Ref U.S. Pharmacist [health system edition] January 2010
Current Management and Prospective Therapies
Basically, it happens when protective barrier for the intestinal tract is compromised from injury, bacterial products, or exogenous agents. These factors cause cell death. Then endothelial cells recruit leukocytes, fibroblasts, and epithelium into the mucosa from the vascular space, resulting in granulomas [which is a histopathologic lanmark of Chrohn's disease damage to the GI tract.]
Chronic inflamation ultimately thickens the bowel wall and eventually narrows the lumen.
Therapeutic Management Options
Aminosalicylates (5-ASA)
1st line therapy for mild - moderate CD.
Sulfasalazine, mesalamine, olsalazine, balsalazine
Be-careful with sulfasalazine since it contains sulfa so it shouldn't be used in patients who allergic to sulfa. In this case, mesalamine would be an option. Only Pentasa [controlled release cap] and Asacol [delayed release tab] are mesalamine forms used for CD treatment.
Adverse effects include headache, nausea, GI distress
Glucocorticoids
to reduce inflammatory and to induce remission of active CD.
Normally use when 5-ASA compounds are ineffective because of lack of efficacy in maintaining CD remission. Common adverse effects are moon face, acne, weight gain, dyspepsia.
Immunosuppressants
Thiopurines can maintain remission of moderate to severe CD.
Azathioprine, 6-mercaptopurine are steroid-sparing agents that induce cell apotosis.
Methotrexate inhibits cytokine synthesis. It is effective for inducing remission and preventing relapse in patients with CD. MTX treatment; 25mg per week has a slow onset [3-6 months] and requires monitoring.
Antimicrobials
mild to moderate CD associated with fistulas and abscesses.
Fluoroquinolones and metronidazole are drug of choice.
Flagyl 500mg po q12hrs
Ciprofloxacin > or equal to 20mg/kg/day
Biological
Infliximab [Remicade]
Adalimumab [Humira]
and new agents such as nataliumab, certolizumab
