3. Introduction
The term in? ammatory bowel disease (IBD) is
used to represent
2 distinctive disorders of idiopathic chronic
intestinal in? amma-
tion: Crohn disease and ulcerative colitis. Their
respective
etiologies are poorly understood, and both
disorders are charac-
4. Introduction
A bimodal distribution has been
shown with an early onset at 10-20 yr of age and
a 2nd, smaller
peak at 50-80 yr of age. About 25% of patients
present before
20 yr of age. IBD may begin as early as the 1st
yr of life, and an
increased incidence among young children has
5. Introduction
The risk of IBD in family members of an
affected person has been reported in the range of
7-30%; a child whose parents both have IBD
has a > 35% chance of acquiring the disorder.
6. Introduction
(16%). Genetic disorders that have been
associated with IBD
include Turner syndrome, the Hermansky-Pudlak
syndrome, gly-cogen storage disease type Ib,
and various immunode? ciency
disorders.
7. Pathogenesis
The gut is under constant immunologic stimulation
from microbial agents and dietary antigens. In
response, the mucosa normally displays
physiologic inflammation.
In IBD, the mechanisms that keep physiologic
inflammation in check fail and pathologic
inflamation ensues.
10. Diagnosis
The diagnosis of ulcerative colitis must be con?
rmed by endo-
scopic and histologic examination of the colon.
Classically,
disease starts in the rectum with a gross
appearance characterized
by erythema, edema, loss of vascular pattern,
granularity, and
11. Diagnosis
There may be some variability in the intensity of
in? ammation even in those areas involved.
Flexible sigmoidos-
copy can con? rm the diagnosis; colonoscopy can
evaluate the
extent of disease and rule out Crohn colitis. A
colonoscopy
should not be performed when fulminant colitis is