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.

TreatmentMesalazine is more useful in UC than in CD. Antibiotics are effective in long-term in CD, but generally not useful in UC. Depending on the level of severity, IBD may require immunosuppression to control the symptom. Often, anti-inflammatory steroids are used to control disease flares. While ulcerative colitis can be treated by performing a total colectomy (removing the entire large intestine), surgery for Crohn’s disease involves removing the damaged parts of the intestine and reconnecting the healthy parts, which does not cure Crohn’s, as it can recur after surgery, mostly at the site of the intestinal anastomosis (connection) or in other areas. 

I personally know two people with this problem. Interestingly, both were in abusive relationships and the prolonged stress was ultimately what made their illness chronic. Since they left that situation they’ve begun to heal slowly but surely. There are experimental protocols that can help patients achieve LT remission. One is a high-dose amino acid therapy involving L-Tyrosine, L‐cysteine‐Adenine, 5-HTP, L-Dopa in addition to using Glycyrrhizic Acid. Gum Mastic can also be tremendously helpful, as it kills H. Pylori and reduces inflammation.

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