In February of 2018, I was diagnosed with Crohn’s Disease. I first started Remicade (Infliximab) which was unable to induce clinical remission. During this time, I was also taking Prednisone and Mercaptopurine (6MP). None of these drugs were able to make me comfortable and at my worst, I weighed 87lbs completely unable to walk. I stopped Remicade and started Humira (Adalimumab) in July 2018.
Although I achieved remission in a single month (which is unheard of), my body was now severely catabolic and beginning to shut down due to starvation. My intestines were so atrophied after months of being unable to eat that my body rejected any form of oral nutrition, necessitating total parenteral nutrition (TPN).
Ultimately, I was hospitalized for a month at the end of August 2018, where I had a PICC (peripherally inserted central catheter) line inserted and remained on TPN for several weeks. I was later released into the care of physical therapy, where I would undergo several hours of therapy daily to help me learn how to walk and eat again.
When I first started taking Humira, there weren’t many resources available to me online. Everything was too clinical or it wasn’t informative enough. I wanted to make a video providing the kind of information I needed that would have put me at ease, or possibly even made the decision to take Humira instead of Remicade. I would have been in remission far faster and ultimately would have recovered faster.
Another important thing I feel like needs to be said is that I have not experienced any hair loss from Humira. My hair loss was diagnosed as Telogen Effluvium, a depressing symptom of malnutrition and stress. Hair loss is frequently experienced with patients with inflammatory bowel disease with surprising frequency. My dermatologist assured me that because she could see my hair growing back even in my bald patches, it was not a side effect of the Humira. If you experience hair loss while taking Humira and it does not grow back, take it as a strong indicator that it is caused by the biologic itself instead of being a symptom of your flare. My hair is growing back beautifully.
How is Crohn’s Disease Diagnosed?
Reliable indicators of any given Crohn’s patient’s prognosis are lacking, so medical intervention is traditionally guided by signs and symptoms.
I was diagnosed with the Anti-Saccharomyces cerevisiae Antibodies (ASCA) blood test because all other traditional methods failed.
Most people think you can only test or confirm Crohn’s with a simple colonoscopy, but that isn’t true. They’re typically only beneficial for chronic patients and not acute patients.
Here are a few of the most common tests (all of which I received) and their shortcomings:
This is a pretty standard test for Crohn’s and other bowel-related conditions. Mine showed inflammation, ulcerated patches, and blunted vili (your vili are supposed to look something like a shag carpet but mine looked like smooth linoleum, which turned out to be a reaction to wheat products due to Celiac Disease). However, this is only a definitive diagnostic if you have chronic Crohn’s, meaning you’ve had symptoms for some time. Your symptoms may have been minor and not enough to cripple your lifestyle, as it did mine. While in hindsight I had many small, otherwise deniable issues for years (abdominal pain and fatigue, primarily), my Crohn’s didn’t fully hit me until September, 2017, and nearly killed me.
Its acute onset meant I had no scarring, abscesses, strictures, or fistulas, which is what a colonoscopy is looking for. Because of this, many specialists simply told me I was having bad periods, was a hypochondriac, or a pill seeker. In the words of one, she had “no reason to believe this was anything more than a passing thing.”
During a colonoscopy, samples will also be taken. Mine didn’t present with the chronic inflammation results gastroenterologist look for when diagnosing Crohn’s.
- Computerized tomography (CT).
I’ve had so many of these damnable things, I can’t even remember them all. CT scans are not sensitive enough to pick up minute inflammation. In the beginning, all my CT scans showed were swollen small bowels. I was asked many times if I had been struck in the abdominal area because my colonoscopy results didn’t have the classic signs my doctors were looking for. Around March, 2018, after I’d been formally diagnosed with Crohn’s (I’ll get to how shortly), I went back to the hospital with rapidly worsening symptoms only to be told that the CT scan picked up no trace signs of inflammation, and was sent home. A second colonoscopy showed that the Crohn’s was, in fact, spreading up my duodenum, which the CT scan failed to detect.
- Magnetic resonance imaging (MRI).
This isn’t a bad method, because it’s more sensitive than a traditional CT scan. However, it just showed more of the same; inflammation with no scarring, abscesses, strictures, or fistulas. They didn’t know why, and I was sent home. Again.
- Capsule Endoscopy.
More of the same, here. This is great for scanning parts of your bowels not reachable by traditional endoscopy or colonoscopy methods, but it’s just as useless if you lack chronic symptoms and scarring.
So, what will work for a prospective patient who has all the symptoms of Crohn’s but lacks its hallmark scarring and fistulae formation?
- Anti-Saccharomyces cerevisiae Antibodies (ASCA) blood test.
After three colonoscopies, countless CT scans, two MRIs and one capsule endoscopy, my then newest gastroenterologist ordered this test. Anti-Saccharomyces cerevisiae antibodies (ASCA) are a specific and sensitive diagnostic marker for the Crohn’s disease phenotype. To understand how this test works, you need to know how Crohn’s works.
Everybody produces a protein cell called Tumor Necrosis Factor Alpha (TNFα). It aids in inducing fevers, inflammation, and the inhibition of viral replication, to name a few. To put it simply, it regulates your immune system’s response to illness and disease. It can also signal a protective immune response to help block certain infections.
TNFα, in healthy folks, regulates immune cells and inflammation in the body. However, if you produce too much of it, your body begins to suffer systemic inflammation—e.g., Crohn’s Disease, and a number of other inflammatory conditions inflicted by an overactive immune system. Excess amounts of TNFα cause your immune system to mistakenly attack healthy cells in the GI tract, leading to the systemic inflammation typical to Crohn’s.
Basically, immunoglobulin (Ig)A and IgG antibodies against Saccharomyces cerevisiae (ASCA) are higher among patients with Crohn’s than those without. TNFα influences the development of IgA-ASCA antibodies in people with Crohn’s Disease.
For reference, these were my ASCA antibodies test results:
Modestly elevated, but this modest elevation got me my diagnosis and treatment after hemming and hawing from professional’s for months who claimed I was simply an attention-seeking hypochondriac because I had acute aggressive symptoms.
If you have any questions about me, Crohn’s, or Humira, please feel free to ask; I am not a medical professional, but I can give you information based on my experience in hopes that it will help you.
I have compiled a list of additional resources regarding this entry and its contents for researching the topics therein:
Humira (Adalimumab): if you’re curious about Humira and want to know more, visit their homepage.
Humira Cost Savings Card: a direct link to one of the most important components of your Humira care.
Support for Humira: for a sharps container, travel case, and more.
Crohn’s Colitis Foundation: the leader in research, education, and support for IBD sufferers and their families.
The Crohn’s & Colitis Foundation of America: a non-profit, volunteer-driven organization dedicated to finding a cure for those living with IBD-related chronic illness.
Crohn’s and Colitis Foundation Forum: a place to share your experiences with Crohn’s and Colitis.
Click the ❤︎ below if you enjoyed this piece and share it with your friends by posting it on your social media! All comments are held in a moderation queue and must be accepted by the administrator.