Conventional Treatment

conventional treatmentHere you’ll learn how to change your lifestyle and regain your health.  If on a doctors treatment plan, you will learn how to change your diet and lifestyle to ensure efficacy of your drug program.  All drugs can fail, so adherence to a change in diet with stress reduction techniques gives you a good chance of helping to put your disease in remission.  

Conventional Treatment

For many people, conventional treatment can fail or the need to increase the dosage becomes risky.   I found the SCD diet after Remicade failed and I did not want to increase the dosage based on the risk factor.   

Here’s an article from the Mayo clinic on the current line of drugs used to treat IBD:

An expanding pipeline for IBD drugs

A number of emerging therapies for inflammatory bowel disease (IBD), as well as new applications of existing drugs, are currently under active investigation or in clinical trials. Unlike existing medications, novel agents are notable for addressing a variety of targets, including:

  • Adhesion molecules beta-7 integrin and mucosal addressing cell adhesion molecule-1
  • The p40 subunit of interleukin 12/23
  • Chemokine receptor 9
  • Janus kinase

That diversity is encouraging, says Edward V. Loftus Jr., M.D., of Mayo Clinic in Rochester, Minn. “We used to have this monolithic view that you treat all patients who have Crohn’s or ulcerative colitis the same way. With the advent of individual or personalized medicine, we’re beginning to appreciate that there is considerable individual variation in response to a particular medication.

“For example, even with the anti-tumor necrosis factor agents, arguably the most effective class of medications for IBD, only 70 to 80 percent of people, at most, respond initially, and many of those patients lose their response over time. So we need multiple drugs with multiple mechanisms of action.”

Old drugs, new applications

With that in mind, some older therapies are being re-purposed or reformulated for use in ulcerative colitis (UC), where therapeutic options are particularly limited.

Adalimumab (Humira) One is the anti-tumor necrosis factor (anti-TNF) monoclonal antibody, adalimumab (Humira), a mainstay of Crohn’s disease therapy that is currently approved only for that IBD subtype. But after demonstrating some efficacy for UC in several large studies, Humira is now likely to receive FDA approval for ulcerative colitis, too.

Golimumab (Simponi) Researchers are also actively studying the arthritis drug golimumab (Simponi), a fully human anti-TNF agent. In preclinical studies, golimumab was more effective at neutralizing TNF-alpha than were other anti-TNF biologics. And unlike other anti-TNFs, golimumab can be administered both intravenously and subcutaneously. The results of a large randomized trial of golimumab in UC will be presented at Digestive Disease Week 2012.

Budesonide Also under study is a modified corticosteroid, budesonide, currently used for induction therapy in Crohn’s disease. The Entocort formulation of the drug is released in the ileum and right colon, but a reworked version using a multimatrix (MMX) formulation that reaches the entire colon may have potential for treating ulcerative colitis. Phase 2 trials were promising, and the drug is now being studied in phase 3 trials. Mayo Clinic in Minnesota will be the site of the Santarus-sponsored trial.

Budesonide has not proved more effective for Crohn’s disease than systemic corticosteroids and is not intended for long-term therapy. But because the drug is metabolized quickly in the liver, it causes fewer side effects and less adrenal gland suppression.

Metronidazole (Flagyl) Metronidazole (Flagyl) is an antibiotic that is often used as an adjunctive therapy in Crohn’s disease patients with perianal fistulas, but the oral formulation is associated with several side effects, such as strong metallic taste, nausea and peripheral neuropathy, which can limit its use in many patients. A metronidazole ointment that is applied topically to the perianal area is currently being assessed in patients with perianal Crohn’s disease. Mayo Clinic in Minnesota is currently a site for that study, which is sponsored by Braintree Laboratories.

Adhesion molecule blockers

Natalizumab Novel agents may show the most promise because their targets are more diverse. Among the new therapies are adhesion molecule blockers, which prevent leukocyte migration into the gut mucosa. The drug natalizumab (Tysabri), a humanized monoclonal antibody to alpha-4 integrin, is the existing agent in this class. Natalizumab is currently approved for both multiple sclerosis and Crohn’s disease refractory to standard therapy, including anti-TNF therapy.

Although natalizumab has shown efficacy in Crohn’s disease, it is rarely prescribed because it increases the risk of progressive multifocal leukoencephalopathy (PML), a viral brain infection that usually results in death or severe disability. The overall rate of PML cases is about 1.16 per 1,000 patients.

“The problem is that natalizumab affects adhesion molecules at the level of the blood-brain barrier system as well as in the gut,” Dr. Loftus explains. “So the goal is to develop more gut-specific targets.”

Vedolizumab Of selective adhesion molecule blockers currently in development, the most prominent is vedolizumab, a humanized monoclonal antibody to the adhesion molecule α4β7-integrin that theoretically inhibits leukocyte migration in the gut without affecting the blood-brain barrier. Vedolizumab has been studied for both Crohn’s disease and UC.

In late February, drugmaker Takeda announced that vedolizumab had met all its primary endpoints in a pivotal phase 3 trial for ulcerative colitis. Trial results will be presented in detail at Digestive Disease Week 2012. To date, more than 1,000 patients have received the drug, with no known cases of PML.

“It’s looking good in terms of safety, but we’re waiting for the results of the big trials,” Dr. Loftus says. “Vedolizumab might be a year-and-a-half to two years away from release.”

Etrolizumab Other monoclonal antibodies affecting the adhesion molecule pathway are several years behind. Genentech’s ulcerative colitis drug etrolizumab  — formerly known as rhuMAb Beta 7 or RG7413 — is selective for the β7 subunit, which is gut-specific and should help eliminate the risk of PML.

Etrolizumab is currently under study in a phase 2 trial of patients with moderate to severe UC who are refractory to anti-TNF therapy. Mayo Clinic in Minnesota is one of the sites for the study. Pfizer is developing PF-00547659, a monoclonal antibody to mucosal addressin cell adhesion molecule-1 (MAdCAM-1). The drug is being assessed in a phase 2 trial of patients with moderate to severe Crohn’s disease at several sites, including Mayo Clinic in Minnesota and Florida.

Chemokine antagonists

Certain chemokines are proinflammatory receptors that attract leukocytes — in a sense, second cousins to adhesion molecules. Chemokine receptor 9 (CCR9) is integral to the migration of immune cells into the intestine, and several drugs that block this receptor are in development. One, GSK-1605786, is an oral agent that may inhibit B and T cell entry into the small gut while maintaining normal immune function. Small, preliminary trials of GSK-1605786 were promising, and a larger trial for treatment of moderate to severe Crohn’s disease is now under way. Mayo Clinic in Minnesota is one of the sites of the GlaxoSmithKline-sponsored study.

JAK inhibitors

Janus kinase (JAK) inhibitors modulate signaling for a number of important proinflammatory cytokines. Tofacitinib is a novel oral JAK inhibitor originally developed for the treatment of rheumatoid arthritis that also appears to have some benefit for ulcerative colitis. A multicenter, phase 2 study of 200 patients with UC presented at Digestive Disease Week 2011 showed significant differences in response rates and mean Mayo scores for tofacitinib compared with placebo.

Although there was little difference in adverse events between tofacitinib and placebo at eight weeks — the length of the study — long-term safety will need to be assessed because of the potential for immunosuppression and perhaps for dyslipidemia. A phase 3 trial of tofacitinib for moderate to severe UC has recently gotten underway, with Mayo Clinic in Minnesota as one of the study sites.

Cytokine blockers

Ustekinumab (Stelara) is a human monoclonal antibody that binds to the p40 subunit shared by the interleukin (IL)-12 and IL-23 cytokines. Both cytokines are involved in inflammatory and immune responses. Ustekinumab is approved for the treatment of plaque psoriasis and has performed well in phase 2 studies for Crohn’s disease. Additional clinical trials for patients with active Crohn’s disease are ongoing, including one at Mayo Clinic in Minnesota sponsored by Janssen Biotech.

Clinical trials at Mayo

Dr. Loftus says, “I want to make it clear that we are always happy to see people on short notice if a referring physician has a patient who seems to be interested in a clinical trial. Ordinarily, we have a waiting list, but will work in potential clinical trial patients as soon as possible.”

He adds, “The fundamental difficulty in treating IBD is that we don’t understand what triggers the inflammatory process. We’re not getting at the root cause; we’re simply targeting nodes in the inflammatory pathways that seem important and blocking inflammation at those points. It stands to reason that not all patients will respond to drug A, so the more drugs with different mechanisms of action, the better. (After all), this isn’t a disease that lasts 26 weeks. It waxes and wanes over the course of a lifetime, and we need to have different ways to treat it.”



If you haven’t yet tried drugs, I can show you how a changing your diet will slow or completely halt the progression of IBD.  The quicker you can catch the disease, the greater your chance of going into remission early.

After 8 months on Remicade, the drug failed and I forced to find alternatives.  Looking back, I realize that I was eating uncontrollably eating junk food – I had become a compulsive greasy chip eater.  I know that I craved salt and sugar.  I am sure I overloaded my system and the drug couldn’t stop the progression.    Now that my system is balanced, I now longer crave greasy salty, sugary foods and my digestion has never been better !

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