Category Archives: Medicines

living with crohn's disease

Understanding Crohn’s Disease

What is Crohn’s Disease?

Crohn’s disease is a chronic inflammatory disease of the bowels in which the gastrointestinal tract is most affected.  The gastrointestinal tract refers to the group consisting of mouth, esophagus, stomach, both small and large intestine, and anus, although symptoms can occur which affects a sufferer’s skin, joints and eyes.  It is not contagious, and you cannot contract Crohn’s through your actions or by an inadequate diet.

How does Crohn’s develop?

First of all, Crohn’s is not contagious, so you didn’t “catch” it from someone or by someplace you’ve been.  You cannot get Crohn’s through an inadequate diet.  Although the exact causes aren’t widely understood, it’s generally thought that Crohn’s disease may be genetically inherited (so if someone in your family has Crohn’s it’s likely that you’ll be more susceptible to getting it.).  Your individual immune system also plays a part; since Crohn’s is thought to be a hyperactive or overactive immune system, sometimes environmental factors beyond your control trigger an abnormal immune response.  This leads to a chronic condition of raw and inflamed intestines, and can lead directly to Crohn’s.

The disease most often affects individuals between the ages of 15 and 35. But it can potentially affect anyone at any age.  It affects both, men and women,  equally. Although interestingly enough, there have been studies showing anover average number of Crohn’s sufferers among the Ashkenazi Jews.

Two reasons to get Crohn’s related testing & common tests:

You’ll want to see your doctor to determine whether you have Crohn’s in the first place. Also, upon a confirmed diagnosis, to re-evaluate your Crohn’s disease on a regular basis.

Common tests are through either blood or imaging.  The blood tests involve a routine procedure to detect infection, anemia, inflammation. Also, to identify (and subsequently treat) any vitamin or mineral deficiencies.  There are also fecal blood tests (to determine if you have blood in your stool). Also, antibody blood tests (to look for antibodies and proteins that will indicate to your doctor which diseases your body is currently trying to fight off).

Imaging tests can include conventional x-rays, contrast x-rays, endoscopy, and endoscopy ultrasound.

Things to do before visiting your doctor:

In order to have all of the pertinent information you’ll need to help your doctor with a diagnosis, there are a few things you can do.  Make a list of all current medications (including herbal varieties) that you’re currently taking.  Keep a diary of your symptoms, how long they lasted, and how severe or mild each one was.  You might also keep track of things you missed because of your symptoms. For example, did you stay home from work, or miss a meal due to discomfort?  If you’re forgetful, or if you’re worried that you’ll be too emotional to relay or receive important information, it might help to bring a friend or family member with you.  The better your doctor understands your symptoms and how they affect you, the better he or she can not only diagnose you. But also prescribe appropriate relief.

Most of all, remember that although some details might lead to embarrassment, your doctor is a professional who deals with many situations like these on a daily basis.  Don’t be afraid to share details!

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Gut Fungus Suspected in Crohn’s Disease

People with Crohn’s disease may have a higher level of a certain fungus in their gut, a new study finds.
Scientists have known that gut bacteria may contribute to the development of Crohn’s, but the new study finds that this fungus may also play a role in the condition.
The findings could lead to new treatments for people with the disease, who may have such symptoms as severe abdominal pain, weight loss, fatigue and diarrhea.
“We already know that bacteria, in addition to genetic and dietary factors, play a major role in causing Crohn’s disease,” study co-author Mahmoud A. Ghannoum, director of the Center for Medical Mycology at Case Western Reserve, said in a statement. Previous research has shown that people with Crohn’s have an abnormal response to certain bacteria that live in the gut, he said. “While most researchers focus their investigations on these bacteria, few have examined the role of fungi, which are also present in everyone’s intestines,” Ghannoum added.
In the study, the researchers analyzed the microorganisms found in fecal samples from 20 people with Crohn’s, 28 of their relatives without the disease, and 21 people without Crohn’s who were not related to the 20 people with Crohn’s or their relatives. All of the participants were residents of Belgium or northern France.
The researchers found that the people with Crohn’s disease had significantly higher levels of two types of bacteria, called Escherichia coliand Serratia marcescens, and one fungus, called Candida tropicalis, compared with their healthy relatives and the other people in the study who did not have the disease, according to the study, published Sept. 20 in the journal mBio.
Although previous research in mice has suggested that this fungus may be involved in Crohn’s, this is the first time it has been linked to the condition in people, the researchers said.
Moreover, when the researchers examined these bacteria and fungus, they found that the three microorganisms worked together to form a so-called biofilm—a thin, sticky layer of microorganisms—that attaches itself to a portion of the gut. This biofilm could trigger the inflammation that causes the symptoms of Crohn’s disease, the researchers said.
The new study “moves the field forward,” said Dr. Arun Swaminath, director of the inflammatory bowel disease program at Lenox Hill Hospital in New York City, who was not involved in the study. “The really neat thing they have done is to show how [these microorganisms] actually interact together,” to form the biofilm, he said.
However, the study was conducted in a small group of patients in France and Belgium, and more research is needed to see if these findings would apply to patients in other countries, Swaminath said.

Credits: By Agata Blaszczak-Boxe, LiveScience

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A New Care Plan for Crohn’s Disease

Combined treatments helped heal patients with Crohn’s disease

Septic perianal Crohn’s disease is a complication that has long been difficult to treat, but a new type of care plan may help.
Researchers at Penn State College of Medicine spent more than 10 years developing and testing a care plan that helps doctors decide how and when to treat patients with septic perianal Crohn’s disease.

Crohn’s disease is one of several inflammatory bowel disorders. Patients have severe abdominal cramping, bleeding and diarrhea. About 41 percent of patients with Crohn’s disease develop infected abscesses that become fistulas–open wounds that are very difficult to treat.

At one time surgery was the preferred treatment, but a medication called infliximab, know by the brand name Remicade, helped suppress the inflammatory condition in about 59 percent of patients. After a year, however, only 25 percent of the patients still experienced healing.

“What was thought to be a silver bullet of sorts for this problem really is not,” lead author Walter A. Koltun, MD, said in a press release.

Dr. Koltun is a professor of surgery at Penn State College of Medicine.

Despite the expense and possibility of significant side effects, many patients with Crohn’s disease stay on infliximab through fear the condition will become worse if they stop the medication. Dr. Koltun and colleagues have developed a care plan that helps doctors determine whether and when to continue the medication or to move to a surgical solution. The care plan is the first of its kind.

An analysis of 135 episodes of septic perianal Crohn’s disease found that 60 percent of the patients treated with the new care plan healed and remained healed for at least six months. Half of the remaining patients improved, but did not heal completely. The remainder did not heal and required surgery.

The researchers also analyzed genetic variations to see how they might affect healing, but results were not statistically significant.

“What we did with this study is look at a combined medical and surgical protocol for managing this problem, recognizing that there’s a role for the medicines, and there’s a role for the surgery,” Dr. Koltun said in the press release. “Our protocol provides a paradigm for when you perhaps should stop the drug and when to consider surgery with or without medication.”

The research and care plan were published in the June issue of the Journal of the American College of Surgeons.

Funding for the care plan was provided by the Carlino Fund for Inflammatory Bowel Disease Research.

None of the authors reported a conflict of interest.

An article from dailyrxnews, by Matt Wilson

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Crohn’s disease: Potential treatment to prevent fibrosis uncovered

Scientists from the University of British Columbia in Canada have found a mutation that switches off a hormone receptor, which prevents mice from developing fibrosis. This discovery could lead to potential treatments to prevent fibrosis in people with Crohn’s disease.

Crohn’s disease is a long-term condition that causes inflammation to the lining of the digestive system. While the disease can affect any part of the gastrointestinal tract, the most commonly affected areas are the end of the small intestine (the ileum) or the large intestine (colon).

One of the main complications of Crohn’s disease is the development of fibrosis, which is where the intestines become blocked – by thickened and scarred connective tissue – and so narrow that food and feces are unable to pass.

Fibrosis takes place due to an overproduction of proteins – including collagens – that are usually involved in the tissue healing process.

Mutation turns off hormone receptor, prevents fibrosis

While there has been some success in treating the inflammation associated with Crohn’s disease, there are no effective drugs to treat fibrosis. Understanding how fibrosis occurs can help scientists to develop new medicines to treat patients.

Surgery and repetitive surgery is common and often required to restore proper digestion. Around 70 percent of people with Crohn’s disease will eventually need surgery. Approximately 30 percent of individuals who have surgery for Crohn’s disease experience recurrence of their symptoms within 3 years, and up to 60 percent will have a recurrence within 10 years.

Scientists infected mice with a type of salmonella that imitates the symptoms – including fibrosis – caused by Crohn’s disease.

The team found that a particular mutation prevented the mice from developing fibrosis and, furthermore, the mutation had switched off a hormone receptor that is responsible for inducing part of the body’s immune response – inflammation.

“We found what we think are the inflammatory cells that drive fibrosis,” says co-author Kelly McNagny, professor at the Department of Medical Genetics and co-director of the University of British Columbia (UBC) Biomedical Research Centre (BRC).

“The gene that was defective in those cells is a hormone receptor, and there are drugs available that may be able to block that hormone receptor in normal cells and prevent fibrotic disease,” he adds.

Reversing fibrosis may promote tissue regeneration

McNagny and colleagues indicate that their breakthrough could also be applied to other tissue types that experience fibrosis.

McNagny notes that the potential fibrosis prevention method could be used for conditions that result in tissue fibrosis such as liver cirrhosis, chronic kidney disease, scarring from heart attacks, and muscle degeneration.

“We think that we can potentially block complications of all these age-related fibrotic diseases by dampening these particular inflammatory cell types,” concludes McNagny.

Future work by McNagny and team will focus on testing drugs to observe if fibrosis can be stopped or reversed in mice.

This article published on http://www.medicalnewstoday.com/ by Hannah Nichols

 

 

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Crohn’s disease scientist knows the disease as a patient, too

Whenever a co-worker has a bad cold, Karen Edelblum wears a mask. Karen Edelblum is an assistant professor at Rutgers New Jersey Medical School studying Crohn’s disease. She also has the bowel disease herself.  Crohn’s disease scientist knows the disease as a patient, too
She has sworn off raspberries and popcorn.

And, although just in her mid-30s, she already has been through a case of shingles, a disease that more typically strikes those over 50.

Such is life for someone with Crohn’s disease, a misery-inducing immune disorder with flare-ups that she likens to having food poisoning for months on end.

But unlike most of the 1.6 million others in the United States who suffer from inflammatory  bowel disease (IBD ), which includes Crohn’s and colitis, Edelblum is fighting the problem not only as a patient, but also as a scientist.

An assistant professor at Rutgers New Jersey Medical School, she has uncovered new clues about specialized cells in the immune system, ingeniously recording microscopic movies of their activity inside a live mouse.
Edelblum also is active in the patient community, having worked nine summers at a camp for children with the condition, and raising money for research. All the while she maintains a sense of humor about a disease.

She gets high marks from former boss Jerrold R. Turner, a senior pathologist at Brigham and Women’s Hospital in Boston.

“She’s really the full package,” said Turner, a faculty member at Harvard Medical School. “She’s not somebody who’s going to go into her lab and close the door.”

It was a course that Edelblum started plotting when she was 13 years old.

An initial misdiagnosis

That’s when the first flare-up happened.

Like others with her condition, Edelblum has a “leaky” gut – a flaw in the lining that separates the intestinal tract from the bloodstream.

But that alone is not enough to cause colitis, which strikes the colon, or Crohn’s, which can occur anywhere in the digestive tract.

Sufferers also have an immune system prone to going into overdrive, so that when bacteria invade, the immune response sets off a vicious cycle of inflammation, leading to further impairment of the intestinal lining.

It is unclear what triggers a flare-up, though stress can contribute. Physicians sometimes fail to read the signs.

Edelblum had a chronic fever and gastrointestinal distress, and one internist suggested she might have leukemia. Her mother was skeptical and sought another opinion, eventually getting a diagnosis of Crohn’s.

The 13-year-old patient then asked her doctor three questions: Am I going to die? (Not from this.) Is there a cure? (No.) If I have kids, would they get it? (Possibly.)

“That’s when I decided this is what I’m going to do with my life,” she recalled last month, sitting in her lab in Newark, N.J. “If I have the capability to change this outcome for myself or others, then why not do that?”

Growing up in the Houston area, she always had been interested in science. When peers recoiled from dissecting worms and other creatures in science class, she would offer to come in early and do it for them.

She studied biology as an undergraduate at Emory University, followed by a doctorate in cell biology at Vanderbilt University and a post-doctoral position with Turner, then at the University of Chicago.

 

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Edelblum was far from the first patient who aspired to study her own disease, Turner said.

“What’s unusual is that she followed through, and she didn’t change her mind later,” he said. “What most people in the world don’t realize is how hard research is.”

Working with Turner, she used sophisticated microscopes to peer inside the gut of a sedated mouse, carefully performing surgery to ease the animal’s intestines onto a glass plate without disrupting their function.

Sitting in front of a computer screen at Rutgers, she called up a series of images recorded through that procedure, revealing the activity of a poorly understood immune soldier called a gamma delta T-cell.

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Highlighted in fluorescent green, the cells can be seen approaching the lining of the animal’s intestine. They remain in position for a few minutes, then retreat and move to another location, a pattern that made Edelblum think of a sentinel on patrol.

Last year in the journal Gastroenterology, she, Turner, and colleagues reported that these sentinels appear to serve an antibacterial function.

The team administered Salmonella bacteria to two kinds of mice: one in which the movement of these sentinels was genetically blocked, and another in which it was enhanced.

“If you block the migration of these cells, more bacteria get in,” Edelblum said. “And if you enhance the migration, fewer of them get in.”

Other researchers have shown that the cells secrete an antimicrobial peptide, though it is not clear that is what keeps the bacteria from getting across.

These sentinels are not compromised in people with Crohn’s or colitis, Edelblum said. Rather, she hopes there might be a way to enhance their activity to strengthen a patient’s defenses against the disease.

They appear to be among the immune system’s first lines of defense, springing into action long before inflammation sets in.

She is intent on finding what causes the sentinels to migrate. Some signal from the bacteria, perhaps.

For now, Edelblum keeps her own disease at bay with immunosupressive drugs, receiving intravenous infusions every 10 weeks. With careful management of her disease, she has not had a flare-up in 14 years.

But the suppressed immune system led to the case of shingles a few years ago, and it makes her wary of sneezing coworkers. And past flare-ups have left her with lesions in her colon, hence the need to avoid popcorn and raspberries – too irritating.

She continues to advise others with inflammatory bowel disease, and in one case went a step further, inviting a patient from the summer camp to come work with her for a few months.

The microscopic sentinels on her computer screen may not end up holding the answer. But Edelblum is determined to serve as a human sentinel so long as the disease poses a threat.

 

“This article is written by Tom Avril for the Philly magazine”

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NZ microbiologist may have cracked Crohn’s disease

Research by NZ microbiologist John Aitken has recorded a major advance in the treatment of Crohn’s disease, which affects 20,000 New Zealanders!

Christchurch gastroenterologist Professor Richard Gearry, who has worked with Aitken on previous studies, says scientists have struggled to grow the MAP-type bacteria and “nobody has had the same sort of success . . . as John”.

“If you can grow it, you can start to explore causation a lot more. Not only that, but that work will translate to Johne’s disease in livestock which is a big problem in NZ.

“People internationally are very interested in that. All of sudden you can get underneath the clinical observations and try and understand those mechanisms as to what is going on.”

Aitken became interested in Crohn’s as a 23-year-old when he was told he had it. He spent the next three years with an image of his colon snapping like a carrot.

It turned out he did not have Crohn’s, but his brush with the disease sharpened his interest.

In 2005, a US colleague, whose wife had Crohn’s, asked him to look at her blood samples and he was able to see the elusive mycobacterium associated with Crohn’s under the microscope.

By 2010, he was able to grow the bacteria and Crohn’s clinicians and researchers were starting to take notice.

A year later, Aitken and others set up a medical laboratory under the banner of Otakaro Pathways Ltd in the old Princess Margaret Hospital mortuary. Funding came from various sources including Callaghan Innovation.

Canterbury’s earthquakes intervened, but Aitken is pushing ahead with his research with renewed vigour and setting up a new laboratory in the Templeton Industrial park.

One of the shareholders is Professor Tom Borody, who runs the Centre for Digestive Diseases in Sydney. He is a controversial figure in his field, but since he invented using antibiotic therapy against the bug that can cause stomach ulcers, he is not taken lightly.

Borody doesn’t need more testing to be convinced Crohn’s is bacterial in origin. He is well known in Australia as a gastroenterologist prepared to treat Crohn’s with a cocktail of antibiotics which Aitken says are achieving 80 to 90 per cent remission rates.

While patients are queuing up to see Borody, the medical world is not exactly beating a path to his door.

“It’s very difficult for experts to prove themselves wrong,” says Aitken, who doesn’t want to be pigeonholed as a bacteria advocate, although it’s clear where his research places him.

He avoids calling the organism he has grown and made visible MAP.

“What we are trying to do is have a test out there that can tell whether therapy against the mycobacterium is working.”

If researchers find out that mycobacteria cause Crohn’s and discover how the mechanism works, the key to curing or treating other diseases like multiple sclerosis might be next.

For the moment, mainstream gastroenterologists like Gearry will not prescribe the cocktail favoured by Borody to Crohn’s patients even if they want them.

He describes the immune system versus bacteria Crohn’s debate as “incredibly polarising”.

“A lot of groups around the world are very strong in using this anti-MAP therapy. They all zealously believe MAP is the cause . . . but the concern is maybe they can’t afford to see [their hypothesis] fail and there are financial interests in it as well.”

Gearry says the best test of anti-MAP therapy so far was a randomised control trial in Australia involving about 200 patients who were given the three antibiotics Borody and others claimed were the key to treating Crohn’s.

Those running the trial, the methodology of which was later criticised, concluded the anti-MAP therapy was no more effective than a placebo.

The results did not discourage large Israeli pharmaceutical company Redhill from funding another randomised control study which got under way this year. Redhill developed a pill which combines the three antibiotics – Clarithromycin, Rifabutin and Clofazimine – used by Borody.

Gearry is supervising the trial in Canterbury and so far has two patients taking part.

“I have no opinion on it. What I have been really worried about is the science behind what has gone on with the clinical aspects of this. It hasn’t been rigorous and it’s been led by people other reasons for it to succeed.”

AITKEN’S LEGACY

The results of the trial are keenly awaited internationally.

Meanwhile, other Crohn’s research groups around the world are making strides into aspects of Crohn’s. Aitken, for instance, is working with a group in Bulgaria. The race is on.

Aitken hasn’t published his work for fear of it being pinched. He not quite ready to tell the world. He certainly doesn’t need more money.

“Instead of going in with circumstantial evidence, you are much better going in with total forensic evidence.”

Aitken comes back frequently to the patients and their mothers.

“The mothers of the children are just unbelievable. I’ve never seen anything like it. It’s like they sense there is something out there they must reach it whatever it takes.”

They send him cards, drawings and letters of thanks.

“This article taken from the magazine stuff.co.nz”

 

A New Normal

603515_3678145960639_647107342_nHi! My name is Alicia and I am the Multimedia Director for Girls With Guts.  I have had UC/Crohns for almost 10 years now.  I have a complicated and LONG history with IBD but I’ll try and spare you with the gritty (and bloody) details. Continue reading

My Journey with LDN

LDNAzulfidine, Dipentum, Flagyl, Imuran, Asacol, Prednisone, Remicade, and Humira.  These are just some of the medicines I have been on for Crohn’s Disease.  Azulfidine was the very first.  Dipentum followed and after I took myself off it for some years, it was the first one I went back on so I did this one twice.  Sadly, none of these meds helped me sufficiently.  Some of them I got really bad side effects.  Most I couldn’t even last a year. Continue reading

The Crohn’s Fairytale

SDing-0149My journey through the trials and tribulations of Crohn’s is something I talk about quite often. I tell the story to small groups, to large audiences, and to individuals one-on-one. I tell the story almost like a fairytale; framing Crohn’s disease as the evil Dragon, myself as the helpless Princess, with the ostomy as my Knight in Shining Armour.

Or… plastic.

And the Princess and the Ostomy lived happily ever after.

I tell my story as if it was just that; a story; a beginning, a middle, and an end. Continue reading