Smoking, the oral contraceptive pill, and Crohn's disease

Wakefield, AJ; Sawyerr, A. M.; Hudson, Mark; Dhillon, A. P.; Pounder, RE

doi:10.1007/bf01297463

Cited by 69 publications

(33 citation statements)

References 44 publications

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“…Interestingly, one of the effects of cigarette smoking is to increase platelet aggregation [44]. It also reduces endothelial prostacyclin synthesis, which normally combats platelet aggregation.…”

Section: Blood Viscositymentioning

confidence: 98%

“…Furthermore, the persistence of the raised serum fibrinogen with disease remission appears to be disease specific [43]. Interestingly, the oral contraceptive pill also increases fibrinogen levels along with other coagulation factors [44]. Prolonged and/or current use of the oral contraceptive pill increases the relative risk of Crohn's disease by four to eight times [45].…”

Section: Blood Viscositymentioning

confidence: 99%

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Crohn's disease: in defense of a microvascular aetiology

Thornton

Solomon

2002

Int J Colorectal Dis

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Proving cause and effect will always be a difficult task given the self-perpetuating nature of the inflammatory and coagulation cascades and our inability at present to identify persons who subsequently develop Crohn's disease at a point prior to mucosal inflammation. Results to date however, are supportive of each of these factors, alone or in combination playing an integral part in the development of microvascular ischaemia, a pathological process which appears to precede the classic changes which characterize Crohn's disease.

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Section: Blood Viscositymentioning

confidence: 98%

Section: Blood Viscositymentioning

confidence: 99%

Crohn's disease: in defense of a microvascular aetiology

Thornton

Solomon

2002

Int J Colorectal Dis

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“…Smoking, a known adult risk factor, may be an important modifiable risk factor in the adolescent population. 40 Evidence suggests that passive smoking is a disease modifier in terms of risk for surgery in IBD, 41 but its effects on TE are as yet unknown. In a small number of selected patients with additional risk factors such as significant family history of TE, formal thrombophilia screening at diagnosis may be warranted.…”

mentioning

confidence: 99%

Cerebral thromboembolic events in pediatric patients with inflammatory bowel disease

Barclay

Keightley

Horrocks

et al. 2010

Inflammatory Bowel Diseases

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“…The relative risk of CD in women taking oral contraceptives is about twice that of controls, although there is no direct evidence for a causative relationship [83,84,85,86]. …”

Section: Diet and Food Additivesmentioning

confidence: 99%

Interaction between Susceptibility and Environment: Examples from the Digestive Tract

Rogler¹

2011

Dig Dis

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During the last few years a significant advance has been achieved in the understanding of the pathogenesis of inflammatory bowel disease (IBD). From twin studies it was evident that there is more that 50% concordance of Crohn’s disease (CD) in monozygotic twin pairs, however it is only 3.6% among dizygotic twins. These data indicate that the genetic background may be responsible for 50% of the risk or ‘susceptibility’ to develop CD. Obviously it is not a sufficient condition as otherwise there would be 100% concordance of disease in monozygotic twin pairs. Environmental factors as well must play an important role. This is further supported by the fact that there is only low development in genetic risk factors over ten thousands of years. In contrast, the incidence of CD and ulcerative colitis (UC) has dramatically increased in Western countries in the last 100 years. This further supports the concept of a ‘Western lifestyle factor(s)’ that triggers chronic intestinal inflammation in a genetically susceptible host. The proof of the concept of a genetic susceptibility was achieved in 2001 with the discovery that NOD2 is the most important susceptibility gene for CD. The function of NOD2 has been investigated in detail. NOD2 is an intracellular ‘alarm button’, a receptor recognizing invading bacteria that entered the mucosal wall. NOD2 mutants associated with susceptibility to CD seem to be deficient in their recognition of bacterial wall products. In a genome-wide association study a disease association was found in the autophagy-related 16-like 1 gene (ATG16L1). The ATG16L1 gene encodes a protein in the autophagosome pathway that processes intracellular bacteria. Based on these findings, CD is now discussed as an impaired and inadequate immune reaction to the gut bacteria which are a part of our environment (or perhaps ‘in-vironment’). In addition to NOD2 and ATG16L1, there are more ‘innate’ pathways by which commensal and pathogenic bacteria can directly interact with cells of the intestinal mucosa. The ‘environment concept’ and the ‘genetic concept’ of IBD pathophysiology are converging. With the finding that most susceptibility genes for CD and UC are involved in innate immune mechanisms and the primary defense against bacteria entering the mucosa, for the first time a unifying concept of the ‘genetic pathophysiology hypothesis’ and the ‘environment pathophysiology hypothesis’ of IBD was possible. Bacteria are the link between the environment and mucosal defense system.

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Smoking, the oral contraceptive pill, and Crohn's disease

Cited by 69 publications

References 44 publications

Crohn's disease: in defense of a microvascular aetiology

Crohn's disease: in defense of a microvascular aetiology

Cerebral thromboembolic events in pediatric patients with inflammatory bowel disease

Interaction between Susceptibility and Environment: Examples from the Digestive Tract

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