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PEDIATRIC IBD Growth and Nutrition

PEDIATRIC IBD Growth and Nutrition. By Karla Au Yeung, MD MAJ, MC, USAR 3 November 2000. Objectives. Epidemiology/Definition Complications/ Mechanisms Malnutrition Medication effects Micronutrient deficiencies Effects unique to pediatrics Specific Nutritional Therapy.

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PEDIATRIC IBD Growth and Nutrition

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  1. PEDIATRIC IBDGrowth and Nutrition By Karla Au Yeung, MD MAJ, MC, USAR 3 November 2000

  2. Objectives • Epidemiology/Definition • Complications/ Mechanisms • Malnutrition • Medication effects • Micronutrient deficiencies • Effects unique to pediatrics • Specific Nutritional Therapy

  3. Definition of Failed Growth • Kleinman, et al • Dec Ht > 0.3 SD per year • growth velocity <5cm/yr • Dec ht velocity > 2cm from preceding yr (during early to mid-puberty) • Bone age and pubertal staging

  4. Our Situation • 25% of all IBD are pediatric --> infants • CD > UC 4:1 • Growth failure is unique to pediatric IBD • 30-50% of CD ped. Pts • 10% of UC ped. Pts • Malnutrition/micronutrient deficiencies more likely due to increased metabolic needs for growth

  5. Our Situation cont. • Sole manifestation of IBD in 5% of pts • Resemble anorexia nervosa • wt loss/anorexia sx more prevalent than GI sx • IBD pts do not have disordered body image or fear becoming fat • Problem: heights (weights) do not get recorded regularly for school-age kids

  6. Problems We Face in This Situation • 1. Growth/Nutrition is a problem before we meet the pt. • Possible direct effects of inflam. mediators • Anorexic effects of inflam. Mediators • 2. Patients don’t feel well • Post-prandial pain --> dec. intake • anorexia (intake 55-80% of RDA of cal. Needs)

  7. Complications cont. • 3. Malabsorption • Protein Losing Enteropathy • Bacterial Overgrowth • Dec. surf. Area for absorption • Lactose intolerance • Micronutrient deficiencies • Rapid transit

  8. Micronutrient Deficiencies • Iron deficiency anemia is most common • Tx with iron dextran if resistant to oral Fe Tx • Folate and B12 • Zinc deficiency (est. up to 40% pts) • lower in growth impaired teens with CD • Zinc repletion does not accelerate growth. • Ca, Mg, Phos, Vit D - esp in adolescent pts.

  9. Complications Cont. • 3. Chronic Dec Energy and Protein intake • not able to keep up with needs • endocrine functions altered • 56% RDA was mean caloric intake in one study

  10. Complications Cont.: Medications • Steroids • alter linear growth • proteolytic/ osteolytic • inhibit bone growth • Sulfasalazine • use folic acid

  11. Complications Cont. • 6. Time is our enemy • Eventual closure of the epiphyses • Stunted growth in 17% of pts with early delay in growth • Especially important in the peripubertal age • 7. Elemental Formulas • Can restore growth velocity • Bad taste, need for NGT/G-tube

  12. Growth Failure at Presentation“Prepatterned” • Motil, et al Gastroenterology 1993 • Regardless of pubertal development, at dx, 23-39% of pts had delayed growth • Delay in linear growth persisted through puberty and was not reversed by surgery • Sig. Neg. assoc. between linear growth and disease activity, but not medication Tx

  13. Ht Velocity According to Severity of Symptoms • Severity GI Sx- Griffiths, et al Gut 1993 Cm/yr

  14. Growth In Pediatric IBDGender Difference • Sentongo, et al. JPGN 2000 • Prospective Study to measure anthropometry, DEXA, genetic potential, PCDAI, lifetime steroid use in relation to gender and disease activity • Results: • Ht age Z inc. in male control compared to CD pt. This difference not seen in females

  15. Endocrinologic Issues • Short stature evaluation: • secondary to IBD • constitutional delay • genetically short stature • Other hormones • thyroid/growth hormone - non-contributory • gonadotropins/estrogen- affected by malnutrition --> delayed pubertal maturation

  16. Endocrine Cont. • Insulin-like growth factor I • mediates growth • nutritionally modulated • low levels during fasting and quickly return to nl w/ feeding • low in CD who are nutritionally impaired

  17. Factors Affecting Bone Mass in IBD • Hyams and others showed mouse calvarium and serum from active CD had impaired mineralization - not in UC or controls • Osteoblast impaired by cytokine in CD serum: IL-1B, TNFa, IL-6 • STEROID • Dec. Formation (inhibit osteoblast) • Inc. Resorption (dec. gut absorption, Inc. PTH)

  18. Risk Factors for Low Bone Mineral Density • Semeao, et al J. Ped 1999 • Life long risk of frax related to peak bone mass • Peak bone mass is achieved during puberty-early adulthood • Reports of up to 70% CD children with dec. BMD • Evaluated several parameters for risks

  19. Inc. # hosp. Days Inc. PCDAI Hypoalbuminemia NGT/TPN Flagyl/Asacol unreliable because such routine use 6MP (32% pts) >7.5 mg/day of steroid exposure >5000mg accum steroid use Duration of steroid >12 mos Risk Factors for Low Bone Mineral Density

  20. NOT Correlated Site of Dz Age Dx Duration DZ H/o surgery Conclusion: Use this as criteria to decide who needs DEXA and when Risk of dec. bone mass is not just due to steroid use. Low BMD Risks cont.

  21. Labs to Evaluate Osteopenia • Serum Ca, Phos, Alk Phos • Vit D, Vit D metabolites, Alk phos isoenzymes, GGT, PTH • BONE AGE • Impt for interpreting BMD • Impt for estimating growth delay • Dual Xray Densitometry/absorptiometry • 1SD below mean = osteopenia

  22. Treatment of Osteopenia • Tx underlying disorder • Nutritional rehabilitation • Consider malabsorption and tx • Bone is mineralized at max dose of steroid of 0.3mg/kg qod • Substitute steroid for immunomod. Asap • Ca supplement when well

  23. Treatment of Osteopenia • Vit D supplement: no evidence that excess beyond RDA is needed • except liver dz, deficiency, dietary restriction • Weight Bearing exercise helps mineralize bone • Bisphosphonates • dec. turnover of bone • side effects/ longterm effects on growing bones

  24. 0-6 months 6-12 months 1-3 years 4-8 years 9-13 years 210mg 270 mg 500 mg 800 mg 1300 mg RDA for Calcium

  25. Dietary Calcium Sources • Dairy products • Meat, fish with bone • Broccoli • Bok choy • Kale

  26. Enteral Nutrition: Intro • Possible Mechanisms: • 1. Dec. Antigen load to the GI tract • 2. Alter intestinal microbial flora • 3. Dec. intestinal synthesis of inflammatory mediators via reduction of dietary fat • 4. Provision of micronutrients to diseased bowel

  27. Enteral Nutrition cont. • Formula composition for protein and/or fat source have not proven to make a difference in studies • Common practice for remission is elemental or semi-elemental formula • Dec. ratio of n-6 to n-3 polyunsat fatty acids • dec. precursors for arachidonate-derived eicosanoid synthesis (n-6) (fish-oil tx)

  28. Enteral Nutrition Intro cont. • Factors for Relative Benefit of Enteral Nutrition as Primary Therapy • Mostly small bowel dz • Prepubertal • Acute Malnutrition/Growth Failure • Motivated patient/family • Not as good as steroid compared in meta-analysis (relapse 70% in one year)- but growth improved on nutrition tx.

  29. Enteral Nutrition Support • Three possible strategies • 1. Begin with nutritional therapy alone • elemental formula only for 4-6 wks • 2. Nutritional supplement to increase caloric intake and reverse growth delay • 3. Prevent relapses • intermittent administration

  30. Supplementary Enteral Nutrition Maintains Remission • Wilschanski, et al Gut 1996 • Tx 65 pts active CD with elemental formula overnight 4-6 weeks: 72% remission • 43% relapse by 6 mos • 60% relapse by 12 mos • If continued NGT fdg with daytime reg. diet, even less relapse rate • Suggest macro/micronutrient effect vs. Ag

  31. Chronic Intermittent Elemental Diet • Belli, et al Gastroenterology 1988 • 7 boys/ 1 girl CD/growth delayed • 1st year observe • 2nd year, elemental diet group/control grp • E. diet q 4months for 1 month • Treat prn with medication (sulfa/pred)

  32. RESULTS • No pt dropped out • Ave caloric intake of 133% during ED Tx compared to 106% between tx. • ED grp grew 7cm the 2nd year • ED grp gained more weight • ED grp dec. prednisone intake (22vs89 mg/kg/year) • ED grp CDAI dec. significantly

  33. Absolute Height Changes Cm/yr

  34. Conclusion to This Study • This is tolerable and effective method for maintaining remission with nutrition tx • Not only did pts have increased height and weight, but they also had dec. steroid use. • In past studies, even though pts achieve longer remission with steroids, linear growth was not improved much • problem: small study

  35. Conclusions • Growth delay is something intrinsic to Crohn’s disease in addition to malnutrition from a multitude of reasons. • Induce remission and minimize daily steroids ASAP - consider nutritional tx • Improve energy/nutrient deficiencies • Account for catch up growth • Limited time available in puberty pt.

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