What is Helicobacter pylori? Helicobacter pylori (H. pylori) is a bacterium that causes chronic inflammation of the inner lining of the stomach (gastritis ) in humans. This bacterium also is considered as a common cause of ulcers worldwide; as many as 90% of people with ulcers have detectable organisms. H. pylori infection is most likely acquired by ingesting contaminated food and water, and through person to person contact. In the United States, about 30% of the adult population is infected (50% of infected persons are infected by the age of 60), but the prevalence of infection is decreasing because there is increasing awareness about the infection, and treatment is common. About 50% of the world population is estimated to have detectable H. pylori in their gastrointestinal tract (GI tract, but stomach, mainly). The infection is more common in crowded living conditions with poor sanitation. In countries with poor sanitation, approximately 90% of the adult population can be infected. Infected individuals usually carry the infection indefinitely (for life) unless they are treated with medications to eradicate the bacterium. One out of every six patients with H. pylori infection may develop ulcers of the duodenum or stomach. H. pylori also is associated with stomach cancer and a rare type of lymphocytic tumor of the stomach called MALT (mucosa-associated lymphoid tissue) lymphoma. In addition, several recent research papers have shown a link between diabetes , infections, elevated hemoglobin A1C levels , and H. pylori. What does H. pylori cause in humans? H. pylori infections start with a person acquiring the bacterium from another person (via either the fecal-oral or oral-oral route). Although the majority of individuals that have these bacteria in their GI tracts have few if any symptoms (see symptoms), most people develop stomach inflammation (gastritis) from the body's response to the bacterium itself and to a cytotoxin termed Vac-A, a chemical that the bacterium produces. Researchers also suggest that the stomach acid stimulates the bacterium in addition to the cytotoxin, and increases invasion of the lining of the stomach, inflammation, and ulcer formation. Other investigators have shown that these bacteria and their products are associated with alterations in the lining cells that are associated with stomach and other cancers, although these are infrequently seen diseases. The frequency of people infected may somehow be related to race. About 60% of Hispanics and about 54% of African Americans have detectable organisms as compared to about 20%-29% of Anglo Americans. In developing countries, children are very commonly infected.
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What is Helicobacter pylori?Helicobacter pylori (H. pylori) is a bacterium that causes chronic inflammation of the inner lining
of the stomach (gastritis) in humans. This bacterium also is considered as a common cause
of ulcers worldwide; as many as 90% of people with ulcers have detectable organisms.
H. pylori infection is most likely acquired by ingesting contaminated food and water, and through
person to person contact. In the United States, about 30% of the adult population is infected
(50% of infected persons are infected by the age of 60), but the prevalence of infection is
decreasing because there is increasing awareness about the infection, and treatment is
common. About 50% of the world population is estimated to have detectable H. pylori in their
gastrointestinal tract (GI tract, but stomach, mainly).
The infection is more common in crowded living conditions with poor sanitation. In countries with
poor sanitation, approximately 90% of the adult population can be infected. Infected individuals
usually carry the infection indefinitely (for life) unless they are treated with medications to
eradicate the bacterium. One out of every six patients with H. pylori infection may develop ulcers
of the duodenum or stomach. H. pylori also is associated with stomach cancer and a rare type of
lymphocytic tumor of the stomach called MALT (mucosa-associated lymphoid tissue) lymphoma.
In addition, several recent research papers have shown a link between diabetes, infections,
elevated hemoglobin A1C levels, and H. pylori.
What does H. pylori cause in humans?H. pylori infections start with a person acquiring the bacterium from another person (via either the
fecal-oral or oral-oral route). Although the majority of individuals that have these bacteria in their
GI tracts have few if any symptoms (see symptoms), most people develop stomach inflammation
(gastritis) from the body's response to the bacterium itself and to a cytotoxin termed Vac-A, a
chemical that the bacterium produces. Researchers also suggest that the stomach acid
stimulates the bacterium in addition to the cytotoxin, and increases invasion of the lining of the
stomach, inflammation, and ulcer formation. Other investigators have shown that these bacteria
and their products are associated with alterations in the lining cells that are associated with
stomach and other cancers, although these are infrequently seen diseases.
The frequency of people infected may somehow be related to race. About 60% of Hispanics and
about 54% of African Americans have detectable organisms as compared to about 20%-29% of
Anglo Americans. In developing countries, children are very commonly infected.
What are the symptoms of H. pylori infections?Most individuals infected with H. pylori have few or no symptoms. They may experience a few
episodes of gastritis (minor belching, bloating, nausea,vomiting, abdominal discomfort), but little
or nothing else. Often, these symptoms simply cease. However, those individuals who have a
more serious infection exhibit symptoms of stomach and duodenal ulcers or gastritis which
include the following:
Abdominal pain and/or discomfort that usually does not wax and wane
Nausea and vomiting sometimes with blood or coffee-ground like vomitus
Dark or tar-like stools (black color of feces due to bleeding ulcers)
Fatigue
Low red blood cell count due to bleeding
Full feeling after a small amount of food; decreased appetite that is more constant
Symptoms of black, tarry stools and fatigue should cause a person to seek medical help or go to
an emergency department to be evaluated for intestinal bleeding.
Is H. pylori contagious?Yes, H. pylori is contagious. However, sometimes there is a grey area between the terms
contagious and colonized. Contagious usually implies a disease-causing agent is transferred
from person to person, while colonization usually implies a non-disease-causing agent simply
populates a body surface but does not cause disease, even when transferred from person to
person. The grey area occurs when many people have the agent that causes disease in some of
them, but not in many others. Some microbiologists consider such organisms as adapting to their
human hosts by slowly changing from infecting humans to colonizing them. Although this is
speculation, it seems to fit the ongoing situation with H. pylori. However, others think the bacteria
become infecting agents when their genes and surrounding environment trigger H. pylori to
produce and release enough toxic chemicals to cause the GI tract to become inflamed.
How is H. pylori infection diagnosed?Accurate and simple tests for the detection of H. pylori infection are available. They include blood
dyspepsia has not been determined, and there is little research in the area. The relationship
between overgrowth and dyspepsia needs to be pursued, however, since many of the symptoms
of dyspepsia are also symptoms of bacterial overgrowth. Overgrowth can be diagnosed by
hydrogen breath testing and is treated primarily with antibiotics.
Other diseases and conditions can aggravate functional diseases, including dyspepsia. Anxiety
and/or depression are probably the most commonly-recognized exacerbating factors for patients
with functional diseases. Another aggravating factor is the menstrual cycle. During their periods,
women often note that their functional symptoms are worse. This corresponds to the time during
which the female hormones, estrogen and progesterone, are at their highest levels. Furthermore,
it has been observed that treating women who have dyspepsia with leuprolide (Lupron), an
injectable drug that shuts off the body's production of estrogen and progesterone, is effective at
reducing symptoms of dyspepsia in premenopausal women. These observations support a role
for hormones in the intensification of functional symptoms.
What is the course of dyspepsia (indigestion)?Dyspepsia is a chronic disease that usually lasts years, if not a lifetime. It does, however, display
periodicity, which means that the symptoms may be more frequent or severe for days, weeks, or
months and then less frequent or severe for days, weeks, or months. The reasons for these
fluctuations are unknown. Because of the fluctuations, it is important to judge the effects of
treatment over many weeks or months to be certain that any improvement is due to treatment
and not simply to a natural fluctuation in the frequency or severity of the disease.
What are the complications of dyspepsia (indigestion)?The complications of functional diseases of the gastrointestinal tract are relatively limited. Since
symptoms are most often provoked by eating, patients who alter their diets and reduce their
intake of calories may lose weight. However, loss of weight is unusual in functional diseases. In
fact, loss of weight should suggest the presence of non-functional diseases. Symptoms that
awaken patients from sleep also are more likely to be due to non-functional than functional
disease.
Most commonly, functional diseases interfere with patients' comfort and daily activities.
Individuals who develop nausea or pain after eating may skip breakfast or lunch because of the
symptoms they experienc. Patients also commonly associate symptoms with specific foods (for
example, milk, fat, vegetables). Whether or not the associations are real, these patients will
restrict their diets accordingly. Milk is the most common food that is eliminated, often
unnecessarily, and this can lead to inadequate intake of calcium andosteoporosis. The
interference with daily activities also can lead to problems with interpersonal relationships,
especially with spouses. Most patients with functional disease live with their symptoms and
infrequently visit physicians for diagnosis and treatment.
How is dyspepsia diagnosed (indigestion)?Dyspepsia is diagnosed primarily on the basis of typical symptoms and the exclusion of non-
(outlet) part of the stomach (the antrum) and the first part of the small intestine (the duodenum).
Pressures are measured with the stomach empty and after a test meal. Abnormally high or low
pressures as well as uncoordinated contractions can be identified. These abnormalities are
believed to be associated with symptoms of dyspepsia. Antro-duodenal motility studies and
expertise in their use are not widely available.
Gallbladder emptying studies
Gallbladder emptying studies determine how well the gallbladder empties. Between meals, the
gallbladder stores bile that is produced by the liver. After meals, the muscles of the gallbladder
contract and squeeze out (empty) most of the bile into the intestine. In the intestine, the bile
assists with the digestion of food.
For a gallbladder emptying study, a radioactive material is injected intravenously. The radioactive
material is removed from the blood by the liver and accumulates with the bile in the gallbladder.
The gallbladder then is stimulated to contract with either a meal or an intravenous injection of a
hormone, called cholecystokinin. A Geiger-counter-like device is placed over the abdomen and
the speed with which the radioactivity leaves the gallbladder and enters the intestine is
monitored. Emptying studies of the gallbladder are widely available since this technology is used
for several purposes other than measurement of gallbladder emptying.
It has been suggested that abnormally slow emptying of the gallbladder may be associated with
abdominal pain. Unfortunately, however, the studies that support the association between slow
gallbladder emptying and symptoms are weak. Moreover, many people have abnormally slow
emptying of the gallbladder but no symptoms. For these reasons, abnormal emptying studies of
the gallbladder have not been widely accepted for diagnosing functional disorders of the
gallbladder. The lack of a clear association between dyspepsia and abnormalities of gallbladder
emptying is important since it means that patients with abnormal emptying may not be improved
by removal of their gallbladders.
How is dyspepsia (indigestion) treated?The treatment of dyspepsia is a difficult and unsatisfying topic because so few drugs have been
studied and have shown to be effective. Moreover, the drugs that have been shown to be useful
have not been substantially effective. This difficult situation exists for many reasons, as follows:
Life-threatening illnesses (for example, cancer, heart disease, andhigh blood pressure)
are the illnesses that capture the public's interest and, more importantly, research funding.
Dyspepsia is not a life-threatening illness and has received little research funding. Because
of the lack of research, an understanding of the physiologic processes (mechanisms) that
are responsible for dyspepsia has been slow to develop. Effective drugs cannot be
developed until there is an understanding of these mechanisms.
Research in dyspepsia is difficult.Dyspepsia is defined by subjective symptoms (such as
pain) rather than objective signs (for example, the presence of an ulcer). Subjective
symptoms are more unreliable than objective signs in identifying homogenous groups of
patients. As a result, groups of patients with dyspepsia who are undergoing treatment are
likely to contain some patients who do not have dyspepsia, which may dilute (negatively
affect) the results of the treatment. Moreover, the results of treatment must be evaluated on
the basis of subjective responses (such as improvement of pain). In addition to being more
unreliable, subjective responses are more difficult to measure than objective responses (for
example, healing of an ulcer).
Different subtypes of dyspepsia (for example, abdominal pain and abdominal bloating)
are likely to be caused by different physiologic processes (mechanisms). It also is possible,
however, that the same subtype of dyspepsia may be caused by different mechanisms in
different people. What's more, any drug is likely to affect only one mechanism. Therefore, it
is unlikely that any one medication can be effective in all-even most-patients with dyspepsia,
even patients with similar symptoms. This inconsistent effectiveness makes the testing of
drugs particularly difficult. Indeed, it can easily result in drug trials that demonstrate no
efficacy (usefulness) when, in fact, the drug is helping a subgroup of patients.
Subjective symptoms are particularly prone to responding to placebos (inactive drugs). In
fact, in most studies, 20% to 40% of patients with dyspepsia will improve if they receive
inactive drugs. Now, all clinical trials of drugs for dyspepsia require a placebo-treated group
for comparison with the drug-treated group. The large placebo response means that these
clinical trials must utilize large numbers of patients to detect meaningful (significant)
differences in improvement between the placebo and drug groups. Therefore, these trials
are expensive to conduct.
The lack of understanding of the physiologic processes (mechanisms) that cause dyspepsia has
meant that treatment usually cannot be directed at the mechanisms. Instead, treatment usually is
directed at the symptoms. For example, nausea is treated with medications that suppress
nausea but do not affect the cause of the nausea. On the other hand, the psychotropic drugs
(antidepressants) and psychological treatments (such as cognitive behavioral therapy) treat
hypothetical causes of dyspepsia (for example, abnormal function of sensory nerves and the
psyche) rather than the symptoms. Treatment for dyspepsia often is similar to that for irritable
bowel syndrome (IBS) even though the causes of IBS and dyspepsia are likely to be different.
Education
It is important to educate patients with dyspepsia about their illness, particularly by reassuring
them that the illness is not a serious threat to their physical health (though it may be to their
emotional health). Patients need to understand the mechanisms (causes) for the symptoms.
Most importantly, they need to understand the medical approach to the problem and the reasons
for each test or treatment. Education prepares patients for a potentially prolonged course of
diagnosis and trials of treatment. Education also may prevent patients from falling prey to the
charlatans who offer unproven and possibly dangerous treatments for dyspepsia. Many
symptoms are tolerable if patients' anxieties about the seriousness of their symptoms can be
relieved. It also helps patients deal with symptoms when they feel that everything that should be
done to diagnose and treat, in fact, is being done. The truth is that psychologically healthy people
can tolerate a good deal of discomfort and continue to lead happy and productive lives.
Diet
Dietary factors have not been well-studied in the treatment of dyspepsia. Nevertheless, patients
often associate their symptoms with specific foods (such as salads and fats). Although specific
foods might worsen the symptoms of dyspepsia, they are not the cause of dyspepsia.
(Intolerance to specific foods, for example, lactose intolerance (milk) and allergies to wheat,
eggs, soy, and milk protein are not considered functional diseases. The common placebo
response in functional disorders such as dyspepsia also may explain the improvement of
symptoms in some people with the elimination of specific foods.
Dietary fiber often is recommended for patients with IBS, but fiber has not been studied in the
treatment of dyspepsia. Nevertheless, it probably is reasonable to treat patients with dyspepsia
with fiber if they also have constipation.
Intolerance to lactose (the sugar in milk) often is blamed for dyspepsia. Since dyspepsia
and lactose intolerance both are common, the two conditions may coexist. In this situation,
restricting lactose will improve the symptoms of lactose intolerance, but will not affect the
symptoms of dyspepsia. Lactose intolerance is easily determined by testing the effects of lactose
(hydrogen breath testing) or trying a strict lactose elimination diet. If lactose is determined to be
responsible for some or all of the symptoms, elimination of lactose-containing foods is
appropriate. Unfortunately, many patients stop drinking milk or eating milk-containing foods
without good evidence that it improves their symptoms. This often is detrimental to their intake of
calcium which may contribute to osteoporosis.
One of the food substances most commonly associated with the symptoms of dyspepsia is fat.
The scientific evidence that fat causes dyspepsia is weak. Most of the support is anecdotal (not
based on carefully done, scientific studies). Nevertheless, fat is one of the most potent influences
on gastrointestinal function. (It tends to slow down the gastrointestinal muscles while it causes
the muscles of the gallbladder to contract.) Therefore, it is possible that fat may worsen
dyspepsia even though it doesn't cause it. Moreover, reducing the ingestion of fat might relieve
symptoms. A strict low fat diet can be accomplished fairly easily and is worth trying. Additionally,
there are other health-related reasons for reducing dietary fat.
Another dietary factor, fructose and fructose-related sugars, has been suggested as a cause of
dyspepsia since many people do not fully digest and absorb them before they reach the distal
intestine. It is diagnosed with a hydrogen breath test using fructose and treated with elimination
of fructose-containing foods from the diet. Unfortunately, fructose and its related sugars are
widespread among fruits and vegetables and are found in high concentrations in many food
products sweetened with corn syrup. Thus, an elimination diet is more difficult to maintain.
Psychotropic drugs
Patients with functional disorders, including dyspepsia, are frequently found to be suffering
from depression and/or anxiety. It is unclear, however, if the depression and anxiety are the
cause or result of the functional disorders or are unrelated to these disorders. (Depression and
anxiety are common and, therefore, their occurrence together with functional disorders may be
coincidental.) Several clinical trials have shown that antidepressants are effective in IBS in
relieving abdominal pain. Antidepressants also have been shown to be effective in unexplained
(non-cardiac) chest pain, a condition thought to represent a dysfunction of the esophagus.
Antidepressants have not been studied adequately in other types of functional disorders,
including dyspepsia. It probably is reasonable to treat patients with dyspepsia with psychotropic
drugs if they have moderate or severe depression or anxiety.
The antidepressants work in dyspepsia and in functional esophageal pain at relatively low doses
that have little or no effect on depression. It is believed, therefore, that these drugs work not by
combating depression, but in different ways (through different mechanisms). For example, these
drugs have been shown to adjust (modulate) the activity of the nerves and to have analgesic
(pain-relieving) effects as well.
Commonly used psychotropic drugs include the tricyclic
antidepressants,desipramine (Norpramine) and trimipramine (Surmontil). Although studies are
encouraging, it is not yet clear whether the newer class of antidepressants, the serotonin-
reuptake inhibitors such as fluoxetine(Prozac), sertraline (Zoloft), and paroxetine (Paxil), are
effective in functional disorders, including dyspepsia.
Psychological treatments
Psychological treatments include cognitive-behavioral therapy, hypnosis, psychodynamic or
interpersonal psychotherapy, and relaxation/stress management. Few studies of psychological
treatments have been conducted in dyspepsia, although more studies have been done in IBS.
Thus, there is little scientific evidence that they are effective in dyspepsia, although there is some
evidence that they are effective in IBS.
Hypnosis has been proposed as an effective treatment for IBS. It is unclear exactly how effective
hypnosis is, or how it works.
Promotility drugs
One of the leading theories for the cause of dyspepsia is abnormalities in the way gastrointestinal
muscles function. The function of muscles may be abnormally increased, abnormally decreased,
or it may by uncoordinated. There are medications, called smooth muscle relaxants, that can
reduce the activity of the muscles and other drugs that can increase the activity of the muscles,
called the promotility drugs.
Many of the symptoms of dyspepsia can be explained on the basis of reduced activity of the
gastrointestinal muscles that results in slowed transport (transit) of food through the stomach and
intestine. (It is clear, as discussed previously, that there are other causes of these symptoms in
addition to slowed transit.) Such symptoms include nausea, vomiting, and abdominal bloating.
When transit is severely affected, abdominal distention (swelling) also may occur and can result
in abdominal pain. (Early satiety is unlikely to be a function of slowed transit because it occurs
too early for slowed transit to have consequences.) Theoretically, drugs that speed up the transit
of food should, in at least some patients, relieve symptoms of dyspepsia that are due to slow
transit.
The number of promotility drugs that are available for use clinically is limited. Studies of their
effectiveness in dyspepsia are even more limited. The most studied drug is cisapride (Propulsid),
a promotility drug that was withdrawn from the market because of serious cardiac side effects.
(Newer drugs that have similar effects but lack the toxicity are being developed.) The few studies
with cisapride for dyspepsia were inconsistent in their results. Some studies demonstrated
benefits whereas others showed no benefit. Cisapride was effective in patients with severe
emptying problems of the stomach (gastroparesis) or severely slowed transit of food through the
small intestine (chronic intestinal pseudo-obstruction). These two diseases may or may not be
related to dyspepsia.
Another promotility drug that is available is erythromycin, an antibiotic that stimulates
gastrointestinal smooth muscle as one of its side effects. Erythromycin is used to stimulate
smooth muscles of the gastrointestinal tract at doses that are lower than those used for treating
infections. There are no studies of erythromycin in dyspepsia, but erythromycin is effective in
gastroparesis and probably also in chronic intestinal pseudo-obstruction.
Metoclopramide (Reglan) is another promotility drug that is available. It has not been studied,
however, in dyspepsia. Moreover, it is associated with some troubling side effects. Therefore, it
may not be a good drug to undergo further testing in dyspepsia.
Domperidone (Motilium) is a promotility drug that is available in the U.S., but requires a special
permit from the US Food and Drug administration. As a result, it is not very commonly
prescribed. It is an effective drug with minimal side effects.
Smooth muscle relaxants
The most widely studied drugs for the treatment of abdominal pain in functional disorders are a
group of drugs called smooth-muscle relaxants.
The gastrointestinal tract is primarily composed of a type of muscle called smooth muscle. (By
contrast, skeletal muscles such as the biceps are composed of a type of muscle called striated
muscle.) Smooth muscle relaxant drugs reduce the strength of contraction of the smooth
muscles but do not affect the contraction of other types of muscles. They are used in functional
disorders, particularly IBS, with the assumption (not proven) that strong or prolonged
contractions of smooth muscles in the intestine-spasms-are the cause of the pain in functional
disorders. There are even smooth muscle relaxants that are placed under the tongue, as
isnitroglycerin for angina, so that they may be absorbed rapidly.
There are not enough studies of smooth muscle relaxants in dyspepsia to conclude that they are
effective at reducing pain. Since their side effects are few, these drugs probably are worth trying.
As with all drugs that are given to control symptoms, patients should carefully evaluate whether
or not the smooth muscle relaxant they are using is effective at controlling the symptoms. If it is
not clearly effective, the option of discontinuing the relaxant should be discussed with a
physician.
Commonly used smooth muscle relaxants are hyoscyamine (Levsin, Anaspaz, Cystospaz,
Donnamar) and methscopolamine (Pamine, Pamine Forte). Other drugs combine smooth muscle
relaxants with a sedativechlordiazepoxide hydrochloride and clidinium bromide (Donnatal,
Librax), but there is no evidence that the addition of sedatives adds to the effectiveness of the
treatment.
What is a reasonable approach to the diagnosis and treatment of dyspepsia (indigestion)?The initial approach to dyspepsia, whether it be treatment or testing, depends on the patient's
age, symptoms and the duration of the symptoms. If the patient is younger than 50 years of age
and serious disease, particularly cancer, is not likely, testing is less important. If the symptoms
are typical for dyspepsia and have been present for many years without change, then there is
less need for testing, or at least extensive testing, to exclude other gastrointestinal and non-
gastrointestinal diseases.
On the other hand, if the symptoms are of recent onset (weeks or months), progressively
worsening, severe, or associated with "warning" signs, then early, more extensive testing is
appropriate. Warning signs include loss of weight, nighttime awakening, blood in the stool or the
material that is vomited (vomitus), and signs of inflammation, such as fever or abdominal
tenderness. Testing also is appropriate if, in addition to symptoms of dyspepsia, there are other
prominent symptoms that are not commonly associated with dyspepsia.
If there are symptoms that suggest conditions other than dyspepsia, tests that are specific for
these diseases should be done first. The reason is that if these other tests disclose other
diseases, it may not be necessary to do additional testing. Examples of such symptoms and
possible testing include:
Vomiting: upper gastrointestinal endoscopy to diagnose inflammatory or obstructing
diseases; gastric emptying studies and/or electrogastrography to diagnose impaired
emptying of the stomach.
Abdominal distention with or without increased flatulence: upper gastrointestinal and
small intestinal x-rays to diagnose obstructing diseases; hydrogen breath testing to
diagnose bacterial overgrowth of the small intestine.
For a patient with typical symptoms of dyspepsia who requires testing to exclude other diseases,
a standard screening panel of blood tests would reasonably be included. These tests might
reveal clues to non-gastrointestinal diseases. Sensitive stool testing (antigen/antibody) for
Giardia lamblia would be reasonable because this parasitic infection is common and can be
acute or chronic. Some physicians do blood testing for celiac disease (sprue), but the value of
doing this is unclear. Moreover, if an EGD is planned, biopsies of the duodenum usually will
make the diagnosis of celiac disease. A plain x-ray of the abdomen might be done during an
episode of abdominal pain (to look for intestinal blockage or obstruction). Testing for lactose
intolerance or a trial of a strict lactose-free diet should be considered. The physician's clinical
judgment should determine the extent to which initial testing is appropriate.
Once testing has been done to an extent that is appropriate for the clinical situation, it is
reasonable to first try a therapeutic trial of stomach acid suppression to see if symptoms improve.
Such a trial probably should involve a PPI (proton pump inhibitor) for 8 to 12 weeks. If there is no
clear response of symptoms, the options then are to discontinue the PPI or confirm its
effectiveness in suppressing acid with 24 hour acid testing. If there is a clear and substantial
decrease in symptoms with the PPI, then decisions need to be made about continuing acid
suppression and which drugs to use.
Another therapeutic approach is to test for Helicobacter pylori infection of the stomach (with
blood, breath or stool tests) and to treat patients with infection to eradicate the infection. It may
be necessary to retest patients after treatment to prove that treatment has effectively eradicated
the infection, particularly if dyspeptic symptoms persist after treatment.
If treatment with a PPI has satisfactorily suppressed acid according to acid testing (or acid
suppression has not been measured) and yet the symptoms have not improved, it is reasonable
to conduct further testing as described above. Esophago-gastro-duodenoscopy, or EGD, (and,
possibly, colonoscopy) would be the next consideration, probably with multiple biopsies of the
stomach and duodenum (and colon if colonoscopy is done). Finally, small intestinal x-rays and
an ultrasound examination of the gallbladder might be done. An abdominal ultrasound
examination, CT scan, or MRI scan can exclude non-gastrointestinal diseases. Once appropriate
testing has been completed, empiric trials of other drugs (for example, smooth muscle relaxants,
psychotropic drugs, and promotility drugs) can be done. (An empiric trial of a drug is a trial that is
not based on an understanding of the exact cause of the symptoms)
If all of the appropriate testing reveals no disease that could be causing the symptoms and the
dyspeptic symptoms have not responded to empiric treatments, other, more specialized tests
should be considered. These tests include hydrogen breath testing to diagnose bacterial
overgrowth of the small intestine, gastric emptying studies, EGG, small intestinal transit studies,
and antro-duodenal motility and barostatic studies. These specialized studies probably should be
done at centers that have experience and expertise in diagnosing and treating functional
diseases.
What is in the future for dyspepsia (indigestion)?The future of dyspepsia will depend on our increasing knowledge of the processes (mechanisms)
that cause dyspepsia. Acquiring this knowledge, in turn, depends on research funding. Because
of the difficulties in conducting research in dyspepsia, this knowledge will not come quickly. Until
we have an understanding of the mechanisms of dyspepsia, newer treatments will be based on
our developing a better 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. Examples of experimental drugs for intestinal
neurotransmission aresumatriptan (Imitrex) and buspirone(Buspar). These drugs are believed to
reduce the responsiveness (sensitivity) of the sensory nerves to what's happening in the intestine
by attaching to a particular 5-HT receptor, the 5-HT1 receptor. The 5-HT1 receptor drugs,
however, have received only minimal study so far and their role in the treatment of dyspepsia, if
any, is unknown.
Promotility drugs similar to cisapride, as previously discussed, are being pursued actively.
Dyspepsia (Indigestion) At A Glance Dyspepsia is a functional disease in which the gastrointestinal organs, primarily the stomach
and first part of the small intestine, function abnormally. It is a chronic disease in which the
symptoms fluctuate in frequency and intensity.
Theories of the cause of dyspepsia include abnormal input from intestinal sensory nerves,
abnormal processing of input from the sensory nerves, and abnormal stimulation of the
intestines by motor nerves.
The primary symptoms of dyspepsia are upper abdominal pain, belching, nausea, vomiting,
abdominal bloating, early satiety, and abdominal distention (swelling). The symptoms most
often are provoked by eating.
Dyspepsia is diagnosed on the basis of typical symptoms and the absence of other
gastrointestinal diseases, particularly acid-related diseases and non-gastrointestinal
diseases that might give rise to the symptoms.
Testing in dyspepsia is directed primarily at excluding the presence of other gastrointestinal
diseases and non-gastrointestinal diseases. Some patients may require specific testing of
certain gastrointestinal functions.
Treatment in dyspepsia is primarily with education as well as smooth muscle relaxant and
promotility drugs. There also may be a role for anti-depressant drugs and dietary changes.
Future advances in the treatment of dyspepsia depend on a clearer understanding of its