Crohn’s disease and ulcerative colitis are disorders of particular importance to
gastroenterologists who care for both children and adults. Although these chronic
inflammatory bowel diseases are still largely of unknown etiology, there is an
increase in knowledge of their immunopathology.
Protein-energy malnutrition, which is a prominent feature of inflammatory
bowel disease [1–5], develops largely as a result of the systemic inflammatory
Inflammatory bowel disease encompasses two different diseases: ulcerative
colitis and Crohn’s disease. Although both are strongly associated with the 20th
century, they are not entirely new entities.
A genetic predisposition to inflammatory bowel disease has long been suspected,
given that there are ethnic and familial aggregations of these disorders [1,
2]. In the 1990s, several genetic epidemiological studies have enabled the risk of
recurrence in families to be better defined.
For over half a century, and despite progressively intensified research efforts,
the etiology of inflammatory bowel disease remains an enigma. The most widely
accepted comprehensive theory suggests that the pathogenesis of Crohn’s disease
and ulcerative colitis is multifactorial, resulting from a complex interplay of
genetic predisposition, environmental and immunological factors .
Man and animals are protected from a wide range of microorganisms (parasites,
bacteria, moulds, yeasts, fungi, and viruses) by a highly complex biological
response which is executed by the immune system .
The term “inflammatory bowel disease” applies to bowel diseases of unknown
etiology characterized by chronic and often relapsing inflammation. They include
ulcerative colitis, Crohn’s disease, indeterminate colitis, pouchitis, and microscopic
Inflammatory bowel disease comprises disorders of unknown etiology. The
diagnosis is made on the association of symptoms and signs and sometimes on the
family history of the subject, since there is at present no specific clinical, morphological,
or biological diagnostic test.
Until the 1970s, Crohn’s disease was considered to be uncommon in children,
although ulcerative colitis had been recognized in children since the 1920s .
The diagnosis of Crohn’s disease is more difficult in children because systemic
manifestation such as growth failure and delayed puberty  may dominate the
early clinical picture.
The genetic basis of diseases is becoming more widely understood. It has long
been known that certain diseases are inherited through genetic defects. However,
other disorders are manifested by alterations in the expression genes central to
Inflammatory bowel diseases, in particular Crohn’s disease, have profound
effects on nutritional status  and malnutrition is common, even in patients with
relatively quiescent disease attending an outpatient clinic (Table 1). In a recent
prospective survey of 154 consecutive patients referred to the gastrointestinal
clinic of a teaching hospital, 11 of 47 (23%) with Crohn’s disease had significant
The appropriate use of nutritional treatment in the management of inflammatory
bowel disease has been an unresolved issue. There is no disagreement that
replacement therapy is indicated when nutrient deficiency is present.
Prepubertal children with Crohn’s disease require special approaches to treatment
because of the propensity for chronic intestinal inflammation to impede
The relative merits of treating Crohn’s disease with corticosteroids or enteral
nutrition remains an area of controversy, particularly following meta-analyses
which implied that corticosteroids were more effective at inducing clinical remission
The inflammatory bowel diseases are chronic inflammatory processes that
may have pathological and clinical manifestation in any part of the alimentary
tract from the mouth to the anus, but mainly in the ileum and the colon.
The molecular mechanisms of intestinal injury in Crohn’s disease and ulcerative
colitis are increasingly being elucidated. These findings have led to new
anticytokine treatments designed to decrease mucosal damage in inflammatory
During the last decade, major advances have been made in therapeutic
approaches to both Crohn’s disease and ulcerative colitis. Nevertheless, many
patients continue to pose a therapeutic challenge because they remain symptomatic
despite standard medical intervention.
This is going to be very brief. Thank you all for attending. I deeply appreciate
your participation. The free flow of ideas that were characteristic of this workshop
will, I believe, have a cytokine-induced cascade response for the expansion of our
knowledge of inflammatory bowel disease.