tag:blogger.com,1999:blog-63903890029467326832024-03-13T01:09:48.428-07:00Fecal Microbiota Transplant and Its Evolving Medical UsesFecal Microbiota Transplant is used in the treatment of the bacterium, clostridium difficile. The transplants have shown promise for diseases and disorders such as colitis (including ulcerative colitis and crohn's disease), multiple sclerosis, parkinson's disease, diabetes, autism, irritable bowel syndrome, acne and even obesity! Subscribe for updates on the latest medical research for fecal microbiota transplantation including medical professionals who perform stool transplants.Unknownnoreply@blogger.comBlogger18125tag:blogger.com,1999:blog-6390389002946732683.post-20407879259054135602021-06-24T23:33:00.001-07:002021-06-24T23:33:17.069-07:00<p> Years later - my son's story. Considered cured. </p><p><a href="https://www.facebook.com/LetsTalkShitBook/posts/272711171304899">https://www.facebook.com/LetsTalkShitBook/posts/272711171304899</a></p>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-6390389002946732683.post-74878726948681573002016-11-20T02:26:00.000-08:002014-01-13T01:38:07.281-08:00"Jake's" Widespread Crohn's Disease Gone Thanks To FMT! 20 November 2013It's been a while since I posted about my son "Jake". For those who haven't read his story, here is the link <a href="http://www.fecalmicrobiotatransplant.com/2013/07/crohns-disease-fmt.html">http://www.fecalmicrobiotatransplant.com/2013/07/crohns-disease-fmt.html</a> . He has been off medication (Imuran) for nine months now and looks and feels well. Unfortunately his cousin who was his donor became unsuitable to donate in mid August due to picking up a parasite, so Jake has gone since then without any<a href="http://www.fecalmicrobiotatransplant.com/p/what-is-fecal-microbiota-transplant.html" target="_blank"> FMT</a>.<br />
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Today he had a colonoscopy and endoscopy and we were thrilled with the news. There is no sign of Crohn's Disease anywhere - <u>not</u> in his intestines, <u>not</u> in his terminal ileum and <u>not</u> in his duodenum!!! In fact, Professor Borody said there was no scarring or ulceration or any indication that the disease had ever existed. It was all perfect, healthy and inflammation-free. When he was first diagnosed with Crohn's three years ago it was very widespread. I am sure that anyone reading who has any experience or understanding of Crohn's Disease will appreciate just how incredible this is! The persistence has paid off.<br />
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It's still too early to say that this is a cure - only time will tell that, but his remission is not just clinical, it's visible and histological remission with no medication. This has completely defied the "odds" so far. It's the miracle we prayed for and it is Jake's wish and mine that this will give hope to others with this terrible disease.<br />
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I am one very, very happy mother! What an absolute "legend" of a doctor Professor Borody is!!<br />
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Oh and by the way, Jake's skin is still clear - his acne never returned :-)Unknownnoreply@blogger.com17tag:blogger.com,1999:blog-6390389002946732683.post-25540690149490815842016-07-27T21:12:00.000-07:002014-01-13T01:37:40.738-08:00Crohn's Disease, Acne and Fecal Microbiota Transplant In Teenager - Remission Without Medication! 27 July 2013I have hesitated in sharing my son's story with Crohn's Disease and the success we have had with <a href="http://www.fecalmicrobiotatransplant.com/p/what-is-fecal-microbiota-transplant.html" target="_blank">FMT</a> <a href="http://www.fecalmicrobiotatransplant.com/p/what-is-fecal-microbiota-transplant.html" target="_blank">(fecal microbiota transplantation)</a> until now because I didn't want to do so prematurely.<br />
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My son is 15 years old. To protect his privacy, I will call him Jake, although that is not his real name :-).<br />
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Jake was diagnosed with Crohn's Disease a few days before his 13th birthday. It was widespread ulceration, inflammation and infection throughout his duodenum, terminal ileum, ascending colon, descending colon and rectum. It was a "gut-wrenching" time for me as a mother to an only child, especially after being told how very serious this disease is, how extensively he had it, that he would have it for the rest of his life, and probably do poorly in the long-term because he was so young at diagnosis. <br />
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I was worried sick with the long term consequences of my son taking immune-suppressive drugs (in his case, Imuran) - on the other hand I was terrified of the consequences of Crohn's Disease and felt we were between a "rock and a hard place". I cannot begin to put into words just how heartbroken and helpless I felt, but I am sure that any parent who reads this will understand.<br />
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Professor Tom Borody was recommended to us by a family friend as being an outstanding gastroenterologist. Unfortunately he was unable to treat Jake until he turned 14 as he was a paediatric patient, however tests he was able to order showed that Jake also had a strain of c-diff (clostridium difficile) - it was not the worst strain, but Prof. Borody felt that we needed to get rid of that first. It was what he called a "super infective".<br />
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Within days of his 14th birthday, Jake had a gastroscopy and colonoscopy. The Imuran had certainly helped to take care of the crohn's in his colon - however his terminal ileum was still swollen, inflamed and pussey. His duodenum, still had some crohn's-like ulcerations. Prof. Borody recommended <a href="http://www.fecalmicrobiotatransplant.com/p/what-is-fecal-microbiota-transplant.html" target="_blank">FMT</a> to kill off the c-diff and we proceeded to have suitable family members tested as potential donors. Jake began a three week course of oral vancomycin to weaken the c-diff and then in April 2012 had his first FMT via colonoscopy- his terminal ileum was still very inflamed and swollen. I continued to administer FMT treatments to Jake at home and his 14 year old cousin was the donor. We also continued his Imuran.<br />
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A remarkable and unexpected bonus to having the FMT was that acne that had plagued Jake for the past year and a half had completely disappeared 7 days after treatment began. It has never returned!!<br />
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In November of 2012 Jake had a colonoscopy and endoscopy. To Prof. Borody's surprise, Jake's colonoscopy was perfect - the terminal ileum looked normal, as if there had never been a problem! The only trace was one single tiny erosion in his duodenum. There was no trace of c-diff either!<br />
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As advised, we reduced his Imuran and gradually over the next few months. Jake was completely off his medication by March 2013, so as at the time of writing, it's been almost five months. Jake is growing tall, his appetite is huge (perfectly normal for a healthy teenage boy) and he is putting on weight appropriately for his age. I still do top-up FMT treatments every 3 to 4 weeks - it's difficult to know exactly when the right time to stop is - in total he has had well over 115 treatments. Prof. Borody says that Jake needs to develop his own microbiota. <br />
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I do not know if FMT offers a cure for crohn's disease - but I do know that there is no way my son would have been able to sustain any remission without medication prior to this as we had tried a couple of times to reduce his Imuran but both times his symptoms came back within two weeks. What I do know is that FMT has tremendous potential for Crohn's and other diseases and definitely needs further studies. I also have to stress the importance of stringent donor testing.<br />
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I will keep you all posted in the months ahead of Jake's progress, but thus far, as a mother, I cannot be more delighted with how well this has gone. I am also so incredibly thankful for Prof. Tom Borody for being one of those scientists who dares to think "outside the box". It is because of doctors like him that medicine advances instead of remaining stagnant. It is because of him that Jake's future is looking good instead of bleak and that I can cry tears of happiness and gratitude instead of despair.<br />
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<a href="http://www.fecalmicrobiotatransplant.com/2013/11/crohns-cure-fecal-transplant.html" target="_blank">(Please click here to read part 2 of "Jake's" Story - November 2013 (One year later) - Colonoscopy/Gastroscopy showing no sign of Crohn's Disease whatsoever - NOT even in his duodenum!)</a>Unknownnoreply@blogger.com18tag:blogger.com,1999:blog-6390389002946732683.post-16726847857169576932014-11-09T20:51:00.002-08:002014-11-09T20:51:36.694-08:00Fecal Microbiota Transplant, or Poop Transplant Explained!<div class="separator" style="clear: both; text-align: center;">
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<span style="font-family: Arial, Helvetica, sans-serif;">I love the simplicity of this video in it's explanation of fecal microbiota transplant! Very worth watching!</span></div>
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<br />Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-6390389002946732683.post-61444873168986632212014-01-29T19:33:00.000-08:002014-01-30T21:29:52.006-08:00Cure For Crohn's Disease - Let's Kill Paratuberculosis Together!I have received information from a Canadian man who's two young children have both been diagnosed with Crohn's Disease - they are currently being treated with an antibiotic regime that is working very well and will hopefully kill MAP (mycobacterium avium paratuberculosis) which is the bacterium implicated for causing Crohn's Disease. There has been much debate in the medical profession about the causation of Crohn's Disease (ie: autoimmune disease vs bacterial origin (MAP being the main player). I believe it's time to put the "autoimmune disease" theory to bed once and for all and so do many others. Please <u><strong><span style="color: blue;"><em>click</em></span></strong><em> <strong><span style="color: blue;">here</span></strong></em></u> to read a brilliant article by Dr Judith Lipton who has been cured of Crohn's for 8 years as at the time of writing. Then, if you are convinced, as I am that MAP causes Crohn's Disease in the majority of cases, come back here and click the link at the end of this post and donate to help end the suffering caused by Crohn's Disease!<br />
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Below is the ground-breaking information I have received<br />
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<strong><em>"Late last year, Dr. Marcel Behr (Microbiologist in Chief in Montreal - MUHC) created a mouse model whereby he is able to infect them with paratuberculosis and they come down with Crohn's 100% of the time. This is the first infectious model of Crohn's disease in the world! We are NOW going to begin testing various combinations of antibiotics to try and achieve a CURE rate of about 95% as is the case with the latest Tuberculosis regimen. We have been raising funding for this project (We need roughly $100,000 CAD). We will keep you posted but in the meantime let us know if you know of anyone who might be willing to contribute to this critical research."</em></strong><strong><em><br /></em></strong><br />
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If we are to progress with <strong>putting an end to Crohn's Disease forever</strong>, donations to enable this to happen are needed <u>NOW!</u> This is not about finding a drug to cover up symptoms or to supress the immune system (with the possibility of horrific side effects) as the majority of drugs for Crohn's Disease do, this is about <strong>KILLING THE ACTUAL BACTERIA THAT CAUSES CROHN'S</strong> in the majority cases.... it's about finding the <strong>very best combination of medication to actually get rid</strong> <strong>of the very slow growing insidious MAP!!</strong>
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I will share the link with you and urge anyone who suffers from or knows someone with Crohn's Disease to spread this message. <strong>PLEASE DONATE</strong> through the link below! Together no matter where you reside in the world, we <strong><u>can conquer Crohn's Disease</u></strong> and put an end to the needless suffering! <span style="color: blue;"><a href="https://www.mghfoundation.com/donate/online-donation" target="_blank"><span style="color: blue; font-size: large;">Click</span></a><span style="font-size: large;"> </span></span><a href="https://www.mghfoundation.com/donate/online-donation" target="_blank"><strong><span style="color: blue; font-size: large;">HERE</span></strong></a><span style="color: blue;"><span style="font-size: large;"> </span><a href="https://www.mghfoundation.com/donate/online-donation" target="_blank"><span style="color: blue; font-size: large;">to <strong>DONATE</strong>, and it's very important that you select the designation to donate to</span></a><span style="font-size: large;"><span style="color: blue;"> </span> <strong><span style="color: red;">"Russell and Gabby Fund to Support Crohn's Research".</span></strong></span></span>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-6390389002946732683.post-16717160440470698412014-01-12T22:36:00.004-08:002014-01-13T02:34:15.979-08:00Colorectal Cancer and Altered Gut Microbiota <xmlns:xlink www.w3.org="" xlink="">
<span style="font-family: Arial; font-size: small;">Is this the reason that people who consume a diet high in fibre from fruit and vegetables and a lower in animal fat and protein (both animal fat and protein diets attract <a href="http://www.cbc.ca/news/health/human-gut-bacteria-seem-to-be-picky-eaters-1.1041404" target="_blank">bacteriodes</a>) have a lower incidence of colon cancer? It would seem that it is every bit as important to provide the food for our microbiota to thrive on as it is to feed ourselves. We and our microbiota would appear to benefit mutually from the same types of food - it's not just about nutrition, it's about feeding our "helpful friends" as well!</span></xmlns:xlink><xmlns:xlink www.w3.org="" xlink="">
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<xmlns:xlink www.w3.org="" xlink=""><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: small;"><u><strong>The Differences in Colonic
Mucosal Microbiota Between Normal Individual and Colon Cancer Patients by
Polymerase Chain Reaction-denaturing Gradient Gel Electrophoresis</strong></u></span>
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<span style="font-size: small;">Authors: Huipeng, Wang MD; Lifeng, Gong MD; Chuang, Ge MD; Jiaying, Zhao MD; Yuankun,
Cai MD</span></span></h4>
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<strong><em>Abstract</em></strong></span><br />
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<span style="font-family: Arial, Helvetica, sans-serif;"><strong>Objective:</strong> The aim of this study was to analyze the differences in the intestinal composition between normal individuals and colon cancer patients.</span><br />
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<strong>Methods:</strong> To establish the criteria for screening a normal individual for colon cancer, human colonic biopsies were obtained at routine colonoscopy. For patients with colon cancer, samples were obtained from cancerous regions. For normal individuals, colonic biopsies were taken from 3 sites of large intestine (descending, transverse, and ascending colon). Thereafter, a comparison of the microbiota structure by polymerase chain reaction-denaturing gradient gel electrophoresis (PCR-DGGE) was carried out. At last, bacterial species were identified by sequencing special bands from DGGE gels and comparing data with sequence databases.</span><br />
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<strong>Result:</strong> With PCR-DGGE, we have discovered that the diversity and richness of the bacterial community from colon cancer patient’s colonic mucosa were lower than that of the normal individual’s sample. Then, a special DGGE band was found in the colon cancer patients. After sequencing, we confirmed that it had a high level of similarity with bacteroides.</span><br />
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<strong>Conclusions:</strong> Colon cancers are closely related with the alteration of intestinal flora such as the reduction of biodiversity and richness of the bacterial community. Furthermore, the increase in proportion of bacteroides may be directly associated with colon cancer.</span><br />
<a href="http://journals.lww.com/jcge/Abstract/2014/02000/The_Differences_in_Colonic_Mucosal_Microbiota.10.aspx" target="_blank">Journal of Clinical Gastroenterology</a>:<br />
February 2014 - Volume 48 - Issue 2 - p 138-144<br />
doi: 10.1097/MCG.0b013e3182a26719<br />
ALIMENTARY TRACT: Original Articles<br />
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<br />Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-6390389002946732683.post-91394373605417502182013-05-28T20:14:00.000-07:002013-05-28T20:14:09.066-07:00Multiple Sclerosis and Fecal Microbiota Transplant<span style="font-family: Arial, Helvetica, sans-serif;">With World MS Day being 29th May, it seems appropriate to post a link to a previous entry about Multiple Sclerosis and Fecal Transplant.</span><br />
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<span style="font-family: Arial, Helvetica, sans-serif;">The link is to three case studies from Centre of Digestive Diseases, Sydney Australia (Professor Borody). Three of his patients who had multiple sclerosis were treated for constipation (one of the many complications of this terrible disease) and to their's and Professor Borody's surprise, their MS symptoms unexpectedly also disappeared, so much so that as at the time of writing the study all patients remained in remission, one of them for 15 years! Professor Borody speculates that a gut pathogen may be responsible for causing the neurological disease and encourages a new direction in medical research of MS.</span><br />
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<a href="http://www.fecalmicrobiotatransplant.com/2012/08/could-multiple-sclerosis-be-caused-by.html"><span style="font-family: Arial, Helvetica, sans-serif;">http://www.fecalmicrobiotatransplant.com/2012/08/could-multiple-sclerosis-be-caused-by.html</span></a>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-6390389002946732683.post-33798749684722542192013-03-27T20:34:00.000-07:002013-03-27T20:34:13.215-07:00Youngest Fecal Transplant Recipient "The Doctor's Exclusive Medical Miracales"<div class="separator" style="clear: both; text-align: center;">
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<span style="font-family: Arial, Helvetica, sans-serif;">This is a video which aired on TV - great news for pediatric (child) patients with c-diff</span> </div>
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<br />Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-6390389002946732683.post-15111466812471632622013-03-27T14:10:00.002-07:002013-03-27T14:14:17.366-07:00FMT Success Story For Pediatric UC Patient!This story comes from a mother who posted as a visitor on <a href="http://thepowerofpoo.blogspot.com.au/" target="_blank">http://thepowerofpoo.blogspot.com.au/</a> - it's a very powerful story showing the tremendous results that FMT can give to a IBD sufferer (a child). It's definitely worth reading!<br />
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<strong><u>Kathy's Success Story</u></strong>
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"Hi, I’m Kathy, mom to a nine-year-old girl diagnosed with Ulcerative Colitis in January 2012 and successfully treated with FMT. I don't want to know where we would be now if we hadn't tried it, or if it hadn’t worked. We went through seven months of hell trying to get her better before we started FMT. Here’s our story:
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E's symptoms appeared out-of-the blue. On Christmas Eve 2011, she called me into the bathroom to look at her wipe, which had some blood on it. Over the next few days, we noticed that her stool, though completely formed, had some visible blood coating the outside of it. I didn't make too much of it, which is surprising since I tend to be a bit of an alarmist when anything seems out of the ordinary. I thought that she had picked up salmonella after playing with a lizard in the yard and that the blood would resolve, and we would move on with our lives. I was totally wrong.
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Within three-and-a-half weeks of the onset of bleeding, E had a colonoscopy, which showed inflammation in her colon. E was diagnosed with IBD, and more specifically, Ulcerative Colitis (and even more specifically, proctosigmoiditis). The good news, or so I thought, was that only her rectum and sigmoid colon were involved. The doctor thought so, too and said E would have to be on Asacol for at least a year, but that it should work to control the symptoms. At that point, I didn’t know anything about IBD, including that it was considered an autoimmune disease whose only “cure” was a colectomy. Yikes.
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Well, Asacol didn’t work. And neither did sulfasalazine, flagyl, prednisone, mesalamine enemas, hydrocortisone enemas, cortifoam and canasa suppositories. What?!?! How could that be? Well, apparently, there are cases of UC that are refractory, or not responsive to medication. But, at that point, we hadn’t hit the big guns yet — 6-MP or Remicade, so we weren’t there yet.
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In the meantime, we met with a surgeon. He told us that E might need a colectomy. It was the worst appointment of our lives. He wasn’t nice or compassionate. It seemed like he just wanted to cut open my kid and take her colon—no big deal. E said there was no way she was having her colon out. She said she didn’t need the surgery. I wanted to believe her, but I wasn’t sure we were going to be able to beat this thing. With more and more meds, she was just getting worse and worse as time went on. Her hemoglobin and hematocrit started dropping. She was getting more and more tired and lying around the house instead of climbing trees and running around. She was looking terrible. She was waking in the night to use the bathroom. I felt like I was losing my daughter.
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I had been frantically doing research all along, searching for alternative things to try. We tried various supplements—bovine colostrum, homeopathic phosphorus, turmeric, fish oil, cod liver oil, vitamin D, VSL, Chinese herbs— acupuncture, and two diets—SCD/paleo/GAPS (though admittedly we only followed it about 90%) and Jini Patel’s “stop intestinal bleeding diet”.
I first heard of FMT from a good friend of mine before E was even diagnosed with UC, when the bleeding had first started. I remember being so afraid to try it. I didn’t want to put anything in her rectum or colon for fear of making things worse. I couldn’t bear the thought of hurting my daughter more than she was already hurting. And I always thought poop was kind of dirty — I mean, we wash our hands after we use the bathroom, after all. Our doctors didn't know anything about it and pretty much changed the subject when I brought it up at appointments. So, I went ahead and purchased a home FMT protocol online.
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Then, I researched more and looked for support from other parents whose children have IBD. FMT looked to me like the most likely treatment to help E. I learned that people were doing FMT for UC and were being helped by it, but many were doing it without support from their doctors. I knew Borody’s research, I read about the Bright Clinic in Oregon, and I was in touch with someone who had successfully done FMT for his seven-year-old son. I read countless IBD forums. I learned that healthy stool is full of healthy bacteria and that if put into the colon of a person with UC, the bacteria would recolonize in the sick person’s colon and help it heal by restoring the balance of bacteria that was likely out of balance. But, I was wary about doing FMT without the support of our doctors. We were dealing with a child, and I was terrified that if I tried something like putting someone else’s poop into my daughter’s colon and she got sicker, I would get in some serious trouble.
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In April 2012, we had plans to travel 1000 miles for a second opinion at one of the top pediatric IBD centers in the country. The day before we left, E’s bleeding was getting worse and worse. Her tummy was aching, her knees were hurting, and she literally had to run to the bathroom every couple of hours. The bowl was red every time she went. I was a mess. We decided to give 6-MP a try, since our doctor at home assured us that our second opinion would give us the same advice. I felt that if she didn’t get better soon, we were going to be in trouble. So far, we had been able to keep E out of the hospital, but just barely. Every few days we were talking with the doctor, deciding whether to hospitalize her or try to keep her home. It was torture.
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At our second opinion appointment, the doctor confirmed what our doctor had said, but he also had statistics. There was a 50% chance that 6-MP would work for E, and a 60% chance that Remicade would (and even if Remicade worked, there was no guarantee it’d work forever). And that was the end of the road. If neither of those medications worked, her colon would have to be removed.<br />
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Shortly after, we decided to try FMT. I got the ball rolling on getting E into the first U.S. clinical trial for FMT in children. It turned out she was a good candidate. Unfortunately, the timing didn’t work out. We could tell by her blood work that she wouldn't be likely to stay on 6-MP even though her symptoms had improved quite a bit. In the end, we decided to take advantage of her improved status on 6-MP and try FMT before she had to discontinue it.
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Fortunately, with some pushing and pleading we finally persuaded our doctors to support us in FMT. They gave us a protocol (it was the protocol for C. Diff written by Silverman) and a list of blood and stool tests for the donor to have done.
We wanted a donor with good digestive and overall health. My husband has IBS, so he was out. I have always had a good gut as far as I know, but I still had all the tests to make sure there were no hidden problems. Two months prior to my first donation I was on antibiotics, but it doesn’t seem to have affected the quality of my donation.
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We started FMT in August last year. We began with a 10 day triple antibiotic therapy followed by 5 consecutive days of FMT, followed by twice-weekly FMT. Within 24 hours of the first enema what little bleeding there was had stopped. Within 3 months, E’s bowel movements reduced to 2-3 times daily. Throughout we have continued with sulfasalazine and FMT twice a week. E continues to do just great and her labs look awesome. The biggest improvement we saw in the labs was six months post-FMT when her calprotecin had dropped from a high of 1014 when she was flaring to her current level of 60.1.<br />
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It’s now seven months since we started FMT and E is 90% better. We are still doing FMT twice weekly and E still has some minimal food restrictions, which is why I don't say she is 100% better. She says she feels better than she ever has. She looks beautifully healthy. We have kept up the FMT because we believe the intestines take a long time to heal, and because we don't think it can hurt. While we have faith in the treatment, we don’t want to stop it yet, either.<br />
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My advice for people considering FMT is to talk to others who have done it and to try to find a doctor who will support you, if that’s important to you. After doing all the research I did, I felt very confident in the potential of FMT and strongly believed that we had nothing to lose by trying it. When the top researchers in the country told us that the best they can do is give your child a dangerous drug that has a 60% chance of working or they can cut out her colon, which has countless potential complications, I felt it was time for us to look at other options, and FMT seemed to be the best one by a longshot.
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My daughter was only sick for seven months, but it was the worst seven months of my life. I cried every day for six of those months. People kept telling me that she would get better, but I stopped believing them. But then, we fixed her. WE brought her back to health! And now our doctors are trying the treatment on other patients, and a family member who is in pediatric gastroenterology convinced her boss to try FMT on patients (they have done two so far!) There is no greater feeling than, even in some little way, to help someone regain the health of his or her child. What a roller coaster it has been — we went from feeling completely lost and scared to feeling like we can point people in the right direction and optimistic that our daughter is going to remain well.
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The best advice I can give someone trying to make a decision about FMT is that you will know if and when it is time for you to do FMT. Nobody can make the choice for you. We are all on our own journeys and have to find our own paths. There are many ways to wellness, and FMT may be yours. There are people out there doing it and doctors are starting to do it. But, these things are slow to get going in the medical field, and sometimes time is not on your side. It certainly wasn’t for us — we just did our research and did what we felt we needed to do for our child, and FMT was it. While it can be overwhelming at first, the prep is easy and the administration is even easier. I would do FMT every day for the rest of my life if that is what we needed to do."<br />
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If you are the parent of a child with UC and need support in making the FMT decision, Kathy is willing to help. Please visit <a href="http://thepowerofpoo.blogspot.com.au/" target="_blank">http://thepowerofpoo.blogspot.com.au/</a> and the blogger, Tracy can send your details to Kathy so that she can contact you.Unknownnoreply@blogger.com1tag:blogger.com,1999:blog-6390389002946732683.post-78367451661797280072013-01-22T11:46:00.004-08:002013-02-10T12:11:16.500-08:00Fecal Microbiota Transplantation Declared "THE ULTIMATE PROBIOTIC"!Following the spectacular results of a randomised study publicised in last week's New England Medical Journal by van Nood et al. (The Netherlands), The Gastroenterological Society of Australia spokesperson, Associate Professor Jane Andrews has declared fecal microbiota transplantation to be <em>"The Ultimate Probiotic".</em> <br />
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"Fecal transplantation for recurrent C.difficile has now got very good evidence behind it" she remarked in the Australian "Gastroenterology update". <br />
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The Australian society has changed their previous view in which they had considered fecal transplant to be unsafe and warned against it's use, and are now looking at setting up a state-based service at the Royal Adelaide Hospital in South Australia next year. The article stated that fecal microbiota transplantation had become mainstream in many centres (overseas). <br />
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This is very exciting news for those suffering from the incredibly debilitating and potentially deadly symptoms of clostridium difficile (estimated to kill over 30,000 Americans each year), and I am sure that it will lead to further research for validation of treatment of other diseases and disorders. <br />
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Read the article <a href="http://www.gastroenterologyupdate.com.au/latest-news/faecal-transplants-wipe-out-c-difficile" target="_blank">here</a>Unknownnoreply@blogger.com1tag:blogger.com,1999:blog-6390389002946732683.post-77619114464136127152013-01-18T00:30:00.001-08:002013-02-12T22:43:31.700-08:00Fecal Microbiota Transplantation - New England Journal of Medicine Reports 94% Cure Rate for C-difficile <p>The results of a randomized controlled study has been published in the New England Journal of Medicine this week which showed a 94% cure rate for clostridium difficile as opposed to 31% of patients taking the antibiotic vancomycin. The study was stopped prematurely becase the results were so outstanding for those who were given fecal transplant that it was considered to be unethical not to offer the treatment to all patients participating in the study. Read more below courtesy of the New England Journal.nbsp; Here is a link to the study: <br />
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<a href="http://www.nejm.org/doi/full/10.1056/NEJMoa1205037#.UPkDN6pY7mY.blogger" target="_blank">Duodenal Infusion of Donor Feces for Recurrent Clostridium difficile — NEJM</a><br />
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and a link to the editorial written by Ciarán P. Kelly, M.D.<br />
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<a href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#.UPkEutrjs3I.blogger" target="_blank">Fecal Microbiota Transplantation — An Old Therapy Comes of Age — NEJM</a><br />
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"Fecal Microbiota Transplantation — An Old Therapy Comes of Age</h1>
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Ciarán P. Kelly, M.D.</div>
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January 16, 2013<span class="doi">DOI: 10.1056/NEJMe1214816</span></div>
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<span class="doi">In 1958, doctors in Denver administered feces by enema to their patients with fulminant, life-threatening pseudomembranous enterocolitis.<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref1" rel="#refLayer" target="_blank">1</a></span> The goal of this infusion of donor feces (also termed fecal microbiota transplantation [FMT]) was to “re-establish the balance of nature” within the intestinal flora to correct the disruption caused by antibiotic treatment. They reported “immediate and dramatic” responses and concluded that “this simple yet rational therapeutic method should be given more extensive clinical evaluation.” During the ensuing 50 years, the association between <em>Clostridium difficile</em> infection and pseudomembranous enterocolitis was established, and effective antimicrobial treatments were identified. Despite these advances, <em>C. difficile</em> became the most commonly identified cause of nosocomial infectious diarrhea in the United States. During the past decade, there has been an alarming increase in the incidence and severity of this disorder, with associated increases in mortality and economic cost.<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref2" rel="#refLayer" target="_blank">2</a></span> </span><br />
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Although most patients with <em>C. difficile</em> infection have a response to antimicrobial therapy, approximately 25% have a recurrence after the initial treatment course.<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref2" rel="#refLayer" target="_blank">2</a></span> Patients with a first recurrence of <em>C. difficile</em> infection are more likely to have a second recurrence (risk, 35 to 45%), and for patients with multiple recurrences, the subsequent recurrence rates surpass 50%.<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref2" rel="#refLayer" target="_blank">2-4</a></span> <br />
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Only patients with the most recalcitrant cases of <em>C. difficile</em> infection are likely to undergo FMT, usually out of desperation after multiple treatment approaches have failed.<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref5" rel="#refLayer" target="_blank">5,6</a></span> Yet, systematic review reveals that the reported efficacy of FMT in treating recurrent <em>C. difficile</em> infection is greater than 90%.<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref6" rel="#refLayer">6</a></span> So why has FMT not become routine therapy for <em>C. difficile</em> infection during the past 50 years? There are three main reasons: it is aesthetically unappealing, it is logistically challenging (in terms of harvesting and processing suitable donor material), and there is a lack of efficacy data from randomized, controlled trials.<br />
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The last impediment is addressed in a report on a randomized, controlled trial by van Nood et al.,<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref7" rel="#refLayer" target="_blank">7</a></span> now in the <em>Journal</em>. In this study, investigators compared the duodenal infusion of donor feces after vancomycin therapy and bowel lavage with vancomycin therapy either alone or with bowel lavage. The study was unblinded and imperfect. Nonetheless, the outcome favors FMT (81% response) above vancomycin therapy either alone (31%, P<0.001) or with bowel lavage (23%, P<0.001) in patients with relapsed <em>C. difficile</em> infection in whom standard therapy with vancomycin has failed. The trial was closed to new enrollment by its data and safety monitoring board after only 43 of a planned 120 patients had undergone randomization because almost all patients in the two control groups had a recurrence. The finding that FMT was effective in 81% of patients with recurrent <em>C. difficile</em> infection is consistent with a systematic review of uncontrolled case series in which FMT through the stomach or small intestine showed an overall response rate of 80%; the anecdotally reported overall response rate for FMT through colonoscopy or enema is 92%.<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref6" rel="#refLayer" target="_blank">6</a></span> Thus, this study and the previous case series yield consistent, strongly positive results.<br />
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The study by van Nood et al. is an important confirmation of the efficacy of FMT for recurrent <em>C. difficile</em> infection. Their findings will provide added stimulus to the ongoing efforts to address the other main impediments to the routine and widespread use of FMT. Natural antipathy toward fecal therapy can be reduced by banking suitable material from anonymous, screened donors.<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref8" rel="#refLayer" target="_blank">8</a></span> Such a system would both distance the recipient from the stool donation and provide physicians with readily accessible, quality-controlled treatment materials. Ultimately, the use of feces may be eliminated in favor of defined mixtures of cultured bacteria that confer colonization resistance against <em>C. difficile</em>, an approach that was pioneered by Tvede and Rask-Madsen in 1989 and is now being examined afresh.<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref9" rel="#refLayer" target="_blank">9</a></span> The later approach can also assuage concern regarding the inadvertent transmission of disease-causing pathogens through FMT. These advances can make intestinal microbiota therapy acceptable and accessible to most patients and their physicians. It will also facilitate the “more extensive clinical evaluation” of FMT for severe, refractory <em>C. difficile</em> infection, as first advocated in 1958.<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref1" rel="#refLayer" target="_blank">1</a></span> <br />
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The significance of the study by van Nood et al. goes far beyond the treatment of recurrent or severe <em>C. difficile</em> infection. The burgeoning field of microbiome research, initially made possible by technologies to identify bacterial 16S ribosomal RNA in complex biologic samples, has alerted us to the abundant, diverse, and influential nature of the gut microbiota.<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref10" rel="#refLayer" target="_blank">10</a></span> Microbiome research has been expanded and complemented by methods to characterize the protein composition (proteomics) and metabolic processes (metabolomics) of the intestinal contents and those from other body sites. The results of this study represent a clear precedent in which planned therapeutic manipulation of the human intestinal microbiota can lead to demonstrable, clinically important benefits, thereby bringing FMT to the mainstream of modern, evidence-based medical practice.<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref1" rel="#refLayer" target="_blank">1,5-9</a></span> The study by van Nood et al. will encourage and facilitate the design of similar trials of intestinal microbiota therapy for other indications, such as inflammatory bowel disease, irritable bowel syndrome, prevention of colorectal carcinoma, and metabolic disorders, to name just a few.<span class="ref"><a class="showRefLayer" href="http://www.nejm.org/doi/full/10.1056/NEJMe1214816#ref10" rel="#refLayer" target="_blank">10</a></span> As such, it heralds the delayed adolescence of a broad and exciting new branch of human therapeutics.<br />
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</span><br /></p>Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-6390389002946732683.post-60844131116037998042012-12-18T22:01:00.000-08:002012-12-29T14:58:28.789-08:00Ulcerative Colitis Long Term Remission After Fecal Transplants<span style="color: black; font-family: Verdana, sans-serif; font-size: large;">The excerpt of six case reports listed below come from the following medical publication. </span><a class="navLink" href="http://www.cdd.com.au/pdf/publications/paper17.pdf" target="_blank"><span style="color: black;"><span style="font-size: large;"><span style="font-family: Verdana, sans-serif;"><em><span style="color: blue;">Treatment of ulcerative colitis using fecal bacteriotherapy</span></em><strong>.</strong></span></span></span></a><span style="color: black; font-family: Verdana, sans-serif; font-size: large;">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)</span><br />
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<a class="navLink" href="http://www.cdd.com.au/pdf/publications/paper17.pdf" target="_blank"><strong><span style="color: black; font-family: Verdana, sans-serif; font-size: large;">Treatment of ulcerative colitis using fecal bacteriotherapy.</span></strong></a><br />
<span style="color: black; font-family: Verdana, sans-serif; font-size: large;">TJ Borody, EF Warren, S Leis, R Surace, O Ashman.<br /> J Clin Gastroenterol 2003; 37(1): 42-7.</span><br />
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<u><strong><span style="color: black; font-family: Verdana, sans-serif; font-size: large;">Patient 1</span></strong></u><br />
<u><strong><br /></strong></u><span style="color: black; font-family: Verdana, sans-serif; font-size: large;">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.</span><br />
<span style="color: black; font-family: Verdana, sans-serif; font-size: large;">Immediately preceding HPI, his symptoms were moderately controlled using prednisone 25 mg/d and salazopyrin 1 g/d. </span><br />
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<span style="color: black; font-family: Verdana, sans-serif; font-size: large;">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.</span><br />
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<span style="color: black; font-family: Verdana, sans-serif; font-size: large;"><strong><u>Patient 2</u></strong></span><br />
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<span style="color: black; font-family: Verdana, sans-serif; font-size: large;">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. </span><br />
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<span style="color: black; font-family: Verdana, sans-serif; font-size: large;">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.</span><br />
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<span style="color: black; font-family: Verdana, sans-serif; font-size: large;"><strong><u>Patient 3</u></strong></span><br />
<strong><u></u></strong><br /><span style="color: black; font-family: Verdana, sans-serif; font-size: large;">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. </span><br />
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<span style="color: black; font-family: Verdana, sans-serif; font-size: large;">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.</span><br />
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<span style="color: black; font-family: Verdana, sans-serif; font-size: large;"><strong><u>Patient 4</u></strong></span><br />
<strong><u></u><br /></strong><span style="color: black; font-family: Verdana, sans-serif; font-size: large;">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. </span><br />
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<span style="color: black; font-family: Verdana, sans-serif; font-size: large;">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.</span><br />
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<span style="color: black; font-family: Verdana, sans-serif; font-size: large;"><strong><u>Patient 5</u></strong></span><br />
<strong><u></u></strong><br /><span style="color: black; font-family: Verdana, sans-serif; font-size: large;">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<br />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.</span><br />
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<span style="color: black; font-family: Verdana, sans-serif; font-size: large;">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.</span><br />
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<span style="color: black; font-family: Verdana, sans-serif; font-size: large;"><strong><u>Patient 6</u></strong></span><br />
<br /><span style="color: black; font-family: Verdana, sans-serif; font-size: large;">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. </span><br />
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<span style="color: black; font-family: Verdana, sans-serif; font-size: large;">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.</span><br />
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<span style="color: black; font-family: Verdana, sans-serif; font-size: large;"></span><br />Unknownnoreply@blogger.com2tag:blogger.com,1999:blog-6390389002946732683.post-90548469967114009692012-12-15T23:17:00.002-08:002013-10-24T03:41:28.094-07:00Clinics and Doctors Who Perform Fecal Microbiota Transplantation<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.</span><br />
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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! </span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.</span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">Doctors from around the world are listed below:</span></div>
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<u><strong><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">Australia</span></strong></u></div>
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<a href="http://www.cdd.com.au/" target="_blank"><span style="color: black;"><span style="font-size: large;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="color: blue;">Professor Thomas Borody</span>,</span></span></span></a><span style="color: black;"></span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">Centre For Digestive Diseases</span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">Five Dock, Sydney </span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;"><strong><u>USA</u></strong></span></div>
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<a href="http://www.einstein.yu.edu/departments/medicine/divisions/gastroenterology-liver-diseases/faculty/profile.asp?id=2519" target="_blank"><span style="color: blue; font-family: Arial, Helvetica, sans-serif; font-size: large;">Dr Lawrence J Brandt</span></a><span style="color: black;"></span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">Montefiore Medical Center<br />111 East 210th Street<br />Rosenthal Pavilion<br />Bronx, NY 10467</span></div>
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<span style="color: blue;"><a href="http://www.sfmc.net/DoctorDetails.htm?physID=321&F2_keywordFilter=x321x" target="_blank"><span style="font-size: large;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="color: blue;">Wilfred </span><span style="color: blue;">Lee, MD</span></span></span></a></span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">Gastroenterology</span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">Internal Medicine</span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">St Francis Medical Centre</span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">2907 Keystone<br />Cape Girardeau, MO 63701</span></div>
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<span style="color: blue;"><a href="http://www.uofmmedicalcenter.org/Providers/Bio/D_121673" target="_blank"><span style="font-size: large;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="color: blue;">Dr. </span><span style="background-color: white;"><span style="color: blue;">Alexander</span> <span style="color: blue;">Kh</span><span style="color: blue;">or</span><span style="color: blue;">uts</span></span></span></span></a></span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">Gastroenterology (GI) Clinic</span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">Phillips-Wangensteen Building<br />Clinic 1E<br />516 Delaware St. SE<br />Minneapolis, MN 55455</span></div>
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<a href="http://www.lifebridgehealth.org/Sinai/SinaiDivisionofGastroenterology.aspx" target="_blank"><span style="color: blue; font-family: Arial, Helvetica, sans-serif; font-size: large;">Sudhir K. Dutta, M.D.</span></a></div>
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<span style="font-family: Arial, Helvetica, sans-serif; font-size: large;">Division Head of Gastroenterology, <br />Sinai Hospital of Baltimore<br />2411 W. Belvedere Avenue, Suite 305<br /> Baltimore, MD 21215<br />Phone: 410-601-5392</span><br />
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<span style="font-family: Arial; font-size: large;"><a href="http://tampaendocenter.com/physicians/r-david-shepard-md" target="_blank">Dr David Shepard</a></span></div>
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<span style="font-family: Arial; font-size: large;">Tampa Endoscopy Center</span></div>
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<span style="font-family: Arial; font-size: large;">4809 North Armenia Avenue</span></div>
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<span style="font-family: Arial; font-size: large;">Suite 100 </span></div>
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<span style="font-family: Arial; font-size: large;">Tampa, Florida, 33603-1436</span></div>
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<span style="font-family: Arial; font-size: large;">Phone: (813) 658-5037</span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><u>Canada</u></span></h2>
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<span style="font-family: Arial; font-size: large;"><u>Dr Michael Silverman</u></span></div>
<span style="font-family: Arial; font-size: large;">Lakeridge Health</span><br />
<span style="font-family: Arial; font-size: large;">1 Hospital Court</span><br />
<span style="font-family: Arial; font-size: large;">Oshowa</span><br />
<span style="font-family: Arial; font-size: large;">Ontario, Canada </span><br />
<span style="font-family: Arial; font-size: large;">905-721-4717</span><br />
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<span style="font-family: Arial, Helvetica, sans-serif; font-size: large;"><strong><u>UK </u></strong></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><span style="color: blue; font-family: Arial, Helvetica, sans-serif;"><a href="http://www.taymount.com/" target="_blank"><span style="font-size: large;"><span style="color: blue;">Taymoun</span><span style="color: blue;">t Clinic</span></span></a></span></span><br />
<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: large;">Clinic Director is Glenn Taylor</span></span><br />
<span style="font-family: Arial, Helvetica, sans-serif; font-size: large;">1/F, 16a High Street</span><br />
<span style="font-family: Arial, Helvetica, sans-serif; font-size: large;">Hitchin, Hertfordshire</span><br />
<span style="font-family: Arial, Helvetica, sans-serif; font-size: large;">SG6 1AT United Kingdom</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: large;">Email Contact: enquiries@taymount.com<br />Website: </span><a href="http://www.taymount.com/" target="_blank"><span style="color: blue; font-family: Arial, Helvetica, sans-serif; font-size: large;">http://www.taymount.com</span></a></span><br />
<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: large;">Telephone: 0044 1462 712500</span></span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.</span></div>
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<span style="font-family: Arial, Helvetica, sans-serif; font-size: large;"></span><br />Unknownnoreply@blogger.com66tag:blogger.com,1999:blog-6390389002946732683.post-521555950830184422012-12-03T00:15:00.001-08:002012-12-30T00:54:32.477-08:00Stool Banks for Stool Doners?<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">According to an article in the </span><a href="http://www.smh.com.au/world/science/blood-bank-sperm-bank--stool-bank-20121203-2aqqc.html" rel="nofollow" target="_blank"><span style="background-color: white; color: blue; font-family: Arial, Helvetica, sans-serif; font-size: large;">Sydney Morning Herald</span></a><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">, 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. </span><br />
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<span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.</span><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">"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.</span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.</span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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 </span></em><a href="http://www.smh.com.au/national/deadly-superbug-hits-australia-20121017-27qbq.html?rand=1354511669644"><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;"><em>the deadly 244</em></span></a><em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">.</span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.</span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.</span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.</span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.</span></em><br />
<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">"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."</span></em><br />
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<em><span style="color: black;"><span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: large;"><strong>Wheel of misfortune</strong><br />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.</span></span></span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.</span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">"This has to be tested in large numbers of people before you unleash it for such a widespread disease," Rubin said.</span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.</span></em><br />
<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.<br /><br />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.</span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.</span></em><br />
<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">"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.<br /><br /><strong>Getting over the 'ick' factor</strong><br />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.</span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.<br /><br />"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."<br /><br />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.</span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.<br /><br />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.<br /><br />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.<br /><br />Dr Mark Pochapin, director of gastroenterology at NYU Langone Medical Center, said fecal transplants had more appeal than emerging anti-toxin approaches.<br /><br />"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."<br /><br />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.</span></em><br />
<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">People, he said, would set aside stools for processing into capsules that would be frozen and stored until needed.</span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">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.</span></em><br />
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<em><span style="color: black; font-family: Arial, Helvetica, sans-serif; font-size: large;">"Look at it as a way to put people's bacterial population back together again after antibiotics, like restoring Humpty Dumpty," said McDonald."</span></em><br />
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<a href="http://www.smh.com.au/world/science/blood-bank-sperm-bank--stool-bank-20121203-2aqqc.html" target="_blank"><span style="color: blue; font-family: Arial, Helvetica, sans-serif; font-size: large;">http://www.smh.com.au/world/science/blood-bank-sperm-bank--stool-bank-20121203-2aqqc.html</span></a>Unknownnoreply@blogger.com5tag:blogger.com,1999:blog-6390389002946732683.post-49375813329400824152012-08-25T14:43:00.001-07:002012-12-30T00:56:44.973-08:00Could Multiple Sclerosis Be Caused By Bacteria?<span class="recView_15" id="sp_15_address"><span class="recView_15" id="sp_15_address"><strong><u><span style="color: black; font-family: Arial, Helvetica, sans-serif;">TITLE: Fecal Microbiota Transplantation (FMT) in Multiple Sclerosis (MS)</span></u></strong></span></span><br />
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<span style="color: black; font-family: Arial, Helvetica, sans-serif;">T.J. Borody, S.M. Leis, J.L. Campbell, M. Torres, A. Nowak, , Centre for</span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif;">Digestive Diseases, Five Dock, New South Wales, AUSTRALIA;</span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif;">Recent evidence implicates the GI microbiota in the progression of neurological diseases such as Parkinsons Disease 1, Multiple Sclerosis and Myasthenia Gravis 2. We report three patients with MS diagnoses who achieved durable symptom reversal with FMT for constipation.</span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif;">Case study observations on three MS cases</span></div>
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<span style="color: black;"><span style="font-family: Arial, Helvetica, sans-serif;"><strong>Case 1:</strong> A 30 yr old male with constipation, vertigo and impaired concentration and a concomitant history of MS and trigeminal neuralgia. Neurological symptoms included severe leg weakness and he required a wheelchair and an indwelling urinary catheter. Previous failed treatments included Mexiletine,</span></span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif;">Tryptanol and 9-interferon. The patient underwent 5 FMT infusions for his constipation, with its complete resolution. Interestingly his MS also progressively improved, regaining the ability to walk and facilitating the removal of his catheter. Initially seen as a ‘remission’, the patient remains well 15 yrs post-FMT without relapse.</span></div>
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<span style="color: black;"><span style="font-family: Arial, Helvetica, sans-serif;"><strong>Case 2:</strong> A 29 yr old wheelchair-bound male with ‘atypical MS’ diagnosis and severe, chronic constipation. He reported parasthesia and leg muscle weakness. The patient received 10 days of FMT infusions which resolved his constipation. He also noted progressive improvement in neurological symptoms, regaining the</span></span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif;">ability to walk following slow resolution of leg parasthesia. Three years on the patient maintains normal motor, urinary and GI function.</span></div>
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<span style="color: black;"><span style="font-family: Arial, Helvetica, sans-serif;"><strong>Case 3:</strong> An 80 yr old female presented with severe chronic constipation, proctalgia fugax and severe muscular weakness resulting in difficulty walking, diagnosed as ‘atypical’ MS. She received 5 FMT infusions with rapid improvement of constipation and increased energy levels. At eight months she reported completere solution of bowel symptoms and neurological improvement, now walking long distances unassisted. Two years post-FMT, the patient was asymptomatic.</span></span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif;">We report reversal of major neurological symptoms in three patients after FMT for their underlying GI symptoms. As MS can follow a relapsing-remitting course, this unexpected discovery was not reported until considerable time had passed to confirm prolonged remission. It is tempting to speculate that </span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif;">FMT achieved eradication of an occult GI pathogen driving MS symptoms.</span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif;">Our finding that FMT can reverse MS-like symptoms suggests a GI infection underpinning these disorders. It is hoped that such serendipitous findings may encourage a new direction in neurological research.</span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif;"><strong>References</strong></span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif;">1. Borody et al Am J Gast 2009;104:S367</span></div>
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<span style="color: black; font-family: Arial, Helvetica, sans-serif;">2. Gower-Rousseau et al Am J Gast 1993;88;1136</span><br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiAFx2eBxbA8-wcwuF0X5V4BSp9PLXOcCwX4NfLYq2Go23R2PAnuE5C0sEG3fTxCbbVU3iFnVfngXMx1Zbceg8pJpcRURsrqv5qt6SXWeOSsT8aiBKA02p-wTTvcxZRfmSBFmZicMHLGlH9/s1600/multiplesclerosisfmt.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img alt="reversal of multiple sclerosis symptoms after fecal microbiota transplantation" border="0" height="384" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiAFx2eBxbA8-wcwuF0X5V4BSp9PLXOcCwX4NfLYq2Go23R2PAnuE5C0sEG3fTxCbbVU3iFnVfngXMx1Zbceg8pJpcRURsrqv5qt6SXWeOSsT8aiBKA02p-wTTvcxZRfmSBFmZicMHLGlH9/s640/multiplesclerosisfmt.jpg" title="fecal microbiota transplant reversal of multiple sclerosis" width="640" /></a></td></tr>
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</span><br />Unknownnoreply@blogger.com5tag:blogger.com,1999:blog-6390389002946732683.post-23485511557323502182012-08-22T21:39:00.001-07:002012-12-29T12:51:52.544-08:00Ulcerative Colitis, Fecal Microbiota Transplant, and Fecal Flora - Medical Literature - Possible Cure?<h2 class="cit">
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<span style="color: black; font-family: Verdana, sans-serif;">Borody TJ, Warren EF, Leis S, Surace R, Ashman O.</span></div>
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<span style="color: black; font-family: Verdana, sans-serif;">Centre for Digestive Diseases, 144 Great North Rd, Five Dock NSW 2046, Australia. </span></div>
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<span style="color: black; font-family: Verdana, sans-serif;">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.</span></div>
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<span style="color: black; font-family: Verdana, sans-serif;">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.</span></div>
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<span style="font-family: Verdana; font-size: x-small;"></span><span style="color: black;"> </span></div>
<div class="abstr">
<span style="color: black; font-family: Verdana, sans-serif;"><strong>Conclusions</strong></span></div>
<div class="abstr">
<span style="color: black;"> </span></div>
<div class="abstr">
<span style="color: black; font-family: Verdana, sans-serif;">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.</span></div>
<div class="abstr">
<span style="font-family: Verdana, sans-serif;"></span><span style="color: blue;"> </span></div>
<div class="abstr">
<a abstractlink="yes" alsec="jour" alterm="J Clin Gastroenterol." aria-expanded="false" href="http://www.ncbi.nlm.nih.gov/pubmed/12811208#" role="button" target="_blank" title="Journal of clinical gastroenterology."><span style="color: blue; font-family: Verdana, sans-serif;">J Clin Gastroenterol.</span></a><span style="color: black; font-family: Verdana, sans-serif;"> 2003 Jul;37(1):42-7.</span></div>
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<dl class="rprtid"><span style="color: black;">
</span>
<dt><span style="color: black; font-family: Verdana, sans-serif;">PMID:</span></dt>
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<span style="font-family: Verdana, sans-serif;"> </span></span><dd><span style="color: black; font-family: Verdana, sans-serif;">12811208</span></dd><span style="color: black; font-family: Verdana, sans-serif;"> </span><dd><span style="color: black;"><span style="font-family: Verdana, sans-serif;"> [PubMed - indexed for MEDLINE]</span> </span></dd></dl>
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<h1>
<span style="color: black;">
<span style="font-family: Verdana, sans-serif; font-size: large;"><u>Reduced Diversity and Imbalance of Fecal Microbiota in Patients with Ulcerative Colitis.</u></span></span></h1>
<div class="auths">
<span style="color: black; font-family: Verdana, sans-serif;">Hideyuki Nemoto, Keiko Kataoka, Hideki Ishikawa, Kazue Ikata, Hideki Arimochi, Teruaki Iwasaki, Yoshinari Ohnishi, Tomomi Kuwahara and Koji Yasutomo</span></div>
<div class="label">
<strong><span style="color: black; font-family: Verdana, sans-serif;">Source</span></strong></div>
<div class="label">
<strong><span style="font-family: Verdana;"></span></strong><span style="color: black;"> </span></div>
<div class="aff">
<span style="color: black; font-family: Verdana, sans-serif;">Department of Immunology and Parasitology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, 770-8503, Japan</span></div>
<div class="aff">
<span style="font-family: Verdana; font-size: x-small;"></span><span style="color: black;"> </span></div>
<div class="abstr">
<span style="color: black; font-family: Verdana, sans-serif;"><strong>Abstract</strong></span></div>
<div class="abstr">
<span style="color: black;"> </span></div>
<div class="abstr">
<span style="color: black;"><span style="font-family: Verdana, sans-serif;"><strong>BACKGROUND:</strong></span> </span></div>
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<span style="color: black;"> </span></div>
<div class="abstr">
<span style="color: black; font-family: Verdana, sans-serif;">Clinical observations and experimental colitis models have indicated the importance of intestinal bacteria in the etiology of ulcerative colitis (UC), but a causative bacterial agent has not been identified.</span></div>
<div class="abstr">
<span style="font-family: Verdana; font-size: x-small;"></span><span style="color: black;"> </span></div>
<div class="abstr">
<span style="color: black;"><strong><span style="font-family: Verdana, sans-serif;">AIM:</span></strong> </span></div>
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<span style="color: black;"> </span></div>
<div class="abstr">
<span style="color: black; font-family: Verdana, sans-serif;">To determine how intestinal bacteria are associated with UC, fecal microbiota and other components were compared for UC patients and healthy adults.</span></div>
<div class="abstr">
<span style="font-family: Verdana; font-size: x-small;"></span><span style="color: black;"> </span></div>
<div class="abstr">
<span style="color: black;"><span style="font-family: Verdana, sans-serif;"><strong>METHODS:</strong></span> </span></div>
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<span style="color: black;"> </span></div>
<div class="abstr">
<span style="color: black; font-family: Verdana, sans-serif;">Fresh feces were collected from 48 UC patients. Fecal microbiota were analyzed by use of terminal-restriction fragment length polymorphism (T-RFLP), real-time PCR, and culture. The concentrations of organic acids, indole, and ammonia, and pH and moisture, which are indicators of the intestinal environment, were measured and compared with healthy control data.</span></div>
<div class="abstr">
<span style="font-family: Verdana; font-size: x-small;"></span><span style="color: black;"> </span></div>
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<span style="color: black;"><strong><span style="font-family: Verdana, sans-serif;">RESULTS:</span></strong> </span></div>
<div class="abstr">
<span style="color: black;"> </span></div>
<div class="abstr">
<span style="color: black; font-family: Verdana, sans-serif;">T-RFLP data divided the UC patients into four clusters; one cluster was obtained for healthy subjects. The diversity of fecal microbiota was significantly lower in UC patients. There were significantly fewer Bacteroides and Clostridium subcluster XIVab, and the amount of Enterococcus was higher in UC patients than in healthy subjects. The fecal concentration of organic acids was significantly lower in UC patients who were in remission.</span></div>
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<span style="font-family: Verdana; font-size: x-small;"></span><span style="color: black;"> </span></div>
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<span style="color: black;"><span style="font-family: Verdana, sans-serif;"><strong>CONCLUSION:</strong></span> </span></div>
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<span style="color: black;"> </span></div>
<div class="abstr">
<span style="color: black; font-family: Verdana, sans-serif;">UC patients have imbalances in the intestinal environment-less diversity of fecal microbiota, lower levels of major anaerobic bacteria (Bacteroides and Clostridium subcluster XIVab), and a lower concentration of organic acids.</span></div>
<div class="resc">
<dl class="rprtid"><span style="color: black;">
</span>
<dt><span style="color: black; font-family: Verdana, sans-serif;">PMID:</span></dt>
<span style="color: black;">
</span><dd><span style="color: black; font-family: Verdana, sans-serif;">22623042</span></dd><dd><span style="color: black; font-family: Verdana, sans-serif;"> [PubMed - as supplied by publisher] </span></dd></dl>
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<div class="aux">
<span style="font-family: Verdana;"></span><span style="color: black;"> </span></div>
<div class="aux">
<a abstractlink="yes" alsec="jour" alterm="Dig Dis Sci." aria-expanded="false" href="http://www.ncbi.nlm.nih.gov/pubmed/22623042#" role="button" target="_blank" title="Digestive diseases and sciences."><span style="color: blue; font-family: Verdana, sans-serif;">Dig Dis Sci.</span></a><span style="color: black; font-family: Verdana, sans-serif;"> 2012 May 24. [Epub ahead of print]</span></div>
<span style="color: black;"><span style="font-family: Verdana, sans-serif;"></span><span style="font-family: Verdana, sans-serif;"></span><span style="font-family: Verdana, sans-serif;"></span><span style="font-family: Verdana, sans-serif;"></span></span><br />
<span style="font-family: Verdana, sans-serif;"><div class="normal">
<div class="secondary">
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<span style="color: black;"> </span></div>
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</span></span><span style="color: black;"></span><br /></div>
Unknownnoreply@blogger.com0tag:blogger.com,1999:blog-6390389002946732683.post-29386050576139771292012-08-21T17:41:00.001-07:002012-12-29T12:53:11.182-08:00Dr Tom Borody Video Fecal Microbiota Transplant for Clostridium Difficle<div class="separator" style="clear: both; text-align: center;">
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<div class="separator" style="clear: both; text-align: center;">
<span style="font-family: Verdana, sans-serif;"><span style="color: black;">Professor Tom Borody, on ABC TV Australia, Catalyst, </span><span class="storyDateTop"><span style="color: black;">Thursday, 14 July 2011 talks about Fecal Microbiota Transplantation (FMT) also known as "human probiotic infusion" for treatment of clostridium difficlile (c-diff). He is the pioneer and leading world expert on FMT.</span> </span></span></div>
<div class="separator" style="clear: both; text-align: center;">
<span style="font-family: Verdana, sans-serif;"><span class="storyDateTop" style="color: blue;"><a href="http://www.fecalmicrobiotatransplant.com/2012/08/dr-tom-borody-video-fecal-microbiota.html#comment-form" target="_blank">Please Click This Link To Leave A Comment!</a></span></span></div>
<div class="separator" style="clear: both; text-align: center;">
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<h1>
<iframe allowfullscreen="allowfullscreen" frameborder="0" height="360" src="http://www.youtube.com/embed/tDcia_uqf3k" width="640"></iframe></h1>
Unknownnoreply@blogger.com1tag:blogger.com,1999:blog-6390389002946732683.post-14164114138899070452012-08-21T00:28:00.000-07:002012-12-29T12:54:12.481-08:00Fecal Microbiota Transplant - From Trash To Treasure!<span style="color: black; font-family: Verdana, sans-serif;">In order to understand why a person would have a Fecal Microbiota Transplant, we first need to understand the incredible history of Fecal Microbiota Transplants.</span><br />
<span style="font-family: Verdana, sans-serif;"><br /></span><span style="color: black;">
<span style="font-family: Verdana, sans-serif;">In 1958, Chief of Surgery at Denver General Hospital, Dr Ben Eiseman, reported in the Journal of Clinical Gastroenterology of four patients who were cured of pseudomembraneous colitis. Enemas containing feces from healthy colons successfully replenished good digestive bacteria. Pseudomenbranous is a painful, extremely debilitating and potentially fatal inflammation of the colon associated with a bacterium called Clostridium difficile. </span></span><br />
<span style="font-family: Verdana, sans-serif;"><br /></span><span style="color: black;">
<span style="font-family: Verdana, sans-serif;">In the mid 1980s, Australian gastroenterologist, Professor Thomas Borody, who invented the triple antibiotic therapy for helicobacter pylori bacterium (the cause of stomach ulcers), was faced with one of the most difficult cases he had seen at that time. His patient was a woman who had developed an incurable colitis through an unidentifiable pathogen after holidaying in Fiji.</span></span><br />
<span style="font-family: Verdana, sans-serif;"><br /></span><span style="color: black;">
<span style="font-family: Verdana, sans-serif;">He searched medical literature for alternative treatments and came across the paper which was published in 1958 by Dr Eiseman. "So I
looked at the method and I kind of made up the rest of it," Borody
said.</span></span><br />
<span style="font-family: Verdana, sans-serif;"><br /></span><span style="color: black;">
<span style="font-family: Verdana, sans-serif;">The woman's brother donated stool which was screened for known pathogens. Using a blender, and mixed with some brine (nowdays he uses normal saline) Professor Borody made a slush which he filtered to remove any solids.</span></span><br />
<span style="font-family: Verdana, sans-serif;"><br /></span><span style="color: black;">
<span style="font-family: Verdana, sans-serif;">He administered it to his patient by enema on two consecutive days.
The results were incredible and her colitis was gone within days! It never returned!</span></span><br />
<span style="font-family: Verdana, sans-serif;"><br /></span><span style="color: black;">
<span style="font-family: Verdana, sans-serif;">This was the beginning of an amazing medical story - one that is still evolving - one that has helped countless people regain normal lives after the ravages of clostridium difficile. Both Dr Ben Eiseman and Professor Thomas Borody have something special as doctors. The ability to "think outside the box". Fortunately others have followed these pioneers into the new fronteer.</span></span><br />
<span style="font-family: Verdana, sans-serif;"><br /></span><span style="color: black;">
<span style="font-family: Verdana, sans-serif;">Fecal Microbiota Transplants are now being used across the USA with increasing frequency. The cure rate for clostridium difficile has been quoted at between 90 and 95% success rate. But it doesn't stop there - there are reports of reversal of symptoms and disease of ulcerative colitis, crohn's disease, parkinson's disease, multiple sclerosis, acne, autism and even obesity! How could FMT possibly help with these diverse diseases and disorders? Look for my next post and find out. :-)</span></span>Unknownnoreply@blogger.com0