[Etiology of Crohn disease. Current data].
Both genetic and environmental factors appear to play an aetiologic role in Crohn's disease. The hypothesis of genetic susceptibility is based on the frequency of familial forms (6-33%) and higher relative risk in first degree relatives (x10 to x21). Three genetic segregation analyses have defined a genetic model favouring autosomal recessive transmission and incomplete penetration. The frequency of the deleterious allele would be 0.01 in the general population. One-third of all patients would be homozygous. To date, no genetic marker has been found for Crohn's disease although in one study, molecular biology techniques revealed a significant association between the HLA-DR1, DQW5 genotypes, and the association DR1/DQW5, and Crohn's disease. There are also many arguments in favour of an environmental cause, including: increased incidence since the Second World War, a north-south incidence gradient (established in the US and probable in Europe), predominance in urban areas. In addition, 21 conjugal forms were recently reported in the US, including 14 which appeared after marriage. We have also observed 10 conjugal forms in a limited area in northern France and in Belgium. Smoking has also been shown to have a detrimental effect, perhaps via modifications in the microcirculation of the intestinal wall. Despite contradictory results, oestrogen-progesterone treatment does not appear to increase the risk of Crohn's disease and there is no convincing evidence that any particular food could be incriminated. In contradiction with a widely believed myth, there is no evidence showing that psychiatric factors have an effect on appearance or aggravation of the disease. Perinatal infection has however been recently shown to affect incidence and subjects born during periods of flu epidemics have a higher relative risk. Still other studies have emphasized the dual role of genetic/environmental factors. Based on current knowledge, the sequence leading to the appearance of Crohn's disease would include one or more perinatal event(s) such as viral infection acting on a genetically susceptible subject and leading to modified immune response in a vulnerable system (perinatal period). Later in life an aggression (environment) would lead to inappropriate immune response. Current research is directed towards identifying infectious agents capable of triggering the disease and on markers of genetic susceptibility.
Colombel
J F
JF
Gower-Rousseau
C
C
D003424:Crohn Disease / Q000453:epidemiology / Q000209:etiology* / Q000235:genetics / Q000382:microbiology; D004927:Escherichia coli Infections / Q000382:microbiology*; D005260:Female; D006801:Humans; D015994:Incidence; D008297:Male; D015995:Prevalence; D012307:Risk Factors; D013290:Streptococcal Infections / Q000382:microbiology*
Etiologie de la maladie de Crohn. Données actuelles.