Sam and her mom, Jackie, answered questions in an online Guest Chat last Wednesday, February 16, 2005 in the Cushing's Chatroom.
Sam was born with Cyclical Cushing's Syndrome on March 22nd 1999 and is thought to be perhaps the ONLY child in medical literature born with Cyclical Cushing's Syndrome.
The Discovery Health Channel aired Sam's show, Mystery Diagnosis, Mon. Nov. 15, 2004 with several repeat performances. This show was the first in a series called Diseases Doctors Miss. Every year, millions of Americans fall prey to ailments that go undiagnosed or misdiagnosed. Medical professionals struggle to understand their baffling conditions.
Sam's story was also presented by Dr. Stratakis in Grand Rounds at Seattle Children's Hospital November 18, 2004.
Read Sam's Bio. It's a truly amazing story about what one determined Mom can do for her child.
The NIH (National Institutes of Health) made a poster of Sam's rare case in Adobe PDF format. If you don't have that, you'll be prompted to add the Adobe program to your computer to view this file. You can view Sam's NIH poster here.
The transcript is available at http://www.cushings-help.com/transcripts/jackieandsam2-9-2005.htm.
Cushing's Awareness Day. We are currently petitioning to have
April 8 be declared as Cushing's Awareness day. This date was chosen
because it was Dr. Harvey Cushing's Birthday.
Print out a sample letter to send to your
congress person or senator or download it in
More information here
See what Jayne has done! She wrote to her representative and she's now in the Congressional Record. She has her first response and it's a fantastic one!
A new Message Board area is being added to discuss ideas for making Cushing's Awareness Day a reality. Please do what you can to help the cause! Thank you for helping to make this
Awareness Day a reality!
welcome your articles, letters to the editor, bios and Cushing's
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By Vicki Wade, R.Ph, Pharm. D..
Have you recently experienced a major stress in your life, be it illness,
job, death, children, etc? After this stress, have you felt as though you
just cannot seem to get yourself together, or at least back to where you
used to be? Are you usually tired when you wake up, but still "too wired" to
fall asleep at night? Is it hard for you to relax or to get exercise? Do you
find that you get sick more often and take a long time to get well? If so,
then you, like many other Americans may be experiencing symptoms of Adrenal
Adrenal fatigue is not a new condition. People have been experiencing this
condition for years. Although there is increasing physician awareness, many
are not familiar with adrenal fatigue as a distinct syndrome. Because of
this lack of knowledge, patients suffer because they are not properly
diagnosed or treated.
Adrenal fatigue is a condition in which the adrenal glands function at a
sub-optimal level when patients are at rest, under stress, or in response to
consistent, intermittent, or sporadic demands. The adrenal glands are two
small glands that sit over the kidneys and are responsible for secreting
over 50 different hormones - including epinephrine, cortisol, progesterone,
DHEA, estrogen, and testosterone. Over the past century, adrenal fatigue has
been recognized as Non-Addison's hypoadrenia, subclinical hypoadrenia,
neurasthenia, adrenal neurasthenia, and adrenal apathy.
Generally patients who present with adrenal fatigue can often be heard
saying, "After______, I was never the same." The onset of adrenal fatigue
often occurs because of financial pressures, infections, emotional stress,
smoking, drugs, poor eating habits, sugar and white flour products,
unemployment and several other stressors. After experiencing many of these
events over a long period of time, the adrenal glands tend to produce less
cortisol, the body's master stress hormone. Cortisol's main role in the body
is to enable us to handle stress and maintain our immune systems. The
adrenal gland's struggle to meet the high demands of cortisol production
eventually leads to adrenal fatigue.
Patients with adrenal fatigue have a distinct energy pattern. They are
usually very fatigued in the morning, not really waking up until 10 AM, and
will not usually feel fully awake until after a noon meal. They experience a
diurnal lull in their cortisol (the stress hormone produced by the adrenal
gland) and as a result, they feel low during the afternoon, generally around
2-4 PM. Patients generally begin to feel better after 6 PM; however, they
are usually tired after 9 and in bed by 11 PM These patients find that they
work best late at night or early in the morning.
Some key signs and symptoms of adrenal fatigue include salt cravings,
increased blood sugar under stress, increased PMS, perimenopausal, or
menopausal symptoms under stress, mild depression, lack of energy, decreased
ability to handle stress, muscle weakness, absent mindedness, decreased sex
drive, mild constipation alternating with diarrhea, as well as many others.
Although there no specific tests that will provide a true diagnosis of
adrenal fatigue there are tests that may contribute to an assessment, such
as a postural hypotension test, an AM cortisol test, or an ACTH stimulation
test. It is customary for a physician to assess the adrenals together with
thyroid tests to rule out insufficiency, which sometimes occurs in
A single determination of plasma cortisol or 24-hour urinary free cortisol
excretion is not useful and may be misleading in diagnosing adrenal
insufficiency. However, if the patient is severely stressed or in shock, a
single depressed plasma cortisol determination is highly suggestive. An
elevated plasma ACTH level in association with a low plasma cortisol level
Treatment for adrenal fatigue is relatively simple. Lifestyle modifications
can be initiated to treat this condition. Simple changes such as more
laughter (increases the parasympathetic supply to the adrenals), small
breaks to lie down, increased relaxation, regular meals, exercise (avoiding
any highly competitive events), early bedtimes and sleeping until at least 9
AM whenever possible can all benefit those experiencing adrenal fatigue.
A diet that would be conducive to treating adrenal fatigue includes one that
combines unrefined carbohydrates (whole grains) with protein and oils (nuts
and seeds) at most meals - olive, walnut, fiber, flax and high-quality fish
oil. It is also important for patients to eat regular meals, chew food well,
and eat by 10 AM and again for lunch. Patients should look to avoid any
hydrogenated fats, caffeine, chocolate, white carbohydrates, and junk foods.
Diets should have a heavy emphasis on vegetables. It may be of additional
benefit that patients add salt to their diet, especially upon rising and at
least a half-hour before their lowest energy point of the day. (Preferably,
1/8 to ˝ teaspoonful of sea salt, Celtic salt, or sea salt w/ kelp powder
added to an 8 oz glass of water). In adrenal fatigue, one should not follow
the USDA's Food Guide Pyramid, as these patients tolerate fewer
carbohydrates and need more protein.
The addition of nutritional supplements may also offer additional benefits
to patients experiencing adrenal fatigue. They should consider the addition
- Vitamin C 2,000-4,000 mg/day Sustained Release
- Vitamin E w/ mixed tocopherols 800 IU/day
- Vitamin B complex
- Niacin (125-150 mg/day)- as inositol hexaniacinate
- B-6 (150 mg/day)
- Pantothenic acid (1200-1500 mg/day)
- Magnesium citrate (400-1200 mg)
- Liquid trace minerals (zinc, manganese, selenium, chromium,
molybdenum, copper, iodine)- calming effect
- If depression is present - Add SAM.e 200 mg bid; DL-Phenylalanine (DLPA)
500 mg bid
Some herbal remedies that have been noted as possible therapies include
Licorice, Ashwagandha, Maca, Siberian Ginseng, Korean Ginseng. Note:
Licorice can and, if taken over time, does have a propensity to elevate
blood pressure. It should not be used in persons with a history of
hypertension, renal failure, or who current use digitalis preparations such
Under the supervision of a physician hormone supplementation with DHEA,
Pregnenolone, and Progesterone may also offer some benefits. There are
several glandular extracts on the market that contain adrenal, hypothalamus,
pituitary, thyroid, and gonadal that are also often recommended. Sometimes
the initiation of hydrocortisone (Cortef®) may be necessary as a replacement
hormone when cortisol is not being produced by the adrenals. While the
initiation of corticosteroids, such as hydrocortisone may have quick and
dramatic results, they can sometimes make the adrenals weaker rather than
stronger. As a result, the initiation of hydrocortisone is usually a last
resort. It is important to note that patients may have to undergo treatment
for 6 month to 2 years.
While a cortisol measurement may be helpful to confirm any thoughts or ideas
that a patient may have decreased adrenal function, typically blood cortisol
levels would be tested along with blood levels of potassium, and sodium. If
the pituitary gland is the cause of adrenal failure electrolyte levels are
usually normal. Practitioners usually pay attention to extremely low
cortisol levels, which generally diagnoses Addison's disease - a condition
in which the adrenal glands are completely depleted, also considered a
medical emergency. If you think you may be experiencing adrenal fatigue or
if you are unsure, feel free to contact Pete Hueseman, R.Ph., P.D. at
1-800-728-0288 or E.mail him directly at
can also your ask your questions of Pete at
Valentine's Day Marks Expansion Of Newborn Screening in Oklahoma
Valentine's Day, Monday, Feb. 14, will have special relevance for Oklahoma
families of newborns born that day and afterward. Effective that date, the
Oklahoma State Department of Health will expand its newborn screening
program to include screening for two additional disorders: cystic fibrosis
and congenital adrenal hyperplasia.
State public health officials say these tests and the provision of
follow-up services to ensure treatment within the first weeks of life for
affected newborns will help saves lives and prevent severe disability.
To commemorate the expansion of the newborn screening program, selected
public health officials and newborn screening program staff will be wearing
a bright blue wristband on Valentine's Day that says, "Breathe." While the
simple act of breathing is something most persons take for granted, it can
be extremely difficult for someone living with cystic fibrosis (CF). Testing
for CF in newborns will allow for early detection of the disorder so
complications can be prevented or improved. Newborns will also be tested for
congenital adrenal hyperplasia (CAH), a disorder that can lead to death if
not treated within the first weeks of life.
The addition of these two tests is an important step in moving Oklahoma
toward meeting March of Dimes recommendations for uniform national newborn
screening. In addition to funding the expansion of the newborn screening
program to include CF and CAH screening, the State Board of Health has added
a third test for implementation later this year. That test will be for the
metabolic disorder medium-chain acyl coenzyme A dehydrogenase deficiency (MCAD).
The Oklahoma State Department of Health has purchased new equipment to allow
for MCAD testing as well as 30 other metabolic disorders.
Oklahoma is one of nine states offering CF screening to all newborns, and
is the 39th state to add CAH screening. Oklahoma's newborn screening program
also screens for the disorders of phenylketonuria (PKU), congenital
hypothyroidism, classic galactosemia, and sickle cell disease. In 2004, the
Oklahoma State Department of Health screened more than 50,000 newborns for
genetic disorders and identified 32 newborns with a disorder. Expanded
screening is expected to identify 17 newborns with CF and two with CAH each
In addition to screening, Oklahoma newborns identified with a disorder
receive comprehensive follow-up program services to ensure optimal healthy
outcomes, a unique service when compared to newborn screening efforts
provided by other states.
"The consequences of not detecting these conditions early are
devastating. Without early detection and subsequent intervention, newborns
may suffer profoundly, and for some of the disorders, there is a risk of
death," said Pam King, director of Genetics. "The cost to screen an infant
is far less than the cost of failing to promptly identify affected infants."
Without the screening test, doctors are often unable to identify these
disorders quickly. Failure to screen one affected infant can result in an
odyssey of frequent hospital stays and invasive procedures trying to
determine a diagnosis. Studies have shown costs for hospitalizations and
diagnostic procedures can easily exceed $500,000 for one infant. The cost
for disability services and in some cases institutionalization for
profoundly affected infants who did not receive prompt treatment can exceed
$1 million annually.
"Even so, these costs are immeasurable when compared to the effect that
the loss of an infant's life has on a family," said State Health
Commissioner Dr. Michael Crutcher. "That's why we are indebted to the Board
of Health and its many partners who were committed to improving the health
of Oklahoma's children."
Crutcher said expansion of the newborn screening program was successful
due to diverse support from legislators, families and health care providers.
"Enhancing newborn screening services is a way to prevent mental
retardation, improve health, and save lives. When we improve the quality of
life for our children, we also improve the quality of life for Oklahoma's
future," Crutcher said.
For more information about newborn screening services, contact Pam King,
director of Genetics, Oklahoma State Department of Health, 405/271-6617.
Published Friday, February 11, 2005 on page a5
Copyright ©1998-2005 The Ponca City News
QUALITIES OF LIFE HEALTH
Beaming in on the brain
New radiation system tackles tumors while bypassing nearby tissue
By Marc Davis
Special to the Tribune
Published February 13, 2005
If it weren't for a unique method of removing residual
brain tumor tissue, a treatment offered by Loyola University Health System,
Craig Fedder might be blind.
Fedder, who lives in Aurora, knew he had a serious problem
when, driving home one evening after work in January 2003, he was suddenly
stricken with double vision.
"I was on the road, speeding along in the middle of
traffic, when it happened," said the 60-year-old Fedder,
training-development manager for the International Truck and Engine Co. in
Warrenville. "I was really scared. I tried to drive with my hand over one
eye. That didn't help. I thought I'd have an accident. I was lucky to make
Fedder sought medical attention, and eventually an MRI and
CT scan revealed a 2.8-centimeter benign tumor on Fedder's pituitary gland.
The tumor created pressure against nerves that control eye movement and
caused his double vision. His tumor was removed in a traditional surgical
procedure in March 2003 by Dr. Thomas Origitano, a neurosurgeon at Loyola
University Chicago Stritch School of Medicine. But Fedder still had a
Microscopic residual tumor tissue remained in Fedder's
brain and had to be removed or the tumor could grow back, causing a
recurrence of his vision problems, Origitano explained.
The usual method of tumor tissue removal is a monthlong
course of external beam radiation. Although the treatment can be effective,
the side effects can be rough: fatigue, nausea, time lost from work. Most
dangerous, however, is the potential damage to brain tissue.
"The danger of injury to adjacent [brain] tissue includes
possible hearing loss, blindness, difficulty swallowing, even paralysis,"
said Dr. Bahman Emami, chairman of the department of radiation oncology at
Loyola University Health System.
In Fedder's case, the potential injury to his optic nerve,
which was being pressured by the tumor, could cause permanent blindness. If
his brain tumor tissue were removed in the traditional way, there was a
chance of damaging the optic nerve. With Loyola's new Novalis system of
radiation, however, the risk was substantially reduced, Emami said.
"What's unique about this [Novalis] method is its ability
to shape the radio beam to the contours of the tumor," Origitano explained.
"This leaves as much healthy tissue as possible untouched. The patient's
exposure to radiation is reduced, and side effects are not as severe. It's
also now used as a surgical method which can treat smaller tumors, reduces
treatment time and causes minimal bleeding. Patients recover more quickly
and with fewer or less-troublesome aftereffects."
Fedder was scheduled for a course of treatment using the
Novalis system in early 2004 at the Loyola University Health System,
Maywood. Loyola is the only Chicago-area medical facility using the system,
Before Fedder's treatment, a plastic mask was made of his
face for use as a precision guide for aiming the beam.
"They put a roll of plastic mesh over my face," Fedder
said, describing the mask-making process. "It was warm and pliable and took
an impression. It was not uncomfortable."
The finished mask was attached with bolts to fixtures on
both sides of Fedder's head that held it steady so that the radiation would
target the same place every time.
The computer recognized the face and made appropriate
targeting adjustments after two X-ray images verified the exact position of
the patient's head. The radiation machine then rotated around Fedder's head,
dispensing a precise dose of radiation to a pinpoint target. The radiation
is a stream of fast-moving subatomic particles generated by a linear
accelerator, a machine that uses electricity to generate the high-energy
radiation beam. Emami supervised the treatment.
After the radiation, about a five-minute exposure, Fedder
returned to work the same day.
The whole thing took about 30 minutes, Fedder said. "That
includes the time it took for me to get ready. After it, I didn't feel
woozy, sick or tired." Only near the end of his 25 days of radiation--five
days a week, with Saturday and Sunday off--did Fedder start to feel some
fatigue. He also lost hair on his head in two small patches. "But I started
to feel normal again pretty soon, and my hair grew back quickly," he said.
The Novalis system is now being used for both initial
brain tumor surgery and the radiation follow-up. The system may also soon be
used to treat other types of tumors, including those of the breast and
prostate, Origitano said.
As for Fedder, "I feel great now," he said. "I have no
eyesight problems, I see Dr. Origitano once a year and everything was
covered by insurance. I feel pretty lucky."
Copyright © 2005, Chicago Tribune
Dental surgery might become easier with new growth
hormone injection technique
Today, when dentists replace a tooth, they also have the
complicated task (painful for the patient) of building a bone structure
around the new tooth. They typically transfer excess bone material to the
tooth from other areas of the patient's face. But some University of
Michigan researchers may have found a better way. The scientist used gene
therapy to inject a growth hormone into the mouths of lab mice, and the
hormone coaxed bones into growing by themselves.
LOS ANGELES, Feb. 2 (Xinhuanet) -- US Researchers have
found that introducing a growth factor protein into a mouth wound, using
gene therapy, helps generate bone around dental implants, according to a
paper in the Molecular Therapy journal published on Tuesday.
US Researchers have found that introducing a growth factor
protein into a mouth wound, using gene therapy, helps generate bone around
dental implants. (yahoo.com) For a patient with a sizable mouth wound,
replacing a tooth means more than simply implanting a new one. The patient
also needs the bone structure to anchor the new tooth in place.
Such reconstructive surgery today involves either taking a
bone graft from the patient's chin or jaw, which leaves a second wound
needing to heal, or using donated bone from a tissue bank, which yields
A team of researchers at the University of Michigan led by
Professor William Giannobile delivered the gene encoding for bone
morphogenetic protein-7 (BMP-7) to large bone defects in rats, in an attempt
to turn on the body's own bone growth mechanisms.
The study showed that the animals produced nearly 50
percent more supporting bone around dental implants after getting BMP-7
BMP-7 is part of a family of proteins that regulates
cartilage and bone formation. Recent studies have shown that BMPs are
present in tooth development and periodontal repair. The Michigan study
mixed BMP-7 genes with an inactivated virus in a gel-like carrier and
injected it into wounds. Researchers said using a virus, with the harmful
effects turned off, harnesses the virus' ability to enter into cells and use
their genetic machinery.
Once inside the cell, the viruses help BMP-7 genes get
where they need to be in the host's cells to boost bone production. Gene
expression producing BMP-7 proteins peaks after a week. The gene acts
quickly to get bone growth started, then disappears within about 28 days.
Scientists said a next step in this process could include
looking for non-viral approaches to delivering gene therapy to the defect
site. Alternatively, they could conduct the gene therapy outside the body
using a tissue biopsy and then transplant the genetically modified cells
back into the patient. But this would require two surgical procedures
instead of one.
"This study represents a proof-of-concept investigation.
We are encouraged about the promise of this treatment," Giannobile said,
adding that more work is necessary before the approach can be tested in
Yuma Sun - Yuma, AZ, USA
Tracking down the cause of women's facial hair
BY PAUL G. DONOHUE, M.D.
Feb 9, 2005
DEAR DR. DONOHUE: You recently wrote about a woman
concerned with losing her hair. I have the opposite problem. I am 43 and
have a mustache and goatee, and I must shave daily. The hair on my legs also
grows rapidly. What are the treatments for this condition? -- D.S.
ANSWER: Some of what I say applies only to premenstrual
women, but most can be applied to women of all ages.
Many women experience hair growth in places where it is a
male feature -- the face, chin, neck or chest. Hair growth in those areas
(and often robust leg-hair growth) depends on the influence of male hormones
or on hair follicles that are extremely sensitive to low levels of male
hormones. Tracking down the cause of the overly abundant supply of the
hormone determines the proper treatment.
One common condition is polycystic ovary syndrome, which,
in its full expression, features large, cystic ovaries, menstrual
irregularities, acne, infertility and the failure to ovulate. Male-pattern
hair growth is another feature.
Tumors of the ovary or adrenal gland that produce male
hormones are a rare but other possible cause. So are thyroid gland disorders
and a condition called the metabolic syndrome, in which blood pressure is
elevated and blood sugar is high, as are blood triglycerides. However, the
greatest number of women with the problem fall into the "idiopathic"
category, meaning no cause can be found.
Shaving is one solution. It doesn't make hair grow faster
or thicker. Creme bleaches, chemical hair removers, electrolysis and laser
treatments are other answers. Weight loss, when applicable, can lower
male-hormone levels. Birth control pills are another way to blunt
male-hormone action. So is the blood pressure medicine spironolactone.
Vaniqa cream doesn't get rid of existing hair, but it prevents new hair
Oh, My Aching Back
By Phyllis Schneider
Back pain affects nearly half of all adults in any given
year and at least two-thirds at some point in their lives. It's so prevalent
that in the United States, back pain is second only to upper respiratory
infections as the reason people visit their doctors.
Unfortunately, many doctors don't have a clue about what
causes back pain, so they order tests, which lead to unnecessary surgery for
many people. But back pain usually doesn't signal a serious illness or
condition, and in most cases, the pain will eventually go away with minimal
treatment. Next time you feel the twinge of backache, here's what you need
to know and do.
Why It Hurts
The mystery of back pain starts in your head, says Dennis C. Turk, Ph.D., a
pain researcher at the University of Washington in Seattle. "Pain doesn't
originate in the body but in the brain," he explains. "Let's say you strain
your back. That information is transferred along nerve pathways to your
brain, where it's interpreted as pain." And each person perceives that pain
Brain chemistry seems to play a role in pain perception.
Recent research at Upstate Medical University in Syracuse, N.Y., found that
chronic back pain triggered changes in several brain chemicals, most notably
one involved in brain cell communication. According to principal
investigator Igor D. Grachev, M.D., Ph.D., a neuroscientist, a reduction in
this chemical resulted in increased feelings of pain. "This could explain
why someone may feel intense pain when an MRI of the spine shows only a
minor problem," he says.
Low back pain can have many causes. It could be a pulled
or strained muscle or ligament. It might be a herniated disk, which happens
when tears in the outer part of a spinal disk release the jellylike
substance that cushions the vertebra above and the one below. The cause
might also be arthritis, osteoporosis, an infection of the spine, or
physical trauma from a car accident or serious fall. Still another
possibility is spinal stenosis, a condition in which bony overgrowths of the
vertebrae narrow the spinal canal and hit nerve roots, notes Andrew J. Haig,
M.D., director of the Spine Program at the University of Michigan in Ann
Arbor. This condition is particularly common in people over 60.
If you have pain, sometimes accompanied by numbness or
tingling that radiates down the back of your leg and below the knee, the
problem may be sciatica. "Sciatica is usually caused by a herniated disk
pressing on nerve roots," Haig says, "but occasionally, it's the result of
Although the potential causes are many, about 85 percent
of the time no reason for the pain is ever found, Haig says. At best,
diagnosis is often a guessing game. Some tantalizing new research, however,
points to a genetic component in a small percentage of cases.
To try to figure out what's going on, doctors may order
X-rays, MRIs, or CT scans. But all too frequently these tests either don't
pinpoint the cause of the pain or they find other back conditions that
aren't related to the pain.
"Studies have shown that an MRI or CT scan will show some
'problem' such as a herniated disk or spinal stenosis in one out of three
people with absolutely no symptoms of back pain," Turk says. And when a test
does show a spinal abnormality in someone with back pain, there's no
guarantee that it's the cause of the pain.
Too Many Tests
"There's a tremendous problem with over-testing in this country," says John
D. Loeser, M.D., a neurosurgeon at the University of Washington.
Unfortunately, that over-testing may lead to unnecessary surgery. This is
especially true for older people because of a misperception of what's
"Radiologists tend to believe that 'normal' equals a
picture of an 18-year-old's spine," he points out. "They label age-related
changes that occur in almost everyone over 65 as 'abnormal.'"
Does that mean testing is never called for? Of course not.
Getting a picture of the spine is necessary for diagnosing low back pain in
a person who has a history of cancer, a fever (which could indicate a spinal
infection), or has undergone severe physical trauma. For others with low
back pain, testing may be advisable if the pain fails to improve after four
to six weeks of conservative treatment.
Saying No to the Knife
Surgeons perform approximately half a million back operations in the United
States each year. Yet some experts suggest that an astonishing 95 to 98
percent of people with back pain do not require surgery.
When is surgery appropriate? If people have failed to get
better after a reasonable period of time or if they have sciatica, they
should consider an operation, Loeser says. "But even in these instances,
surgery may not be the best choice," he adds. "If you leave disk disease
alone, most people will get better with nothing more than physical therapy
and other conservative treatment. The problem is that if there's a lot of
pain, some people simply can't or won't endure it. A surgical procedure can
reduce the pain quickly."
About one out of three people with back pain will improve substantially in a
week, and two out of three will feel better after seven weeks. So a
wait-and-watch approach plus some simple pain-management strategies are the
best course for most people, Haig says.
But that doesn't mean taking to your bed, he adds. In
spite of the once-prevailing belief that bed rest is the best therapy for an
aching back, doctors now advise just the opposite. "When people are confined
to bed, they lose muscle mass, coordination, and balance," Haig says. "For
every week you spend in bed, you need six to eight weeks to regain lost
muscle and get yourself back in shape." If you feel you must rest, don't
stay in bed for more than a couple of days and even then try to get up
periodically and move around.
To reduce inflammation and pain, apply an ice pack for 20
to 30 minutes several times a day for the first day or two. After that, a
heating pad set on low may offer some relief. Over-the-counter pain
relievers such as acetaminophen, aspirin, or ibuprofen can also help.
If you don't feel any improvement after a month, see your
doctor or seek help from a center that specializes in treating back pain.
These programs combine the techniques of several specialists. In many of
them, a physiatrist (a physician who specializes in rehabilitation medicine)
or other expert, such as an osteopath (whose training emphasizes
musculoskeletal disorders), works with a physical therapist to develop an
exercise regime that will stretch and strengthen the muscles and ligaments
of the back and other parts of the body.
In some cases doctors recommend antidepressants, even if
the person isn't depressed. "Antidepressants seem to regulate the brain's
neurotransmitters that control sensory perceptions," Haig explains.
Anti-seizure medications may also relieve pain. "We don't
know exactly why," Haig continues, "but when back pain becomes chronic, it
cycles like a reverberating circuit in your brain, sending signals that say,
'I hurt, I hurt.' An anti-seizure drug may interrupt that cycle."
But, he cautions, these and other drugs have side effects.
"People need to understand that they have a choice to use or not use
medicine for pain," he says. "No medicine cures all back pain. You and your
doctor have to make a judgment based on the cost and side effects of a drug
versus the amount of pain you're in."
If you have pain, especially from sciatica, that's so
severe it keeps you from exercising, you may benefit from an epidural
cortisone injection, Haig says. "These have been used for 15 or 20 years to
reduce the inflammation and swelling around nerve roots, but until recently,
doctors weren't able to inject the cortisone in exactly the right place.
Today, however, some doctors use fluoroscopes to locate the site of the
inflammation, so the injections are more accurate." Although no research
shows that these epidural cortisone injections cure back pain, and relief
lasts only two or three months, that may be enough time to begin an exercise
program and start benefiting from it.
What Doesn't Work
Some common treatments for back pain either don't work at all or provide
minimal relief at best. Traction, for example, has been shown to be
ineffective. And a recent large-scale study found that back braces and
support belts (items often sold through mail-order health products catalogs
and magazine ads) not only do not relieve pain or prevent injury but may
actually increase the risk of damage. These devices tend to give their
wearers a false sense of security, making them more likely to move
incorrectly and put undue strain on their backs.
Transcutaneous electrical nerve stimulation (TENS), a mild
application of electrical current to the skin over the painful area, which
attempts to block pain signals traveling to the brain, has also proved
ineffective. On the other hand, a related procedure, percutaneous electrical
nerve stimulation (PENS), in which acupuncture needles are used to deliver
electricity, may offer some relief, according to preliminary research.
Traditional acupuncture may relieve pain over the short term, but there's no
evidence that the improvement lasts, according to Haig. The same goes for
massage therapy. "We need careful research on both procedures," he says. "So
far, the jury's still out."
As for magnet therapy? "It's a complete scam," Loeser
says. "Don't waste your money."
To reduce your risk of developing back pain or to prevent a recurrence,
"Stay strong, flexible, and coordinated," Haig says. That means committing
yourself to a program of stretching, aerobics, and strength training.
Also, if you still smoke, quit. "Research shows that
cigarette smoking is a significant risk factor for back pain," Haig notes.
The way you sit or the mattress you sleep on may play some
role in back pain, but not for reasons you might imagine. "There's no
'right' way to sit," Haig says. "What's important is that you are able to
move around in your chair, to flex your back, and stretch your legs." An
ideal chair has arms, provides support for your back (a lumbar cushion can
be useful), and isn't so high that your legs dangle.
While folklore holds that a hard mattress is better for a
bad back, you can sleep on whatever kind of mattress feels best, Haig says.
It's a matter of individual choice. One may like to sleep on their side with
a pillow between her knees or on her back with a pillow under her knees.
Pillows work for some but not for others.
Ultimately, preventing back pain means staying active and
exercising. And if you suffer from back pain, don't look to the experts for
a quick fix. "Over the years, we've found that one of the major problems is
that people with back pain have been misled into thinking that they can get
rid of their symptoms if they find a smarter, better doctor," Loeser says.
"But the truth is that they need to make themselves better."
Other Issues: Diabetes and Menopause
DDAVP: Court Rules for Barr in Patent Suit
02.09.2005, 12:47 PM
Barr Pharmaceuticals Inc. on Wednesday said a federal
court rules in its favor in a lawsuit involving antidiuretic patents held by
Ferring BV and Aventis Pharmaceuticals Inc.
The generic drug maker said the District Court of Southern
New York found that the patents for DDAVP tablets in doses of 0.1 milligrams
and 0.2 milligrams are unenforceable and not infringed by a product made by
the company's Barr Laboratories Inc. unit.
The court's decision clears the way for the Food and Drug
Administration to approve Barr's pending application to market a generic
version of DDAVP, or desmopressin acetate. Barr said it is the first to file
an abbreviated new drug application for the doses and has 180 days of
exclusivity on the products.
Barr filed the application in July 2002, and was sued Dec.
13, 2002 by Ferring and Aventis. Ferring manufactures DDAVP for Aventis,
which markets the product in the United States. Barr filed for summary
judgment in April 2004.
DDAVP tablets had annual sales of $177 million last year.
They are indicated as antidiuretic replacement therapy in the management of
central diabetes insipidus - a disorder of the pituitary gland characterized
by intense thirst and by the excretion of large amounts of urine - and for
the management of the temporary excessive urination and thirst following
head trauma or surgery in the pituitary region. They are also indicated for
the management of primary nocturnal enuresis, or bed-wetting.
Barr shares rose $1.07, or 2.3 percent, to $47.005 in
midday trading on the New York Stock Exchange.
Menopause and Mood Disturbance
By Claudio N. Soares, M.D., Ph.D
Psychiatric Times January 2005 Vol. XXII Issue 1
Gonadal steroids appear to affect brain systems known to mediate
depression and anxiety on multiple levels (Leibenluft, 1999). The sexual
dimorphism seen in hypothalamic-pituitary-adrenal (HPA) axis regulation and
the response to stress observed in animal studies and in humans corroborate
this observation. The impact of sex hormones on brain functioning has been
associated with gender differences observed in the prevalence, outcome and
response to treatment of mental disorders. It is noteworthy that such
differences become more noticeable with the onset of puberty; young females
undergoing physical and hormonal changes frequently report affective
instability, as well as high levels of emotional distress. After puberty,
gender proportions of depression and anxiety significantly change, with an
increase in female to male ratio up to 2:1 to 3:1 (Born and Steiner, 2001;
Kessler et al., 1994; Steiner, 1992). Some women seem to be particularly
vulnerable for developing depression during periods of marked hormonal
variability (i.e., premenstrual periods, puerperium and perimenopause)
(Harlow et al., 2003, 1999; Soares et al., 2001b; Stewart and Boydell,
Menopausal Transition and Mood
The mechanism by which neuroregulatory changes modulate the transition to
menopause is still largely unknown (Wise et al., 1996). Generally,
perimenopause or menopause transition begins in a woman's 40s, with a mean
age of 47.5 years and an average duration of four to eight years. Menopause
usually occurs at a mean age of 51.2 years. Reproductive aging may occur as
early as 10 years prior to menopause and is evidenced by a rising
follicle-stimulating hormone (FSH) level in the early follicular phase of
the cycle and a decrease in inhibin B. Therefore, for several years, women
transitioning to menopause may face marked biological variability, with
subsequent endocrinologic and clinical changes (e.g., irregular/anovulatory
cycles, vasomotor symptoms).
The interaction between these hormonal changes, the subsequent onset of
menopause-related clinical symptoms, and the emergence of mood symptoms and
cognitive deficits constitute a complex puzzle. Epidemiological studies have
shown mixed results with respect to the association between depression and
menopause (McKinlay, 1996; Porter et al., 1996). Initial data obtained in
1994 from a cross-sectional population survey of 2,103 women from the
Netherlands were compared to data from the same population obtained three
and one-half years later (range=2.8 to 4.7 years) (Maartens et al., 2002).
By using a cutoff score of 12 on the Edinburgh Depression scale (EDS) to
define presence of depression, the investigators found a significant
association between the transition from pre- to perimenopause (mainly based
on menstrual history) and a higher increase in EDS scores (odds ratio=1.8,
95% confidence interval=1.1-3.3). Other independent factors contributing
significantly to an increase in depressive symptoms over time included prior
depression, financial problems, unemployment, transition from peri- to
postmenopause and death of a partner. A prospective study by Freeman et al.
(2004) also found an increased likelihood of depressive symptoms during
transition to menopause and a decreased likelihood after menopause, after
adjusting for other predictors of depression.
The Harvard Study of Moods and Cycles is an ongoing community-based,
prospective study designed to explore some of the characteristics involving
the association between depression and ovarian failure. After screening more
than 4,000 premenopausal women (ages=36-44), subgroups of women with (n=332)
and without (n=644) history of depression were enrolled for prospective
assessments of serum hormone levels, menstrual characteristics and
standardized psychiatric evaluations (Harlow et al., 2003). Findings of this
study demonstrated that women with a history of depression (assessed by
standardized psychiatric interview--Structured Clinical Interview for DSM-IV
[SCID]) are more likely to develop greater hormonal fluctuations (serum
levels of FSH, luteinizing hormone [LH] or estradiol [E2]) over time, even
while still being premenopausal, than women without depression. In addition,
women with a history of depression are more likely to present with symptoms
that characterize an earlier transition to menopause (menstrual
irregularities, presence of hot flushes and night sweats) (Harlow et al.,
2003). More recent findings derived from the Harvard Study of Moods and
Cycles also suggest that women approaching menopause (i.e., presenting with
irregular cycles and significant vasomotor symptoms) are at significantly
greater risk for developing depressive symptoms, even in the absence of
prior episodes of depression (Soares, 2003). This putative association could
consolidate the view of an existing intrinsic connection between disrupted
hormone milieu and brain functioning.
A study of more than 500 pre-, peri- and postmenopausal women in a
primary care clinic demonstrated that marital disruption and unemployment,
as well as somatic symptoms and past history of depression, may influence
the likelihood of depressive symptoms in this population, regardless of
menopausal status (Joffe et al., 2002). The presence of severe hot flushes,
however, was a risk factor for depression only among perimenopausal women,
even though hot flushes occurred in all three menopausal groups. This
correlation between hot flushes and depression corroborates one of the
physiological theories commonly employed to explain the occurrence of
depressive symptoms among menopausal women--the so-called domino effect
(Campbell and Whitehead, 1977). This theory proposes that the discomfort
caused by night sweats and hot flushes provokes physical changes (e.g.,
sleep disturbance) and, consequently, affects mood stability. Hence,
investigators have speculated that the capacity of estrogen to improve mood
is secondary to providing relief of somatic menopausal symptoms and
normalization of sleep.
Despite accumulating evidence that hormonal fluctuations exert a
psychological destabilizing action during certain reproductive cycle-related
events, clinical studies have also demonstrated that sex hormones may in
fact help to prevent or even treat depressive symptoms. This correlation has
already been shown in studies that examined the effects of treatment with
estradiol for premenstrual depressive symptoms (Smith et al., 1995) and
during puerperium (Ahokas et al., 2001; Gregoire et al., 1996).
Double-blind, placebo-controlled studies have shown significant
antidepressant benefit with the use of transdermal estradiol in
perimenopausal women suffering from major depressive disorder, dysthymia or
minor depression (Schmidt et al., 2000; Soares et al., 2001a). Results
obtained with the use of estradiol for postmenopausal depressed women were
less promising (Cohen et al., 2003). Transdermal testosterone, on the other
hand, has been shown to be efficacious for the treatment of psychological
distress and decreased libido in some surgically induced menopausal women (Shifren
et al., 2000). These were mostly small studies, so larger studies are needed
to corroborate these promising findings.
Hormones and the Brain
The complex interactions between estrogens and brain functioning have
gained greater understanding over the last decade (Joffe and Cohen, 1998).
The distribution of various E2 receptors (named and E2 receptors, to date)
in different brain regions (such as the medial amygdala, hippocampus and
limbic system) and their distinct up- or downregulation by estradiol
contribute to the complexity of estrogen's effects on the central nervous
system (Genazzani et al., 1997; Maggi and Perez, 1985; Silva et al., 2001;
Woolley, 1999). Estrogens interact with membrane and nuclear receptors.
Through nuclear receptors, they act as transcription factors regulating the
expression of targeted genes. In addition, estrogens affect membrane
receptors by possibly modulating the synthesis, release and metabolism of
monamines (McEwen and Alves, 1999; Stahl, 2001). Estrogens exert an agonist
effect on serotonergic activity by increasing the number of serotonergic
receptors and the transport and uptake of the neurotransmitter. They also
increase synthesis of serotonin, upregulate 5-HT1 receptors, downregulate
5-HT2 receptors and decrease monoamine oxidase activity (Halbreich and Kahn,
2001). Estrogens appear to increase noradrenergic (NA) activity by
increasing NA turnover, decreasing NA reuptake, and decreasing the number
and sensitivity of dopamine D2 receptors (Garlow et al., 1999). Lastly,
estrogens induce new dendritic spine formation and synapses in hippocampal
neurons, and they regulate neurotropic factors and neuropeptides (e.g.,
neuropeptide Y [NPY] and corticotropin-releasing hormone [CRH]). Estrogen
availability may also modulate the binding affinity of 5-HT receptors, as
shown in animal models (Bethea et al., 2002) and neuroimaging clinical
studies (Kugaya et al., 2003).
Estrogens are available in many preparations: transdermal patches and
creams, oral tablets, intranasal or sublingual formulations, injections, and
subdermal implants (Ramachandran and Fleisher, 2000; Stahl, 2001). Most data
on the efficacy and safety of estrogens in the United States have been based
on studies using oral conjugated estrogens. Differences in the
pharmacokinetic aspects of estrogen preparations may contribute to the lack
of consistency across studies regarding the effect of estrogen treatment on
mood (Halbreich and Kahn, 2001). Treatment studies of transdermal estradiol
for perimenopausal depression (randomized, placebo-controlled studies, 50
g/day or 100 g/day) have shown positive results (Schmidt et al., 2000;
Soares et al., 2001a). Most estrogen trials that failed to detect an
antidepressant efficacy in comparison with placebo used either oral
preparations of conjugated equine estrogen or piperazine sulfate estrone (Coope
et al., 1975; Strickler et al., 1977; Thomson and Oswald, 1977).
The use of transdermal estradiol (50 g/day) showed superior efficacy
compared to placebo in 34 perimenopausal women with major and minor
depression, in the presence or absence of hot flushes (Schmidt et al.,
2000). These findings corroborate the idea that the effects of estrogen on
mood and on vasomotor symptoms, the latter possibly resulting from
hypothalamic thermoregulatory dysfunction, are independent. Similar results
were found in a larger sample of perimenopausal women suffering from
depressive disorders (mostly major depression) who were treated with
transdermal estradiol (100 µg/day) or placebo (Soares et al., 2001a). In
this study, most women were able to sustain an antidepressant benefit after
a four-week washout period, despite the re-emergence of vasomotor symptoms,
again suggesting the existence of independent effects of estradiol on mood
and vasomotor symptoms.
Studies on postmenopausal subpopulations have shown less compelling
evidence of estrogen's antidepressant efficacy. Negative results have been
reported when conjugated estrogen (George et al., 1973) or estrogen sulfate
(Coppen et al., 1977) were given to surgically induced menopausal women. In
addition, the use of transdermal estradiol (50 µg/day) in postmenopausal
women did not show superior efficacy when compared with placebo for the
treatment of depressive symptoms (Saletu et al., 1995). Antidepressant
benefit of estrogen for postmenopausal women appears to be limited even when
examined in open clinical trials (Cohen et al., 2003). It is possible that
postmenopausal women would require a higher dose and/or prolonged treatment
with E2 to obtain a satisfactory antidepressant response to estrogen
treatment, possibly due to the altered sensitivity of their estrogen
receptors. Also, it is possible that perimenopausal women with depression
are uniquely responsive to the mood-enhancing effects of E2.
Studies of the efficacy of estrogen as an adjunctive therapy for major
depression in postmenopausal women have had mixed results. Retrospective
analyses of older women have shown greater improvement in depressive
symptoms among those who received fluoxetine (Prozac) plus hormone therapy,
which may include estrogen preparations, progestogens or both, than those
receiving the antidepressant alone (Amsterdam et al., 1999; Schneider et
al., 1997). However, in these studies, women were not randomly assigned to
hormone therapy, which might have contributed to a selection bias. A similar
study with sertraline (Zoloft) did find a positive effect of hormone therapy
augmentation (Schneider et al., 1998). A pooled analysis of women treated
with venlafaxine (Effexor) with or without concomitant use of hormone
therapy for depression found no evidence suggesting a significant change in
efficacy associated with hormone therapy use (Entsuah et al., 2001).
However, that concomitant use of hormone therapy could maximize some of the
benefits obtained with the selective serotonin reuptake inhibitors in
perimenopausal women, particularly in promoting greater well-being (Soares
et al., 2003).
The Women's Health Initiative Study, a randomized, controlled, primary
prevention trial (planned duration, 8.5 years), randomly assigned 16,608
postmenopausal women 50 to 79 years of age (mean age=63 years) with an
intact uterus at baseline to receive estrogen plus progestin (0.625 mg/day
of conjugated equine estrogen [CEE] plus 2.5 mg/day of medroxyprogesterone
acetate [MPA]; n=8,506) or placebo (n=8,102). The primary outcome measure
was coronary heart disease, with invasive breast cancer as the primary
adverse outcome. Other measures included cases of stroke, pulmonary
embolism, endometrial cancer, colorectal cancer and hip fracture. In May
2002, the trial was stopped by recommendation of the data and safety
monitoring board, as the overall health risks associated with combined
estrogen plus progestin had exceeded the benefits (Rossouw et al., 2002). In
February 2004, the estrogen alone arm (or placebo), including postmenopausal
women with hysterectomy, was also stopped because the burden of incident
disease events was showing similar impact on both groups and, therefore,
would not result in any significant benefit (Anderson et al., 2004). Lastly,
although not specifically designed to examine the benefits of hormone
therapy for psychological symptoms, mood or cognition, the Women's Health
Initiative Study also reported the impact of estrogen (plus progestin) on
quality of life, including questions on general health, vitality, mental
health, depressive symptoms and sexual satisfaction. At three years, there
were no significant benefits in terms of any quality-of-life outcomes (Hays
et al., 2003).
The results from this study should be carefully interpreted. In fact,
various menopause societies have expressed their concerns about the
generalization of its findings; investigators and seasoned clinicians have
pointed out that some of these results were a "direct consequence of
unsuitable population selection [e.g., older, postmenopausal women],
terribly wide inclusion criteria [e.g., subjects with various pre-existing
medical conditions], lack of adequate assessments [e.g., lack of adequate
assessment for menopause-related somatic symptoms, and the incongruous
treatment choice [CEE + MPA]" (Notelovitz, 2003). The main criticism,
however, relies on the fact that this study was designed essentially to
examine the impact of a specific hormone formulation (CEE + MPA) on the
relative risk for developing coronary heart disease, cancer or fractures in
older, postmenopausal women. The study was not designed to address the
impact/safety of using CEE + MPA (or any other hormone preparation) for the
management of menopause-related somatic and/or psychological complaints in
younger, perimenopausal women--for example, for the treatment of hot flushes
and depressive symptoms in this population.
Clinicians and health care professionals should continue to consider many
factors when advising treatment choices for women approaching menopause or
for those who are postmenopausal. It has been speculated that hormone
therapy discontinuation could increase the risk for mood instability,
anxiety and insomnia, especially in women with a past history of these
The Women's Health Initiative study yielded data only on the use of
conjugated estrogens and medroxyprogesterone; long-term data on other
hormone therapy regimens are sparse and certainly overdue. As already seen
with various antidepressants, hormonal therapies differ with respect to
absorption, metabolism and bioavailability. Nonetheless, in the absence of
more data, we cannot ensure the safety of switching patients to another
hormone combination. Moreover, clinicians and health care professionals
should continue to weigh the risks and contraindications for using short- or
long-term estrogen/progestin preparations, particularly in light of updated
data on the impact of such treatments for the risk of developing new
thromboembolic events, breast cancer or endometrial cancer.
Androgens might have important neuroprotective properties (Wolf and
Kirschbaum, 1999), as well as an essential role in the organization or
programming of brain circuits (Rubinow and Schmidt, 1996). Androgens are
produced by the adrenal glands and ovaries in women, and they include
testosterone, androstenedione, dehydroepiandrosterone (DHEA) and
dehydroepiandrosterone sulfate (DHEA-S). The latter two are adrenal steroids
and are available in higher concentrations than other androgens (Morrison,
The impact of testosterone on mood and behavior in women has been well
described. Depressive symptoms and anxiety, as well as decreased libido,
have been described among postmenopausal women who present with decreased
testosterone, particularly after oophorectomy; however, testosterone
supplementation has been shown to alleviate these symptoms (Sherwin and
Gelfand, 1985). Shifren and colleagues (2000) examined the impact of
transdermal testosterone in 75 surgically induced postmenopausal women (ages
31 to 56). They received patches containing 150 g or 300 g of testosterone
or placebo for 12 weeks. All participants received concomitant treatment
with oral conjugated estrogens. When compared with placebo, women who
received testosterone reported greater psychological well-being and a
significant improvement in mood and anxiety. Treatment with testosterone was
well tolerated without significant occurrence of acne or hirsutism.
There is accumulating evidence suggesting a complex interaction between
sex hormones and brain functioning. The transition to menopause serves as an
interesting model for the understanding of this interaction and its
implication for the development of mood disturbances during the menopausal
years. The extent to which the use of hormone interventions (particularly
estrogen and testosterone preparations) may help to improve treatment
outcomes among women who present with depressive symptoms or cognitive
decline is still debatable given the methodological limitations of the
existing data. Antidepressants, mood stabilizers and psychotherapy will
continue to be well-established treatments for mood disturbances. It is
plausible, however, that subgroups of menopausal women will benefit from the
combined use of hormonal and nonhormonal strategies. The search for an
improved quality of life for our female patients will certainly stimulate
further studies to define strategies for ameliorating depressive symptoms
with fewer side effects. Psychiatrists and other health care professionals
should, therefore, be aware of the accumulating data on the psychotropic
effects of sex hormones.
Dr. Soares is assistant professor of psychiatry at Harvard Medical School
and is associate director for research at Massachusetts General Hospital
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Topical Corticosteroid Rx-To-OTC Switch Safety Data
Will Be Topic Of Joint Cmte. Meeting
Safety data needed for prescription-to-over-the-counter
switches of topical corticosteroid products will be discussed at a joint
meeting of FDA’s Nonprescription Drugs and Dermatologic & Ophthalmic Drugs
Advisory Committees on March 24.
The committees will focus particularly on the database to
evaluate the potential for hypothalamic, pituitary, adrenal (HPA) and growth
suppression and other systemic and local adverse events.
The potential for HPA axis and growth suppression with
topical corticosteroids is considered a potential stumbling block for the
Rx-to-OTC switch of topical corticosteroids. Studies on various
corticosteroids indicate use of the drugs can slow children’s growth. Data
are not yet available on whether the impact is reversible.
The development of a risk management program for topical
corticosteroids to prevent hypothalamic pituitary axis suppression in
pediatric patients being treated for atopic dermatitis was discussed by
FDA’s Pediatric Subcommittee of its Anti-Infective Drugs Advisory Committee
at an Oct. 29, 2003 meeting.
The subcommittee recommended a boxed warning be added to
topical corticosteroids concerning the HPA axis suppression risk. Other
recommendations by the advisory committee included additional studies to
determine risk, patient package inserts, “Dear Health Care Provider” letters
and provider educational programs.
While HPA axis suppression from topical steroid use will
often resolve without consequence, FDA has noted that “pediatric patients
who are suppressed from topical steroid use and experience a significant
physiologic stress (such as trauma, surgery, or serious infection) may have
life-threatening complications from their suppression (including death)
which are preventable if the suppression is recognized and treated
appropriately with stress doses of glucocorticoids."
On March 23, the Nonprescription Drugs Advisory Committee
will consider microbiologic surrogate endpoints for demonstrating the
effectiveness of antiseptic products in health care settings. To watch a
live or archived webcast of this meeting,
click here. To arrange for live videoconferencing or to order videotapes
& DVDs, email
firstname.lastname@example.org or call 800-627-8171.
This meeting will be held March 24, 2005 at the Hilton in
Gaithersburg, Md. beginning at 8 a.m.
Posted: Friday, February 11, 2005
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please click here »
Janelle had her right adrenal gland removed. The tumor was
bigger than the gland.
Clyde Kansas and is a freshman at Wichita State University in
Jo Ellen V
Jo Ellen had usuccessful transphenoidal (pituitary) surgery the day before
Thanksgiving, 2004. Due to Empty Sella the tumor cannot be seen by MRI. She
had a 2nd surgery in January, 2005 which did locate and remove the pituitary
ACTH secreting tumor.
suburb of Indianapolis, IN
Rhonda had Transsphenoidal Pituitary Surgery May 1001. She
also has vascular Necrosis or Osteonecrosis from longterm, high steroid use
for asthma and paralyzed vocal cord in 1980's
• If you've been diagnosed with Cushing's, please
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and will be shared with the medical world. It would not be used
for other purposes without your expressed permission. Note:
This information will not be sold or shared with other
Lynne Clemens, Secretary of
CUSH Org is be the
person responsible for the creation of this register. If you
have any questions you may contact her at
do not have to be a member of CUSH to fill out this
questionnaire, as long as you are a Cushing’s patient. We do not
believe that the world has an accurate accounting of Cushing’s
patients. The only way to authenticate accuracy is with actual
numbers. Your help will be appreciated. Thank you."