Medical Treatment of Pituitary Tumors
A. Prolactin producing tumor (Prolactinoma):
- What are the benefits and limitations of medical treatment?
- How do the medications work?
- Is there a way to measure a tumor's "receptors"?
- Why don't these medications always reduce prolactin
to normal?
- Do these medications "cure" the
tumor? Can I stop the medication later?
- Is one medication more effective than another?
- If my prolactin level returns to normal, will I be
able to get pregnant?
B. Growth hormone producing tumor (Acromegaly):
- Why should I have treatment
after I’ve
had surgery to remove the tumor and I feel better?
- My tumor makes growth hormone, what is the IGF-1 test
and why is it important?
- What is Somatomedin C?
- What is the role of medical treatment for a growth
hormone producing tumor?
- What medications are available for treatment of Acromegaly?
- How do the medications differ?
- What are the side effects of these medications?
- Can medical treatment be used instead of surgery for Acromegaly?
- Does medical treatment shrink the tumor?
- Can patients receive financial assistance in receiving these medications?
- I have had surgery, why do I still have a problem and have to have
radiation treatment and take medication?
C. ACTH producing tumor (Cushing's Disease) :
- Are there any medical treatments for ACTH producing tumors?
- What are the side effects of ketoconazole (Nizoral)?
- I had surgery for Cushing's, why do I have to take steroid (cortisol)
replacement (hydrocortisone (Cortef), prednisone or dexamethasone)?
- I have been cured of my Cushing's - why don't I feel normal, 6 months
after my surgery?
D. Non functioning pituitary tumor :
- Is there any medical treatment for this type of tumor?
- Should I try medication before surgery?
E. TSH producing tumor:
- Is there a medical treatment for these tumors?
F. Craniopharyngioma:
- Is a craniopharyngioma
a pituitary tumor?
- Is there medical treatment for a craniopharyngioma?
II. Medical Treatment of Pituitary Tumors
Any medical therapy for a pituitary tumor should reduce hormone overproduction
by the tumor, and, ideally, decrease the size of the pituitary tumor so that
if there is a visual abnormality, this is corrected. Reduction in tumor size
should improve or relieve headache associated with the tumor. Because not all
pituitary tumors produce an excessive amount of a hormone or hormones, the
only measure of successful medical therapy for a non hormone-producing tumor
is the effect on tumor size and clinical symptoms (visual problems, headache).
A. Prolactin producing tumor (Prolactinoma):
1.
What are the benefits and limitations of medical treatment?
Medical therapy is usually more effective than surgery for this tumor
type, particularly for large tumors (macroadenoma, > 10 mm). In patients
with large tumors, surgery results in normal prolactin levels in < 20% of
patients. Surgery is effective in removing the bulk of the tumor, but prolactin
levels remain elevated; surgery does not produce a "cure". In this
situation, if the patient has had surgery and still has an elevated prolactin,
medical treatment is necessary. In patients who have a small tumor (< 10
mm), the chances of a "cure" with surgery are greater, on the order
of 80% to 90%. However, even with successful surgery, there is a risk of recurrence
of the tumor at a later date (months, years); approximately 13 to 20% of patients
have a recurrence of elevated prolactin within 5 years of surgery. The limitations
of medical therapy are that most patients require long term therapy, side effects
of therapy, cost, and a lack of response in a small percentage of patients.
2.
How do the medications work?
Prolactin is normally inhibited (suppressed) by the hypothalamic (brain)
hormone, dopamine. This hormone, dopamine normally travels down the pituitary
stalk (connects the brain to the pituitary gland) in the blood vessels
to inhibit prolactin production. Drugs known as dopamine agonists act like
dopamine to inhibit prolactin production. Dopamine agonists available in the
U.S. include cabergoline (Dostinex), bromocriptine (Parlodel) and pergolide
(Permax). A very effective drug, quinagolide (Norprolac), is only available
in Europe and Canada. Dostinex is a long acting drug and can be taken once
or twice a week; bromocriptine is given up to 3 times a day; pergolide is usually
given once each day.
All of these drugs act on the tumor in the same way - by inhibiting
or reducing the amount of prolactin made by the tumor and thus causing the
tumor to shrink. Over 90% of patients treated with one of these medications
have a decrease in prolactin and a decrease in tumor size. Some patients are
not able to take these medications because of side effects (nausea, vomiting,
nasal stuffiness, and constipation). Cabergoline causes fewer side effects
than bromocriptine or pergolide, but cabergoline is more expensive than the
other drugs. Some studies indicate that cabergoline may be more effective than
bromocriptine or pergolide in reducing prolactin and tumor size in some patients.
A minority of patients do not have a good response to these drugs.
Why? These drugs act on dopamine "receptors" which are on the surface
of the tumor. A receptor can be visualized as a keyhole, the drug is the key
- in order for the drug (“key”) to be effective, the tumor must
have an adequate number of receptors ("keyholes") and the drug must
be able to bind (attach) to the receptor (keyhole). In patients who do not
have a good response to medication, there are not enough receptors (keyholes)
on the tumor surface or the binding to the receptors (keyholes) is not adequate.
In this situation, alternative treatments such as surgery and/or radiation
therapy may be necessary.
3.
Is there a way to measure a tumor's "receptors"?
No blood tests can determine this. Research studies have been done
which have demonstrated this principle by measuring the number of receptors
on tumors removed by surgery. The only way to judge the effect of medical treatment
is a trial of a dopamine agonist drug (bromocriptine, pergolide, or cabergoline)
4. Why
don't these medications always reduce prolactin to normal?
Although these medications are effective in lowering prolactin and
reducing tumor size, the prolactin level may not decrease to normal (< 20).
Why?
When a tumor is large and produces a very high prolactin level (several hundred,
in the thousands), the medication may lower prolactin by 90%; if the level
before treatment level is 10,000, a 90% reduction lowers prolactin to 1,000,
certainly not normal (normal is usually < 20), but a substantial reduction.
The tumor size is decreased but it does not disappear. This may be acceptable
if there are no other ill effects of the tumor such as headache or loss of
vision. The most frequent hormonal problem resulting from an elevated prolactin
is hypogonadism (loss of hormone production by the ovaries or testes). Hypogonadism
in a pre-menopausal woman results in loss of menstrual periods and difficulty
becoming pregnant. Hypogonadism in men causes impotence (difficulty obtaining
an erection) and infertility. Hypogonadism is treatable with hormone replacement,
testosterone in men, estrogen and progesterone in women, even if the prolactin
level is reduced to normal. Restoration of fertility may require additional
treatments with injections of the pituitary hormones, LH and FSH.
5. Do
these medications "cure" the tumor? Can I stop the medication later?
Usually not. These medications control the tumor; they do not destroy
the tumor. The medications are only effective as long as they are taken. If
the medication is stopped, the prolactin will usually increase and the tumor
will also increase in size. In a patient with a prolactin-producing tumor – the
medication must be taken regularly as prescribed, to control the problem.
In the situation of a very small tumor (< 10 mm), the medication
is often stopped after a year or more to see if the prolactin stays normal.
In a minority of patients, this is successful and the prolactin remains normal.
The possible reason for this is that the small tumor has somehow self-destructed
(this occurs in a few patients). If the prolactin is normal after stopping
the medication, the level should be monitored every few months to make sure
it remains normal. A recent study showed that approximately 15% of patients
who had a large tumor (> 10 mm, macroadenoma) continued to have a normal
prolactin when the medication was stopped after 5 years of treatment. If the
medication is stopped, regular medical follow up and measurement of the blood
prolactin level is necessary to determine if restarting medical treatment is
necessary.
6.
Is one medication more effective than another?
The different
drugs act the same way. However, cabergoline is more effective than the other
drugs. All dopamine agonists reduce prolactin and tumor size in the majority
of patients. Most commonly, the benefits of one drug over another are related
to:
(b)
cost,
(c)
ease of taking the medication.
Some patients have side effects with one drug and little to no side
effects with another drug. The best way to determine this is a trial of a different
medication. The most important thing about avoiding side effects is to always
take the medication with food and preferably at night. This will minimize side
effects such as nausea or vomiting.
The issue of cost is particularly important for patients who do not
have insurance plan to cover the costs or if there is high co-pay for medications.
Pergolide is only approved in the U.S. for another indication (Parkinson's
disease), it is not FDA approved for treatment of a prolactin producing pituitary
tumor. Therefore, women who wish to become pregnant should be treated with
bromocriptine. Bromocriptine, ha been given to several thousand women who wished
to become pregnant. A worldwide surveillance has shown there that there is
no increased risk (above the normal risk in the general population) of birth
defects (there is always some risk of birth defects, even for a woman taking
no medications). Cabergoline is also not approved for pregnancy; information
on several hundred women who became pregnant while taking cabergoline reveals
no increase (above the normal risk) of birth defects for the baby. Until there
is more experience with cabergoline in women who become pregnant, bromocriptine
should be used
7.
If my prolactin level returns to normal, will I be able to get pregnant?
Yes - if the only reason for infertility is the high prolactin level.
There are many causes of infertility, but if high prolactin is the only reason,
lowering prolactin to normal results in the same chances for pregnancy as the
general age-matched population (fertility declines with increasing age, especially
after 32 years).
B. Growth hormone producing tumor (Acromegaly):
1. Why should I have treatment after I’ve had surgery
to remove the tumor and I feel better?
An unfortunate fact is that when most patients are diagnosed with acromegaly
(usually a delay of 7 to 8 years after beginning of symptoms), the pituitary
tumor is large and may invade areas that the surgeon cannot go into (the arteries
on each side of the pituitary gland) or where the tumor has invaded surrounding
structures (bone below the gland or coverings near the pituitary gland). The
reported surgical remission rates (normal growth hormone, normal IGF-1) range
from 57% to about 75%, depending on the size of the tumor and expertise of
the surgeon. Surgery is usually effective in removing the bulk of the tumor
and reliving headaches and improving visual problems, but it maynot
be possible to remove the entire tumor. Additional treatments are necessary
to lower growth hormone and IGF-1 levels to normal in order to reduce the risk
of the complications of continued excessive growth hormone production.
2. My tumor makes growth hormone, what is the IGF-1 test
and why is it important?
While the tumor makes growth hormone, its action and effect is dependent
on production of IGF-1 (insulin-like growth factor-1); Blood IGF-1 is produced,
primarily in the liver, in response to the amount of growth hormone made by
the pituitary gland. Growth hormone works primarily through IGF-1. The blood
IGF-1 level is also a very reliable indicator of overall growth hormone
production. Since blood growth hormone levels fluctuate every few minutes over
24 hours, a single growth hormone level is only a “snapshot” in
time and does not reflect overall growth hormone production. The blood IGF-1
level is the most reliable indicator of overall growth hormone production and
is a reliable measure of activity in a patient with acromegaly. A normal blood
IGF-1 level indicates remission or, in patients taking medication, control
of acromegaly.
3. What is Somatomedin C?
Somatomedin C and IGF-1 are the same hormone, with different names.
4.
What is the role of medical treatment for a growth hormone producing tumor?
Medical treatment is usually given if patients are not cured by surgery.
In addition, medical therapy may also be used as the first line of therapy.
This depends on the size and location of the tumor. Although medications can
lower growth hormone and/or IGF-1 levels, they do not always shrink the tumor.
Because of the long-term complications of excessive growth hormone (joint problems,
diabetes, high blood pressure, facial changes, sweating, risk of colon polyps
and colon cancer, and premature heart disease and premature death), it is important
to reduce growth hormone and/or IGF-1 to normal. Most often, medical therapy
is given to lower GH and IGF-1 to normal after unsuccessful surgery. Radiation
therapy to the remaining tumor is another option. Since it may take months
or years before the radiation therapy is effective, medical treatment is used
to control excessive growth hormone production while waiting for the effects
of radiation. Medications do not cure the problem - they control it. The medication
is effective only as long as it is taken as prescribed.
5.
What medications are available for treatment of Acromegaly?
Currently used drugs include:
- Dopamine agonist: bromocriptine (Parlodel), cabergoline (Dostinex),
pergolide (Permax)
- Somatostatin analogs: octreotide (Sandostatin), octreotide LAR (Sandostatin
LAR), lanreotide or lanreotide (Autogel; not currently available in the
U.S.).
- Growth
hormone receptor antagonist, pegvisomant (Somavert).
6.
How do the medications differ?
The dopamine agonist drugs, bromocriptine, pergolide and cabergoline
may improve symptoms but are not very effective, resulting in a normal hormone
levels in less than 10%. Cabergoline may be more effective than the other drugs.
In addition, patients more likely to respond are those in whom IGF-1 and GH
levels are only slightly elevated.
Octreotide-LAR and lanreotide lower growth hormone, and therefore,
IGF-1 levels. Octreotide-LAR is given as an injection in the buttock
every 28 days or sometimes less frequently; this is usually administered in
a doctor’s office.
Octreotide-LAR and lanreotide reduce growth hormone and IGF-1 levels in approximately
90% of patients. However lowering of these hormone levels to normal occurs
in approximately 45% to 60% of patients. The reason is the same as that which
occurs with medical treatment of prolactin producing tumors - the number of "receptors" on
which the medication can act. Short acting octreotide must be given at least
every 8 hours by a subcutaneous (under the skin) injection. A very small needle
(insulin syringe and needle) is used and the discomfort is usually not a problem
for most patients. Some patients have a better response giving the injection
every 6 hours; others use a small pump (worn on the belt or in a shirt pocket)
which delivers the medication continuously (the needle under the skin is changed
every 2 or 3 days). The long acting preparation, Sandostatin LAR is more convenient
to take (once every 28 days) but requires a visit to the doctor’s office.
Lanreotide (not currently available in the U.S.) is usually administered every
14-30 days depending on the response.
Some patients have a better response to the combination of a dopamine agonist
and octreotide. In patients who still have mild elevations of IGF-1 levels
during octreotide treatment, the addition of a dopamine agonist may reduce
IGF-1 levels to normal. Regardless of which regimen in used, these medications
do not cure the disease; they control excessive growth hormone production by
the tumor. Therefore, the medication(s) is effective only as long as it is
taken regularly.
Pegvisomant (Somavert): This medication does not act on the pituitary tumor
- it blocks the action of growth hormone at the liver to reduce production
of IGF-1. Up to 97% of patients treated with Somavert have a reduction in IGF-1
to normal. Because the medication doesn’t act on the tumor, the tumor
itself is not treated. Although most tumors that secrete growth hormone grow
slowly, there is a risk of continued growth of the tumor in Somavert-treated
patients.. This medication therefore is not typically used without other treatments
if the tumor is large or showing signs of growth. Regular MRI scans are necessary
to find out if there is growth of the pituitary tumor in patients treated with
Somavert.. This medication is given as an injection under the skin with a small
needle similar to the one patients with diabetes use to give insulin and is
self-administered once a day.
7. What are the side effects of these medications?
All dopamine agonists have similar side effects. However, some drugs may
cause mild or no side effects in patients who may have side effects from other
similar drugs.
Bromocriptine (Parlodel): nausea, vomiting, dizziness (especially with standing
up quickly), headache, nasal stuffiness, constipation. Side effects are minimized
by always taking the medication with food.
Pergolide (Permax): nausea, vomiting, dizziness (especially with standing
up quickly) ,headache, nasal stuffiness, constipation. Side effects are minimized
by always taking the medication with food. Liver function tests need to be
checked in the blood as some patients may develop an abnormality.
Cabergoline (Dostinex): occasional nausea, vomiting, dizziness (especially
with standing up quickly) ; fewer or less noticeable side effects than bromocriptine
or pergolide.
Sandostatin LAR, lanreotide: when beginning treatment: loose stools, light-colored
stools, occasional diarrhea and abdominal cramping. This side effect usually
lessens or disappears within 1 to 2 weeks. The long-term side effect is the
risk of developing gallstones - approximately 18% of people develop gallstones
or gall bladder sludge seen on ultrasound testing.. The gallstones usually
do not cause a problem, and in most patients do not cause symptoms. However,
there is always a small risk of developing problems.
When beginning treatment with Sandostatin LAR, the recommendation is to first
take the short acting preparation (octreotide) as an injection 3 times a day
for a week in case side effects are too bothersome. If there are bothersome
side effects, the long acting preparation, Sandostatin LAR, may not be suitable.
In some centers, the patient is given a single or a few injections of the shorting
acting Sandostatin to make sure there are not side effects and then the patient
is given an injection of long acting Sandostatin - Sandostatin LAR.
Pegvisomant (Somavert): Development of abnormal liver tests occurred in 2
of approximately 150 patients treated with this drug. The tests returned to
normal when the medication was stopped. The reason for this side effect is
not known. It is recommended that liver tests be measured before beginning
treatment and every month for the first 6 months of pegvisomant treatment and
at regular intervals afterward. Growth of the remaining tumor has occurred
in a few patients; this means that regular MRI studies are necessary to detect
this. Previous radiation treatment to the tumor appears to make it less likely
that there will be tumor growth, but regular MRI scans are necessary to make
sure there is no growth.
8. Can medical treatment be used instead of surgery for Acromegaly?
Occasionally, but not usually. Most patients have a macroadenoma (tumor greater
than 1 cm) at the time of diagnosis. In this situation, surgery to remove as
much of the tumor as possible is usually the first treatment. This is particularly
important if the tumor is close to the eye nerves (optic chiasm). If the patient
cannot undergo surgery, or there is no clear benefit of surgery, medical treatment,
preferably with Sandostatin, is used. Again, this is not a cure; medical treatment
with a somatostatin drug controls the problem, optimally in approximately 45
to 60% of patients. If a patient has a microadenoma tumor less than 1cm), the
cure rate with an experienced pituitary surgeon is usually excellent and therefore
surgery is typically recommended.
9. Does medical treatment shrink the tumor?
Octreotide, Sandostatin LAR and lanreotide: Approximately one-third of patients
have a reduction in tumor size. The amount of tumor shrinkage is usually modest,
approximately 30% shrinkage. In patients with a large tumor, especially when
close to the optic nerve, causing symptoms because of the large size of the
tumor and/or is in an area a surgeon can safely remove, surgery is recommended
as the first treatment to remove as much as possible with medical treatment
afterward if there is continued excessive growth hormone production.
Pegvisomant (Somavert): No; this medication does not act directly on the
growth hormone producing tumor - it acts to block the action of growth hormone
on the liver and reduces IGF-1 production and does not cause reduction in tumor
size.
10. Can patients receive financial assistance in receiving these medications?
Sandostatin LAR: Novartis has an assistance program for patients who qualify.
The Novartis patient assistance telephone number is: 1-877-LAR-INFO. If the
patient has Medicare - this cost is covered by Medicare since the injection
of Sandostatin LAR must be administered at a doctor's office.
Pegvisomant (Somavert): The Pfizer Bridge program works with PSI, and independent
company, to provide assistance for patients who qualify. The Bridge program
telephone number is 1-800-645-1280, The PSI telephone number is 1-800-366-7741.
11. I have had surgery, why do I still have a problem and have to have radiation
treatment and take medication?
Some patients are not cured with surgery. The reasons for this are most commonly
related to the size of the tumor: the larger the tumor, the less likely it
can be removed completely. Additionally, the tumor may have spread to nearby
structures such as bone, the cavernous sinus (location of carotid artery and
nerves controlling eye movements) and the membrane surrounding the gland (dura
mater). In this situation, the surgeon removes all that can be safely removed,
but if the tumor has invaded surrounding structures such as bone or the cavernous
sinus or the membrane covering the pituitary, excessive growth hormone production
may persist. Surgery is usually the first step to remove as much of the tumor
as possible, since the medical treatments do not always shrink the tumor and
if present, relieving pressure on the optic nerve.
C. ACTH producing tumor (Cushing's Disease) :
1. Are there any medical treatments for ACTH producing tumors?
No. There are no approved medical treatments for the pituitary tumors that
cause Cushing’s. However, there are medications that can reduce cortisol
production by the adrenal glands, but do not have any effect on the pituitary
overproduction of the hormone ACTH (the pituitary hormone that stimulates the
adrenal glands to make too much cortisol). Thus, medications are used to control
adrenal gland cortisol overproduction, but do not treat the source of the problem
- the pituitary gland. However, by blocking the production of cortisol by the
adrenal glands they can reduce many of the problems such as hypertension, weight
gain, diabetes, tendency to infection, depression and many of the other problems
that are caused by too much cortisol. Ketoconazole (Nizoral) is a medication
that reduces adrenal gland cortisol production. This medication is most often
used in patients who are not cured of Cushing's after surgery, are too ill
to be operated on and need to have cortisol levels quickly lowered before surgery
and while waiting for therapy to become effective in patients treated with
radiotherapy. If a drug to lower cortisol is prescribed, careful monitoring
is necessary to determine if the dose is effective (measure 24 hour urine cortisol
level), to make sure it does not reduce cortisol to below normal (measure morning
blood cortisol level and sometimes urine cortisol tests as well.) and to make
sure there is no ill effect on the liver. This drug is usually given twice
a day. Sometimes, when giving the exact amount of ketoconazole is difficult,
a very small amount of a steroid, for example dexamethasone, is used together
with ketoconazole to keep the adrenal glands blocked down but to prevent the
patients from having too little cortisol.
Another drug that may be used in patients who cannot tolerate ketoconazole
is metyrapone. This medication blocks the production pathway of cortisol by
the adrenal glands. It may stimulate ACTH from the tumor and therefore is not
usually the first drug used unless ketoconazole cannot be given.,
2. What are the side effects of ketoconazole (Nizoral)?
Ketoconazole (Nizoral): the most common side effect is nausea and abnormalities
in liver function. Before this medication is taken, a blood test should be
measured to make sure there are no significant liver abnormalities. If the
patient develops fatigue or jaundice, liver tests should be measured again
and the medication stopped immediately. If liver tests become abnormal, they
usually return to normal after the ketoconazole is stopped. Other side effects
include vomiting, abdominal pain and itching.
Metyrapone: the most common side effects are nausea and sometimes vomiting.
3. I had surgery for Cushing's, why do I have to take steroid (cortisol)
replacement (hydrocortisone (Cortef), prednisone or dexamethasone)?
.A patient cured of Cushing’s disease should have very little if any
measurable cortisol. Once the tumor has been removed completely ,the rest of
the pituitary gland is still suppressed (relatively "asleep"). Because
the high cortisol levels from Cushing’s will cause the normal part of
the pituitary gland that makes ACTH to shut down. it may take several months
for the normal ACTH producing cells to start functioning again. In the mean
time, steroid replacement is necessary to protect against too little cortisol
(adrenal insufficiency). In patients cured of Cushing’s disease, taking
cortisol replacement is essential for life. At a later date, the need for continued
steroid replacement is determined by blood tests. Most, but not all patients
who are cured of Cushing’s disease will not need steroids after a year
is over and sometimes sooner
If a person has to take steroid replacement (hydrocortisone, prednisone,
dexamethasone) he/she should wear a medical alert bracelet or necklace, which
identifies the need for steroid treatment.
4. I have been cured of my Cushing's - why don't I feel normal, 6 months
after my surgery?
This is a common question and a very common problem. Cushing's affects every
system of the body; it causes problems gradually, particularly its effect on
muscles and body fat. With Cushing's, muscles become thin and weak. It takes
a long time for the body to "repair" itself, usually 9 to 12 months.
It is quite common for patients to still feel weak and have achy muscles several
months after successful surgery or successful radiation treatment. More positively,
the problems with depression, concentration and memory may improve fairly soon
successful pituitary surgery. Usually most patients have improvement in mood
and depression 6 months after successful treatment. However, they are still
frustrated that they are not “back to normal”. Unfortunately, the
excess weight does not "magically" disappear - it takes time and
a weight reduction diet to return to normal body weight. The important word
here is: patience. Occasionally some patients may experience an increase in
depression and anxiety after cure of Cushing’s as the body re-adjusts
to large changes in cortisol going from very high to low levels.
D. Non functioning pituitary tumor :
1. Is there any medical treatment for this type of tumor?
Generally, no. There are no specific medical treatments for this type of
tumor. The best treatment is surgery to remove the tumor. Dopamine agonists
such as bromocriptine or cabergoline have been used in a few patients who cannot
have surgery. A small minority of patients have had some improvement in vision
because of slight reduction in tumor size and relief of pressure on the optic
chiasm (eye nerves above the pituitary gland). However, this medicine does
not cause dramatic tumor shrinkage - the best treatment is to remove as much
of the tumor as possible with surgery.
2. Should I try medication before surgery?
Not if there loss of vision. Unless there is a reason surgery cannot be performed,
the best treatment is removal of as much of the tumor as possible. Additional
treatment such as pituitary radiation may be necessary to treat any remaining
tumor and to prevent re-growth. It is important to have an MRI scan once a
year to detect any tumor re-growth. Since there is no blood test to indicate
excessive hormone production, the MRI scan is the only way to determine if
there is re-growth of the tumor.
E. TSH producing tumor:
1. Is there a medical treatment for these tumors?
Surgery to remove this type of tumor is the most common therapy used. In
some patients, residual tumor tat cannot be removed by surgery is treated with
octreotide and this therapy may improve the hyperthyroidism ( too much thyroid
hormone ) that results when the TSH from the tumor stimulates the thyroid gland
to make too much thyroid hormone. In some patients, medication to lower thyroid
hormone levels may be used before, and in some cases after surgery. These medications
are methimazole (Tapazol) or PTU ( propylthiouracil). These medications do
not work on the tumor but work directly on the thyroid to block thyroid hormone
production. Both of these medications work in the same way although methimazole
is about 10 times stronger so that much lower doses are needed. These drugs
are usually well tolerated although very rarely, effects on blood counts may
occur and liver problems rarely occur.
F. Craniopharyngioma:
1. Is a craniopharyngioma a pituitary tumor?
No although the tumor may be in the area of the pituitary. A craniopharyngioma
arises from abnormal development of the pituitary gland during fetal (in the
womb) development. It may be located within the pituitary gland or above the
pituitary gland. This is a tumor that one is born with and may enlarge at any
time even in people over 60 years of age. It is not a cancer although some
tumors can grow quickly and may return after surgery. A craniopharyngioma may
be discovered in childhood or at any age in adulthood. This type of tumor does
not produce hormones but frequently interferes with normal pituitary gland
function and may cause diabetes insipidus (a disorder of water balance with
frequent urination and excessive thirst, this is not sugar diabetes).
2. Is there medical treatment for a craniopharyngioma?
No, there are no medicines to treat this type of tumor. Most patients require
hormone replacement(s) because of damage to the normal pituitary gland. Surgery
is the first choice because radiation treatment does not cause an immediate
decrease in tumor size. A craniopharyngioma may be large and invade brain tissue
and because of this, removal of as much as possible is often necessary. Some
patients also require radiation treatment if there is remaining tumor after
surgery; radiation treatment is used to prevent growth of any remaining tumor.
