The Chronic Crohns Campaign UK. ( TCCC.UK ).
The Chronic Crohns Campaign UK - Why We Are Here !!!
TCCC.UK & TNHC.UK Campaign Literature.
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TCCC.UK - Funds To Kings College London.
TCCC.UK - Action Medical Research details.........
TCCC.UK Campaign News ,Updates and Success !!!
The Chronic Crohns Campaign UK- The Breaking News.
TCCC.UK &The 3 Natural Alternatives In Sarah's Story
The New DNA Crohns Vaccine @ Kings College London.
TCCC.UK & Aloe Vera - Nature's Silent Healer. Books
TCCC.UK Raising Awareness - Press Coverage 1996 to 2006.
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Sarah's Crohns Success Story From 1989 to 2006.
Sarah's Crohns Success Story From 2001 to 2006.
Over 90 Degrees Still Does Not Kill Map Bacteria In Milk.
Tim Page - My Side Of The Story In All This Campaigning.
How To Order Aloe Vera, As We Do, At A Lower Price In The UK.
How To Get A Glyconutrient Powder Here In The UK
"Give Us A Quid Or Two" -The DNA Crohns Vaccine Appeal
PARA'S Medical Advisory Council
PARA'S Scientific Advisory Council.
A Message To Internet Hackers / Spammers !!
In Loving Memory Of Hadge Elliott 1956 To 2005.
The New DNA CrohnsVaccine Summary 2006.
TCCC.UK Consultation with DEFRA in 2002 & 2004.
The Chronic Crohns Campaign UK Press Info 1996 to 2006.
The Orkney Islands Crohns & U.C. N A C Group
Glyconutrients - What Are They ?
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Birmingham Contact For TCCC.UK - Stuart Morris IIHHT ICHT dip
MMR = Crohns or Autism ?
How To Get Aloe Vera & Other Aloe Vera Items Outside UK.
Other People'sTestimonials.........
Crohns & Contraception.
More On MAP - The 2 AntibioticsTreatment By Prof JHT.
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More On The Bacteria MAP - 2
Scottish News On Crohns
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Baby Milk - The FSA Update December 2006.
Prof John Hermon Taylor's New Update In March 2008.
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Crohns Research or IBD or IBS Stories In The News
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Further Water And Milk Press Coverage.
Can MAP Cause Ulcerated Colitis, As It Does Crohns..
TCCC.UK - Why We Are Here In 2008, To Help & Advise You.
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Prof John Hermon -Taylor Updates In 2008.
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Crohns Disease Research Group
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Crohn's Disease Research Group
Crohn's Disease Research Group
Head of Group
Professor John Hermon-Taylor
Senior Scientist
Dr. Tim Bull
Post Doctoral Research Scientists
Dr. Karim Sidi Boumedine
Dr. Liz Mcminn
Clinical Research Fellow
Miss Angela Skull
The Crohn's Research Group has been researching the involvement of Mycobacterium avium subspecies paratuberculosis (MAP) in the causation of disease in animals and transmission of these pathogens to humans in retail pasteurised milk. Genomic research has identified additional DNA present in MAP but not in Mycobacterium avium subspecies avium (MAA). This 'extra' DNA includes 14-18 copies of an insertion sequence 'IS900', the 6496bp cassette of low % G+C DNA designated GS, and about 11Kb of additional DNA in the region of IS900 Locus 6. This extra DNA influences the expression of genes in MAP and provides the genetic machinery for coating the surface of MAP with derivitized fucose. This may assist the organism in its ability to adopt a protease-resistant ZN-negative non-bacillary form present in animals with paucimicrobial Johne's Disease and humans with Crohn's Disease.
The 11 Kb of extra DNA around IS900 Locus 6 is found in virulent MAP strains from animals and humans with Crohn's Disease and is absent from some vaccine strains of MAP. This region includes three tetR transcriptional regulators and genes encoding polyketide synthase and an apparently MAP specific catalase.
New methods exploiting the extraordinary physical robustness of MAP have been exploited by the group to develop much improved procedures for detecting low abundance MAP in humans, both in endoscopic ileocolonic mucosal biopsies and in full thickness surgical gut samples. These studies are still in progress but already confirm the presence of MAP in a minority proportion of normal people consistent with widespread exposure, and show unequivocally that MAP is present in over 90% of people with Crohn's Disease.
Studies are also in progress using state-of-the-art DNA vaccine technologies to develop a therapeutic DNA vaccine for treating Crohn's Disease sufferers by assisting in immune-mediated microbial clearance. Such therapy is expected to complement the use of new combinations of anti-MAP drugs currently under development for the treatment of active Crohn's Disease.
The group is working with Government agencies in the UK to assist in a co-ordinated program relevant to animal health and food safety, designed to reduce exposure of the human population to MAP. The group has active collaborations with science laboratories involved in parallel research throughout the world, including Prof. Roger Pickup (CEH, Lake Windermere, UK) in environmental studies, Prof. Marcel Behr (Div. Infectious Diseases, McGill University, Canada) Microarray analysis of MAP transcriptomes, Prof. Raul Barletta (University of Nebraska-Lincoln, USA) generation and study of specific MAP gene knockouts by transposon mutagenesis, Prof. Saleh Naser/ Dr Ira Shafran (University of Central Florida, USA) studies of MAP from humans in the US, Prof. Ivo Pavlik (Central Veterinary Research Institute, Brno, Czech Republic) MAP typing and as well as clinical gastroenterologists from the Dept. Medicine University Tampere Finland and Dept. Medicine University Umea, Sweden. Our major study of MAP in surgical resection samples is being carried out in collaboration with large acute hospitals in Carmarthen, Llanelli, Swansea and Llandough in South Wales, UK which has a high incidence of Crohn's Disease.
The work is supported by 5-year Group and Component research grants from UK Medical Research Council and National Environment Research Council, medical research charities Action Medical Research and The UK Ileostomy Association, as well as other charities and private donors. |
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What Is In Your Glass Of Milk ?
 | What Does Your Glass of Milk Contain ?
MAP - Mycobacterium Avium sub species Paratuberculosis ?
2 x Bovine Sugars ?
Mucus ?
Faeces ?
Antibiotic ?
Steroids ?
Growth / Yield Hormone ?
Please Boil Your Milk Before You Consume.
Please Do Not ReInfest Your Body With MAP.
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Unraveling The Mystery Of Crohns Disease
 | Prof.John Hermon-Taylor.
Saturday Evening Post - USA.
Unraveling the mystery of Crohn's disease: could bacteria found in dairy products play a key role in Crohn's disease?
Saturday Evening Post, March-April, 2004 by Patrick Perry
In November 2000, German veterinarian Dr. Heinrich Dahmen began to suffer the unrelenting symptoms of severe pain, cramping, diarrhea, weight loss, and blood loss. After meeting with a gastroenterologist, Dahmen was diagnosed with Crohn's disease and started on conventional treatments for the disease, including immunosuppressive agents and the steroid prednisone.
After brief relief, Dahmen's condition worsened, and he faced invasive surgery to remove part of his inflamed digestive tract. Before undergoing the procedure, he followed up on a tip about the promising work of London investigators who were working on a new radical approach to the disorder. In July 2001, he traveled to London, where the research team found that Dahmen harbored an infectious agent believed to be involved in Crohn's disease. They began treating Dahmen with an antibiotic regimen that proved effective against the pathogen, and his condition slowly improved. Today, Dr. Dahmen is back in his busy veterinary practice, free of symptoms and feeling "cured" of the disease. Follow-up endoscopy and other tests confirm that Dahmen is in remission--his life has returned to normal.
"From that time I felt better and better," Dr. Dahmen told the Post. "I think I'm totally cured now after a two-year therapy."
In the United States, a Florida woman after years of unsuccessful treatments is also experiencing a rebirth after undergoing antibiotic therapy two years ago, which has since eliminated the unpredictable, yet ever-present pain of Crohn's disease,
On the Trail of Crohn's Disease.
For decades, researchers have debated the link between an infectious agent and Crohn's, a disease that affects millions of people around the world often in the prime of life. Crohn's numbers among a group of mysterious ailments known as autoimmune disorders, where for as yet unknown reasons the body begins to attack itself, wreaking havoc on normal bodily functions. While scientists are working hard to unravel the cause, of great concern is the fact that the rates of autoimmune disorders, like Crohn's and multiple sclerosis, have more than doubled in the last four decades.
Current treatments focus on the symptoms, but do little to address the root cause of Crohn's, including the potential role of bacteria. Whether infection plays a role remains a hotly contested area among experts. The theory, however, is gaining ground as evidence mounts supporting the connection.
Infection has emerged as a causative agent in other diseases, but not without resistance. Con sider Australian researcher Dr. Barry Marshall, who faced an uphill battle when challenging the medical doctrine by suggesting that a bacterium causes most ulcers--a discovery that has changed the course of treatment and quality of life for millions, At that time, the then-radical notion and its proponents were widely ridiculed. Dr. Marshall believes that infectious agents may play a role in other diseases, including Crohn's.
"My hunch is that they are infectious diseases, and we haven't found the germ yet," Dr. Marshall said in a Post interview several years ago for the book The Saturday Evening Post Investigates Digestive Diseases.
But if a microorganism causes Crohn's, what is it and how is it transmitted?
Researchers point to a persuasive body of evidence linking the bacterium, called Mycobacterium avium subspecies paratuberculosis (MAP), to the disease and underscore the route of transmission into the human population through one of our most popular drinks--milk.
MAP infection causes a debilitating disorder called Johne's disease that commonly occurs in cattle throughout the world, including the United States. Cows with Johne's share similar symptoms to people with Crohn's. infected cows secrete the mycobacterium in their milk. Individuals with a genetic susceptibility to Crohn's may thus pick up the disease. Supporters of the theory note that Crohn's is most frequently found in developed countries where milk consumption is high, except in countries where milk is boiled prior to consumption--an extra measure of precaution that some suggest would be prudent today.
The dairy industry, however, vigorously maintains that current pasteurization techniques are adequate to eliminate the bacteria, while critics highlight studies of the milk supply where MAP survived conventional pasteurization processes. Several European countries, such as Britain, have called for more stringent pasteurization procedures to ensure eradication of the microorganisms from the milk supply.
In 2003, British scientists at St. George's Hospital Medical School in London offered more support for the link between Crohn's and the milk-borne bug. Their study reports that over 90 percent of patients with Crohn's had MAP.
"The rate of detection of MAP in individuals with Crohn's disease is highly significant," said the researchers, writing in the Journal of Clinical Microbiology. "The discovery that the MAP bug is present in the vast majority of Crohn's sufferers means it is almost certainly causing the intestinal inflammation."
Lead researcher of the study, Dr. John Hermon-Taylor, has been studying the MAP and Crohn's connection for many years and successfully treated Crohn's patients with an antibiotic regimen that is restoring health and quality of life in his patients.
The Post spoke with Dr. Hermon-Taylor, chairman, department of surgery, St. George's Hospital Medical School in London, to learn more about his research into the milk and Crohn's connection, as well as how antibiotics are bringing new hope to individuals suffering from the devastating disorder.
Post : When did Mycobacterium avium subspecies paratuberculosis (MAP) emerge as a potential causative agent of Crohn's disease?
Hermon-Taylor : The idea was first suggested by Thomas Kennedy Dalziel in a paper published in the British Medical Journal in 1913. The reason that it has taken so long for the issue to become clarified is because the Mycobacterium avium subspecies paratuberculosis, or MAP, doesn't grow consistently in culture, much like the leprosy bacillus which belongs to the same family of organisms. The methods normally used for identifying a bacterium--namely, seeing it through a microscope, growing its culture, or doing a blood test for it--do not work with MAP.
Post : Endoscopy and other techniques would not detect its presence?
Hermon-Taylor : Endoscopy as done in the past wouldn't detect it, but the paper that we published in the U.S. in the July 2003 Journal of Clinical Microbiology shows that if you take endoscopic mucosal biopsies fresh from the endoscopy suite into the lab--and test them by the methods that our science has very carefully optimized and perfected--you can detect MAP with great accuracy.
Using the polymerase chain reaction (PCR) technique, you can show that virtually everyone with chronic inflammation of the Crohn's disease type is infected with the MAP bug. MAP is an organism that is a specific cause of chronic inflammation of the intestine in many different species of animals, including primates.
Post : Could you tell us about your research used to discover the bug in infected individuals?
Hermon-Taylor: We used the PCR test between 1989 and 1992 and found that about two-thirds of people with Crohn's disease were infected with the MAP bug. We published the findings in 1992 in Gut.
In 2000 I at last received a large grant from the U.K. Medical Research Council--our equivalent of the NIH in the United States. This five-year award has enabled us to go back to the beginning and really look at the methods to see why there have been so many conflicting results in the field. Apart from some people actually just not doing the procedures properly, the main problem is that the MAP bug is present in Crohn's disease in a very tough "Teflon-coated" invisible form. Standard laboratory reagents that would break open ordinary bugs, even tuberculosis bacilli, and release their DNA don't work for MAP. We found that you had to include a special mechanical disruption step in processing the tissue sample to access MAP DNA reliably.
When we did this, we found that virtually everyone with Crohn's disease is infected with MAP. We verified this absolutely by sequencing the DNA amplification products. Furthermore, using improved liquid cultures developed by Becton, Dickinson and Company in the U.S. and applying our DNA test to the cultures, we were able to show that 60 percent of the Crohn's disease-derived cultures incubated for more than 38 weeks contained MAP growing very, very slowly.
Post : Where do the MAP bacteria originate?
Hermon-Taylor: The MAP bug belongs to the group of organisms called mycobacteria. The most notorious mycobacteria are those causing tuberculosis and leprosy. But there is another "basket" of mycobacteria called Mycobacterium avium, so called because they were first found in birds.
MAP is, however, a clandestine bug, and it can live in animals and humans for years without necessarily causing disease. But in animals who become susceptible or inherit a susceptibility, or in humans who become susceptible or inherit a susceptibility, MAP infection can slowly lead to the emergence of chronic inflammation of the intestine. MAP demonstrates what scientists call "tissue tropism"; that is to say, if it is inhaled or ingested, it homes in on the gut and ends up causing chronic inflammation of the intestine.
Post : Does this eventually lead to Crohn's disease?
Hermon-Taylor: Our evidence and that of others suggests that the MAP bug causes most Crohn's disease. Expressed in a different way, if there were no MAP bugs in the world, there would hardly be any Crohn's disease at all.
Post : What led to the spread of the organisms?
Hermon-Taylor: The MAP bug was first identified in 1895, causing chronic inflammation of the intestine, in a cow in Germany. What MAP has done almost certainly is to take ad vantage over the last 150 years or so of the opportunities created by the rapidly expanding human populations of Western Europe and North America. This has been accompanied by increasing populations of domestic animals. They are, after all, our food animals. Instead of each sparsely distributed family having one cow, sheep and goat, we congregate in cities, and one family owns 300 cows and 300 sheep. Crowded farm environments, particularly in temperate regions with the animals housed in winter, create biological opportunities for amplification of the MAP organisms. When circumstances provide an ecological opportunity for bacteria in this way, they undergo what is called an adaptive radiation, and they change. This has happened with the cholera bacillus, salmonella bacillus, meningitis bacillus, Helicobacter pylori bacillus, and so on. The MAP which have emerged over the last 100 years have diverged into strains that prefer to infect cows, although they can infect sheep, and strains which prefer to infect sheep but can infect cows. We have evidence of the emergence of a humanized strain of these organisms.
Post : How do MAP bugs spread into humans?
Hermon-Taylor: The herd prevalence of MAP infection--that is to say, the percentage of herds which have two or more animals infected with the MAP bug--in Western Europe and North America runs between about two and 70 percent of herds. The infection is often subclinical, so you don't know the herd is infected. There is a huge regional variation, but herd prevalence in the range of 25 to 55 percent is common. Individual animal infection rates range between about one and eight percent. What all this says is, the domestic livestock of Western Europe and North America are extensively infected with the MAP bug.
And there are wildlife reservoirs. Research in Scotland, for example, has shown that rabbits on farms with infected domestic animals get infected with MAP. The organism is amplified and shed in the rabbit pellets. Grazing cattle will not eat grass contaminated with fox or dog feces, but they eat rabbit droppings. A short-range cycle of reinfection develops. This gives the organism a further opportunity to change. In addition, MAP goes up the rabbit predator chain to the foxes, carrion birds and so on.
Infected animals secrete the organism in their milk. We showed from 1990 to 1994 that there was a very high risk in Britain, that the MAP bug was being transmitted to the human population in retail pasteurized cow's milk supplies. This has since been confirmed by research carried out for the U.K. government's Food Standards Agency. The results of the work done by Dr. Irene Grant were published in 2002 in Applied and Environmental Microbiology. Using the DNA test and our optimized methods, she found that 11.8 percent of hundreds of bottles and cartons of milk from all over Britain tested positive for the MAP bug. She actually cultured live MAP from two percent of milk samples. She DNA-fingerprinted the MAP isolates, and they were not common laboratory strains.
But because MAP is so reluctant to grow in culture, the true proportion of retail cartons and bottles of pasteurized cow's milk in Britain contaminated with live MAP is much more likely to be closer to 10 percent than two percent.
Post : Would the same hold true in the United States?
Hermon-Taylor: Research carried out by the Institute for Food Safety and Hygiene, Faculty of Veterinary Medicine at the University of Zurich in Switzerland, using the methods we provided them, found that 19.7 percent of 1,384 bulk tanks of milk from all over Switzerland tested positive for the MAP bug. Work from the Veterinary Research Institute in Brno in the Czech Republic has reproduced the U.K. work of Dr. Irene Grant and cultured live MAP from two percent of samples of retail pasteurized milk in the Czech Republic.
Given what has been found in other countries, there is likely to be a similar risk that the MAP bug is also conveyed to people in the U.S. in milk supplies.
Post : Is milk then the primary mode of transmission of Crohn's?
Hermon-Taylor: It would be a major route of transmission. Another potential route is from the environment. Unlike the tuberculosis bacillus, tough MAP bugs can survive for months or years in the environment. Organisms that survive in the environment, which are already known to cause disease in animals and humans, include organisms like Cryptosporidium and Legionella, for example. Infected animals shed millions of the MAP bugs onto pastures. We have been doing research over the past 2 1/2 years which shows, as you would predict, that MAP bugs are flushed into surface waters like rivers. Where a river heavily contaminated with MAP runs through a population center, there is a risk that the organisms--which will aerosol off the water--may reach the human population by inhalation.
Post : Would boiling the milk to a certain temperature kill the bacterium?
Hermon-Taylor: Yes, it would almost certainly kill it. However, we do not know exactly if there is a commercially acceptable time-temperature combination that will ensure the destruction of all live MAP. Finding out what will kill MAP is particularly difficult because the only established method we have at present for telling whether MAP bugs are alive or dead is to try to culture them. And as we have already seen, even when MAP has not been heat-shocked, it is very reluctant to grow in culture.
But the probability is that if you took a kitchen thermometer and heated milk to 80 to 85 degrees Centigrade (177 to 185 degrees Fahrenheit) and set it aside to let it cool, it would substantially reduce or remove the risk of consuming live MAP bugs.
Post : In this way, are we doing everything possible to kill the organisms in milk?
Hermon-Taylor: That's right. I have been living with this knowledge for a long time. I knew MAP bugs were in milk in Britain in 1991. It's necessary to get the problem in perspective.
In the first half of the 20th century, most of the population of Western Europe and North America drank live, virulent tuberculosis bacilli before pasteurization of milk was generally implemented. Only a very small percentage of the people exposed to the bacilli came down with TB. The same thing is happening with the MAP bug. You have either to inherit or acquire a susceptibility to be at risk of developing disease. Alternatively you might get a huge dose of MAP just after having had the flu, or you may be exposed to a particularly nasty strain of the MAP bug. We know that even in human isolates, there are differences in the genomes and behavior of different human isolates of MAP.
Post : But susceptibility and milk must be present at the same time?
Hermon-Taylor: The key factor is the MAP bug. Susceptibility is an enabling co-factor. There has been some very good genetic research identifying the CARD 15/NOD2 gene abnormality, affecting about 15 percent of people with Crohn's disease. These people are mostly of Caucasian or Western European origin, living in North America and Western Europe and elsewhere. We should note, however, that 85 percent of people living in North America and Western Europe who have Crohn's disease don't have a defective CARD 15/NOD2 gene. Furthermore, the CARD 15/NOD2 abnormality doesn't work for people in China, Japan, or Korea who have Crohn's disease. In these countries the incidence of Crohn's disease is rising steeply, as also is the consumption of cow's milk.
Post : Are conventional therapies used to treat Crohn's today rendered useless if the cause is MAP? And if so, what is the treatment strategy?
Hermon-Taylor: In 1992, I came up with the following cascade of reasoning in the search for anti-MAP treatments for people with Crohn's disease whom I knew to be infected with the MAP bug. First is the knowledge, widely available in the chemotherapeutic literature, that clinical infections with any M. avium complex organisms like the MAP bug are poorly responsive to standard unmodified Streptomyces antibiotics. Drugs like streptomycin and rifamycin, which have worked wonderfully for TB and leprosy, don't work well with M. avium complex and MAP bugs.
Next, we also knew that the MAP bug divided very slowly, so that drugs like ciprofloxacin, which work by inhibiting DNA replication, would also not be much use.
The next group of drugs used in the standard treatment of TB--like isoniazid, ethambutol, and pyrazinamide--mostly acts by blocking the synthesis of lipid molecules in the cell walls of classical bacillary-form mycobacteria. These lipid molecules are responsible for the pink-staining ZN reaction. But I knew that the MAP bugs in Crohn's disease are not in their ZN-positive pink-staining form, so treatment with these drugs wasn't going to work, either.
In the early 1990s, new drugs were becoming available. One of those was rifabutin, a chemical modification of rifamycin. Another was clarithromycin from Abbott in Chicago. Clarithromycin is a native erythromycin molecule produced by Streptomyces, with a small chemical modification. These two drugs are much more active both in the lab, and in animals, against organisms of the M. avium complex. Also, they concentrated inside the cells where MAP was predicted to be. They had to be used together. If you use single agent therapy to treat MAP infections, you will get drug resistance within weeks or months. I began treating people with rifabutinclarithromycin combinations in 1992. Sometimes I also used another potentiating drug called clofazimine. We published the results in 1997.
There are now four open-label clinical studies carried out independently--one more in the U.K.; one by Tom Borody, M.D., in Sydney, Australia; and one by Ira Shafran, M.D., at the University of Central Florida--which essentially all say the same thing. That is, that somewhere between 50 to 75 percent of people with active Crohn's disease who can take rifabutin and clarithromycin treatment will get better and heal--sometimes like magic. The people who do not respond are infected with MAP bugs that are already resistant. Still, a majority of people--in my hands about 70 percent can take this treatment--get better. MAP infections are very difficult to eradicate.
Post : How many gastroenterologists are using this therapy to treat Crohn's patients?
Hermon-Taylor: Very few--less than one percent.
Post : If effective, why is the therapy not being used to treat such a severe disease?
Hermon-Taylor: There are several reasons. First, gastroenterologists don't believe MAP causes Crohn's disease, although most of them don't know the scientific evidence out there. Second, these drugs are not approved for use in Crohn's disease, although they are approved for the treatment of infections caused by nontuberculous mycobacteria. Third, these are only open studies and not the results of randomized, placebo-controlled clinical trials. From 1997 to 1999, I helped set up a randomized, controlled trial in several centers throughout Australia. It began in September 1999 and finished in September 2003. Four years later and at a cost of millions of dollars, the trial now has to run another year before the code is broken and the results analyzed.
Post : Any preliminary data that you can share?
Hermon-Taylor : Not publicly available, but it is highly likely that the randomized controlled trial will confirm the consistent results of the open label studies. This is, that a substantial proportion of people sick with Crohn's disease will heal when treated with these agents.
I have a cohort of people, some of them quite young, who had end-stage colonic Crohn's and were facing irreversible surgery and a lifetime of living with an abdominal stoma. Today they are walking around living normal lives because of these anti-MAP drugs.
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