Tobacco and Public Health - TCSC Indonesia

ALLAN HACKSHAW 595
several mechanisms have been proposed. Smoking affects factors that can promote the
development of ulcers, for example by increasing gastric secretions such as pepsin and
causing the reflux of contents in the duodenum back into the stomach. It also has a
detrimental effect on the defensive mechanisms in the gastroduodenal mucosa, which in
the absence of smoking would aid ulcer healing. There have been several reviews on this
topic, for example, see Ashley (1997), Eastwood (1997), Parasher and Eastwood (2000).
However, with the recent discovery of the micro-organism Helicobacter pylori as an
important cause of peptic ulcer, it is possible that the effect of smoking as an independent
risk factor is less than originally thought. It is proposed that smokers are only
more susceptible to H. pylori infection and that smoking enhances the adverse effects of
the infection (Parasher and Eastwood 2000). Furthermore, there is evidence that once
the infection has been eradicated, smoking has little or no effect on ulcer development
or recurrence (Marshall et al. 1988; Borody et al. 1992; O’Connor et al. 1995; Chan et al.
1997; Kadayifci et al. 1997). Whatever the true mechanism may be, smoking is an
important risk factor, either by causing some ulcers directly or indirectly by leading to
H. pylori infection.
Inflammatory bowel disease
It is well documented that smoking increases the risk of Crohn’s disease but decreases
the risk of ulcerative colitis, and this has been consistent between studies, most of
which have been case–control studies. Table 34.3 shows the results of these studies,
including two cohort studies which allowed for oral contraceptive use (associated with
both smoking and inflammatory bowel disease, Vessey et al. 1986). Current smokers
have about half the risk of ulcerative colitis compared to never-smokers and more than
twice the risk of Crohn’s disease, though the risk is higher in women than in men
(Table 34.4). It is estimated that about one-third of all cases of Crohn’s disease could be
attributed to smoking (Logan 1990). In ex-smokers, whilst the risk for Crohn’s disease
is lower than that in current smokers (former vs. never; relative risk 1.5, 95% CI
1.1–1.9 and current vs. never; relative risk 2.4, 95% CI 2.0–2.9), the association with
ulcerative colitis is unclear; there seems to be an increased risk. The pooled result in the
eight case–control studies is 1.9 (95% CI 1.6–2.3) and it is similarly raised, though not
so greatly, in the cohort study by Vessey et al. 1986 (relative risk 1.25). If similar results
are found in further cohort studies it would indicate that the timing of smoking plays
some part in the development of ulcerative colitis.
The biological mechanism for inflammatory bowel disease and its association with
smoking are not yet fully understood, and it is still unclear why current smoking would
have opposite effects on these two disorders, that is, it seems to promote Crohn’s
disease but protect against ulcerative colitis. Nicotine (in the form of patches or chewing
gum) has been proposed as a possible treatment for ulcerative colitis though its effectiveness
remains to be confirmed. Reviews of smoking and inflammatory bowel disease
can be found in Ashley (1997), Logan (1990), and Rubin and Hanauer (2000).