The etiology of inflammatory bowel disease (IBD) is still unknown. However,
a satisfactory solution cannot be far away. IBD actually encompasses two d
iseases, i.e. Crohn's disease (CD) and ulcerous colitis (UC). These disease
s resemble each other so closely that they cannot be distinguished even pat
hologically, but differ from each other sufficiently to regard them as inde
pendent entities. Epidemiological observations may be helpful in identifyin
g the true causative factors of this evasive disease. Geographically, the p
revalence of the disease has a slope from North to South and, to a lesser d
egree, from West to East. The Western-Eastern discrepancy can be attributed
to a difference in Western life styles. The incidence of the disease has b
een increasing world-wide of late, but its spread has been slowing down in
highly affected countries. Racial and ethnic relations in different populat
ions and immigration studies offer interesting data which can reflect genet
ic, inherited, environmental and behavioural factors. The disease seems to
have a characteristic racial-ethnic distribution: the Jewish population is
highly susceptible everywhere, but its prevalence in that population nears
that of the domestic society in which they live. In Hungary, the Roma (Gyps
ies) have a considerably lower prevalence than the average population. This
can be: attributed to a genetic or environmental influence. According to a
ge, the onset of the disease occurs more often in the second or the third d
ecade of life, but there also is another peak in the 60s. Regarding sexual
distribution, there is a slight preponderance of colitis ulcerosa in men an
d of Crohn's disease in women. It may correspond to the stronger auto-immun
e affection in the process of Crohn's disease. Environmental factors and be
havioural influences also are investigated. Diet, the role of the early age
s, smoking habits and the influence of hormonal status and drugs are viewed
as useful contributing factors in the manifestation of the disease. Geneti
c studies show that one-fourth of IBD patients have an affected family memb
er. HLAB27 histocompatibility also plays an important, but not determining
role in the development of the disease. Genetic factors seem to have a stro
nger influence in Crohn's disease than ulcerative colitis. The existence of
multiple sclerosis-IBD families may reflect the common genetic background
or the similar microbial effect as well. A great number of bacterial and vi
ral factors has been suspected of being infectious factors in IBD, mostly i
n CD. Mycobacteria, Yersinia, Campylobacter, Clostridium, Clamidias, etc. a
s well as bacteria and some viruses such as herpes and rotavirus and the pr
imary measles virus. None of them has been proven as a real and exclusively
pathogenic factor. Immunological background has an important function in t
he manifestation of the disease. If an individual has a genetic susceptibil
ity to infections, the down regulation of an inflammation in the bowel wall
does not occur in a proper way. This initiates the auto-immune process whi
ch is a self-increasing cycle. Extra-intestinal manifestations of IBD are o
f high importance because they can not only follow intestinal symptoms, but
precede them by years. Hepatic and biliary disturbances (primary sclerosin
g cholangitis), are the most serious complications. Mucocutaneous manifesta
tions can be the first appearance of the main disease (in the mouth). Auto-
immune consequences (erythema nodosum) or complications caused even by the
therapy can occur. Ocular and musculoskeletal manifestations supposedly hav
e the same genetic background and often precede the intestinal symptoms.
Considering the epidemiological, genetic and immunological data, we can con
clude that ulcerative colitis and Crohn's disease are heterogeneous disorde
rs of mutifactorial etiology in which hereditary (genetic) and environmenta
l (microbial, behaviour) factors interact to produce the disease. (C) 2000
Elsevier Science Ireland Ltd. All rights reserved.