Ulcerative Colitis Long Term Remission After Fecal Transplants

The excerpt of six case reports listed below come from the following medical publication.  Treatment of ulcerative colitis using fecal bacteriotherapy.These are examples of long term remission achieved by using fecal microbiota transplants to treat Ulcerative Colitis.  The report was published in 2003 - if you are interested in reading the report in more detail, please click the following link which will open up a new window at the site for the Centre For Digestive Diseases. Please note that HP in the case studies refers to "human probiotics" (or fecal microbiota transplantation)

Treatment of ulcerative colitis using fecal bacteriotherapy.
TJ Borody, EF Warren, S Leis, R Surace, O Ashman.
J Clin Gastroenterol 2003; 37(1): 42-7.


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 Prednisone was withdrawn stepwise at a rate of 5 mg per week over 5 weeks.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.

Clinics and Doctors Who Perform Fecal Microbiota Transplantation

We are compiling a list of doctors and hospitals around the world who have performed fecal microbiota transplants - the list will grow as more doctors start to use this procedure on their ailing patients.

We would love your help in compiling this list, so a comment with a name of a doctor/physician/medical professional and any information you can give would be very much appreciated!

Please don't try this procedure without qualified medical guidance and advice. It is essential that fecal doners be screened for various diseases including some which are contageous. This is why a list of doctors who are familiar with the procedure is important, so that those of you who feel fecal microbiota transplantation could be beneficial to you can seek out appropriate medical advice.

Doctors from around the world are listed below:

Australia

Professor Thomas Borody,

Centre For Digestive Diseases

Five Dock, Sydney

USA

Dr Lawrence J Brandt

Montefiore Medical Center
111 East 210th Street
Rosenthal Pavilion
Bronx, NY 10467

 

Wilfred Lee, MD

Gastroenterology

Internal Medicine

St Francis Medical Centre

2907 Keystone
Cape Girardeau, MO 63701

Dr. Alexander Khoruts

Gastroenterology (GI) Clinic

Phillips-Wangensteen Building
Clinic 1E
516 Delaware St. SE
Minneapolis, MN 55455

Sudhir K. Dutta, M.D.

Division Head of Gastroenterology,
Sinai Hospital of Baltimore
2411 W. Belvedere Avenue, Suite 305
Baltimore, MD 21215
Phone: 410-601-5392

 

Dr David Shepard

Tampa Endoscopy Center

4809 North Armenia Avenue

Suite 100

Tampa, Florida, 33603-1436

Phone:  (813) 658-5037

 

Canada

Dr Michael Silverman

Lakeridge Health
1 Hospital Court
Oshowa
Ontario, Canada
905-721-4717

UK 

Taymount Clinic
Clinic Director is Glenn Taylor
1/F, 16a High Street
Hitchin, Hertfordshire
SG6 1AT United Kingdom
Email Contact: enquiries@taymount.com
Website: http://www.taymount.com
Telephone: 0044 1462 712500

 

If you are trying to find a doctor who has had past experience in performing fecal microbiota transplants please comment in the box stating the area you live and how far you would be willing to travel for treatment and we will endeavour to locate an appropriate medical professional for you.

Stool Banks for Stool Doners?

According to an article in the Sydney Morning Herald, stool transplants (fecal microbiota transplantation) are being used increasingly in the USA to successfully combat the deadly C.diff.  Reminds me of how the evolution of fungi into penicillin has saved the lives of so many since it's introduction. 

Antibiotics are powerful in their ability to kill bacteria, but the problem is that friendly bacteria are also killed.  Fecal transplant appears to restore the normal balance.  One wonders if down the track fecal transplant will be used in some modified way to negate these harmful effects of antibiotics.

"Drugmakers racing to develop medicines and vaccines to combat a germ that ravages the gut and kills thousands have a new challenger: the human stool.

For patients hit hardest by the bacterium Clostridium difficile, getting a "stool transplant" could become a standard treatment within just a few years. Just as blood banks and sperm banks are now commonplace, stool banks may soon dot the landscape.

About 3 million Americans are infected annually with the bacterium - also known as C. diff - which spreads mainly through hospitals, nursing homes and doctors' offices. It is common in Australia in various strains, including the deadly 244.

Most people have no symptoms, but 500,000 Americans - more than half of them 65 and older - develop abdominal cramps, fever, diarrhea and inflamed colons. As many as 30,000 die each year from the bacterium, usually after recurrences of infection.

 

The infections are typically the result of taking antibiotics, which wipe out friendly bacteria in the colon that normally keep C. diff under control. Transplants of stool from screened donors - given by enema, colonoscopy or a tube down the throat - restore these bacteria.

Although the vast majority of C. diff infections occur in healthcare settings, more and more cases are occurring in younger adults and children who have not recently taken antibiotics or been hospitalised. They include people who take proton pump inhibitors - a leading class of heartburn drugs.

Costly treatments from Merck & Co and other drugmakers, and a vaccine from Sanofi, are on the horizon. But growing numbers of gastroenterologists are more excited about the use of human stool transplants, which in experimental settings have consistently cured 85 percent to 90 per cent of patients who have had multiple episodes of C. diff.
"Until recently, fecal transplants have been on the fringes of mainstream medicine," said Dr Cliff McDonald, an epidemiologist with the US Centers for Disease Control and Prevention. "It could become the primary mode of therapy within a year or two for patients with multiple recurrences."

Wheel of misfortune
The first recorded stool transplants were given in 1958 to four patients with inflamed colons. The procedures won more attention in the mid-1980s, when Australian gastroenterologist Thomas Borody began using them to treat his C. diff. patients.

Dr Moshe Rubin, head of gastroenterology at New York Hospital Queens, said most patients prefer the simplicity of a pill or injection, but for those with multiple bouts the fecal transplants could become a mainstay treatment.

"This has to be tested in large numbers of people before you unleash it for such a widespread disease," Rubin said.

C. diff medicines and vaccines could eventually claim total annual sales of $2 billion, according to Morningstar analyst David Krempa, or 10 times current sales.
Fecal transplants might initially be appropriate for patients who have had a third recurrence - or about 25,000 Americans each year, according to Dr. Sahil Khanna, a Mayo Clinic gastroenterologist. That number could rise as the procedure becomes more widely accepted, and pose perhaps the biggest threat to sales of Merck's experimental drug, which is expected to target a similar patient group.

About 90 per cent of C. diff patients initially treated with vancomycin, and 60 percent of those treated with another standard oral drug called metronidazole, recover within weeks. But 20 percent suffer recurrences, as surviving bacteria spores become activated or as patients become re-infected with spores that cling to clothing and furniture and can survive for months.

With each recurrence, risk of another rises, with more weight loss, diarrhea and fatigue. After a third recurrence, the risk of suffering a fourth is 60 per cent to 70 per cent.
"It's a constant wheel of misfortune," said Eric Kimble, a senior executive for Cubist Pharmaceuticals Inc, which is developing a C. diff treatment called CB-315.

Getting over the 'ick' factor
Fecal transplants have proved a godsend to such patients. They are given to those who have not benefited from metronidazole or vancomycin - or who have suffered repeat recurrences of C. Diff after being temporarily helped by the treatments.

In more than 100 of the experimental procedures performed by Dr Christine Lee, the transplants cured the infections and prevented recurrences in 90 percent of patients, said the infectious disease physician at St Joseph's Healthcare (hospital) at McMaster University in Hamilton, Ontario.

"Their energy level and appetite bounce back within a week, sometimes within 48 hours," Lee said. "They can't believe how simple and effective the procedure is."

In a five-minute bedside procedure, Lee introduces about 50 grams (1.75 ounces) of donated fecal matter into the rectum, using an inexpensive plastic plunger. A single procedure re-establishes the balance of bacteria.

Friends and family of patients, as well as doctors and nurses, provide without pay the stool used in Lee's procedures. They are screened to ensure they do not have viruses, such as HIV or hepatitis C, or other pathogens that can be transmitted to patients. She said some donate stool on a regular basis, which can be used for a great number of patients.

Once transplants are approved by health regulators, Lee predicted, enema procedures will be less costly than two other delivery methods now used for stool transplants. They include colonoscopy, in which doctors sedate the patient and insert stool into the colon, or through a different procedure in which a plastic feeding tube is passed through the nose, down the throat and into the stomach.

In the meantime, gastroenterologists say doctors and hospitals can help prevent C. diff by being more restrained in the use of antibiotics and ensuring that hospital rooms are diligently cleaned with bleach wipes to kill C. diff spores.

Dr Mark Pochapin, director of gastroenterology at NYU Langone Medical Center, said fecal transplants had more appeal than emerging anti-toxin approaches.

"They appear effective, balance the normal intestinal flora, are inexpensive and are safe when done with appropriate testing," he said. "They will far and away revolutionise how we treat this disease."

Many patients might benefit most from transplantation of their own stool, rather than relying on donors. They would include those undergoing chemotherapy or hip or knee replacements, all of which involve use of antibiotics, said the CDC's McDonald.
People, he said, would set aside stools for processing into capsules that would be frozen and stored until needed.

Such "bacterial treatment" after antibiotics might eventually also lower the risk of developing asthma, allergy, obesity or other conditions that may be partly linked to loss of helpful bacteria, McDonald said.

"Look at it as a way to put people's bacterial population back together again after antibiotics, like restoring Humpty Dumpty," said McDonald."


http://www.smh.com.au/world/science/blood-bank-sperm-bank--stool-bank-20121203-2aqqc.html