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

antibody tests, urea breath tests, stool antigen tests, and endoscopic biopsies.

Blood tests for the presence of antibodies to H. pylori can be performed easily and rapidly.

However, blood antibodies can persist for years after complete eradication of H. pylori with

antibiotics. Therefore, blood antibody tests may be good for diagnosing infection, but they are not

good for determining if antibiotics have successfully eradicated the bacterium.

The urea breath test (UBT) is a safe, easy, and accurate test for the presence of H. pylori in the

stomach. The breath test relies on the ability ofH. pylori to break down the naturally occurring

chemical, urea, into carbon dioxide which is absorbed from the stomach and eliminated from the

body in the breath. Ten to 20 minutes after swallowing a capsule containing a minute amount of

radioactive urea, a breath sample is collected and analyzed for radioactive carbon dioxide. The

presence of radioactive carbon dioxide in the breath (a positive test) means that there is active

infection. The test becomes negative (there is no radioactive carbon dioxide in the breath) shortly

after eradication of the bacterium from the stomach with antibiotics. Since some individuals are

concerned about even minute amounts of radioactivity the breath test has been modified so that

it also may be performed with urea that is not radioactive.

Endoscopy is an accurate test for diagnosing H. pylori as well as the inflammation and ulcers that

it causes. For endoscopy, the doctor inserts a flexible viewing tube (endoscope) through the

mouth, down the esophagus, and into the stomach and duodenum. During endoscopy, small

tissue samples (biopsies) from the stomach lining can be removed. A biopsy specimen is placed

on a special slide containing urea (for example, CLO test slides). If the urea is broken down by H.

pylori in the biopsy, there is a change in color around the biopsy on the slide. This means that

there is an infection with H. pylori in the stomach.

Biopsies also may be cultured in the bacteriology laboratory for the presence of H. pylori;

however, this is done infrequently since other simpler tests are available.

A recently-developed test for H. pylori is a test in which the presence of the bacterium can be

diagnosed with a sample of stool. The test uses an antibody to H. pylori to determine if H.

pylori is present in the stool. If it is, it means that H. pylori is infecting the stomach. Like the urea

breath test, in addition to diagnosing infection with H. pylori, the stool test can be used to

determine if eradication has been effective shortly after treatment.

In 2012, the FDA gave approval for the urea breath test to be done in children aged 3 years to 17

years old.

Why treat H. pylori?Chronic infection with H. pylori weakens the natural defenses of the lining of the stomach to the

ulcerating action of acid. Medications that neutralize stomach acid (antacids), and medications

that decrease the secretion of acid in the stomach (H2-blockers and proton pump inhibitors or

PPIs) have been used effectively for many years to treat ulcers.

H2-blockers include

ranitidine  (Zantac),

famotidine  (Pepcid),

cimetidine  (Tagamet), and

nizatidine  (Axid).

PPIs include

omeprazole  (Prilosec),

lansoprazole  (Prevacid),

rabeprazole  (Aciphex),

pantoprazole  (Protonix), and

esomeprazole  (Nexium).

Antacids, H2-blockers and PPIs, however, do not eradicate H. pylori from the stomach, and

ulcers frequently return promptly after these medications are discontinued. Hence, antacids, H2-

blockers or PPIs have to be taken daily for many years to prevent the return of the ulcers and the

complications of ulcers such as bleeding, perforation, and obstruction of the stomach. Even such

long-term treatments can fail. Eradication of H. pylori, however, usually prevents the return of

ulcers and ulcer complications even after appropriate medications such as PPIs are stopped.

Eradication of H. pylori also is important in the treatment of the rare condition known as MALT

lymphoma of the stomach. Treatment of H. pylori to prevent stomach cancer is controversial and

discussed later in this article.

What is the treatment for H. pylori?H. pylori is difficult to eradicate from the stomach because it is capable of developing resistance

to commonly used antibiotics. Therefore, two or more antibiotics usually are given together with a

PPI and/or bismuth containing compounds to eradicate the bacterium. (Bismuth and PPIs have

anti-H. pylori effects.) Examples of combinations of medications that are effective are:

a PPI, amoxicillin (Amoxil) andclarithromycin (Biaxin)

a PPI, metronidazole (Flagyl),tetracycline and bismuth subsalicylate(Pepto-Bismol, Bismuth)

These combinations of medications can be expected to cure 70% to 90% of infections. However,

studies have shown that resistance of H. pylori (failure of antibiotics to eradicate the bacterium)

to clarithromycin is common among patients who have prior exposure to clarithromycin or other

chemically similar macrolide antibiotics (such as erythromycin). Similarly, H. pyloriresistance to

metronidazole is common among patients who have had prior exposure to metronidazole. In

these patients, doctors have to find other combinations of antibiotics to treat the H.

pylori. Antibiotic resistance is another reason why antibiotics should be used carefully and

judiciously for the right reasons, and indiscriminate use of antibiotics for improper reasons should

be discouraged. First-line regimens for Helicobacter pylorieradication are taken from the

guidelines developed by the American College of Gastroenterology as follows:

1. Standard dose of a *PPI (proton pump inhibitor) *b.i.d. (esomeprazole is *q.d.),

clarithromycin 500 mg b.i.d., amoxicillin 1,000 mg b.i.d. for 10-14 days

2. Standard dose PPI b.i.d., clarithromycin 500 mg b.i.d. metronidazole 500 mg b.i.d. for 10-14

days

3. Bismuth subsalicylate 525 mg p.o. q.i.d. metronidazole 250 mg * p.o. *q.i.d., tetracycline 500

mg p.o. q.i.d., ranitidine 150 mg p.o. b.i.d. or standard dose PPI q.d. to b.i.d. for 10-14 days

4. PPI + amoxicillin 1 g b.i.d., for 5 days, followed by PPI, clarithromycin 500 mg, tinidazole

500 mg b.i.d. for 5 days (used mainly in other countries)

*PPI = proton pump inhibitor; pcn = penicillin; p.o. = orally; q.d. = daily; b.i.d. = twice daily; t.i.d. =

three times daily; q.i.d. = four times daily.

Some doctors may want to confirm eradication of H. pylori after treatment with a urea breath test

or a stool antigen test, particularly if there have been serious complications of the infection such

as perforation or bleeding in the stomach or duodenum. Endoscopic biopsies to determine

eradication of the bacterium are not necessary, and blood tests are not good for determining

eradication since it takes many months for the antibodies to H. pylori to decrease. The best tests

for determining eradication are the breath and stool tests discussed previously. Patients who fail

to eradicate H. pylori with treatment are retreated, often with a different combination of

medications.

Who should receive treatment forH. pylori?There is a general consensus among doctors that patients should be treated if they are infected

with H. pylori and have ulcers. The goal of treatment is to eradicate the bacterium, heal the

ulcers, and prevent the ulcers' return. Patients with MALT lymphoma of the stomach also should

be treated. MALT lymphoma is rare, but the tumor often quickly regresses upon successful

eradication of H. pylori.

There currently is no formal recommendation to treat patients infected with H. pylori without ulcer

disease or MALT lymphoma. Since antibiotic combinations can have side effects, and stomach

cancers are infrequent in the United States, it is felt that the risks of treatment to eradicate H.

pylori in patients without symptoms or ulcers may not justify the unproven benefits of treatment

for the purpose of preventing stomach cancer. On the other hand, H. pylori infection is known to

cause atrophic gastritis (chronic inflammation of the stomach leading to atrophy of the inner lining

of the stomach). Some physicians believe that atrophic gastritis can lead to cell changes

(intestinal metaplasia) that can be precursors to stomach cancer. Studies have also shown that

eradication of H. pylori may reverse atrophic gastritis. Thus, some doctors are recommending

treatment of ulcer- and symptom-free patients infected with H. pylori.

Many physicians believe that dyspepsia (non-ulcer symptoms associated with meals) may be

associated with infection with H. pylori. Although it is not clear if H. pylori causes the dyspepsia,

many physicians will test patients with dyspepsia for infection with H. pylori and treat them if

infection is present.

Scientists studying the genetics of H. pylori have found different strains (types) of the bacterium.

Some strains of H. pylori appear to be more prone to cause ulcers and stomach cancer. Further

research in this area may help doctors to intelligently select those patients who need treatment.

Vaccination against H. pylori is unlikely to be available in the near future.

Can H. pylori infections be prevented?With at least 50% of the world population with detectable H. pylori in their stomachs, it seems

likely that with no vaccine available, it will be very difficult or impossible for people to have no

exposure to these bacteria. The chance of the organisms causing symptomatic infection is low,

but certainly not absent. Currently, suggestions have been made to prevent ulcers, but the

effectiveness of these recommendations are unknown. The following is a list of

recommendations to help prevent ulcers:

reduce or stop the intake of alcohol

stop smoking

substitute acetaminophen (Tylenol and others) for aspirin for pain control

substitute acetaminophen or other drugs for nonsteroidal anti-inflammatory drugs (NSAIDs)

avoid caffeine in coffee and many "power" drinks

check for GI symptoms and treat immediately during or after radiation therapy

identify and reduce or avoid stress

wash hands with uncontaminated water to avoid contracting the bacterium

if infected with H. pylori, antimicrobial treatment may avoid ulcer formation and extension of

disease

Currently, there is no commercially available vaccine to prevent either infection or colonization of

the stomach by H pylori. However, research is ongoing, and the NIH is funding vaccine studies in

conjunction with vaccine makers (For example, Helicovax to prevent H. pylori colonization of

human GI tracts by EpiVax, Inc.).

What is the prognosis for H. pyloriinfections?Many infections are mild and produce few, if any, symptoms. The prognosis of these infections is

excellent. Patients with more serious symptoms that are treated appropriately usually have a

good prognosis although up to 20% may have reoccurrence of the infection. Those with ulcers

who have effective eradication of their infection heal their ulcers well (with usually minor scarring

in the tissue).

Untreated and severe infections have a more guarded prognosis because extensive damage can

occur with bleeding, scarring,anemia, and hypotension (low blood pressure) occurring. Some

patients with these symptoms will die if not treated quickly.

REFERENCES: 

Cancer.gov. Helicobacter pylori and Cancer. 

Chey, W, Wong, B and the Practice Parameters Committee of the American College of

Gastroenterology, American College of Gastroenterology Guideline on the Management

of Helicobacter pylori Infection, Amer. J. Gastro, 102:1808-1825, 2007 

FDA.gov. FDA approves first Helicobacter pylori breath test for children.

Reviewed by Jay W. Marks, MD on 5/17/2012

http://www.medicinenet.com/helicobacter_pylori/article.htm

What is dyspepsia (indigestion)?Dyspepsia is one of the most common ailments of the bowel (intestines), affecting an estimated

20% of persons in the United States. Perhaps only 10% of those affected actually seek medical

attention for their dyspepsia. Dyspepsia is not a particularly good term for the ailment since it

implies that there is "dyspepsia" or abnormal digestion of food, and this most probably is not the

case. In fact, another common name for dyspepsia is indigestion, which, for the same reason, is

no better than the term dyspepsia! Doctors frequently refer to the condition as non-ulcer

dyspepsia.

Dyspepsia (indigestion) is best described as a functional disease. (Sometimes, it is called

functional dyspepsia.) The concept of functional disease is particularly useful when discussing

diseases of the gastrointestinal tract. The concept applies to the muscular organs of the

gastrointestinal tract-esophagus, stomach, small intestine, gallbladder, and colon. What is meant

by the term, functional, is that either the muscles of the organs or the nerves that control the

organs are not working normally, and, as a result, the organs do not function normally, and the

dysfunction causes the symptoms. The nerves that control the organs include not only the nerves

that lie within the muscles of the organs but also the nerves of the spinal cord and brain.

Some gastrointestinal diseases can be seen and diagnosed with the naked eye, such as ulcers

of the stomach. Thus, ulcers can be seen at surgery, on X-rays, and by endoscopy. Other

diseases cannot be seen with the naked eye but can be seen and diagnosed under the

microscope. For example,gastritis (inflammation of the stomach) can be diagnosed by

microscopic examination of biopsies of the stomach. In contrast, gastrointestinal functional

diseases cannot be seen with the naked eye or with the microscope. In some instances, the

abnormal function can be demonstrated by tests (for example, gastric emptying studies or antro-

duodenal motility studies). However, the tests often are complex, are not widely available, and do

not reliably detect the functional abnormalities. Accordingly, and by default, functional

gastrointestinal diseases are those that involve abnormal function of gastrointestinal organs in

which the abnormalities cannot be seen in the organs with either the naked eye or the

microscope.

Occasionally, diseases that are thought to be functional are ultimately found to be associated

with abnormalities that can be seen. Then, the disease moves out of the functional category. An

example of this would beHelicobacter pylori (H. pylori) infection of the stomach. Some patients

with mild upper gastrointestinal symptoms who were thought to have abnormal function of the

stomach or intestines have been found to have stomachs infected with H. pylori. This infection

can be diagnosed under the microscope by identifying the bacterium. When patients are treated

with antibiotics, the H. pylori and symptoms disappear. Thus, recognition of infections

with Helicobacter pylori has removed some patients' systems from the functional disease

category.

The distinction between functional disease and non-functional disease may, in fact, be blurry.

Thus, even functional diseases probably have associated biochemical or molecular abnormalities

that ultimately will be able to be measured. For example, functional diseases of the stomach and

intestines may be shown ultimately to be associated with reduced or increased levels of normal

chemicals within the gastrointestinal organs, the spinal cord, or the brain. Should a disease that

is demonstrated to be due to a reduced or increased chemical still be considered a functional

disease? In this theoretical situation, we can't see the abnormality with the naked eye or the

microscope, but we can measure it. If we can measure an associated or causative abnormality,

should the disease no longer be considered functional, even though the disease (symptoms) are

being caused by abnormal function? The answer is unclear.

Despite the shortcomings of the term, functional, the concept of a functional abnormality is useful

for approaching many of the symptoms originating from the muscular organs of the

gastrointestinal tract. To repeat, this concept applies to those symptoms for which there are no

associated abnormalities that can be seen with the naked eye or the microscope.

While dyspepsia is a major functional disease(s), it is important to mention several other

functional diseases. A second major functional disease is theirritable bowel syndrome, or IBS.

The symptoms of IBS are thought to originate primarily from the small intestine and/or colon. The

symptoms of IBS include abdominal pain that is accompanied by alterations in bowel movements

(defecation), primarily constipation or diarrhea. In fact, dyspepsia and IBS may be overlapping

diseases since up to half of patients with IBS also have symptoms of dyspepsia. A third distinct

functional disorder is non-cardiac chest pain. This pain may mimic heart pain (angina), but it is

unassociated with heart disease. In fact, non-cardiac chest pain is thought to result from a

functional abnormality of the esophagus.

Functional disorders of the gastrointestinal tract often are categorized by the organ of

involvement. Thus, there are functional disorders of the esophagus, stomach, small intestine,

colon, and gallbladder. The amount of research that has been done with functional disorders is

greatest in the esophagus and stomach (for example, non-cardiac chest pain, dyspepsia),

perhaps because these organs are easiest to reach and study. Research into functional

disorders affecting the small intestine and colon (IBS) is more difficult to conduct and there is

less agreement among the research studies. This probably is a reflection of the complexity of the

activities of the small intestine and colon and the difficulty in studying these activities. Functional

diseases of the gallbladder (referred to as biliary dyskinesia), like those of the small intestine and

colon, also are more difficult to study, and at present they are less well-defined. Each of the

functional diseases is associated with its own set of characteristic symptoms.

What are the symptoms of dyspepsia (indigestion)?We usually think of symptoms of dyspepsia as originating from the upper gastrointestinal tract,

primarily the stomach and first part of the small intestine. These symptoms include:

upper abdominal pain  (above the navel),

belching ,

nausea  (with or without vomiting),

abdominal bloating  (the sensation of abdominal fullness without objective distention),

early satiety (the sensation of fullness after a very small amount of food), and,

 abdominal distention (swelling as opposed to bloating).

The symptoms most often are provoked by eating, which is a time when many different

gastrointestinal functions are called upon to work in concert. This tendency to occur after meals

is what gave rise to the notion that dyspepsia might be caused by an abnormality in the digestion

of food.

It is appropriate to discuss belching in detail since it is a commonly misunderstood symptom

associated with dyspepsia. The ability to belch is almost universal. Belching, also known as

burping or eructating, is the act of expelling gas from the stomach out through the mouth. The

usual cause of belching is a distended (inflated) stomach that is caused by swallowed air or gas.

The distention of the stomach causes abdominal discomfort, and the belching expels the air and

relieves the discomfort. The common reasons for swallowing large amounts of air (aerophagia)

or gas are gulping food or drink too rapidly, anxiety, and carbonated beverages. People often are

unaware that they are swallowing air. Moreover, if there is not excess air in the stomach, the act

of belching actually may cause more air to be swallowed. "Burping" infants during bottle

or breastfeeding is important in order to expel air in the stomach that has been swallowed with

the formula or milk.

Excessive air in the stomach is not the only cause of belching. For some people, belching

becomes a habit and does not reflect the amount of air in their stomachs. For others, belching is

a response to any type of abdominal discomfort and not just to discomfort due to increased gas.

Everyone knows that when they have mild abdominal discomfort, belching often relieves the

problem. This is because excessive air in the stomach often is the cause of mild abdominal

discomfort; as a result, people belch whenever mild abdominal discomfort is felt-whatever the

cause.

If the problem causing the discomfort is not excessive air in the stomach, then belching does not

provide relief. As mentioned previously, it even may make the situation worse by increasing air in

the stomach. When belching does not ease the discomfort, the belching should be taken as a

sign that something may be wrong within the abdomen and that the cause of the discomfort

should be sought. Belching by itself, however, does not help the physician determine what may

be wrong because belching can occur in virtually any abdominal disease or condition that causes

discomfort.

What causes dyspepsia (indigestion)?It's not surprising that many gastrointestinal diseases have been associated with dyspepsia.

However, many non-gastrointestinal diseases also have been associated with dyspepsia.

Examples of the latter include diabetes, thyroid disease,hyperparathyroidism (overactive

parathyroid glands), and severe kidney disease. It is not clear, however, how these non-

gastrointestinal diseases might cause dyspepsia. A second important cause of dyspepsia is

drugs. It turns out that many drugs are frequently associated with dyspepsia, for

example, nonsteroidal anti-inflammatory drugs (NSAIDs such asibuprofen), antibiotics,

and estrogens). In fact, most drugs are reported to cause dyspepsia in at least some patients.

As discussed previously, most dyspepsia (not due to non-gastrointestinal diseases or drugs) is

believed to be due to abnormal function of the muscles of the organs of the gastrointestinal tract

or the nerves controlling the organs. The nervous control of the gastrointestinal tract, however, is

complex. A system of nerves runs the entire length of the gastrointestinal tract from the

esophagus to the anus in the muscular walls of the organs. These nerves communicate with

other nerves that travel to and from the spinal cord. Nerves within the spinal cord, in turn, travel

to and from the brain. (The gastrointestinal tract is exceeded in the numbers of nerves it contains

only by the spinal cord and brain.) Thus, abnormal function of the nervous system in dyspepsia

might occur in a gastrointestinal muscular organ, the spinal cord, or the brain.

The nervous system controlling the gastrointestinal organs, as with most other organs, contains

both sensory and motor nerves. The sensory nerves continuously sense what is happening

(activity) within the organ and relay this information to nerves in the organ's wall. From there,

information can be relayed to the spinal cord and brain. The information is received and

processed in the organ's wall, the spinal cord, or the brain. Then, based on this sensory input

and the way the input is processed, commands (responses) are sent to the organ over the motor

nerves. Two of the most common motor responses in the intestine are contraction or relaxation

of the muscle of the organ and secretion of fluid and/or mucus into the organ.

As already mentioned, abnormal function of the nerves of the gastrointestinal organs, at least

theoretically, might occur in the organ, spinal cord, or brain. Moreover, the abnormalities might

occur in the sensory nerves, the motor nerves, or at processing centers in the intestine, spinal

cord, or brain.

Some researchers argue that the cause of functional diseases is abnormalities in the function of

sensory nerves. For example, normal activities, such as stretching of the small intestine by food,

may give rise to sensory signals that are sent to the spinal cord and brain, where they are

perceived as painful. Other researchers argue that the cause of functional diseases is

abnormalities in the function of motor nerves. For example, abnormal commands through the

motor nerves might produce painful spasm (contraction) of the muscles. Still others argue that

abnormally functioning processing centers are responsible for functional diseases because they

misinterpret normal sensations or send abnormal commands to the organ. In fact, some

functional diseases may be due to sensory dysfunction, motor dysfunction, or both sensory and

motor dysfunction. Others may be due to abnormalities within the processing centers.

An important concept that is relevant to these several potential mechanisms (causes) of

functional diseases is the concept of "visceral hypersensitivity". This concept states that diseases

affecting the gastrointestinal organs (viscera) "sensitize" (alter the responsiveness of) the

sensory nerves or the processing centers to sensations coming from the organ. According to this

theory, a disease such as colitis (inflammation of the colon) can cause permanent changes in the

sensitivity of the nerves or processing centers of the colon. As a result of this prior inflammation,

normal stimuli are perceived (felt) as abnormal (for example, as being painful). Thus, a normal

colonic contraction may be painful. It is not clear what prior diseases might lead to

hypersensitivity in people, although infectious diseases (bacterial or viral) of the gastrointestinal

tract are mentioned most often. Visceral hypersensitivity has been demonstrated clearly in

animals and people. Its role in the common functional diseases, however, is unclear.

Another potential cause of dyspepsia is bacterial overgrowth of the small intestine (small

intestinal bacterial overgrowth or SIBO), although the frequency with which this condition causes

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-

functional gastrointestinal diseases (including acid-related diseases), non-gastrointestinal

diseases, and psychiatric illness. There are tests for identifying abnormal gastrointestinal function

directly, but they are limited in their ability to do so.

Exclusion of other diseasesExclusion of non-functional gastrointestinal disease

As always, a detailed history from the patient and a physical examination frequently will suggest

the cause of dyspepsia. Routine screening blood tests often are performed looking for clues to

unsuspected diseases. Examinations of stool also are a part of the evaluation since they may

reveal infection, signs of inflammation, or blood and direct further diagnostic testing. 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 EGDis planned, biopsies

of the duodenum usually will make the diagnosis of celiac disease.) If bacterial overgrowth of the

small intestine is being considered, breath hydrogen testing can be considered.

There are many tests to exclude non-functional gastrointestinal diseases. The primary issue,

however, is to decide which tests are reasonable to perform. Since each case is individual,

different tests may be reasonable for different patients. Nevertheless, certain basic tests are

often performed to exclude non-functional gastrointestinal disease. These tests identify anatomic

(structural) and histological (microscopic) diseases of the esophagus, stomach, and intestines.

Both X-rays and endoscopies can identify anatomic diseases. Only endoscopies, however, can

diagnose histological diseases because biopsies (samples of tissue) can be taken during the

procedure. The X-ray tests include:

The esophagram and video-fluoroscopic swallowing study for examining the esophagus

The upper gastrointestinal series for examining the stomach and duodenum

The small bowel series for examining the small intestine

The barium enema for examining the colon and terminal ileum.

The computerized tomography (CT) scan for examining the small intestine

The endoscopic tests include:

Upper gastrointestinal endoscopy (esophago-gastro-duodenoscopy or EGD) to examine the

esophagus, stomach and duodenum

Colonoscopy  to examine the colon and terminal ileum

Endoscopy also is available to examine the small intestine, but this type of endoscopy is

complex, not widely available, and of unproven value in dyspepsia.

For examination of the small intestine, there is also a capsule containing a tiny camera and

transmitter that can be swallowed (capsule endoscopy). As the capsule travels through the

intestines, it transmits pictures of the inside of the intestines to an external recorder for later

review. The capsule is not widely available and its value, particularly in dyspepsia, has not yet

been proven.

Newer endoscopes, similar to those used for EGD and colonoscopy are available that allow the

entire small intestine to be examined. Unlike the capsule, however, the endoscope has channels

in it that allow instruments to be passed into the intestine to collect samples of tissue (biopsies)

and to treat abnormal findings such as polyps.

X-rays are easier to perform and less costly than endoscopies. The skills necessary to perform

gastrointestinal X-rays, however, are becoming rare among radiologists because they are doing

them less often. Therefore, the quality of the X-rays often is not as high as it used to be, and, as

a result, CT scans of the small intestine are replacing small intestinal X-rays. As noted

previously, endoscopies have an advantage over X-rays since at the time of endoscopies,

biopsies can be taken to diagnose or exclude histological diseases, something that X-rays

cannot do.

Exclusion of acid-related gastrointestinal diseases

Because they are so common, the most important non-functional gastrointestinal diseases to

exclude are acid-related diseases that cause inflammation and ulceration of the esophagus,

stomach, and duodenum. Infection of the stomach with Helicobacter pylori, an infection that is

closely associated with some acid-related diseases, is included in this group. It is not clear,

however, how often Helicobacter pylori causes dyspepsia. Moreover, the only way of excluding

this bacterium as a cause of dyspepsia in a particular patient is by eliminating the infection (if it is

present) with appropriate antibiotics. If dyspepsia is substantially improved by eradication, it is

likely that the bacterium was responsible. Helicobacter pylori infection also can be diagnosed (or

excluded) by blood tests, biopsy of the stomach,urea breath test, or a stool test.

Endoscopy is a good way of diagnosing or excluding acid-related inflammation. If no signs of

inflammation are present, acid-related diseases are unlikely. Nevertheless, some patients without

signs of inflammation respond to potent and prolonged suppression of acid, suggesting that acid

is causing their dyspepsia. Therefore, many physicians will use potent suppression of acid in

dyspepsia as a means to both treat and diagnose. Thus, if dyspepsia improves substantially

(more than 50% to 75%) with suppression of acid, they consider it likely that acid is responsible

for the dyspepsia. For this purpose, it is important to use potent acid suppression with proton

pump inhibitors (PPIs), such as:

omeprazole   (Prilosec, Zegerid),

lansoprazole  (Prevacid),

rabeprazole  (Aciphex),

pantoprazole   (Protonix) or

esomeprazole  (Nexium).

Treatment often is given at higher than recommended doses for 12 weeks or more before a

decision is made about the effect of treatment on the symptoms. (A short course for just a few

days or weeks is not enough.) If the symptoms of dyspepsia do not improve, it even may be

reasonable to check the amount of acid produced by the stomach (and also the reflux of acid into

the esophagus) by 24 hour ph monitoring to be certain that the acid-suppressing drugs are

effectively suppressing acid. (Up to 10% of patients are resistant to the effects of even the PPIs.)

Exclusion of non-gastrointestinal disease

Patients with dyspepsia often undergo abdominal ultrasonography (US), computerized

tomography (CT or CAT scans), or magnetic resonance imaging (MRI). These tests are used

primarily to diagnose non-intestinal diseases. (Although the tests also are capable of diagnosing

intestinal diseases, their value for this purpose is limited. X-ray and endoscopy are better.) It is

important to realize that US, CT, and MRI are powerful tests and may uncover abnormalities that

are unrelated to dyspepsia. The most common example of this is the finding of gallstones that, in

fact, are causing no symptoms. (Up to 50% of gallstones cause no symptoms.) This can cause a

problem if the gallstones are assumed to be causing the dyspepsia. Surgical removal of the

gallbladder with its gallstones (cholecystectomy) is unlikely to relieve the dyspepsia.

(Cholecystectomy would be expected to relieve only the characteristic symptoms that gallstones

can cause.) Additional tests to exclude non-gastrointestinal diseases may be appropriate in

certain specific situations, although certainly not in most patients.

Exclusion of psychiatric disease

The possibility of psychiatric (psychological or psychosomatic) illness often arises in patients with

dyspepsia because the symptoms are subjective and no objective abnormalities can be

identified. Psychiatric illness may complicate dyspepsia, but it is unclear if psychiatric illness

causes dyspepsia. If there is a possibility of psychiatric illness, a psychiatric evaluation is

appropriate.

Specific tests of gastrointestinal functionEsophageal motility study

Functional disorders of the esophagus can be identified with esophageal motility

studies(manometry). For these studies, a pressure-sensing tube is swallowed and positioned

within the esophagus. Contractions of the esophageal muscle normally cause increases in

pressure within the esophagus that can be monitored by the catheter during and between

swallows of water. Among the abnormalities that can be seen are abnormally high or abnormally

low pressures during swallow-associated contractions and/or during spontaneous contractions

unassociated with swallows.

Gastric emptying study and electrogastrogram

Slow emptying of the stomach is a common functional abnormality that can lead to bloating,

nausea, and vomiting. Rapid emptying of the stomach is relatively uncommon and can lead to

abdominal pain and diarrhea. Both of these abnormalities--slow and rapid emptying--can be

identified by a gastric emptying study.

The most common type of emptying study is a nuclear medicine study. In this test, patients drink

or eat food labeled with radioactive material. A Geiger counter-like device then is placed over the

abdomen and the speed with which the radioactive drink or food empties from the stomach is

monitored.

The electrogastrogram (EGG) is like the electrocardiogram (ECG) for the heart. Electrodes that

are taped to the upper abdomen monitor the electrical activity generated by the muscle of the

stomach. Abnormalities of the electrical rhythm of the stomach frequently are associated with

dyspeptic symptoms, particularly nausea and vomiting. EGGs are not commonly available and

are considered a research tool.

Barostatic study

A barostat is an instrument that is used to measure pressure and determine the compliance

(flexibility) of a gastrointestinal organ. Compliance is a term that describes the effect that internal

stretching has on the organ. The greater the compliance of an organ, the less there is tension

(pressure) generated when the organ is stretched from within.

Compliance is important to the normal function of gastrointestinal organs. For example, as food

fills the stomach during a meal, the muscles of the stomach must relax (comply) to accommodate

the increasing volume of food. If the stomach does not relax properly, the pressure in the

stomach increases abnormally. It is believed that abnormally high pressures within the stomach

(due to reduced compliance) can lead to symptoms such as early satiety (the feeling of

abdominal fullness or pain after only a small amount of food has been ingested).

The barostat includes a balloon that is placed within a gastrointestinal organ through the mouth

or anus. As the balloon is progressively blown up and stretches the organ, the pressure within

the organ is measured by the barostat. In this way, abnormal compliance can be identified.

Barostats can be placed in the esophagus, stomach, small intestine or colon. Barostatic studies,

however, probably should be considered experimental. In fact, barostats and expertise in their

use are available in only a limited number of centers.

Small intestinal transit study

Small intestinal transit studies measure the speed with which food travels through the small

intestine. In the most common type of transit study, a test meal that has been labeled with a

radioactive material is ingested. A Geiger-counter-like device is placed over the abdomen and is

used to follow the radioactive material through the small intestine and into the colon. Rapid

transit is associated with abdominal pain and diarrhea. Slow transit also may be associated with

abdominal pain. Although transit studies are not difficult to conduct, they are not frequently used

because experience with their use is not wide-spread. They probably should be considered

experimental.

Antro-duodenal motility study

Antro-duodenal motility studies measure the pressures that are generated by the contractions of

the muscles of the antrum (outlet) of the stomach and the duodenum. For these studies, a

pressure-sensing tube is swallowed or passed through the nose and positioned in the distal

(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

cause(s).

REFERENCE: MedscapeToday.com. Functional Dyspepsia.

Reviewed by William C. Shiel Jr., MD, FACP, FACR on 4/18/2012

http://www.medicinenet.com/dyspepsia/page9.htm

Gastritis

Gastritis facts**Gastritis disease facts medically written by: Charles Patrick Davis, MD, PhD

Gastritis is inflammation of the stomach lining (stomach mucosa) that may be acute or

chronic and erosive (loss of mucosal tissue) or nonerosive; the term gastritis is mistakenly

used to describe discomfort or pain in the upper abdomen

The most common cause of nonerosive chronic gastritis is infection with Helicobacter pylori.

The most common cause of both acute and chronic erosive gastritis is prolonged use

of nonsteroidal anti-inflammatory drugs (NSAID's). There are many other causes of various

subtypes of gastritis.

The person with nonerosive gastritis may have no symptoms, but the most common

symptoms are upper abdominal discomfort or pain,nausea and vomiting (all together termed

dyspepsia); erosive gastritis may additionally have symptoms of bloody vomit, black or tarry

stools or bloody stools

Complications of gastritis are infrequent but may include ulcers, polyps, benign and

malignant tumors, and cancer

Gastritis is diagnosed most commonly by endoscopy; other tests are often used (tests for H.

pylori, upper GI X-ray series, blood, and stool tests)

Treatments for gastritis may include antacids, histamine blockers (H2 blockers), proton

pump inhibitors (PPI's), antibiotics, stoppage of NSAID's and alcohol intake.

What is gastritis?Gastritis is a condition in which the stomach lining - known as the mucosa - is inflamed. The

stomach lining contains special cells that produce acid and enzymes, which help break down

food for digestion, and mucus, which protects the stomach lining from acid. When the stomach

lining is inflamed, it produces less acid, enzymes, and mucus.

Gastritis may be acute or chronic. Sudden, severe inflammation of the stomach lining is called

acute gastritis. Inflammation that lasts for a long time is called chronic gastritis. If chronic gastritis

is not treated, it may last for years or even a lifetime.

Erosive gastritis is a type of gastritis that often does not cause significant inflammation but can

wear away the stomach lining. Erosive gastritis can cause bleeding, erosions, or ulcers. Erosive

gastritis may be acute or chronic.

The relationship between gastritis and symptoms is not clear. The term gastritis refers

specifically to abnormal inflammation in the stomach lining. People who have gastritis may

experience pain or discomfort in the upper abdomen, but many people with gastritis do not have

any symptoms.

The term gastritis is sometimes mistakenly used to describe any symptoms of pain or discomfort

in the upper abdomen. Many diseases and disorders can cause these symptoms. Most people

who have upper abdominal symptoms do not have gastritis.

What causes gastritis?Helicobacter pylori (H. pylori) infection causes most cases of chronic nonerosive gastritis. H.

pylori are bacteria that infect the stomach lining. H. pylori are primarily transmitted from person to

person. In areas with poor sanitation, H. pylori may be transmitted through contaminated food or

water.

In industrialized countries like the United States, 20 to 50 percent of the population may be

infected with H. pylori.1 Rates of H. pylori infection are higher in areas with poor sanitation and

higher population density. Infection rates may be higher than 80 percent in some developing

countries.1

The most common cause of erosive gastritis - acute and chronic - is prolonged use of

nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin and ibuprofen. Other agents that

can cause erosive gastritis include alcohol, cocaine, and radiation.

Traumatic injuries, critical illness, severe burns, and major surgery can also cause acute erosive

gastritis. This type of gastritis is called stress gastritis.

Less common causes of erosive and nonerosive gastritis include

autoimmune disorders in which the immune system attacks healthy cells in the stomach

lining

some digestive diseases and disorders, such as Crohn's disease andpernicious anemia

viruses, parasites, fungi, and bacteria other than H. pylori1Lee Y, Liou J, Wu M, Wu C, Lin J. Review: eradication of Helicobacter pylori to prevent

gastroduodenal diseases: hitting more than one bird with the same stone. Therapeutic Advances

in Gastroenterology. 2008;1(2):111–120.

What are the symptoms of gastritis?Many people with gastritis do not have any symptoms, but some people experience symptoms

such as

upper abdominal discomfort or pain

nausea

vomiting

These symptoms are also called dyspepsia.

Erosive gastritis may cause ulcers or erosions in the stomach lining that can bleed. Signs of

bleeding in the stomach include

blood in vomit

black, tarry stools

red blood in the stool

What are the complications of gastritis?Most forms of chronic nonspecific gastritis do not cause symptoms. However, chronic gastritis is

a risk factor for peptic ulcer disease, gastric polyps, and benign and malignant gastric tumors.

Some people with chronicH. pylori gastritis or autoimmune gastritis develop atrophic gastritis.

Atrophic gastritis destroys the cells in the stomach lining that produce digestive acids and

enzymes. Atrophic gastritis can lead to two types of cancer: gastric cancer and gastric mucosa-

associated lymphoid tissue (MALT) lymphoma.

How is gastritis diagnosed?The most common diagnostic test for gastritis is endoscopy with a biopsy of the stomach. The

doctor will usually give the patient medicine to reduce discomfort and anxiety before beginning

the endoscopy procedure. The doctor then inserts an endoscope, a thin tube with a tiny camera

on the end, through the patient's mouth or nose and into the stomach. The doctor uses the

endoscope to examine the lining of the esophagus, stomach, and first portion of the small

intestine. If necessary, the doctor will use the endoscope to perform a biopsy, which involves

collecting tiny samples of tissue for examination with a microscope.

Other tests used to identify the cause of gastritis or any complications include the following:

Upper gastrointestinal (GI) series . The patient swallows barium, a liquid contrast material

that makes the digestive tract visible in an x ray. X-ray images may show changes in the

stomach lining, such as erosions or ulcers.

Blood test . The doctor may check for anemia, a condition in which the blood's iron-rich

substance, hemoglobin, is diminished. Anemia may be a sign of chronic bleeding in the

stomach.

Stool test . This test checks for the presence of blood in the stool, another sign of bleeding

in the stomach.

Tests for H. pylori infection. The doctor may test a patient's breath, blood, or stool for

signs of infection. H. pylori infection can also be confirmed with biopsies taken from the

stomach during endoscopy.

What is the treatment for gastritis?Medications that reduce the amount of acid in the stomach can relieve symptoms that may

accompany gastritis and promote healing of the stomach lining. These medications include

antacids, such as aspirin, sodium bicarbonate, and citric acid (Alka-Seltzer); alumina and

magnesia (Maalox); and calcium carbonate and magnesia (Rolaids). Antacids relieve

mild heartburn or dyspepsia by neutralizing acid in the stomach. These drugs may produce

side effects such as diarrhea or constipation.

histamine 2 (H2) blockers, such asfamotidine (Pepcid AC) and ranitidine(Zantac 75). H2

blockers decrease acid production. They are available both over the counter and by

prescription.

proton pump inhibitors  (PPIs), such as omeprazole (Prilosec,

Zegerid), lansoprazole (Prevacid), pantoprazole (Protonix), rabeprazole(Aciphex), esomepra

zole (Nexium), and dexlansoprazole (Kapidex). All of these drugs are available by

prescription, and some are also available over the counter. PPIs decrease acid production

more effectively than H2 blockers.

Depending on the cause of the gastritis, additional measures or treatments may be needed. For

example, if gastritis is caused by prolonged use of NSAIDs, a doctor may advise a person to stop

taking NSAIDs, reduce the dose of NSAIDs, or switch to another class of medications for pain.

PPIs may be used to prevent stress gastritis in critically ill patients.

Treating H. pylori infections is important, even if a person is not experiencing symptoms from the

infection. Untreated H. pylori gastritis may lead to cancer or the development of ulcers in the

stomach or small intestine. The most common treatment is a triple therapy that combines a PPI

and two antibiotics—usually amoxicillin and clarithromycin—to kill the bacteria. Treatment may

also include bismuth subsalicylate (Pepto-Bismol) to help kill bacteria.

After treatment, the doctor may use a breath or stool test to make sure theH. pylori infection is

gone. Curing the infection can be expected to cure the gastritis and decrease the risk of other

gastrointestinal diseases associated with gastritis, such as peptic ulcer disease, gastric cancer,

and MALT lymphoma.

SOURCE: National Digestive Diseases Information Clearinghouse, National Institutes of Health.

Gastritis.

<http://digestive.niddk.nih.gov/ddiseases/pubs/gastritis/index.htm>

Reviewed on 4/23/2012http://www.medicinenet.com/gastritis/discussion-313.htm

Peptic Ulcer Disease

Peptic ulcer facts Peptic ulcers are sores in the lining of the stomach or duodenum.

Peptic ulcer formation is related toH. pylori   bacteria  in the stomach and nonsteroidal anti-

inflammatory medications (NSAIDs) in 50% of patients. For the remaining 50% there are

miscellaneous or unknown causes.

Ulcer pain may not correlate with the presence or severity of ulceration.

The main symptom of peptic ulcer is upper abdominal pain which can be dull, sharp, or

burning. (Bloating and burping are not symptoms of peptic ulcer, andvomiting, poor appetite,

andnausea are uncommon symptoms of peptic ulcer.)

Diagnosis of ulcer is made withupper GI series or endoscopy.

Treatment of ulcers involves antibiotic combinations along with stomach acid suppression to

eradicate H. pylori, eliminating precipitating factors such as NSAIDs and stomach acid

suppression with medications alone .

Complications of ulcers include bleeding, perforation, and blockage of the stomach (gastric

obstruction).

If a person with peptic ulcerssmokes or take NSAIDs, the ulcers may recur after treatment.

What is a peptic ulcer? A peptic ulcer is a break in the inner lining of the esophagus, stomach, or duodenum. A

peptic ulcer of the stomach is called a gastric ulcer; of the duodenum, a duodenal ulcer;

and of the esophagus, an esophageal ulcer. Peptic ulcers occur when the lining of these

organs is corroded by the acidic digestive (peptic) juices which are secreted by the cells

of the stomach. A peptic ulcer differs from an erosion because it extends deeper into the

lining of the esophagus, stomach, or duodenum and excites more of an inflammatory

reaction from the tissues that are eroded.

Peptic ulcer disease is common, affecting millions of Americans yearly. Moreover, peptic

ulcers are a recurrent problem; even healed ulcers can recur unless treatment is directed

at preventing their recurrence. The medical cost of treating peptic ulcer and its

complications runs into billions of dollars annually. Recent medical advances have

increased our understanding of ulcer formation. Improved and expanded treatment

options now are available.

What are the causes of peptic ulcers? For many years, excess acid was believed to be the major cause of ulcer disease.

Accordingly, the emphasis of treatment was on neutralizing and inhibiting the secretion of

stomach acid. While acid is still considered necessary for the formation of ulcers, the two

most important initiating causes of ulcers are infection of the stomach by a bacterium

called "Helicobacter pyloricus" (H. pylori) and chronic use of anti-inflammatory

medications, commonly referred to as NSAIDs (nonsteroidal anti-inflammatory drugs),

including aspirin. Cigarette smoking also is an important cause of ulcer formation as well

as failure of ulcer treatment.

Infection with H. pylori is very common, affecting more than a billion people worldwide. It

is estimated that half of the United States population older than age 60 has been infected

with H. pylori. Infection usually persists for many years, leading to ulcer disease in 10%

to 15% of those infected. In the past,H. pylori was found in more than 80% of patients

with gastric and duodenal ulcers. With increasing appreciation, diagnosis and treatment

of this infection, however, the prevalence of infection with H. pylori as well as the

proportion of ulcers caused by the bacterium has decreased; it is estimated that currently

only 20% of ulcers are associated with the bacterium. While the mechanism by which H.

pylori causes ulcers is complex, elimination of the bacterium by antibiotics has clearly

been shown to heal ulcers and prevent the recurrence of ulcers.

NSAIDs are medications used for the treatment of arthritis and other painful inflammatory

conditions in the body. Aspirin, ibuprofen (Motrin), naproxen(Naprosyn),

and etodolac (Lodine) are a few of the examples of this class of medications.

Prostaglandins are substances which are important in helping the linings of the

esophagus, stomach, and duodenum to resist damage by the acidic digestive juices of

the stomach. NSAIDs cause ulcers by interfering with prostaglandins in the stomach.

Cigarette smoking not only causes ulcers, but it also increases the risk of complications

from the ulcers such as ulcer bleeding, stomach obstruction, and perforation. Cigarette

smoking also is a leading cause of failure of treatment for ulcers.

Contrary to popular belief, alcohol, coffee, colas, spicy foods, and caffeinehave no

proven role in ulcer formation. Similarly, there is no conclusive evidence to suggest

that life stresses or personality types contribute to ulcer disease.

What are symptoms of a peptic ulcer?Symptoms of ulcer disease are variable. Many ulcer patients experience minimalindigestion,

abdominal discomfort that occurs after meals, or no discomfort at all. Some complain of upper

abdominal burning or hunger pain one to three hours after meals or in the middle of the night.

These symptoms often are promptly relieved by food or antacids that neutralize stomach acid.

The pain of ulcer disease correlates poorly with the presence or severity of active ulceration.

Some patients have persistent pain even after an ulcer is almost completely healed by

medication. Others experience no pain at all. Ulcers often come and go spontaneously without

the individual ever knowing that they are present unless a serious complication (like bleeding or

perforation) occurs.

How are peptic ulcers diagnosed?The diagnosis of an ulcer is made by either a barium upper gastrointestinal X-ray (upper GI

series) or an upper gastrointestinal endoscopy (EGD or esophagogastroduodenoscopy). The

barium upper GI X-ray is easy to perform and involves no risk (other than exposure to radiation)

or discomfort. Barium is a chalky substance that is swallowed. It is visible on X- rays, and allows

the outline of the stomach to be seen on X-rays; however, barium X-rays are less accurate and

may miss ulcers in up to 20% of the time.

An upper gastrointestinal endoscopy is more accurate than X-rays, but involves sedation of the

patient and the insertion of a flexible tube through the mouth to inspect the esophagus, stomach,

and duodenum. Upper endoscopy has the added advantage of having the capability of removing

small tissue samples (biopsies) to test for H. pylori infection. Biopsies are also examined under a

microscope to exclude a cancerous ulcer. While virtually all duodenal ulcers are benign, gastric

ulcers can occasionally be cancerous. Therefore, biopsies often are performed on gastric ulcers

to exclude cancer.

What is the treatment for peptic ulcers?The goal of ulcer treatment is to relieve pain, heal the ulcer, and prevent complications. The first

step in treatment involves the reduction of risk factors (NSAIDs and cigarettes). The next step is

medications.

Antacids

Antacids neutralize existing acid in the stomach. Antacids such as Maalox, Mylanta, and

Amphojel are safe and effective treatments. However, the neutralizing action of these agents is

short-lived, and frequent dosing is required. Magnesium containing antacids, such as Maalox and

Mylanta, can cause diarrhea, while aluminum containing agents like Amphojel can

causeconstipation. Ulcers frequently return when antacids are discontinued.

H2 blockers

Studies have shown that a protein released in the stomach called histamine stimulates gastric

acid secretion. Histamine antagonists (H2 blockers) are drugs designed to block the action of

histamine on gastric cells and reduce the production of acid. Examples of H2 blockers

are cimetidine (Tagamet),ranitidine (Zantac), nizatidine (Axid), and famotidine (Pepcid). While H2

blockers are effective in ulcer healing, they have a limited role in eradicatingH. pylori without

antibiotics. Therefore, ulcers frequently return when H2 blockers are stopped.

Generally, H2 blockers are well tolerated and have few side effects even with long term use. In

rare instances, patients report headache, confusion, lethargy, or hallucinations. Chronic use of

cimetidine may rarely causeimpotence or breast swelling. Both cimetidine and ranitidine can

interfere with the body's ability to handle alcohol. Patients on these drugs who drink alcohol may

have elevated blood alcohol levels. These drugs may also interfere with the liver's handling of

other medications like phenytoin(Dilantin), warfarin (Coumadin), and theophylline. Frequent

monitoring and adjustments of the dosages of these medications may be needed.

Proton-pump inhibitors (PPIs)

Proton-pump inhibitors such

as omeprazole (Prilosec), lansoprazole(Prevacid), pantoprazole (Protonix), esomeprazole (Nexiu

m), andrabeprazole (Aciphex) are more potent than H2 blockers in suppressing acid secretion.

The different proton-pump inhibitors are very similar in action and there is no evidence that one is

more effective than the other in healing ulcers. While proton-pump inhibitors are comparable to

H2 blockers in effectiveness in treating gastric and duodenal ulcers, they are superior to H2

blockers in treating esophageal ulcers. Esophageal ulcers are more sensitive than gastric and

duodenal ulcers to minute amounts of acid. Therefore, more complete acid suppression

accomplished by proton-pump inhibitors is important for esophageal ulcer healing.

Proton-pump inhibitors are well tolerated. Side effects are uncommon; they include headache,

diarrhea, constipation, nausea and rash. Interestingly, proton-pump inhibitors do not have any

effect on a person's ability to digest and absorb nutrients. Proton-pump inhibitors have also been

found to be safe when used long term, without serious adverse health effects. Although they may

promote loss of bone (osteoporosis) and low magnesium levels, both of these side effects are

easily identified and treated.

Sucralfate (Carafate) and misoprostol (Cytotec)

Sucralfate (Carafate) and misoprostol (Cytotec) are agents that strengthen the gut lining against

attacks by acidic digestive juices. Sucralfate coats the ulcer surface and promotes healing.

Sucralfate has very few side effects. The most common side effect is constipation and the

interference with the absorption of other medications. Misoprostol is a prostaglandin-like

substance commonly used to counteract the ulcerogenic effects of NSAIDs. Studies suggest that

misoprostol may protect the stomach from ulceration among people who take NSAIDs

chronically. Diarrhea is a common side effect. Misoprostol can cause miscarriages when given

to pregnant women, and should be avoided by women of childbearing age.

H. pylori treatment

Many people harbor H. pylori in their stomachs without ever having pain or ulcers. It is not

completely clear whether these patients should be treated with antibiotics. More studies are

needed to answer this question. Patients with documented ulcer disease and H. pylori infection

should be treated for both the ulcer and the H. pylori. H. pylori can be very difficult to completely

eradicate. Treatment requires a combination of several antibiotics, sometimes in combination

with a proton-pump inhibitor, H2 blockers, or Pepto-Bismol. Commonly used antibiotics

are tetracycline, amoxicillin,metronidazole (Flagyl), clarithromycin (Biaxin),

and levofloxacin (Levaquin). Eradication of H. pylori prevents the return of ulcers (a major

problem with all other ulcer treatment options). Elimination of this bacteria also may decrease the

risk of developing gastric cancer in the future. Treatment with antibiotics carries the risk of

allergic reactions, diarrhea, and sometimessevere antibiotic-induced colitis (inflammation of the

colon).

Diet

There is no conclusive evidence that dietary restrictions and bland diets play a role in ulcer

healing. No proven relationship exists between peptic ulcer disease and the intake of coffee and

alcohol. However, since coffee stimulates gastric acid secretion, and alcohol can cause gastritis,

moderation in alcohol and coffee consumption is recommended.

What are the complications of peptic ulcer?Patients with ulcers generally function quite comfortably. Some ulcers probably heal even without

medications (though they probably recur as well). Therefore, the major problems resulting from

ulcers are related to ulcer complications. Complications include bleeding, perforation, and

obstruction of the stomach.

Patients with ulcer bleeding may report passage of black tarry stools (melena),weakness, a

sense of passing out upon standing (orthostatic syncope), and vomiting blood (hematemesis).

Initial treatment involves rapid replacement of lost blood intravenously, usually with fluids.

Patients with persistent or severe bleeding may require blood transfusions. An endoscopy is

performed to establish the site of bleeding and to stop active ulcer bleeding with the aid of

specialized endoscopic instruments.

Perforation through the stomach leads to the leakage of stomach contents into the abdominal

(peritoneal) cavity, resulting in acute peritonitis (infection of the abdominal cavity). These patients

report a sudden onset of extreme abdominal pain, which is worsened by any type of motion.

Abdominal muscles become rigid and board-like. Urgent surgery usually is required. A duodenal

ulcer that has perforated can burrow into adjacent organs such as the pancreas or behind the

abdomen and into the back. An esophageal ulcer that perforates can cause severe inflammation

of the tissues that surround it and the heart, and those that lie between the lungs (mediastinitis).

If an ulcer occurs in the narrow outlet from the stomach, it can obstruct the flow of stomach

contents into the duodenum. Duodenal ulcers sometimes also may obstruct the flow of intestinal

contents. Patients with obstruction often report increasing abdominal pain, vomiting of

undigested or partially digested food, diminished appetite, and weight loss. The obstruction

usually occurs at or near the pylorus that separates the stomach from the duodenum. Endoscopy

is useful in establishing the diagnosis of obstruction from an ulcer and excluding gastric cancer

as the cause of the obstruction. In some patients, gastric obstruction can be relieved by suction

of the stomach contents with a tube for 72 hours, along with intravenous anti-ulcer medications,

such as cimetidine (Tagamet) and ranitidine (Zantac). Patients with persistent obstruction require

surgery.

Peptic ulcer summaryWith modern treatment, patients with ulcer disease can lead normal lives without lifestyle

changes or dietary restrictions. Cigarette smokers have been found to have more complications

from ulcers and treatment failure. Eradication of the bacteriaH. pylori not only heals ulcers but

also prevents the recurrence of ulcer disease.

REFERENCE: MedscapeReference. Peptic Ulcer Disease.

Reviewed by Bhupinder Anand, MD on 5/16/2012http://www.medicinenet.com/peptic_ulcer/page6.htm

Upper Endoscopy

(Esophagogastroduodenoscopy, EGD)

What is upper endoscopy?

Upper endoscopy is a procedure that enables the examiner (usually a gastroenterologist) to

examine the esophagus (swallowing tube), stomach, and duodenum (first portion of small bowel)

using a thin, flexible tube through which the lining of the esophagus, stomach, and duodenum

can be viewed using a TV monitor.

How do I prepare for endoscopy?

To accomplish a safe and complete examination, the stomach should be empty. The patient will

most likely be asked to have nothing to eat or drink for six hours or more prior to the procedure.

Prior to scheduling the procedure, the patient should inform his or her physician of any

medications they are currently taking, any allergies, and all of their health problems. This

information will remind the doctor whether the patient may need antibiotics prior to the procedure,

what potential medications should not be used during the exam because of the patient'sallergies,

and will provide the individual scheduling the procedure an opportunity to instruct the patient

whether any of the medications they are taking should be held or adjusted prior to the

endoscopy.

Knowledge whether the patient has any major health problems, such as heart or lung diseases,

will alert the examiner of possible need for special attention during the procedure.

Why have you been scheduled for an endoscopy?

Upper endoscopy usually is performed to evaluate possible problems with the esophagus,

stomach or duodenum, and evaluate symptoms such as upper abdominal

pain, nausea or vomiting, difficulty in swallowing, intestinal bleeding anemia, etc.. Upper

endoscopy is more accurate than X-ray for detecting inflammation or smaller abnormalities such

as ulcers or tumors within the reach of the instrument. Its other major advantage over X-ray is the

ability to perform biopsies (obtain small pieces of tissue) or cytology (obtain some cells with a

fine brush) for microscopic examination to determine the nature of the abnormality and whether

the abnormality is benign or malignant (cancerous).

Biopsies are taken for many reasons and may not mean that canceris suspected. Upper

endoscopy also can be used to treat many conditions within its reach. The endoscope's channels

permit passage of accessory instruments enabling the examiner to treat many of the conditions

such as stretching areas of narrowing (strictures), removal of benign growths such as polyps,

accidentally swallowed objects, or treating upper gastrointestinal bleeding as seen in ulcers tears

of the lining. These capabilities have markedly reduced the need for transfusions or surgery.

What can I expect during endoscopy?

It is most likely that before the procedure the doctor will discuss with the patient why the

procedure is being done, whether there are alternative procedures or tests, and what possible

complications may result from the endoscopy. Practices vary amongst physicians but the patient

may have the throat sprayed with a numbing solution and will probably be given a sedating and

pain alleviating medication through the vein. While lying on your left side the flexible endoscope,

the thickness of a small finger, is passed through the mouth into the esophagus, stomach, and

duodenum. This procedure will NOT interfere with your breathing. Most patients experience only

minimal discomfort during the test and many sleep throughout the entire procedure.

What happens after the endoscopy?

After the test the patient will be observed and monitored by a qualified individual in the

endoscopy or a recovery area until a significant portion of the medication has worn off.

Occasionally a patient is left with a mild sore throat, which promptly responds to saline gargles,

or a feeling of distention from the insufflated air that was used during the procedure. Both

problems are mild and transient. When fully recovered the patient will be instructed when to

resume their usual diet (probably within a few hours) and the patient's driver will be allowed to

take you home. (Because of the use of sedation, most facilities mandate that the patient be taken

by a driver and not drive, handle machinery, or make important decisions for the remainder of the

day.)

When do I get the results of the endoscopy?

Under most circumstances the examining physician will inform the patient of the test results or

the probable findings prior to discharge from the recovery area. The results of biopsies or

cytology usually take 72-96 hours and the doctor may only give the patient a presumptive

diagnosis pending the definitive one, after the microscopic examination.

What are the risks of endoscopy?

Endoscopy is a safe procedure and when performed by a physician with specialized training in

these procedures, the complications are extremely rare. They may include localized irritation of

the vein where the medication was administered, reaction to the medication or sedatives used,

complications from pre-existing heart, lung, or liver disease, bleeding may occur at the site of a

biopsy or removal of a polyp (which if it occurs is almost always minor and rarely requires

transfusions or surgery). Major complications such as perforation (punching a hole through the

esophagus, stomach, or duodenum) are rare but usually require surgical repair.

What if there are still remaining questions about endoscopy?

If the patient still has any questions about their need for this exam, the cost of this procedure and

whether it is covered by the patient's insurance, methods of billing, or any concerns about this

exam, do not hesitate to speak to the doctor or his staff about them. Most endoscopists are

highly trained specialists and will be happy to discuss with the patient their qualifications and

answer any questions.

Last Editorial Review: 2/27/2009

Medical Author:

Jay W. Marks, MD 

Medical Editor:

William C. Shiel Jr., MD, FACP, FACR 

http://www.medicinenet.com/endoscopy/page3.htm