to be due to associated sclerosing cholangitis.

Immediately preceding HPI, his symptoms were moderately controlled using prednisone 25 mg/d and salazopyrin 1 g/d.

The patient was infused with bowel flora donated by his female partner via retention enemas. He ceased taking salazopyrin on the final day of infusion. Prednisone was withdrawn stepwise at a rate of 5 mg per week over 5 weeks. One week following HPI, his symptoms had improved markedly with an accompanying reduction in stool frequency and rectal bleeding. Four months post-HPI, he remained asymptomatic without treatment, defecating 2 to 3 times per day with no bleeding. The patient had not experienced a recurrence of symptoms since the infusion. Serum ALT, ALP, GGT and iron levels progressively returned to normal. He claimed markedly increased energy levels and regained weight. On his most recent review after 13 years follow-up without other therapy he had no clinical or colonoscopic evidence of UC and histopathology samples from several sites around the colon were normal.

 

Patient 2

This 53-year-old woman had a 20-year history of chronic UC, initially diagnosed at another institution. She had previously used salazopyrin, prednisone orally and steroid enemas in various combinations with inadequate follow-up. Treatment on review included prednisone 25 mg/d, metronidazole 200 mg tid together with salazopyrin 2 g/d which was subsequently self-administered with fluctuating doses (highest doses reached over the years remained unclear). On presentation, she complained of rectal bleeding and diarrhea (2–3 motions per day) with intermittent constipation, abdominal cramping, urgency, and flatulence. She referred to self-treat, refused trial of azathioprine, and requested information on alternative therapies favoring the flora manipulation approach of Bennett and Brinkman.11 Prior to HPI and in symptomatic remission colonoscopy revealed patchy inflammatory changes indicative of ongoing IBD. Histology was consistent with UC of moderate-grade activity.

HP retention enemas were administered over 5 consecutive days. The fecal flora originated from an unrelated adult male donor. Salazopyrin, the only concurrent medication at that time, was ceased immediately and within days symptoms had improved markedly. At 4 months post-HPI, colonoscopy and histology showed no active and greatly reduced chronic inflammation. The patient had an entirely normal bowel habit consisting of 1 to 2 formed stools per day with no associated symptoms. At follow-up consultation 10 years later she continued to be asymptomatic. Twelve years post-HPI, there was no clinical or colonoscopic evidence of ulcerative colitis. Histology was negative for both active and chronic inflammation.

 

Patient 3

A 27-year-old male engineer presented with a 5-year history of severe UC symptoms including 10 to 15 bloody motions with mucus per day with intermittent abdominal pain, urgency, nausea, flatulence, and fatigue. These symptoms were particularly difficult to control on maximal standard available medications including high-dose steroids 50 mg/d, mesalamine 4 to 6 g/d, olsalazine 3 to 4 g/d, salazopyrin 3 g/d, azathioprine 200 mg/d, vancomycin 1 g/d and ultimately cyclosporine (dose unknown). An anti-mycobacterial combination of rifabutin (300 mg/d), clarithromycin (500 mg/d), clofazimine (100 mg/d), and ethambutol (800 mg/d) had also previously been administered on the basis of the possibility of Mycobacterium avium subspecies paratuberculosis involvement but was ceased due to fevers. In spite of these therapies, the patient was unable to reduce his daily prednisone dosage below 20 mg in conjunction with other drugs without symptom recurrence. Colonoscopy at this time confirmed gross active colitis with contact bleeding and histology typical of active chronic IBD. Blood tests revealed mild lymphopenia and neutrophilia. Attempts to control symptoms with prednisone, azathioprine, mesalamine, and loperamide hydrochloride before HPI were unsuccessful.

Despite the persistence of diarrhea and rectal bleeding, HPI was commenced using flora donated by the patient’s brother and continued for 5 consecutive days. One week post-HPI, the patient noted decreased pain, urgency and bleeding. While still taking azathioprine and mesalamine, prednisone was reduced stepwise at a rate of 5 mg per week. One month after HPI, all medications were ceased. After 4 months, the patient was defecating twice daily with minimal blood and no urgency. He had gained 5 kg since the infusions and claimed profound improvement in symptoms and general health. One year post-HPI, the patient was asymptomatic and continued to require no medication, having 1 to 2 formed stools per day without bleeding or pain. After a 4-year follow-up period, he remained in complete clinical and colonoscopic remission with biopsies of the distal rectum showing minor architectural changes consistent with past chronic inflammation but without any active inflammation.

 

Patient 4

A 28-year-old woman presented with a 14-year history of UC including diarrhea with mucus and bleeding (3–5 motions per day), cramping, nausea, vomiting, sensation of fever at times, and fatigue. Despite therapy, severe symptoms recurred every few months, especially during times of stress. Intense inflammation was visible colonoscopically with active chronic inflammation on histology. Symptoms were partly controlled over several months on prednisone 40 mg/d, olsalazine 3 g/d, azathioprine 175 mg/d (above which thrombocytopenia developed), and later changed to mercaptopurine 75 mg/d. Prior to HPI, prednisone was reduced to 20 mg/d at a rate of 5 mg/wk.

HPI was administered using flora donated by the patient’s brother-in-law over 5 consecutive days. Mercaptopurine was ceased immediately, while olsalazine was continued for a further 6 weeks. Immediate improvements included reduced bleeding, urgency, nausea, and vomiting, while abdominal cramping persisted for 1 week. The patient experienced 1 episode of bleeding 3 weeks post-HPI and the total withdrawal of prednisone was delayed until week 6. Two months following HPI, the patient was well, with no urgency or bleeding. Colonoscopy and histopathology was normal 1 year after HPI. At 2 years follow-up, she had had no more UC relapses despite episodes of stress and continued to be clinically, colonoscopically, and histologically disease-free without treatment.

 

Patient 5

A 40-year-old woman presented with a 15-year history of severe UC involving frequent episodes of diarrhea with rectal bleeding and mucus (>6 motions per day) with abdominal pain, arthralgia, anorexia, and weight loss. She was treated for over 2 years with prednisone 40 mg/d, azathioprine 200 mg/d, metroni- 44 J Clin Gastroenterol, Vol 37, No. 1, 2003

dazole at times (max. 800 mg), prednisolone sodium phosphate enemas, and olsalazine 3 g/d combined with mesalamine 1.5 g/d or salazopyrin 2 g/d and reached good clinical control. At each review however, she desired to cease all medications. She attempted this periodically, but symptoms relapsed on withdrawal of treatment. Pre-HPI colonoscopy (see Fig. 1) showed intense colitis to mid-transverse colon with contact bleeding and histologically active and chronic inflammation consistent with UC.

Using fecal flora donated by the patient’s brother, HPI was administered via enema over 5 consecutive days. An improvement in symptoms was observed immediately and all concurrent standard medications (prednisone 25 mg/d, azathioprine 200 mg, and mesalamine 1.5 mg/d) were withdrawn over the next 6 weeks. Four months after HPI, the patient was defecating once a day with no bleeding, although abdominal discomfort and minor arthralgia persisted. This abdominal discomfort and arthralgia progressively recovered to normal over the course of 1 year, the patient’s appetite improved and she was consequently able to gain weight. At 1 year following HPI, the patient was clinically disease-free without treatment and at colonoscopy inflammation was absent with the presence of some scarring (see Fig. 2). Histology showed no evidence of active or chronic UC.

 

Patient 6

A 42-year-old man had suffered severe, active UC for 10 years with diarrhea and rectal bleeding (4–5 motions per day) cramping, fatigue, and weight loss diagnosed and treated at another institution.Adequate control of his disease was reached using maximum tolerated therapies, including prednisone 50 mg/d, azathioprine 125 mg/d (adverse effects, including hair loss, with higher dose), mesalamine 1 to 2 g/d and salazopyrin 2 g/d, although he desired to use an alternate approach with few or no drugs. Colitis to mid-sigmoid was re-confirmed on colonoscopy and histology as active, chronic colitis. Prior to HPI, prednisone was withdrawn step-wise to zero at 10 mg per week, while azathioprine and mesalamine were continued.

HPI consisted of 5 consecutive daily infusions and the use of his brother’s fecal flora. Six weeks following HPI, symptoms had regressed to normal and all medications were ceased. At 6 months the patient’s weight had increased by 4 kg. After 1 year without treatment normal bowel habit continued with 1 formed motion per day with no bleeding or urgency. Colonoscopy showed a normal bowel to the cecum with no evidence of colitis. Histopathology was negative for both active and chronic inflammation.

 

Conclusions

 

… To our knowledge these 6 cases document for the first time the total disappearance of chronic UC without the need for maintenance treatment…. Our cases differ from the remissions commonly seen in clinical practice. Remission in UC is a term describing significant clinical improvement often measured by an activity index. There is currently no definition of remission that demands colonoscopic and histologic normality with no recurrence after a long period without maintenance drugs.  Perhaps in the future, if such a therapy can achieve prolonged absence of UC without maintenance drugs, the result should be considered a “cure.”

Comments

  1. Please, I need to know: Is it true that the FDA has temporarily suspended fecal transplants until further notice, nationwide?

    Thanks, Margaret

    • No the FDA has not suspended fecal transplants. They can’t stop people from doing what they want with their own bodies and many people who are currently having them are doing them themselves because of cumbersome FDA regulations.

      What is true is that the FDA’s rules which require an Investigational New Drug (IND) permit for doctors to do these is now being more well publicized than it was before. Unfortunately this is discouraging and effectively preventing many doctors from doing fecal transplants, which is unfortunate especially since there is nothing investigational or new about this procedure. There are also already well publicized guidelines published in medical journals regarding testing to make sure donor stool is safe.

      Ironically people using enemas at home might be using the most safe procedure for fecal transplants, if they are using safe donor stool. This is because even with a trained doctor using a colonoscope, there is always a risk, even if it is low, of an instrument damaging the colon walls.

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