My Child Has Inflammatory Bowel Disease : Why? What now? What s next?
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1 My Child Has Inflammatory Bowel Disease : Why? What now? What s next? George M. Zacur, M.D., M.S. Clinical Assistant Professor Department of Pediatrics and Communicable Diseases Division of Gastroenterology University of Michigan C.S. Mott Children s Hospital
2 Disclosures No disclosure Thank you Crohn's & Colitis Foundation
3 Objectives What is Inflammatory Bowel Disease (IBD)? Crohn Disease or Ulcerative Colitis? WHY? I don t have IBD. How did my child get it? The perfect storm of IBD Genetics and the environment WHAT NOW? How do we treat it? (Currently) Are these medications safe? What about surgery? Diet, probiotics, and fecal transplant. WHAT S NEXT? What should we expect? Disease course Future directions Transition of care
4 What is IBD? IBD is comprised of two distinct entities: Ulcerative Colitis (UC) and Crohn Disease (CD). About 15% with IBD have only colonic involvement, but cannot be distinguished between CD and UC, and this is termed Indeterminate Colitis (IC). IBD Ulcerative colitis Crohn Disease Indeterminate Colitis
5 What is IBD? Ulcerative Colitis (UC): Relapsing episodes of superficial mucosal inflammation, almost always affecting the rectum, in a continuous fashion Crohn Disease (CD): Characterized by transmural inflammation rather than superficial, skip lesions, fibrosis/strictures, fistulas, microperforations, and abscesses
6 What is IBD? Crohn Disease: Any part of the GI tract Can skip areas Rectal sparing Non-caseating granulomas Transmural inflammation Fistulas and abscesses Strictures (scar) common Ileum commonly involved Perianal disease 20% colon-only involved Ulcerative Colitis: Colon only Continuous No rectal sparing No granulomas Mucosal inflammation Can have inflammation in the stomach and duodenum Can have relative rectal sparing, cecal patch, or back-wash ileitis
7 What is IBD? Signs/Symptoms Crohn Disease Ulcerative Colitis Rectal Bleeding Abdominal Pain Diarrhea Weight loss Growth Failure Perianal Disease ++ Mouth Ulcers ++ + Erythema Nodosum + + Fevers ++ + Anemia Arthritis + + Adapted from CHDNF/NASPGHAN 2007
8 Geographic Distribution Cosnes, IBD 2011
9 IBD in the USA >1 million Americans have IBD (>1.5 million?) Incidence in the pediatric age group has doubled over the past decade Current estimates report more than 50,000 children have IBD (some report more than 80,000) % of adults with IBD developed symptoms or were diagnosed as children Rare before age 5 yrs, but reported as young as infancy Very Early Onset (VEO)-IBD
10 Percent of Cases Age of Onset 25 Years Loftus, Gastro 2003; 124:abstract 278
11 Gastro 2006 Age of Onset
12 WHY? I don t have IBD How did my child get it? The perfect storm of IBD Genetics and the environment
13 How did my child get IBD? The perfect storm of IBD Genetics ( 200 IBD genes) Immune System (Mucosal) IBD Gut Environment (Microbiome)
14 How did my child get IBD? The new perfect storm of IBD Genetics Immune System IBD Gut Flora Environmental Triggers
15 Genetics The most important risk factor for IBD is a positive family history (15-30%) Genetic influence is greater in CD than UC Genetically complex Genetic defects Mucosal barrier function Mucosal immune system 200 genes isolated more than half are common to both diseases Schreiber, Semin Immunology 2009 Williams, Inflamm Bowel Dis 2002 Orholm, Scand J Gastroenterol 2000
16 Gut Microbiome (Gut Bacteria) Frank, PNAS 2007
17 How did my child get IBD? Different theories: Hygiene theory? Early antibiotics? Vaginal birth vs C-Section? Breast feeding vs formula feeding? Environmental triggers?
18 Environmental Triggers Smoking: CD Oral contraceptives: CD & UC NSAIDs: CD & UC Vitamin D deficiency: CD Perinatal & childhood infections/microbial exposures? Stress? Food or food additives?
19 Theories of Triggers Genetics Triggers affecting the microbiome: Delivery method, Early diet Triggers that start inflammation: Infections, Antibiotics, NSAID s, Smoking Diet and lack of nutrients can influence inflammation IBD
20 WHAT NOW? How do we treat it? (Currently) Are these medications safe? What about surgery? Diet, probiotics, and fecal transplant.
21 How do we treat it? Principles of Medical Management Enhance quality of life while avoiding long-term toxicity Induction of Remission start the healing process Pitfall is premature withdrawal of inductive therapy: failure to complete induction virtually guarantees failure of maintenance Maintenance of Remission keep healing going Clinically resolution of symptoms (bleeding, urgency, passage of mucous and diarrhea) Endoscopically gut lining without ulcers/exudate/friability/ granularity Clinical remission precedes endoscopic remission which in turn precedes histologic remission and vice versa for flare
22 Therapy (old way) Disease Severity Resection/Diversion Colectomy Severe Moderate Surgery Biologics Methotrexate Azathioprine/6-MP Prednisone Anti-TNF s: Infliximab, Adalimumab, Certolizumab Ustekinumab Vedolizumab Mild CD Enteral Nutrition Budesonide Antibiotics Aminosalicylates UC
23 Therapy Disease Severity Severe Moderate Surgery Methotrexate Azathioprine/6-MP Prednisone Biologics Anti-TNF s: Infliximab, Adalimumab, Certolizumab Ustekinumab Vedolizumab Mild CD Enteral Nutrition Budesonide Antibiotics Aminosalicylates UC
24 Are Aminosalycilates safe? Aminosalycilates: Mesalamine, Sulfasalazine, Balsalazide Effective induction and maintenance of mild to moderate UC; effective maintenance for moderate UC after induction with steroids; do not work for Crohn Disease Tolerated well Headaches; Worse diarrhea/rectal bleeding Kidney disease (very rare) Oral and rectal combination better than oral alone, especially for distal UC (end of the colon)
25 Are Immunomodulators safe? Azathioprine (Imuran)/Mercaptopurine (6-MP) Effective for maintenance of CD and UC (earlier is better); need a bridging medication Pancreatitis, Rash, Flu-like symptoms, GI intolerance Lower white blood cell count Liver damage (temporary) rare Skin Cancer rare Lymphoma extremely rare (4 per 10,000) Methotrexate Used as monotherapy or combination with anti-tnf s better for CD Nausea Liver and lung damage (temporary and rare) Birth defects Risk of cancer is small to negligible (need more data)
26 Are Biologics safe? Anti-TNF s: Infliximab (Remicade), Adalimumab (Humira), Certolizumab (Cimzia), Golimumab (Simponi) Effective for induction and maintenance of remission in CD and UC Highly effective for fistula therapy in CD (best!) Rash, fever, headache Low risk of serious infections, except for TB, Varicella, and Influenza Antibodies and/or loss of response Little evidence for increase risk of cancer with Anti-TNF alone
27 Are Biologics safe? Ustekinumab (Stelara) Initially used for psoriasis found to be effective for CD Slightly better side effect profile than the anti-tnf s Effective for CD only One infusion, then every 8 week injection Still need more data fistulae, strictures, recurrence post-op Vedolizumab (Entyvio) Both take months to work. Significantly better side effect profile Effective for both UC and CD (UC>CD) Infusion schedule similar to other biologics Still need more data fistula, stricture
28 Are Steroids safe? Corticosteroids: Prednisone, Prednisolone, Methylprednisolone, Hydrocortisone Extremely effective anti-inflammatory Not to be used alone, but rather as a bridge NOT MAINTENANCE DRUGS! Short and long-term side effects: Skin problems, stretch marks Infections! Growth failure! Bone disease osteoporosis, degenerative joint disease Hypertension, Diabetes, Cataracts, Glaucoma Gastritis, ulcers
29 What about surgery? Surgery is not necessarily a failure of medication >70% of CD patients will undergo one surgery;? 1/3 UC Colectomy (colon removal) UC more than CD Severe UC, refractory to steroids/medications, severe Crohn colitis Pouchitis, cuffitis, diarrhea Diversion (Temporizing Ileostomy) CD more than UC Severe perianal CD, severe Crohn colitis, severe UC Diarrhea, dehydration Small bowel resection Ileocecal resection Most common surgery of CD Resume/reinitiate therapy Recurrence (Crohn Disease returns where ends are connected)
30 Do we have to use medications? Risks of poor outcomes from the diseases themselves are higher than the side effects of medical or surgical therapy Crohn Disease: Growth failure, short stature, poor nutrition Fistula, abscess, infection Stricture, small bowel obstruction Colon cancer Death Ulcerative Colitis: Profuse diarrhea, severe rectal bleeding, anemia, transfusions Growth failure, infection Toxic megacolon, perforation Colon cancer Death
31 Diet Theory: A regular diet contains harmful components and can alter the gut microbiome which can lead to inflammation. High dietary intakes of total fats, polyunsaturated fatty acids, omega-6 and meat were associated with an increased risk of CD and UC High fiber and fruit intakes were associated with decreased CD risk (but not UC) High vegetable intake was associated with decreased UC risk. Hou, Am J Gastroenterol 2011 Ananthakrishnan, Gastro 2013
32 Enteral Nutrition Elemental (formula) diet: % for 6-8 weeks for induction of remission of CD Study that compares partial vs exclusive enteral nutrition: GREAT! Greater mucosal healing with a more formula diet Decreased fecal calprotectin THEN WHAT? PLEASE study, AIBD, Orlando 2014 Study looking at partial enteral nutrition with a CD exclusion diet: Improvement in labs and disease severity scoring High remission rate Sigall-Boneh, IBD 2014
33 Specialized Diets Gluten-free Low FODMAPS No/Low dairy Low roughage Paleo Diet There is no evidence that these diets improve inflammation or prevent disease complications, although they may improve symptoms for some patients.
34 Probiotics Probiotics: "live microorganisms, which when consumed in adequate amounts, confer a health effect on the host No good evidence that they improve CD or UC Some good evidence they are effective in prevention of pouchitis after colectomy with pouch formation May help symptoms, but not the disease (can t hurt unless there is hardware) Joint FAO/WHO Expert Consultation on Evaluation of Health and Nutritional Properties of Probiotics in Food Including Powder Milk with Live Lactic Acid Bacteria, October 2001
35 Fecal Transplant Fecal Microbiota Transplant (FMT): stool is collected from a tested donor, mixed with saline or other solution, strained, and placed in a patient, by endoscopy, enteral tube (NG or NJ), or enema. May work in some specific cases (C. diff) No good evidence for use in IBD need more studies Harmful if not done correctly (Do not try this at home!)
36 WHAT S NEXT? What should we expect? Disease course Future directions Transition of care
37 What should we expect? 1 st year may be rough Many medications initially Labs Good and bad days Flares Scopes Imaging, MRI Surgery GOAL: NORMAL LIFE!
38 Future Directions Goal of therapy: Optimizing efficacy while minimizing toxicity fancy way of saying finding the right medication, with minimal side effects, and best at treating the disease Individualized therapy based on multiple factors such as disease location, genetics, molecular makeup Altering the diet to modify the gut microbiome as a potential for disease prevention and/or therapy Maybe immunization against bacteria causing IBD?
39 Research
40 Transition of care Know: Your disease Your medications what, why, how much, side effects, interactions Your test results and what they mean Develop Independence and Assertiveness: Take responsibility for knowing medications and adherence Make your own appointments with your doctor tell your history, don t rely on your parents Plan for the future how will you manage your disease at school? Work? Health Insurance? Transition not Transfer: Make introductions dialogue between docs, not just records
41 Transition: goals and milestones
42 Prior to transitioning Patients: Speak up! Take ownership of your health and your treatment. Parents: Allow child to lead the appointment.
43 When transitioning Do your research Have pediatric doctor speak with new doctor Prepare yourself before appointments GET TO KNOW Familiarize yourself with insurance information Read all medical documents YOUR SOCIAL WORKER!
44 THANK YOU!
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