There are several hot button issues in the world of IBD research and treatment (and yes, I realize how lame that sounds, but to the people that are fighting these diseases every day…yeah, okay, even to us “hot button” still seems lame. Sorry.) I recently attended an educational symposium at Mount Sinai hospital and they were talking about the future of IBD research. The focus of these particular presentations was on the role of genetics in both Crohn’s Disease and Ulcerative Colitis – in terms of both predictors for those at risk (i.e. people like my sister who is at a higher risk because I have such bad Colitis), as well as anticipating if someone who has UC or CD will have mild, moderate or severe disease presentation (information, I might argue, that would have been helpful three years ago.) Luckily for my sister, if not for people who are relatives of someone who has Crohn’s, CD has been found to have a much more prominent genetic element than UC.*
Other questions plaguing IBD researchers seem to be focusing on the big one: why do people get UC or CD? What causes it? Why are auto-immune conditions on the rise while other diseases, such as Polio and Smallpox, are being routed out and eradicated throughout the world? Why do 5% of UC patients get PSC, while 70% of PSC patients have UC? What is the connection between the two diseases? Is the hygiene hypothesis correct in questioning whether it is a lack of exposure to infectious agents and microorganisms during childhood in the Western world that is to blame for the skyrocketing incidence rates of auto-immune conditions such as UC and CD? Thankfully for me, and everyone else in the world who suffers from IBD and PSC, I am not in charge of figuring this stuff out. I give money and time when I can, but that is pretty much the extent of my involvement, aside from the portion of my day/week/ month/life that I spend in treatment and getting stuck with the dreaded needles…
In this, the first of the “Enormo Face Series”, I wanted to go over the traditional treatments used for the treatment of UC. Some of this may also apply to Crohn’s patients, but my experience has been with UC so the focus will be on that.
As you can see, the treatment protocols rely on the disease presentation and whether it is classified as mild, moderate or severe. From what I understand, doctors try to use the least amount of medication that they can to alleviate the symptoms, by first promoting remission and then finding maintenance dosage to keep patients in remission for as long as possible.
At the bottom “rung” of treatment options lie Aminosalicylates, the main anti-inflammatory drugs used to treat UC. The anti-inflammatory action in these drugs is produced by 5-ASA and include the following types: Mesalazine (aka Azulfidine and including brand names Asacol, Pentasa, Salofalk, Ipocol and Mezavant); Sulfasalazine (aka Azulfidine); Balsalazide (aka Colazal); and Olsalazine (aka Dipentum). 5-ASA is poorly absorbed by the intestine and hence provides topical relief within the intestine. It is a non-systemic drug and is related to non-steroidal inflammatory drugs (NSAIDS) such as Aspirin and Ibuprofen.
Next up the rung are Corticosteroids. They are often used in conjunction within 5-ASA drugs to bring about remission of UC. After remission is achieved, it is sometimes possible to maintain it with 5-ASAs alone, but more often than not both drugs have to be taken for the maintenance of satisfactory health. Corticosteroids work by reducing inflammation (through a medical process I do not understand). They act as immune suppressants to get the immune system to “stand down” and stop attacking the large bowel. A variety of steroids are used, including: Cortisone, Prednisone, Hydrocortisone, Methlyprednisolone, and Budesonide (aka Entocort).
On the third rung you have Immunosuppressive drugs which generally suppress the immune system by altering the body’s immune response. These drugs are generally understood to work in three broad streams: Mercaptopurine, Azathoprine and Methotrexate. I do not know much about them, as I have never been prescribed them.
Near the top of our ladder lies the new holy grail of UC and CD medications: TNF Inhibitors. These drugs are also understood as biologics or designer drugs because they were created in a lab. The two big guns used under this heading, Remicade (aka Infliximab) and Humira (aka Adalimumab), work to inhibit TNF (which are proteins that somehow trigger more inflammation in inflammatory diseases such as auto-immune conditions). Neither drug can be ingested; Remicade is infused over approximately 2-3 hours via IV, while Humira is injected directly into the patient.
Obviously, if none of these treatments work the only respite for patients with severe Ulcerative Colitis is for them to have their colon removed. In my case, when I was originally diagnosed with Proctitis (January 2006), I was prescribed Salofalk (a brand of Mesalazine) suppositories. They were a very good maintenance dose for me, meaning my UC did not get considerably worse once I began taking them as directed. (In the spirit of full disclosure I should probably admit that I had several bouts of pancreatitis in the ensuing years, was kept overnight at the hospital several times and once had an historic stretch where I didn’t go to the bathroom for almost a month.)
Following my mom’s death, my UC got really bad, really quickly. When I was hospitalized they tried several Corticosteroids; mainly Hydrocortisone and Prednisone. The Hydrocortisone was given via IV, but I have had the pleasure of Prednisone (affectionately “the Pred” or “the ‘zone”) both through IV and by mouth at various times over the last few years. The side effects I experienced were intense and hard to miss: my face got GIANTer (a common side effect of corticosteroid use is known as “Cushing’s Syndrome” which often exhibits itself as “moon face”), which for someone who is already blessed with an abnormally large head, was torture. Aside from giantfaceitis, I became a superhero overnight. One of my biggest complaints since illness-palooza began has been my depressed energy levels: I feel like I can nap all the time, sleep all night and then sleep all day. It is often a challenge to push myself to get moving throughout the day. Not so while I was in “the ‘zone”: I had the energy of 10 (athletic) men. I also apparently transitioned to being Gaston from “Beauty and the Beast” and wanted to eat hard-boiled eggs and nothing else (except for the occasional tub of salsa, piece of Tilapia and 5-tonne bucket of sour keys). These cravings were indescribably immediate: I had to have eggs and I had to have them now. I often joked about chewing on the tables as well, as my appetite seemed to grow in direct correlation to my expanding “moon face.” So, all things being equal, “the ‘zone” can be murderous. Especially on my family, whom I dragged hiking at all hours and who I woke when I began vacuuming at 3 in the morning. I suppose I should be grateful that all I got was an enormous face and a desire to gnaw on the furniture; some people find latent bipolar(ism) on prednisone, or become increasingly manic while contemplating suicide....
Tune in tomorrow for a continuation of this discussion entitled “Enormo Face and the Mischief of Mice.”
*This information is based on statistics provided at the educational symposium. They are contained in forth-coming journal articles (called Gastrointestinal Health and How It Sucks For You. But probably not. Scientists seem to take this stuff way too seriously). If I hear anything further about their publication in an open-source platform, I will update and link accordingly. The CCFC website is really good about keeping up to date on cutting edge research, so if you're crazy excited about this development, I would recommend checking there.
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