Inflammatory Bowel Disease (IBD) is an umbrella term
referring to two chronic diseases that cause inflammation
of the intestines: ulcerative colitis (UC) and Crohn's
disease (CD). Though UC and CD are different diseases
they do have features in common but there are important
distinctions also. Frequently, the symptoms caused by UC
and CD are similar.
Both diseases are chronic and most frequently have
their onset in early adult life. Some patients have
alternating periods of relative health (remission)
alternating with periods of disease (relapse or flare),
while other patients have continuous symptoms from
continued inflammation. Fortunately, as treatment has
improved the proportion of people with continued symptoms
appears to have diminished significantly .
The severity of the diseases varies widely between
individuals. Some suffer only mild symptoms, but others
have severe and disabling symptoms. Some have a gradual
onset of symptoms, some develop them suddenly. About half
of patients have mild symptoms, the other half suffer
frequent flare-ups. Medical science has not yet
discovered a cause or cure, but numerous medications are
now available to control symptoms with many more on the
horizon.
Ulcerative colitis (UC) is an inflammatory disease of
the large intestine, commonly called the colon. UC causes
inflammation and ulceration of the inner lining of the
colon and rectum. This inner lining is called the mucosa.
Crohn's disease (CD) causes inflammation that extends
into the deeper layers of the intestinal wall.
The inflammation of UC is usually most severe in the
rectal area with severity diminishing (at a rate that
varies from patient to patient) toward the cecum, where
the large and small intestine join. Significant
deviations from this pattern may be a clue to the
physician to suspect CD rather than UC. Such deviations
may include either "skip areas" and/or "sparing
of the rectum". Skip areas are patches of healthy
tissue separating segments of diseased tissue. They are
often seen in CD, but rarely in UC. Inflammation of the
rectum is called proctitis. Inflammation of the sigmoid
colon (located just above the rectum) is called
sigmoiditis. Inflammation involving the entire colon is
termed pan-colitis.
The inflammation causes the colon to empty frequently
resulting in diarrhea. As the lining of the colon is
destroyed ulcers form releasing mucus, pus and blood.
UC is relatively common in the western world and at
least 250,000 in the United States alone have the disease.
It occurs most frequently in people ages 15 to 30
although children and older people occasionally develop
the disease.
About 50% of patients are free of symptoms at any
given time but the vast majority suffer at least one
relapse in any 10 year period.
Drug treatment is effective for about 70-80% of
patients; surgery becomes necessary in the remaining 20-30%.
Crohn's disease (CD) is an inflammatory process that
can affect any portion of the digestive tract, but is
most commonly seen (roughly half of all cases) in the
last part of the small intestine otherwise called the
terminal ileum and cecum. Altogether this area is also
known as the ileocecal region. Other cases may affect one
or more of: the colon only, the small bowel only (duodenum,
jejunum and/or ileum), the anus, stomach or esophagus. In
contrast with UC, CD usually doesn't affect the rectum,
but frequently affects the anus instead.
This is CD of the ileum which is the third part of the
small intestine. At one time, CD was thought to affect
only the ileum, and for this reason the name "ileitis"
was at one time synonymous with CD but now simply refers
to CD of the ileum.
This is CD affecting part or all of the colon. This
form comprises about 20% of all cases of CD. Various
patterns are seen. In about half of these cases CD
lesions may be seen throughout one continuous subsegment
of the colon. In another quarter, skip areas are seen
between multiple diseased areas. In the remaining
quarter, the entire colon is involved, with no skip areas.
Unlike UC, in which inflammation is usually confined
to the inner mucosal surface, CD typically involves all
layers of the affected tissues.
Ulcerative proctitis is a form of UC that affects only
the rectum.
This is another name for Crohn's disease that affects
the colon.
This is *NOT* a variant of UC and Crohn's. UC and
Crohn's disease are defined by the presence of
inflammation in the intestine. There is no inflammation
in the intestine in Irritable Bowel Syndrome. Irritable
Bowel Syndrome (IBS) is also known as Functional Bowel
Syndrome (FBS), Functional Bowel Disease (FBD) or spastic
colon . Older terms for IBS are spastic or mucous colitis
or even simply "colitis". These terms are no
longer used because they cause people to confuse IBS with
UC.
IBS is characterized by a variety of symptom patterns
which include diarrhea, constipation, alternating
diarrhea/constipation and abdominal pain. Fever and/or
bleeding are NOT features of IBS.
IBS is much more common than CD or UC and many people
with symptoms of IBS do not seek medical attention. Some
patients with Crohns or UC can also have concurrent IBS.
The most common symptom of both UC and CD is diarrhea,
sometimes severe, that may require frequent visits to a
toilet (in some cases up to 20 or more times a day).
Abdominal cramps are often present, the severity of which
may be correlated with the degree of diarrhea present.
Blood may also appear in the stools, especially with UC.
Fever, fatigue, and loss of appetite may accompany
these symptoms (with consequent weight loss).
At times, some UC and CD patients experience
constipation during periods of active disease. In CD this
can result from a partial obstruction usually of the
small intestine. In UC constipation is most often a
consequence of inflammation of the rectum (also known as
proctitis); the colon has a nervous reaction and stasis
of stool occurs upstream .
Inflammation can affect gut nerves in such a way as to
make the patient feel that there is stool present ready
to be evacuated when there actually is not. That results
in the symptom known as tenesmus where there is an
uncomfortable urge to defecate but nothing comes out. The
feeling of urgency to pass stool is a frequent
consequence of proctitis also. Inability to retain stool
is an extreme manifestation of urgency. It is important
to bring these symptoms to the attention of your
physician because they may improve dramatically with
appropriate local therapy.
Pain usually results from intestinal cramping or
inflammation causing reflex irritability of the nerves
and muscles that control intestinal contractions. Pain
may also indicate the presence of severe inflammation or
the development of a complication such as an abscess or a
perforation of the intestinal wall. Generally, new onset
pain or a significant change in the character of pain
should be brought to the attention of your physician. The
pain of CD is often in the lower right area of the
abdomen. This is where the terminal ileum is located and
pain there usually indicates inflammation of the terminal
ileum.
Location and intensity of abdominal pain vary from
patient to patient, depending upon the location and type
of disease in the affected tissues. Because of a
phenomenon known as "referred pain", the
location where pain is produced may not be the same as
the location where it is experienced.
These are symptoms of IBD that occur outside of the
digestive tract.
Many IBD patients experience a wide variety of extra-intestinal
manifestations of their disease. The most common is joint
pain due to inflammation of the joints (arthritis).
Others include various types of eye inflammation (iritis,
conjunctivitis and episcleritis), skin inflammation (erythema
nodosum and pyoderma gangrenosum) liver inflammation (hepatitis
and sclerosing cholangitis). Other diseases and
complications may be associated with IBD but less
frequently.
At present there is no satisfactory explanation for
the occurence of these extra-intestinal complications of
IBD. Some researchers consider them to be secondary to
the primary disease, while others see both the extra-intestinal
manifestations *and* the primary disease as symptoms of a
"systemic" condition. Resolution of this will
depend on clarification of the cause of IBD.
Fatigue is the most common complication. Fever usually
indicates active disease and/or a complication such as an
abscess. Severe diarrhea, blood loss or infection can
lead to rapid heartbeat and a drop in blood pressure.
Continued loss of small amounts of blood in the stool (which
may not be visible) may lead to anemia (reduced blood
count); this may result in fatigue.
CD frequently results in the development of fistulas
which are abnormal connections between loops of intestine.
These may even involve other organs such as the urinary
bladder or open onto the skin. CD inflammation also
frequently results in the formation of scar tissue with
narrowed segments known as strictures. These strictures
frequently cause bowel obstructions the symptoms of which
will depend on the severity. The presence of a
significant stricture is a common reason for surgery in
CD.
Hemorrhoid-like skin tags and anal fissures may also
develop.
Growth may be retarded in children with both forms of
IBD and/or there may be a delay in the onset of puberty.
Toxic megacolon is a severe dilation of the colon
which occurs when inflammation spreads from the mucosa
through the remaining layers of the colon. It is much
more commonly a complication of UC though it can be seen
occasionally in CD. The colon becomes paralyzed which can
lead to it eventually bursting; this is known as a "perforation".
Such perforation is a dire medical emergency with a 30%
mortality rate. Many patients with toxic megacolon
require surgery.
Anyone with UC or CD serious enough to be at risk for
toxic megacolon should be hospitalized and closely
monitored. Warning signs include abdominal pain/tenderness,
abdominal distention, fever, large numbers of stools with
obvious blood and a rapid (more than 100/minute) pulse
rate.
Fortunately, this grave complication appears to be
decreasing in frequency which probably reflects more
effective treatment.
Use of certain drugs (opiates, opioids and/or
antispasmodics) may predispose to this complication. This
is one of the reasons that these drugs should be used
very carefully in both UC and CD.
Fistulas are hollow tracts running from a part of one
organ (such as the colon) to other organs, adjacent loops
of bowel, and or the skin. They occur in CD as a result
of deep ulceration.
Fistulas between loops of bowel can interfere with
nutrient absorption. This is especially true for fistulas
between the small and large bowel.
Fistulas can also become infected forming abscesses.
Abscesses are collections of pus that may be accompanied
by significant pain, and which can become life
threatening emergencies. Simple treatment of abscesses
resulting from fistulas can sometimes be accomplished via
a procedure called "incision and drainage" (I/D),
in which an incision is made, through which the abscess
is drained. However this procedure does not deal with the
underlying fistula which gave rise to the problem.
Accordingly, a more elaborate procedure, known as a
fistulectomy, is usually necessary for more definitive
treatment.
Fistulas are relatively common in CD patients and are
very rare in patients with UC.
Patients with CD in the small intestine may develop
bowel obstructions which can result in severe cramps and
vomiting. These obstructions can result from narrowing of
the intestine due to inflammation as well as from scar
tissue (stricture) from healed lesions. If the
obstruction is a consequence of inflammation then it can
usually be relieved by medical therapy such as steroids.
However if the obstruction is due to a fibrous stricture
then surgical resection may be necessary. In others, it
may be possible to clear some of these obstructions via a
technique known as stricturoplasty, which attempts to
expand the narrowed segment of the intestine.
Strictures can also occur in the large intestine, but
are much less common.
For patients who have had UC longer than ten years,
the risk of colon cancer is greater than that for
comparable people without UC. There is data that suggests
a risk of 5-10% at that point increasing to a range
between 15 and 40% after 30 years, depending upon the
particular study one looks at. If only the rectum and
lower (sigmoid) colon are involved, the risk of cancer is
not significantly increased. Patients that exhibit
dysplasia (pre-cancerous changes in cells that can be
detected by a biopsy) are at much higher risk.
There is some data suggesting that the risk of colon
cancer in patients with colonic CD is similar to that of
UC patients with disease of similar extent.
Other cancers, such as lymphoma or carcinoma of the
small intestine or anus, may be slightly more common in
Crohn's disease but the risk is not high.
In the presence of longstanding (> 7-8 years) UC
which involves more than the rectum and sigmoid colon or
extensive Crohn's colitis then the consensus of informed
medical opinion is that the patient should have a regular
(yearly or every second year) screening colonoscopy to
look for evidence of dysplasia. If that is found then the
safest option is for a colectomy to be performed. This
strategy does not guarantee that cancer can be avoided
but seems to significantly increase the probability that
it is not life threatening if and when it is detected.
Patients who have both UC and sclerosing cholangitis
may be at even greater risk of developing colon cancer.
Accordingly screening should be done with particular
vigilance in these patients.
There is also some data suggesting that low folic acid
levels may predispose to the development of colon cancer
in UC patients.
The only certain way is to have a colectomy: in other
words to have the colon removed surgically.
However, there is circumstantial evidence that taking
5-ASA drugs drugs such as azulfidine [See
Section 2.1.1] might reduce the risk of colon cancer
also.
Also there is some data that eating a diet rich in
fruit and vegetables (five servings a day) and low in red
meat is associated with a reduced risk of colon cancer in
people without colitis. Regular exercise also seems to be
associated with a reduced risk of colon cancer. These
associations may also be true for UC and CD patients but
they have not been studied.
The answer, unfortunately, is that no cause is yet
known.
Many researchers believe these diseases may be result
of an "inherited predisposition" combined with
a triggering environmental agent (possibly a bacteria or
a virus). There is no simple, predictable pattern of
inheritance though there is certainly some evidence to
suggest that heredity has some role to play. For example,
when two immediate family members both have IBD, the most
common combination is mother-child, followed by sibling-sibling,
with father-child being least common. About 15 to 20% of
people with IBD have immediate family members with IBD.
Heredity factors seem to be more important in CD than
UC.
Up to 2,000,000 Americans are estimated to suffer from
IBD with males and females affected equally.
The diseases can appear at any age, but the age at
which patients are usually first diagnosed falls neatly
onto a bell curve centered at about 24 years old, falling
off quickly in the late teens and early thirties.
However, there are also a significant number of patients
in whom the diseases first occur in later life.
There are significantly more cases in western Europe
and North America than in other parts of the world.
Smoking appears to enhance the likelihood of
developing CD.
Smoking appears to protect against the development of
UC.
There is data that surprisingly few UC patients have
had their appendix removed (appendectomy). This suggests
that removal of the appendix may protect against the
subsequent development of UC. There is no apparent
relationship between appendectomy and CD.
Diagnosis is made based on symptoms and the exclusion
of other diseases by observation of typical findings at
endoscopy and failure to find evidence of infection. The
presence of often bloody diarrhea will prompt your doctor
to perform an endoscopic examination; either a
sigmoidoscopy and/or colonoscopy (described below). If
inflammation is seen by these techniques, the physician
will then attempt to rule out an infectious cause with
stool cultures and blood tests.
Usually it is possible to tell the difference between
CD and UC but not always. Particularly, there may be some
uncertainty between a diagnosis of UC and CD affecting
the colon; this is termed indeterminate colitis.
Occasionally a diagnosis of UC will eventually turn out1.
to be CD.
Flexible sigmoidoscopy and colonoscopy are endoscopic
procedures that allow doctors to examine the lining of
the large intestine. In both procedures, the physician
inserts a flexible tube known generically as an endoscope
through the anus. The doctor is able to move this tube
through the gut to view the mucosal lining of the
intestines. This also enables him to take tiny samples of
the lining using a forceps passed through the endoscope.
These samples (called biopsies) can then be viewed under
a microscope by a pathologist. Examination of these
biopsies by a pathologist is particularly helpful in
making the distinction between CD and UC and also for
detecting the early evidence of cancerous change
indicated by dysplasia.
Flexible sigmoidoscopy is an endoscopic procedure done
without sedation which examines the rectum, sigmoid colon
and often a little bit more of the colon reaching as far
as the splenic flexure (the bend at which point the
descending colon and transverse colon meet).
Colonoscopy is a more elaborate procedure that is used
to examine the entire length of the colon which is
usually done with sedation.
>From the patient's perspective, the main
difference between the two procedures is that flexible
sigmoidoscopy may be performed in the doctors office and
does not normally reach farther than the splenic flexure.
Biopsies, or tissue samples may be taken during either
procedure.
Diagnosis of Crohn's disease of the colon is similar
to diagnosis of ulcerative colitis. The differences
between the two are found by studying the nature and
location of the specific inflammation.
Colonic CD has larger, deeper, thicker ulcers than UC
(which instead has an even "micro-carpet" of
tiny ulcers on the surface lining of the inner mucosa).
In CD, areas of ulceration are often separated by skip
areas, a phenomenon not seen in UC. There is a marked
contrast between the "cobblestone" appearance
often seen with CD and the even "micro-carpet"
seen with UC. Sometimes, "granulomas", a
microscopic indicator of CD may be seen on biopsy samples.
A diagnosis of probable small bowel CD is frequently
made by clinical observations of small bowel Crohn's
symptoms accompanied by the detection on physical
examination of a palpable mass (which may be tender) in
the right lower part of the abdomen. To confirm the
diagnosis an upper GI barium x-ray with small bowel
follow through is generally performed. In small bowel
follow through the small bowel is radiographed as barium
passes through it producing silhouette images of the
lining. The barium can be introduced either by
swallowing, or via a "small-bowel enema" (in
which the barium is pumped to the small bowel through a
tube). The former method, while more comfortable for the
patient and much more commonly used, produces inferior
results because the barium is diluted by gastric juices.
The latter method is generally used in more perplexing
cases. A small bowel enema is also know as an "enteroclysis."
Lots. The two most widely used drug families are
steroids and 5-aminosalicylic acid (5-ASA) drugs , both
of which reduce inflammation of the affected parts of the
intestines.
Immunosuppressive drugs such as 6-mercaptopurine (Purinethol)
are being increasingly used for long-term treatment of
IBD. They are particularly useful in the setting of a
patient who is dependent on chronic high-dose steroid
therapy with its severe and predictable side effects.
5-aminosalicylic acid (5-ASA), also called mesalamine,
is an anti-inflammatory drug used in treating IBD. 5-ASA
has a similar chemical structure to aspirin, but has a 5-amino
group in place of aspirin's acetyl group (aspirin is
acetylsalicylic acid).
Pure unmodified 5-ASA is easily absorbed in the upper
GI tract. To enable its delivery to the lower GI tract
where it is needed it must be chemically modified or
packaged. Different 5-ASA drugs are formulated to allow
delivery to different locations.
Because of the chemical similarities to aspirin,
patients allergic to aspirin should not take 5-ASA drugs.
Sulfasalazine (Azulfidine, Azulfidine EN-Tabs in
the US; Salazopyrin EN-Tabs, SAS in Canada;
salazosulfapyridine, salicylazosulfapyridine):
This is the "staple" drug generally first
prescribed for IBD patients. It is taken by mouth and is
intended to first reduce inflammation of the intestinal
lining and then to maintain remission in mild to moderate
cases.
Sulfasalazine is a combination of sulfapyridine and an
aspirin-like compound, 5-aminosalicylic acid (5-ASA). The
bond between the two is broken by intestinal bacteria,
making the 5-ASA available in the terminal ileum and
colon. A significant amount of the sulfapyridine
component is absorbed, metabolized by the liver, and
excreted in urine. Side effects are experienced by some
patients and can include nausea, heartburn, headache,
dizziness, anemia, and skin rashes. It is also known to
cause a reduced sperm count in men, but only for the
duration of treatment. It may also turn urine a bright
orange-yellow color. The side effects generally result
from the sulfapyridine component. Hence the efforts to
develop formulations of 5-ASA which do not contain
sulfapyridine or other sulfa drugs.
Azulfidine was developed in the 1930's for the
treatment of rheumatoid arthritis. During clinical trials
in the 1940's, arthritis patients who also suffered from
IBD reported improvements in their IBD symptoms while
taking it. This led to its current use as the mainstay
IBD treatment.
For active disease initially, 1 gram every 6-8 hours
is taken by mouth. Adverse effects may be lessened by
reducing the dosage to 500 mg every 6-12 hours.
Maintenance dose is usually 500 mg every 6 hours,
adjusted to patient response and tolerance. Total doses
of more than 4 g/day may increase the risk of adverse
effects and toxicity but some patients may benefit from
taking up to 6 g/day. Azulfadine is generally taken with
a full glass of water after meals or with food to
minimize indigestion.
When indigestion is a problem enteric-coated tablets
may be used which are frequently better tolerated.
Olsalazine Sodium (Dipentum)
Olsalazine is a drug that uses a different mechanism
to deliver 5-ASA to the terminal ileum and colon. Whereas
sulfasalazine links a 5-ASA molecule with a sulfapyridine
molecule, olsalazine links two 5-ASA molecules. This
compound passes through the stomach and upper ileum. It
is then broken down by intestinal bacteria in the
terminal ileum, making 5-ASA available there and also in
the colon.
The major side effect is watery diarrhea, seen in many
patients. Patients with UC or CD affecting the entire
colon seem especially susceptible. Increased cramping and
audible bowel sounds are also commonly reported.
The usual dose of olsalazine is 500 mg by mouth twice
a day.
Mesalamine, USA; Mesalazine, Europe :
Asacol is essentially "Azulfidine without the
sulfa". The Asacol formulation of 5-ASA places 5-ASA
in an acrylic resin coating which dissolves at pH greater
than 7. The tablets are then able to pass through the
stomach and upper ileum before the coating is dissolved,
releasing the drug in the terminal ileum and colon where
the pH is typically greater than 7.
Asacol is generally well tolerated. The recommended
dose is 2.4 g a day though patients frequently seem to
tolerate and benefit from taking up to 4.8 g daily.
Mesalazine,Europe (Salofalk)
Similar to Asacol, but dissolves at pH greater than 6.
Mesalamine, USA; Mesalazine, Europe (Pentasa):
Yet another "Azulfidine without the sulfa"
formulation, this drug packages 5-ASA in a time-release
capsule. This method of delivery is thought to make the
drug available throughout most of the intestines and
provide better release in the small intestine than the
other 5-ASA drugs. For this reason Pentasa is the 5-ASA
preparation of choice for Crohn's disease involving the
small intestine.
Pentasa is generally well tolerated. The recommended
dose is 2g a day though patients frequently seem to
tolerate and benefit from taking up to 4g daily. There is
data that the higher dose may be more effective.
Balsalazide:
Another 5-ASA drug that uses a variant on
sulfasalazine's delivery mechanism, Balsalazide contains
5-ASA joined to an inert vehicle. This combination passes
through the stomach and upper ileum. It is then broken
down by intestinal bacteria in the terminal ileum, making
5-ASA available in the terminal ileum and colon.
Mesalamine (Rowasa) :
Rowasa is 5-ASA in enema form and is effective in
treating distal UC, which is simply UC affecting the
lower part of the colon, near the rectum, and the rectum
itself. One enema contains 4 g of 5-ASA.
Rowasa also comes in suppository form for treating
proctitis (rectal inflammation). Each suppository
contains 500 mg of 5-ASA.
Metronidazole (Flagyl) :
Metronidazole is an antibiotic that is most frequently
used for treating vaginal infections. However, there is
some evidence (much of it anecdotal rather than derived
from formal studies) that it is useful in treating CD.
Some studies have shown that it has an anti-inflammatory
action on CD that is at least as effective as
sulfasalazine. The mechanism of this action is unknown,
and it has not been found in other antibiotics having the
same antibiotic spectrum. Metronidazole appears to be
particularly effective in the treatment of CD in the
colon. The dose is generally 250 mg three times a day.
Some patients are unable to tolerate alcohol while taking
metronidazole; accordingly it is generally recommended
that patients avoid alcohol while taking it.
Though it has been shown to cause cancer in laboratory
rodents exposed to very high doses (much, much higher
than used in humans) there is NO evidence that it has any
similar effect in humans.
The major side effect of metronidazole is irritation
of nerves which can result in permanent nerve damage if
the medication is not promptly stopped. The first hint of
this problem is usually a sensation of "pins and
needles" in the finger tips and toes. If this is
noted the medication should be stopped immediately.
Current issues of the PDR contain the disclaimer
"Crohn's disease is not an approved indication for
metronidazole".
Ciprofloxacin ("Cipro") is another
antibiotic frequently used in the treatment of CD. Many
physicians and patients report positive results from a
trial of cipro, although the formal evidence to justify
its use is limited. An infrequent side effect of
prolonged use is the development of inflammation of
tendons (tendonitis) which may result in rupture
especially of the achilles tendon.
Another antibiotic used in the treatment of CD. As
with the others there is currently little formal evidence
to justify its use.
Prednisone, Prednisolone, Hydrocortisone:
When 5-ASA drugs fail or when symptoms are more
severe, the next therapeutic step usually involves
steroids which are very powerful anti-inflammatory drugs.
These are available in oral, enema, or suppository forms.
The topical forms are useful in treating distal colitis,
the oral forms are useful for achieving remission in mild
to moderate active UC and CD. They are NOT useful for
continued use in order to maintain a remission. The oral
forms can, however, be effective in suppressing active CD
to the point where it appears to be in remission.
Side effects from steroids vary widely between
patients, but are generally pretty severe particularly
when used at moderate to high doses (> 15mg prednisone
daily). Common side effects include rounding of the face
(moon face) and increase in the size of fat pads on the
upper back and back of the neck (buffalo hump), acne,
increased appetite with consequent weight gain, increased
body hair, osteoporosis (especially in women),
compression fractures in vertebrae, diabetes,
hypertension, cataracts, increased susceptibility to
infections, glaucoma, weakness of arm, leg, shoulder, and
pelvic muscles, personality changes including depression
(suicidal tendencies are not uncommon), irritability,
nervousness, and insomnia. Children's growth may also be
affected, even by small doses.
An important and serious complication of steroid
therapy is avascular necrosis of the hip. This results in
death of the bone in the hip joint resulting in arthritis
and severe pain. Fortunately, it is a rare complication.
Side effects are not as severe with the topical forms
in the short term, but increase to about the level of the
oral drugs with long term use.
Some people report inconsistent response to treatment
with Prednisone, saying they respond better at some times
to a particular treatment course than they do at others.
Corticosteroids suppress the activity of the adrenal
glands, which must be restored gradually when the drug is
discontinued. This requires gradual tapering of the
steroid. Most physicians will not taper long term steroid
users faster than roughly 1mg per week or 5 mg per month.
For short term users, dosage may be lowered at a faster
rate, such as 5 to 10 mg per week.
Withdrawal symptoms can occur when the dosage is
lowered too quickly. These may include fever, malaise,
and joint pains. Since these can also be symptoms of IBD,
it is often difficult to tell whether they are the result
of insufficient steroid levels, or a true relapse of IBD.
If IBD symptoms begin to return during tapering,
standard procedure is to return to a slightly higher
dose, which is maintained until symptoms subside.
Tapering may then be resumed at a slower rate.
Long term use of steroids (more than a few days)
suppresses the adrenal gland's normal production of
steroids and can affect its function for a long time (up
to a year, or in some cases even two) even after steroid
use has stopped. During this period, the body may not be
able to produce an adequate supply of steroids during
extreme stress, such as surgery or severe infection.
If you've been taking steroids for a while you should
probably wear a MEDIC-ALERT necklace or bracelet
indicating the quantity and duration of steroid use. (Some
suggest carrying a note in the wallet, but such a note
will likely never be seen because standard operating
procedure for emergency medical personnel is to avoid any
contact with a patient's valuables for liability reasons).
If you require emergency surgery, this information can be
of vital importance since you'll need to be administered
additional steroids. Your body isn't capable of producing
enough steroids on its own to help survive the stress.
Because of the potential problems it is very important
that steroid therapy is closely supervised by a physician.
Increasing the period of time between steroid doses
can allow the adrenal glands to recover somewhat.
Alternate day therapy is simply taking double the daily
dose on every other day. Due to the duration of the
effects of steroids such as Prednisone, this can have the
same therapeutic results with fewer side effects.
Budesonide is currently in "beta testing".
It is a steroid that is processed by the liver so that
there are less severe side effects. Oral and enema forms
are available, depending upon the location of the disease
to be treated. Its role compared to the more established
steroid agents has yet to be defined. The impression of
many is that though it may be safer it may also be less
effective.
Adreno-cortico-tropic hormone is a drug that
stimulates the adrenal gland to release cortisone. It is
seldom used any more.
Steroid drugs unfortunately can cause osteoporosis.
Osteoporosis is a disease which results in the
destruction of bones causing them to become weak and much
more likely to fracture. Without protection within the
first six months of steroid therapy a person can lose 10
percent to 20 percent of bone mass. As many as one in
four of these people may eventually suffer a fracture as
a result. Unlike osteoporosis associated with aging,
steroid-induced osteoporosis can occur at any age, even
in children. For many years it was thought that only high
(>20mgs a day) doses of steroids were a problem, more
recent studies have shown that chronic use of low oral
doses -- as little as 7.5 milligrams a day -- can cause
significant though gradual bone loss.
Steroids reduce the amount of calcium the body absorbs
from food and increase calcium loss through the kidneys.
These actions result in a tendency for the level of
calcium in the blood to fall. To prevent this happening
the body responds by producing increased amounts of
parathyroid hormone. Parathyroid hormone is released to
remove calcium from storage in the bone and restore a
normal level. In addition steroids also cause bone
breakdown directly.
The best strategy is to avoid the problem entirely by
using the lowest effective dose of steroid. Also to use
topical steroids if possible instead of systemic steroids
by mouth.
Recently the American College of Rheumatology
recommended that either before or at the very start of
steroid therapy, patients should ideally be given a bone
density test, especially of the lower spine and the neck
of the thigh bone near where it meets the pelvis. This
test should be repeated every six to 12 months to monitor
the effectiveness of preventive measures and, if
necessary, to modify the course of treatment.
Everyone who must take corticosteroids should consume
at least 1,500 milligrams of calcium and 800
international units of vitamin D a day, either through
diet or supplements. Vitamin D is needed to enhance the
body's ability to absorb calcium and use it to build bone.
Patients on steroids should get regular weight-bearing
exercise, preferably for 30 to 60 minutes a day as this
can help prevent bone loss. They should should not smoke
or drink more than moderate amounts of alcohol as these
are associated with increased rates of bone loss.
Consideration should be given to hormone replacement
therapy in woman who are post menopause. Women who have
not yet reached menopause whose periods become irregular
or stop while on steroids should take oral contraceptives
unless there is a medical reason for not taking them. For
men on steroids consideration should be given to
measuring their testosterone level and, if found to be
low, given testosterone replacement.
Immunosuppressives such as 6-mercaptopurine (6-MP or
purinethol) or azathioprine (imuran) are increasingly
used in treating more severe IBD that does not respond to
5-ASA therapy and short term steroid therapy. The most
frequent use of these drugs is in the context of
inability to reduce the steroid dosages in steroid
dependent patients without causing a disease flare.
Physicians without significant experience in their use
can be reluctant to try them because they rarely can have
extreme side effects. Generally these side effects occur
at higher doses than are used in the treatment of IBD.
However, the emphatic opinion of most physician experts
in the management of IBD is that they are significantly
safer and more effective than long term use of high dose
steroids. The side effects that occur in a small minority
of the patients who take them can include various blood
problems, bone marrow suppression, extensive immune
suppression, kidney damage, liver damage and others.
There is no convincing evidence that they predispose to
the development of cancer at the doses used in treating
IBD patients. Usage of these drugs requires frequent
monitoring by blood tests; ideally a complete blood count
should be obtained every 3 months.
Azathioprine(Imuran) 6-Mercaptopurine (6-MP,
Purinethol ) :
Azathioprine is a drug that was originally used to
prevent rejection in organ transplant patients. 6-MP is
one of the metabolites of Azathioprine; that means that
Azathioprine is converted into 6-MP in the body.
Both drugs have shown some degree of efficacy when
used in combination with prednisone. Because they
facilitate the use of lower steroid doses they are
frequently called "steroid sparing" drugs. Most
people can tolerate these drugs without difficulty thus
helping avoid long term high dose steroids and the
predictable associated side effects. At this time it is
the consensus of experts in the management of IBD that it
is clearly preferable to treat a patient with long term
Azathioprine or 6-MP rather than with continued or even
intermittent high dose steroids.
Despite impressive data from clinical trials
supporting the use of 6-MP and azathioprine in both CD
and UC many patients are still treated with prednisone
for longer periods than are appropriate because of the
erroneous perception that Azathioprine and 6-MP are more
hazardous.
This perception is derived in part from the side
effect profile seen when these drugs were originally used
in preventing transplant rejection and also in the
treatment of leukemia. The important difference is that
significantly higher doses were used in these situations
than are now used in the treatment of both CD and UC.
These drugs were developed in the 1950s and were first
used for the treatment of IBD 30 years ago! Obviously a
lot has been learned about how to use them to maximum
advantage over the intervening years.
The minimum time to respond to the drug is about three
months and can be as long as 12 months. These drugs are
effective in maintaining remission in 60 - 80% of
patients.
An important side effect that occurs in 3-5% of
patients is pancreatitis. This usually occurs within a
few weeks of starting treatment and is manifested by
upper abdominal pain which may radiate to the back and be
associated with nausea and vomiting. If pancreatitis
occurs then the patient cannot take either Azathioprine
or 6-MP in the future.
Because of occasional problems with a reduced white
blood cell count it is recommended that patients have
complete blood counts on a regular basis; every three
months is recommended though they should be more frequent
during the first few months of therapy.
The issue of how long these drugs can safely be used
for has not been definitively resolved. An increasing
number of patients have been maintained on these drugs
for several years (> 3) without any significant long
term side effects noted.
Methotrexate (Folex, Mexate in the US) :
Like the other immunosuppressants, methotrexate may
have some benefit in treating active Crohn's disease.
Methotrexate has not been used as extensively as
Azathioprine or 6-MP but there is increasing data that it
may be useful. Methotrexate may be a useful option in
patients who are intolerant of Azathioprine or 6-MP.
Because of the occurence of liver disease in patients
taking methotrexate over a sustained period careful
monitoring of liver function is necessary. Patients
should not drink alcohol while taking methotrexate.
Methotrexate should not be used in pregnancy. Patients
taking methotrexate should not get pregnant.
Cyclosporine is another immunosuppressant drug that
was originally and is still used extensively for
preventing rejection of organ transplants such as kidney
and liver transplants.
Though initial hopes were high that it would be a very
good drug for severe and complicated CD the results have
been somewhat disappointing.
In severe CD particularly complicated by fistulas
there is data that high dose intravenous cyclosporine may
be useful in the short term. Low dose therapy for
maintenance of remission does not seem to be effective
and has unacceptable side effects.
In severe UC, particularly when a patient is on the
threshold of requiring urgent surgery there has been some
success with cyclosporine in inducing a remission. These
patients are generally treated simulataneously with high
dose steroids also and are started on 6-MP or
azathioprine also. After 3-6 months of therapy, when 6-MP
or azathioprine has hopefully become effective,
cyclosporine is stopped and simultaneously steroids are
reduced and stopped if possible. This approach seems to
be effective in the short term with a significant
proportion of patients with severe UC. However, a
significant proportion of these patients subsequently
have surgery because of inability to maintain them in
remission.
There are several different drugs in various stages of
development for IBD.
Many UC patients have reported that their symptoms
began after quitting smoking. In fact in the vast
majority of studies where it has been checked a
significantly lower proportion of UC patients smoke in
comparison to controls. This data is clearly consistent
with smoking having a preventive effect in UC. The
mechanism of this is not understood.
In marked contrast a higher proportion of CD patients
smoke compared to controls and continued smoking is a
predictor of post surgical recurrence of CD. This data
suggests that smoking may be a co-factor predisposing to
the development of CD. The mechanism of this
predisposition is not understood.
Due to the health risks of smoking, doctors have been
skeptical of this data. Recently more attention has been
devoted to understanding the relationship between smoking
and IBD. One question that has stimulated considerable
work has been whether nicotine is responsible for the
apparently protective effect of smoking in UC?
Two relevant articles were recently published in The
New England Journal of Medicine looking at the potential
therapeutic benefit of nicotine patches, normally used to
help people stop smoking, to induce remission of active
UC and to maintain remission. The patches were helpful in
some patients in the induction of remission but were not
helpful in the maintenance of remission. Most non smoking
patients in the studies suffered some side effects from
the nicotine, including nausea, vomiting,
lightheadedness, headache and sleeplessness. More work
needs to be done to clarify the role of nicotine in
therapy of UC.
It is important to note that IBD has features in
common with inflammatory diseases that involve other
parts of the body such as rheumatoid arthritis and
psoriasis for example. So therapies that are being
developed for these diseases may also be useful for
treating IBD. There has been considerable publicity
recently given to the new data about the treatment of CD
with antibodies against Tumor Necrosis Factor (TNF).
These antibodies are also being evaluated in the
treatment of rheumatoid arthritis.
When the immune system is activated resulting in
inflammation many chemical messengers are released. These
chemical messengers are produced by the cells of the
immune system and are called cytokines. These cytokines
interact with other cells encouraging them to become
activated and thus make the inflammation worse. TNF is
one of the most important cytokines involved in this
process. The term Tumor Necrosis Factor refers to one of
its actions which led to its discovery.
In the setting of an infection TNF frequently plays an
important role in helping the immune system respond
promptly and effectively. However, it is believed that
excessive and inappropriate production of TNF may be an
important contributory factor in the development of
several diseases characterized by inflammation and
activation of the immune system such as multiple
sclerosis, rheumatoid arthritis and others.
Various strategies have been used to evaluate the
importance of TNF in both CD and ulcerative colitis (UC).
Though some data does support a role it has been
difficult to convincingly demonstrate that there is
excessive production of TNF in either disease. The
available data does seem to suggest that TNF may be of
more importance in CD than UC. The fact that the new anti-TNF
treatments seem effective in some patients is the best
evidence that TNF is important in the disease process of
CD.
There has been one small study of an anti-TNF antibody
in UC and a preliminary report did not show impressive
results.
The treatment consists of an antibody which is a
protein that neutralizes the action of TNF. Originally,
the antibody was made by a mouse when it was injected
with human TNF. The immune system of the mouse recognized
the foreign nature of the human TNF and made antibodies
against it. One of these mouse antibodies was modified or
humanized so that it would be less likely to provoke an
adverse reaction when injected into a human. There are
two antibodies that have been used to treat CD. The
first, named cA2, was developed by the biotechnology
company Centecor. The cA2 antibody was initially used in
the treatment of severe infection. More recently it has
been evaluated for the treatment of rheumatoid arthritis.
Because of promising results in the arthritis studies a
group of Dutch physicians gave the antibody to a child
with severe CD and there was a dramatic response. This
encouraged more comprehensive studies of the
effectiveness of the cA2 antibody to treat CD in Europe
and the United States. The second anti-TNF antibody has
been developed by the biotechnology company British
Biotechnology and is called CDP571.
The antibodies blocks the action of TNF. The fact that
it is so effective in some patients has raised the
question whether it is having some additional effects on
the immune system; however this remains to be clarified.
The most important aspect of its use is that it implies
that TNF does indeed seem to have an important role in
the development of inflammation of CD in a significant
percentage of patients.
Like most treatments for IBD it does not seem to work
in all patients. In the recently reported studies most
patients who received the treatment had a beneficial
response about half of whom actually went into remission.
In those patients who have a response the effect is
temporary, lasting several months at best. The antibody
is given by intravenous infusion and cannot be given by
mouth. It is not clear whether it can be given safely to
the same patient more than once. If indeed it can be
given repeatedly it remains to be seen whether it will
continue to have a beneficial effect or whether
resistance will emerge.
The treatment will only be available as part of formal
clinical studies for the next few years. If it continues
to have positive results and becomes available as a
standard therapy in the next few years it is likely to be
expensive.
CD patients with active disease despite therapy with
steroids; this is a prerequisite for enrollment in the
studies. Those patients who may particularly be suitable
for the anti-TNF therapy are those who cannot tolerate 6-mercaptopurine
or in whom 6-mercaptopurine has not worked or have just
been started on 6-mercaptopurine and a therapeutic effect
is not expected for several months. IMPORTANT: the anti-TNF
antibodies are only available as part of formal studies
at present.
2.2.2.8 Q: What are the
alternatives available at present?
The best tested and most effective medications at
present are 6-MP and methotrexate. Other medications are
also being developed which block the action of TNF which
may be useful in the treatment of IBD in the future.
IL-10 is another cytokine like TNF. Cytokines are
chemical messengers produced by the cells of the immune
system that regulate its activity. Unlike TNF, IL-10
suppresses the immune system and is presently being
studied in the treatment of CD. The results of this study
are eagerly awaited.
There is some evidence that fish oil (attributed to
the eicosapentaenoic acid) has anti-inflammatory
properties which may be useful in the treatment of IBD
and rheumatoid arthritis. In addition it may also be
helpful in preventing atherosclerotic cardiovascular
disease. Patient acceptance of fish oil therapy has been
poor because of the indigestion and bad breath associated
with therapy. An Italian study last year using coated
capsules containing fish oil showed evidence of benefit
in preventing recurrences of CD with miminal side-effects.
However, these capsules are not widely available at
present. In the interim various fish oil preparations
containing eicosapentaenoic acid are available from
pharmacies and health food stores which may be of
therapeutic benefit despite the possible side-effect of
increased susceptibility to bleeding. Alternatively it
may be helpful to simply eat more fish in one's diet!
Many patients require treatment with more than one
medication to adequately control their symptoms.
Frequently, several different combinations are tried
before the best one is found. Once symptoms are brought
under control then attempts are made to reduce the
medications to a minimum.
At this point in time because there is no cure for IBD
(except removal of the colon for patients with UC) it is
advisable for many patients to continue taking
medications to keep them in remission. The reason for
this, which is supported by some studies, is that it is
much easier to keep a patient in remission rather than
treat a flare of the disease. Similarly, it is much
easier to use sun screen to prevent sunburn rather than
try to treat sunburn after it has happened.
Drug treatments are ineffective in about 20% of UC
patients. These patients must have their colons removed
due to debilitating symptoms. The colon may also removed
because of the threat of cancer. Removal of the colon
permanently cures the UC and usually all related symptoms.
Patients having these surgeries are generally
hospitalized for about a week and return to work in three
to six weeks.
There is NO role for resections of only part of the
colon in UC even when the disease is limited in extent as
it inevitably recurs in the colonic remnant.
Once the colon is removed there are several options
which may avoid the need to wear a bag appliance to
collect waste.
The entire colon and rectum are removed and a small
opening, about the size of a quarter, called an ileostomy
is made in the lower right corner of the abdominal wall.
The small intestine is then connected to this opening and
a colostomy bag is worn over the opening to collect waste.
The patient then empties the bag about four times a day.
Another operation that gained popularity over an
ileostomy avoids the use of a colostomy bag by forming a
pouch from the last 15-40 cm of ileum inside the wall of
the lower abdomen. A nipple valve in the abdominal wall
allows the patient to empty the pouch by inserting a
catheter through the ileostomy. Initially, the pouch must
be emptied frequently, eight to ten times daily. The
pouch stretches and, after several months it will only
have to be emptied four to five times a day. This
operation used to be performed in two separate steps and
the patient would have to wear a colostomy bag for
several months before the pouch could be attached. The
operation is now generally performed in one step, though
it may be performed as two steps if the patient is
severely ill at the time of surgery.
This procedure is generally not performed because it
has many of the possible complications and none of the
benefits of the Ileoanal Anastomosis, described below.
Since UC inflames only the innermost layer of the
colon, the rectum can be stripped of this layer and
attached to the ileum after the colon is removed. Early
attempts to perform this surgery were frustrating as
patients predictably suffered from incapacitating
diarrhea. The operation was modified in 1980, adding an S
or J shaped pouch just above the rectum and patients
achieved continence. The patient can then pass stools
normally, though bowel movements are more frequent and
watery than in an otherwise healthy individual without
IBD. Like the Kock pouch, eight to ten bowel movements a
day are typical immediately after the surgery. The pouch
continues to stretch for several years and eventually
it's only necessary to have four or five bowel movements
a day. In rare cases (around 5% when the surgery is
performed by an appropriately trained surgeon) when other
complications, such as infection occur, the pouch may
need to be converted to an ileostomy.
The most common complication of these operations is
inflammation of the pouch, called pouchitis. Symptoms
include pain, bloating, and diarrhea. Most patients can
control this by irrigating the pouch with saline solution
and taking antibiotics. In a few cases, a diagnosis of CD
is confirmed in patients thought originally to be
suffering from UC.
Problems with the nipple valve in a continent
ileostomy can cause leakage of stool and an inability to
insert the catheter. About 10% of patients require a
second operation to repair the nipple valve.
Remember that these have the same risks as any
surgery, but that's outside the scope of this FAQ.
Unlike in UC, there is no surgical cure for CD.
Physicians use the phrases "minimalist surgery"
and "surgery avoidance" when discussing
surgical options for CD. This is because new Crohn's
lesions can appear after previously diseased areas have
been removed and even diseased tissue may be functionally
useful. Many surgeons also feel that "surgery in
Crohn's patients just leads to more surgery".
Surgery for CD is usually a resection of the small
intestines.
Severely affected portions of the intestine are
removed and the healthy ends are sewn together. This in
no way prevents inflammation from recurring later and is
generally performed only when the inflammation is unable
to be controlled by medical therapy.
Smoking is associated with recurrent disease following
surgery in CD patients. Clearly, CD patients must be
strongly encouraged to stop smoking.
There is some evidence that 5-ASA drugs (especially
Pentasa for small bowel disease) may be useful in
preventing disease recurrence after surgery. Some experts
use 6-MP following surgery in patients with a high risk
of recurrence and there is a trial in progress to see if
it works in this setting. There is also some limited
evidence that metronidazole may be helpful in preventing
disease recurrence following surgery. Fish oil may also
be a relatively safe option though it is not of proven
benefit.
Most patients find that certain foods are tolerated
less well than others when symptoms are active, but there
is no evidence that these foods directly affect the
inflammation. The most common offenders are milk products
(see the section on lactose intolerance below), spicy
foods, fats, and sugars. In general, a bland low fiber
diet avoiding fruits, vegetables, nuts, and whole grains
is preferable when the disease is active. A high fiber
diet is to be recommended when symptoms aren't present.
Due to reduced appetite, malabsorption of nutrients,
and increased nutritional needs, it's important to make
sure you follow a proper diet. Since the small intestine
is where the body absorbs nutrients from food, CD
patients may have problems absorbing these nutrients. If
more than two or three feet are either diseased or
surgically removed,malabsorption, especially of fats, the
minerals calcium and magnesium, and the fat soluble
vitamins A,E, and D, can be a problem. Resection of at
least two feet may also increase absorption of oxalate,
which reacts with calcium to form kidney stones. A low
oxalate and low fat diet will help prevent kidney stones.
Spinach, cocoa beans, rhubarb, beets, instant coffee,
diet sodas and tea are all high in oxalate. If only the
terminal ileum, the last two to three feet of the small
intestine, is diseased or resected, absorption will be
normal except for vitamin B-12 which can be supplemented
by monthly injections. Iron supplements are helpful in
treating the anemia and patients should drink plenty of
fluids to replace those lost from diarrhea.
Astronaut diets (for example Ensure, Sustacal and
Peptamen) are liquids meeting all nutritional needs and
are almost completely absorbed in the upper intestinal
tract. Because they don't require much digestive effort
by diseased bowel they often seem to be better tolerated
than regular food by patients with active and/or severe
disease. Elemental diets (for example Vivonex) consist
mainly of pure amino acids (the building blocks that make
up proteins) and are even easier to digest. There is some
evidence that elemental diets may be helpful
therapeutically in CD. However, these diets are expensive
and patients find it difficult to comply with them on a
long term basis so they have not evolved into a practical
treatment.
In contrast there is no evidence that elemental diets
are of benefit in UC.
Total parenteral nutrition (TPN), or hyperalimention,
delivers a concentrated solution of nutrients
intravenously. This is used in very active disease either
giving it time to subside, or to nourish the patient
before surgery.
People with Crohn's Disease generally benefit more
than those with UC because CD usually affects the small
intestine, which is where nutrients are absorbed. TPN
may, however, occasionally be warranted in critically ill
people with UC.
It's commonly estimated that about 30% of the world's
adult population suffers from lactose intolerance, though
this may be even higher in patients with IBD. A much
higher than normal fraction of Asians suffer from lactose
intolerance.
Lactose is a sugar found in milk, milk products, and
foods made with milk. The enzyme lactase, normally
produced in our intestines, breaks down lactose during
digestion. Lactose intolerant people don't produce enough
lactase and therefore cannot digest lactose.
Symptoms of lactose intolerance include a bloated
feeling, abdominal pain, flatulence, and diarrhea shortly
after consuming milk or milk products. Sound familiar?
It's not something that you want to subject yourself to
in addition to the symptoms of Crohn's or UC. A simple
laboratory test can determine whether one is lactose
intolerant or not. The severity of symptoms is highly
individual and most people do not need to eliminate
lactose from their diet entirely.
1. Reduce or Remove milk and milk containing foods
from your diet. These include milk chocolate, butter,
cheeses, ice cream and lactose--it's an ingredient by
itself in some foods. Check the label! 2. Eat foods
containing lactose with meals containing protein and fat,
not alone. 3. Use a lactose reducing product available
over the counter at most pharmacies (Dairy Ease or
Lactaid). These contain lactase and are either consumed
with lactose rich food or added to it before eating. Some
dairy products have reduced lactose content. These
include yogurt and Lactaid Milk. 4. Fermented milk
products, such as aged cheeses, contain less lactose and
are usually better tolerated. Cottage and ricotta cheese
are OK, cheddar has about the least. Buttermilk contains
as much lactose as milk. 5. A calcium supplement may be
needed if dairy products are reduced or eliminated from
your diet.
Emotional stress plays a large part in the health of
some patients and is often cited as the trigger of a
relapse, though there is no clear cause and effect
relationship proven. It may be more likely be that stress
is one result of a flare-up rather than being a factor
contributing to one. Treatment of IBD sometimes may
usefully include the teaching of stress reduction
techniques such as meditation.
This is a controversial subject with somewhat "political"
overtones. Many patients resent the assumption of family
and friends and even some doctors that stress is a cause
of their illness, when in fact it is just an exacerbating
factor (as is the case with other illnesses, as well).
Many people need reassurance that all this is not their
fault or "all in their head". It's been proven
that stress does NOT cause IBD, although with IBD as with
any illness stress can exacerbate symptoms.
Because of the nature of these illnesses and the
unpleasant symptoms that result patients frequently feel
very uncomfortable about discussing them even with close
friends and family. Denial may be a factor that inhibits
patients from getting appropriate evaluation and therapy.
Many patients find patient support groups to be
extremely helpful in addressing these issues and enabling
patients to constructively and positively learn how to
live with these chronic illnesses. Many patients not
comfortable with group discussions have found it
particularly helpful to consult with a psychologist
experienced in the evaluation of patients with IBD.
Significant anecdotal evidence suggests that flares of
IBD often occur after increased use of non-steroidal anti-inflammatory
drugs (NSAID's), such as aspirin and ibuprofen.
Accordingly, patients should be very careful about taking
these medications and be aware that they may cause a
flare of their disease. In fact, some physicians who are
very experienced in managing IBD feel these drugs should
rarely if ever be used by IBD patients.
For your physician to treat you most effectively it is
vital that you adequately describe your symptoms. Many
patients are reticent about describing urgency and
episodes of incontinence for example which may be readily
treated with local topical therapy. If despite the best
efforts of your physician you are not doing well either
having continued symptoms or requiring continued high
dose steroids then it may be appropriate to consider
asking for a second opinion. This is best done in
conjunction with your regular physician.
Back to Main
Page