Genetic factors appear to be particularly important in the pathogenesis of
childhood inflammatory bowel disease (IBD). The major presenting feature of
ulcerative colitis in young patients is almost uniformly bloody diarrhea,
whereas the initial symptoms of Crohn's disease are more varied. In compari
son to adults, childhood ulcerative colitis is more often extensive. Anatom
ic distribution of Crohn's disease is similar to adult cohorts. Two serolog
ical tests, antineutrophil cytoplasmic antibody (ANCA) and anti-Saccharomyc
es antibody (ASCA) have been suggested to be helpful in differentiating the
type of pediatric IBD. However, only Crohn's colitis and ulcerative coliti
s present difficulties in differentiation; yet such patients demonstrate co
nsiderable overlap with respect to ANCA and ASCA status. The clinical cours
e of IBD occurring in childhood is variable, as in adults. Unique to pediat
ric populations, and to Crohn's disease particularly, is the potential comp
lication of growth impairment and accompanying pubertal delay. Direct growt
h-inhibiting effects of cytokines released from the inflamed bowel, as well
as chronic undernutrition, and effects of corticosteroid therapy on the gr
owth hormone-insulin growth factor I axis contribute to its pathogenesis. O
ptimization of treatment of intestinal inflammation, and provision of adequ
ate nutrition are of paramount importance in preventing or remedying growth
impairment. Growth is a measure of the success of therapy. Control of gast
rointestinal symptoms by long-term corticosteroid use, which impedes linear
growth, does not constitute successful medical management. Optimal treatme
nt of intestinal inflammation encompasses immunomodulatory therapy, nutriti
onal therapies, and if appropriate, resection of the diseased bowel. (C) 20
00 Prous Science. All rights reserved.