immunomodulators and biologic therapy for inflammatory

Inflammatory Bowel Disease
◦ Subgroups or types of IBD:
 Crohns Disease (CD)
 Ulcerative Colitis (UC)
◦ Onset across all ages reported in as young as
◦ More commonly onset in adolescent age
Environmental Trigger
Genetic Predisposition
Immune Response
Manifestations of IBD:
Crohn’s Disease (CD)
◦ Extends throughout the GI tract: from mouth to anus;
◦ Commonly affects the terminal ileum & colon (terminal
◦ Involves all layers of bowel wall (transmural)
◦ Pain characteristic to RLQ
◦ Fistula/fissure/stricture development
◦ Extra-intestinal symptoms, uveitis, large joint / arthritis,
mouth ulcers, liver disease, renal calculi, cutaneous
manifestations (erythema nodosum)
◦ May require surgery to manage complications
◦ Medical management, life long condition
Manifestations of IBD:
Ulcerative Colitis (UC)
Limited to colon & rectum
Involves the mucosa & submucosal layer
Pain characteristic to LLQ
Extraintestinal symptoms as with Crohn’s
except for apthous lesions
◦ Medical management
◦ Curative surgery is a colectomy
IBD: Signs and Symptoms
Abdominal pain / cramps
 Fatigue
 Anorexia, weight loss and decreased growth velocity
 Nocturnal symptoms
 Systemic symptoms may be present for months or years
prior to GI symptoms and diagnosis (CD)
 Diarrhea (bloody more common with UC)
 Extraintestinal involvement: joint and muscle pains, apthous
oral ulcers (CD), uevitis
 Periods of exacerbations and remissions
 Sometimes differentiation between CD and UC may be
difficult to determine. When differentiation is not obvious
the IBD may be classified as “Indeterminate Colitis”
Diagnostic Workup
Abdominal series to evaluate structure and anatomy
Labs: CBC, Inflammatory markers (ESR and CRP)
Stool studies to rule out infectious origin
Endoscopy (upper & lower may be indicated for CD) with
biopsy and histiologic evaluation
Serum antibody markers help to confirm diagnosis
(perinuclear antineutrophil cytoplasmic antibodies [PANCA] and anti-Saccharomyces cerevisiae antibodies
[ASCA]); Testing + for P–ANCA more likely to have UC
while children who test + for ASCA are more likely to have
Nutrition as Treatment
Low residue diet
Nutrition is a significant first line therapy for CD
◦ (nutrition delivered by mouth, NG/G-tube or parenteral
Nutrition is a supplemental therapy for UC
Vitamin and mineral supplementation
(vitamin B12, folic acid, calcium, Vitamin D, iron)
Pharmaceutical Treatment
Aminosalicylics – anti-inflammatory; induces remission,
administered topically PR
Antibiotics-reduce bacterial burden in the gut
Steroids-induces remission and control inflammation for
maintenance therapy
Immunomodulators- suppress activated inflammation;
maintenance and remission
Biologics-antibodies act on specific molecules in the
immune cascade; maintenance and remission
IBD Pharmacologic
BIOLOGICS (moderate-severe disease)
IMMUNMODULATORS (moderate-severe disease)
ANTIBIOTICS (mild to moderate disease)
STEROIDS (moderate to severe disease)
AMINOSALICYLATES (mild to moderate disease)
1st three levels are mainstay of a traditional step up approach
for pharmacological therapy. A combination of these agnets
may be administered. This approach starts with the least
toxic medical regime and advances in therapy are
determined based on response. Immunomodulators and
biologics are added when there has been a lack of response
or side effects/ toxicities are manifested.
Indications for Immunomodulators
and/or Biologics
Unresponsive to aminosalicyclates, steroids and
Steroid refractory/ steroid dependence
Perianal disease not responding to antibiotics
Fistula / stricture formation
Maintenance of remission
May combine therapies with lower dose steroids
to achieve a “steroid sparing” effect
Crohn’s and Colitis Foundation of America.
Lichtenstein, G.R., Abreu, M.T., Cohen, R., and Tremaine, W. (2006). American
Gastroenterological Association Institute: American gastroenterological
association institute medical position statement on corticosteroids,
immunomodulators, and infliximab in inflammatory bowel disease.
Gastroenterology 130 935-939.
MacDermott, R.P, (2008) 6-mercaptopurine (6-MP) metabolite monitoring and
TMPT testing in the treatment of inflammatory bowel disease with 6-MP or
azathioprine. UpToDate retrieved 1/14/09
Prometheus® 2008. Prometheus thiopurine management.
Prometheus laboratories. San Diego CA
Sanborn, W.J. (1996). A review or immunomodifier therapy for inflammatory
bowel disease: Azathioprine, 6-mercaptoputine, cyclosporine, and
Snapper, S.B. and Podolsky, D.K. (2008 Immune and microbial mechanisms in the
pathogenesis of inflammatory bowel disease. UptoDate retrieved 1/14/09
Su, C. & Lichtensteien, G.R. (2004). Treatment of inflammatory bowel disease with
azathioprine and 6-mercaptopurine. Gastroenterology Clinics of North America
33 209-234.
Taketomo, C.K. Hodding, J.H. and Kraus, Donna, M. (2008-2009). Pediatric dosage
handbook. 15th edition LEXI-COMP
Van Deventer, S.J. (1999). Anti-TNF antibody treatment of Crohn’s disease. Annals
of Rheumatic Diseases 58 S-, 1140-1120
Wyneski, M.J., Green, A., Kay, M., Wyllie, R., Mahajan, L. (2008).
Safety and efficacy of adalimumab in pediatric patients with Crohn disease.
Journal of Pediatric Gastroenterology and Nutrition47(1) 19-25
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