Irritable Bowel Syndrome (cont.)
What is in the future for IBS?
The future of IBS depends on our increasing knowledge of the processes
(mechanisms) that cause IBS. Acquiring this knowledge, in turn, depends on
research funding. Because of the difficulties in conducting research in IBS,
this knowledge will not come quickly. Until we have an understanding of the
mechanisms of IBS, newer treatments will be based on our developing
understanding of the normal control of gastrointestinal function, which is
proceeding more rapidly. Specifically, there is intense interest in intestinal
neurotransmitters, which are chemicals that the nerves of the intestine use to
communicate with each other. The interactions of these neurotransmitters are
responsible for adjusting (modulating) the functions of the intestines, such as
contraction of muscles and secretion of fluid and mucus.
5-hydroxytriptamine (5-HT or serotonin) is a neurotransmitter that stimulates
several different receptors on nerves in the intestine, including one called the
5-HT4 receptor. Stimulation of these receptors by 5-HT increases muscle
contractions in the colon. An example of an experimental drug that affects
intestinal neurotransmission is tegaserod. This drug mimics the effect of 5-HT
on the 5-HT4 receptor. Thus, because it increases intestinal muscle
contractions, tegaserod is being tested for effectiveness in treating
constipation-predominant IBS as well as constipation in general.
Another drug that affects neurotransmission is ondansetron. This drug blocks
a different receptor, the 5-HT3 receptor, and thereby reduces colonic
contractions. Thus, ondansetron (Zofran) has been effective in treating
diarrhea-predominant IBS in initial studies. There are drugs that stimulate
another receptor, the 5-HT1 receptor. Examples of this type of drug are
sumatriptan (Imitrex) and
buspirone. These drugs are
believed to reduce the responsiveness (sensitivity) of the sensory nerves to
what's happening in the intestine. The 5-HT1 receptor stimulators, however, have
not yet been tested for effectiveness in IBS. Finally, in preliminary studies,
fedotozine has been shown to improve functional gastrointestinal symptoms. The
mechanism of action of fedotozine is not known, but it also may act by reducing
the sensitivity of the sensory nerves.
Finally, there is the issue of a relationship between IBS and intestinal
bacteria. Over the next few years, much information will accumulate on this
potential relationship.
- IBS is a functional disease, that is, a disease in
which the intestine (bowel) functions abnormally.
- Theories of the cause of IBS include abnormal input
from intestinal sensory nerves, abnormal processing of input from the sensory
nerves, and abnormal stimulation of the intestines by the motor nerves.
- The primary symptoms of IBS are constipation,
diarrhea, and abdominal pain. Secondary symptoms include abnormal passage of
stool, abnormal form of stool, increased amounts of mucus in the stool, and a
subjective feeling of abdominal distention (bloating).
- IBS is diagnosed on the basis of typical symptoms
(Rome II Criteria) and the absence of other intestinal and non-intestinal
diseases that might give rise to the symptoms. Testing in IBS is directed
primarily at excluding the presence of other intestinal diseases and
non-intestinal diseases.
- Treatment of IBS consists primarily of medications to
control constipation, diarrhea, and abdominal pain. Anti-depressant medication
and psychological treatments also may be used. It is not clear if dietary
alterations have much effect on the symptoms of IBS except for increases in
dietary fiber, which may improve constipation.
- Although it has been hypothesized that IBS may be
caused by intestinal bacteria, specifically by small intestinal bacterial
overgrowth, there is little rigorous scientific support for the hypothesis.
- Future advances in the treatment of IBS depend on a clearer
understanding of its cause(s).
Last Editorial Review: 4/2/2007
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