#ibds

My partner and I had a discussion recently about the possibility of children in our future. 

Now, I know what you’re thinking. Why are two 22-year-olds, fresh out of college, talking about having children? The answer is: Because I don’t want to have children (biologically, at least). I want to make it clear to my partner that I can’t consciously pass down my DNA to a child, if it means they will have to go through everything I went through with my Ulcerative Colitis. And even if my child doesn’t have it, how do I know that he or she won’t pass down the genes for an IDB to their children? Or their children’s children? 

I can’t even think about having a child go through the colonoscopies, the hospital stays, the thousands of pills a year. How could I do that to another human being? How I could knowingly give a child the possibility for a lifetime of constant pain? 

Some people may say that if I knew it was a possibility for my child, wouldn’t I observe his/her health, and make sure it wasn’t as bad as when i flared? The simple answer is, it can flare for many reasons, and a lot for those reasons can’t be controlled by the patient. 

The last time I was hospitalized, it was because my colitis had gotten worse, and my doctor had no explanation, after running dozens of tests, other than my mild ulcerative colitis had decided to become a severe case of ulcerative colitis. I hadn’t changed my diet, I wasn’t much more stressed than usual, I was taking all of the same doses of medications, and I was even on a very high dosage of immune system suppressants. 

There’s this part of me that feels guilty and sad at my decision to not have any biological children, but at the same time, I will continue to feel this way, until there is a cure for IBD’s. 

Now, I know that not all IBD patients feel this way, but I can’t think of a single enjoyable part of this wicked illness. I can’t think of a single reason why I would risk passing this on to a child. I know it sounds selfish, and in some ways, it is. I don’t want to have to go through that distress and emotional turmoil that my parents have to go through. I don’t want to wake up at 3 am and take my child to a hospital. I don’t want to drive six hours to another state to see my child in a hospital, for 5 nights. 

An endless fight against ourselves: the IBDs.

The inflammatory bowel disease is a group of inflammatory conditions of the colon and small intestine. Crohn's disease and ulcerative colitis are the principal types of inflammatory bowel disease. 

Crohn's disease may affect any part of the gastrointestinal tract from mouth to anus. Symptoms often include: abdominal pain, diarrhea (which may be bloody if inflammation is severe), fever and weight loss. Other complications may occur outside the gastrointestinal tract and include: anemia, skin rashes, arthritis, inflammation of the eye, and tiredness. During a colonoscopy, biopsies of the colon are often taken to confirm the diagnosis. Certain characteristic features of the pathology seen point toward Crohn's disease; it shows a transmural pattern of inflammation, meaning the inflammation may span the entire depth of the intestinal wall. There is usually an abrupt transition between unaffected tissue and the ulcer - a characteristic sign known as skip lesions. Under a microscope, biopsies of the affected colon may show mucosal inflammation, characterized by focal infiltration of neutrophils into the epithelium. This typically occurs in the area overlying lymphoid aggregates. These neutrophils, along with mononuclear cells, may infiltrate the crypts, leading to inflammation (crypititis) or abscess (crypt abscess). Granulomas, aggregates of macrophage derivatives known as giant cells, are found in 50% of cases and are most specific for Crohn's disease. Biopsies may also show chronic mucosal damage, as evidenced by blunting of the intestinal villi, atypical branching of the crypts, and a change in the tissue type (metaplasia). Cytokine response is associated with Th17. Terminal ileum is commonly involved, colon is usually involved, rectum is rarely involved. Stenosis is common. Bowel obstruction also commonly occurs (due to stenosis).

Ulcerative colitis is a form of colitis, a disease of the colon, that includes characteristic ulcers, or open sores. The main symptom of active disease is usually constant diarrhea mixed with blood, of gradual onset. Ulcerative colitis only attacks the large intestine and it is an intermittent disease, with periods of exacerbated symptoms, and periods that are relatively symptom-free. Although the symptoms of ulcerative colitis can sometimes diminish on their own, the disease usually requires treatment to go into remission. Endoscopic findings in ulcerative colitis include the following: loss of the vascular appearance of the colon; erythema (or redness of the mucosa) and friability of the mucosa; superficial ulceration, which may be confluent; pseudopolyps. Biopsies of the mucosa are taken to definitively diagnose UC and differentiate it from Crohn's disease, which is managed differently clinically. Microbiological samples are typically taken at the time of endoscopy. The pathology in ulcerative colitis typically involves distortion of crypt architecture, inflammation of crypts (cryptitis), frank crypt abscesses, and hemorrhage or inflammatory cells in the lamina propria. In cases where the clinical picture is unclear, the histomorphologic analysis often plays a pivotal role in determining the diagnosis and thus the management. By contrast, a biopsy analysis may be indeterminate, and thus the clinical progression of the disease must inform its treatment. The degree of involvement endoscopically ranges from proctitis or inflammation of the rectum, to left sided colitis, to pancolitis, which is inflammation involving the ascending colon. Terminal ileum is rarely involved, colon is usually involved, rectum is always involved. Stenosis is rare. Cytokine response is vaguely associated with Th2.

Causes: while the exact cause is unknown, IBD seems to be due to a combination of environmental factors and genetic predisposition. It is increasingly thought that alterations to enteral bacteria can contribute to inflammatory gut diseases. IBD affected individuals have been found to have 30-50 percent reduced biodiversity of commensalism bacteria. Further evidence of the role of gut flora in the cause of inflammatory bowel disease is that IBD affected individuals are more likely to have been prescribed antibiotics in the 2-5 year period before their diagnosis than unaffected individuals. The genetic contribution is poorly understood and seems to arise from the small contribution of dozens of genes. In 2012 163 IBD susceptibility loci were confirmed which means that 163 alleles that can increase the susceptibility to the disease.