Saturday, April 30, 2011

Cushing’s syndrome in pregnancy

    BMJ Case Reports   2011;  doi:10.1136/bcr.01.2011.3720

    * Rare disease

   1. Margarita Victoria B Holgado-Galicia1,
   2. Jose Donato Magno2,
   3. Czarlota Acelajado-Valdenor3,
   4. Iris Thiele Isip-Tan1,
   5. Mary Anne Lim-Abrahan1

   1. Correspondence to Dr Margarita Victoria B Holgado-Galicia,


A 22-year-old G1P0 was admitted at 26 weeks gestation for preeclampsia, hyperglycaemia and cushingoid features. Elevated 24-h urine free cortisol (UFC) and suppressed plasma adrenocorticotrophic hormone (ACTH) suggested ACTH-independent Cushing’s syndrome. Ultrasound showed left adrenal mass. She delivered preterm at 28 weeks due to severe preeclampsia and fetal distress. The infant expired after 4 days. Blood pressure was controlled after delivery and the patient was discharged on ketoconazole. Adrenalectomy was planned postpartum; however, she withdrew consent and was lost to follow-up.

A 33-year-old G1P1 presented with gestational diabetes. Pregnancy was complicated by premature delivery at 31 weeks for fetal distress. The baby improved and survived. Three months postpartum, she was evaluated for osteoporosis after sustaining a fracture from a fall. Cushingoid facies, elevated 24-h UFC, suppressed ACTH and a right adrenal mass on MRI confirmed an ACTH-independent Cushing’s syndrome. She underwent adrenalectomy and improved.


Thursday, April 28, 2011

Radiation Therapy in the Management of Pituitary Adenomas

Jay S. Loeffler and Helen A. Shih

Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School (J.S.L., H.A.S.), Boston, Massachusetts 02114

Address all correspondence and requests for reprints to: Helen A. Shih, M.D., M.S., M.P.H., Massachusetts General Hospital, 100 Blossom Street, Cox 3, Boston, Massachusetts 02114.

Context: Optimal management of pituitary adenomas involves consideration of the roles of medical therapy, surgery, and radiation therapy. The different forms of radiation therapy and their results are reviewed here.

Evidence Acquisition: A literature search through the U.S. National Library of Medicine was used to identify and review clinical experiences of radiation therapy in the management of pituitary adenomas. Emphasis was placed on studies within the last 5–10 yr, with 5 or more years of follow-up data, and of reasonable quality of data. Older studies with larger numbers or particular significance are also highlighted.

Evidence Synthesis: Success of radiation therapy in controlling tumor growth is high, 90–100% in most series, regardless of radiation technique and adenoma subtype. Success in achieving hormonal normalization in secretory tumors is more variable because of differences in patient population, radiation technique, and doses employed and variation of the definition of success. Complete biochemical remission is generally achieved in 50% of patients at 10 yr after treatment for most adenomas. Higher rates of normalization can be achieved with additional medical therapy. Hypopituitarism is an expectant result of radiation therapy. Overall rate of other treatment-related adverse effects is low.

Conclusions: Radiation therapy should be considered in the management of patients with pituitary adenomas, particularly when medical and surgical options have been exhausted. Because response evolves slowly over many years and because hypopituitarism is likely to occur, patients should be counseled on the importance of continued endocrinological surveillance and medical management.


More on last article: Additional autoimmune disease found in one-third of patients with type 1 diabetes

At diagnosis of type 1 diabetes, approximately 33% of patients are positive for at least one additional organ-specific autoantibody, according to new data.

Researchers at the Barbara Davis Center for Childhood Diabetes assessed 491 children diagnosed with type 1 diabetes from 2004 to 2009 for other autoimmune conditions. They measured thyroid peroxidase autoantibodies (TPOAb) to screen for autoimmune thyroid disease, tissue transglutaminase autoantibodies (TTGAb) for celiac disease and 21-hydroxylase autoantibodies (21OHAb) for Addison’s disease.

“We sought to define the prevalence of nonislet, organ-specific autoantibodies at the diagnosis of type 1 diabetes and to determine the prevalence of comorbid autoimmune diseases,” the researchers wrote.

Of the 491 children, 82.7% were white and 53.4% were boys. At the time of diagnosis with type 1 diabetes, mean age was 9.6 years and the average HbA1c level was 11.6%. Measurements of TPOAb, TTGAb and 21OHAb were collected within 16 days, on average, and patients were diagnosed with autoimmune thyroid disease, celiac disease or Addison’s disease within 45 days.

Overall, 32.6% of the children had at least one nonislet, organ-specific autoantibody. Of these, 18.6% were diagnosed with additional autoimmune disease. Results revealed that 24.8% were positive for TPOAb, of whom 12.3% had autoimmune thyroid disease. Of the 11.6% with TTGAb, 24.6% had celiac disease. Just 1% of children had 21OHAb, and the researchers found only one case of Addison’s disease.

“Ongoing follow-up of this cohort will be important to determine the natural history of organ-specific autoimmunity in patients with type 1 diabetes,” the researchers wrote. “Key questions remain, including the incidence of autoantibodies over time, the evolution from positive antibodies to disease, the genetic influences on autoimmunity and disease, and patient characteristics that may influence antibody or disease development.”

For more information:

Disclosure: The researchers report no relevant financial disclosures.



Type 1 Diabetes, Celiac or Addison’s?

After noticing a growing trend in children diagnosed with Type 1 Diabetes, doctors and medical researchers have announced a new study measuring the correlation between this autoimmune disorder as well as three others. Addison’s disease, celiac disease, and autoimmune thyroid disease often have antibodies present in children at the same time that they are diagnosed with Type 1 Diabetes.

It has recently been reported that fifteen to thirty percent of people with Type 1 diabetes have also been diagnosed, and about 4 to 9 percent have been diagnosed with celiac disease. Addison’s disease is at the bottom of the list with less than one percent being diagnosed. Children who have been confirmed to have diabetes should be tested yearly for an autoimmune thyroid disease, and for celiac disease if other symptoms become apparent. There is no real screening schedule for Addison’s disease.



Wednesday, April 27, 2011

PNA Webinar: "Diagnosed with a Pituitary Tumor: What Next?" Available OnLine

The webinar presentation by Aaron A. Cohen-Gadol, M.D., M.Sc. on April 21st, entitled, "You Have Been Diagnosed with a Pituitary Tumor: What Next?” was a rousing success!

Participants from around the country included patients and physicians alike. Unique to this presentation was the technology he employs with hi def camera and the ability for the audience to view not only his slide presentation but to see him as! His presentation included valuable information specifically about surgical options for treatment. In addition, participants were able to type questions during the presentation so Dr. Cohen-Gadol could respond. It is a rare opportunity to be able to ask poignant questions of a physician with such a level of expertise! And, being able to actually see the presenter live as he is talking made for so much more of a personal encounter! Very positive feedback was received from those who signed-on saying such things as, "This is amazing!" "The picture quality is wonderful!" ...and many more praises.

This presentation covered the following:

Dr. Cohen's one-hour presentation explains the diagnosis of a pituitary tumor. He briefly reviews the medical and surgical treatments available, in order to help you make better decisions.

Meet the Webinar Presenter:

Aaron A. Cohen-Gadol, MD, MSc
Neurosurgeon, Goodman Campbell Brain and Spine
Indiana University Department of Neurosurgery
Indianapolis, Indiana

Dr. Cohen is a neurosurgeon at Goodman Campbell Brain and Spine and Indiana University Department of Neurological Surgery. He has a special expertise in surgery of pituitary/skull base tumors and cerebral aneurysms. Dr. Cohen completed his medical school at the University of Southern California (USC) and Neurological Surgery Residency at Mayo Clinic. He also completed fellowships in aneurysm and skull base tumor surgery.

Dr. Cohen tackles some of the most challenging brain tumors and aneurysms microsurgically using advanced minimally invasive technologies with an expectation of best results for the patient. He was voted the Health Care Hero of the Year in the State of Indiana for leading the efforts to advance surgical care of brain aneurysms and tumors previously considered inoperable. He leads numerous research efforts to advance the care of the patients with brain tumors and aneurysms.

Pituitary Tumors: General Information for Patients from Aaron Cohen-Gadol on Vimeo.


(Gamma Knife) Noninvasive brain surgery

EIGHT months after giving  birth to her first child, Orange Feliciano discovered that she had a tumor on her pituitary gland. She was worried about her condition as she was only 26 years old and starting to build a family.

Hannah Pimentel, on the other hand, was only 16 when she learned about the 1.8-centimeter arteriovenous malformation on the motor area of her brain.

But both Orange and Hannah now feel that they had a second chance at life, thanks to the Gamma Knife. Undergoing this non-invasive neurosurgical procedure was truly a life-changing experience for them.

The Gamma Knife is a revolutionary breakthrough in brain surgery. It uses radiation produced by 201 beams of cobalt-60 to treat brain tumors, AVMs, and trigeminal neuralgia, among brain diseases. The radiation is so precise that normal brain tissue is unaffected.

The Philippine Gamma Knife Center made the procedure available locally. Being a noninvasive technique, Gamma Knife does not cause complications such as hemorrhage, infection or other injuries associated with conventional brain surgery.

Hannah and Orange were impressed by Gamma Knife . They were also happy that the treatment took only a few hours. After a few days of rest, both Gamma Knife patients went back to their routines.

Know more about the Gamma Knife by visiting the Philippine Gamma Knife Center at the Cardinal Santos Medical Center compound or calling 7259254, 7237575, and 7260776.


Cushing's Diagnosis ~ Think Like a Doctor: A Litany of Symptoms Solved!

On Wednesday I challenged readers to solve a complicated case of a 76-year-old woman who became physically and mentally debilitated over a matter of months.

More than 500 readers weighed in with diagnoses that included porphyria, thrombotic thrombocytopenic purpura and lupus. As of late Wednesday night, 15 readers had come up with the right diagnosis. And the winning answer is:

Diagnosis: Cushing’s syndrome.

The first answer came early. At 12:54 a.m. Eastern time, Dr. Elizabeth Neary, a pediatrician in Madison, Wis., was the first reader to put all the patient’s symptoms together and reach the correct diagnosis.

The wide range of complaints that characterize Cushing’s syndrome was first described by Dr. Harvey Cushing in 1932. In this disease, the adrenal glands churn out too much cortisol, an essential hormone involved in our body’s response to stress. Cortisol helps maintain blood pressure, reduces the immune system’s inflammatory response and increases blood sugar levels — all vital processes for helping our bodies cope with biological and environmental stress.

But long-term exposure to high levels of cortisol can cause osteoporosis, diabetes, high blood pressure, muscle weakness, memory loss and psychiatric disease. It causes the skin to thin and weaken, making it susceptible to bruises that are often dark and dramatic looking. The lesions on this patient’s arms and legs were signs of this.

Cushing’s syndrome is unusual, but a milder version of the disease can be seen in patients who use steroid hormones like prednisone for the treatment of asthma, rheumatoid arthritis or other inflammatory diseases. However, in this case, the syndrome is believed to have been caused by a tiny tumor that was triggering the constant release of high doses of cortisol.

How the Diagnosis Was Made:

When the patient and her two daughters arrived at Waterbury Hospital, Dr. Rachel Lovins met them in the emergency room. She had been introduced to their mother some years earlier, but now she didn’t recognize the woman who sat before her in the wheelchair.

She had gained a lot of weight, her face was much rounder than Dr. Lovins remembered, and her hair, which had been dark and curly, was thin, gray and uncombed. Over the past year or so, Dr. Lovins had heard her friends talk about their mother’s weakness and decline. Seeing her now, it was clear that her illness had taken its toll. Dr. Lovins excused herself to allow the patient to change into her hospital gown. She would see her again once she had been evaluated in the E.R. and admitted to the hospital.

When she returned later, she stood in the doorway and watched as Dr. Chris Mikos, an E.R. physician, lifted the woman’s hospital gown to examine her abdomen. When he did that, Dr. Lovins saw that the woman had red, almost purple stretch marks on her abdomen.

Suddenly the whole case made sense. Dr. Lovins realized the patient might have Cushing’s syndrome. These stretch marks, known as striae, are the result of the thinning of the skin caused by the excess cortisol. It’s a classic finding in Cushing’s. The patient’s primary doctor may not have seen these marks because she probably didn’t have this debilitated elderly woman change into a gown for every visit.

The test used to look for Cushing’s syndrome is called the dexamethasone suppression test. In this test, you give the patient a dose of a steroid hormone, dexamethasone. If the patient has a normal stress hormone system, then the amount of cortisol in the body will drop dramatically as the body reacts to the steroid and begins to suppress its own cortisol production. A normal patient would post a reading of less than five when it’s measured several hours into the test. This patient’s cortisol was eight times that.

Most of the time, Cushing’s syndrome is caused by a tumor in the pituitary gland in the brain, which in turn causes the adrenal gland to overproduce cortisol. In these cases, surgical removal of the tumor will cure Cushing’s.

But in this case, no tumor was found in the pituitary or elsewhere in the patient’s body. Even so, her doctors still believe that a tumor is triggering the excessive cortisol release, but the tumor is too small to locate.

This patient was started on a medication that prevents the overproduction of cortisol, but she had to stop because of side effects. She is waiting to start the next medicine. If that fails, she will have surgery to remove her adrenal glands. When I saw her last she was doing better but wondered out loud whether she would ever walk again.

Why It Was a Difficult Case:

Because cortisol is a hormone that affects every part of the body, the effects of Cushing’s syndrome are wide ranging, and there is no single symptom that announces that a patient has the disease.

Some of this patient’s complaints were pretty common for a woman her age. She’d gained weight. She was tired. She was depressed. She had high blood pressure. She had cataracts. She had swelling in her legs. All of these are symptoms of Cushing’s, but they are also common in patients without Cushing’s.

On the other hand, she had some unusual problems as well. Her muscles were weak. She had a high white blood cell count. She’d had a gastrointestinal bleed. Still, it wasn’t until you put it all together that it became clear that this woman’s many health problems were all related to Cushing’s.

The patient’s oldest daughter sent an e-mail to her friends telling the story of her mother’s ordeal and of her own frustration in pursuing this unifying diagnosis.

We were told that her psychological state, her neurological problem, her circulation issues and her excessive bleeding were an unrelated bunch of unfortunate circumstances conspiring to make this woman ill. “It happens when you are old,” we were told more than once.

With a disease like Cushing’s, our specialist approach to medicine makes us seem like the proverbial blind men examining the elephant. Each specialist can identify what he is seeing, and yet the whole picture will be missed.

Most of the time, that kind of piecemeal medicine works just fine. But the problem is that the cases in which a different approach is required often are tough to distinguish from the bread-and-butter stuff we see every day.

Readers who come to this column already know it will highlight an unusual case, and as a result, you are ready to take on all the exotic possibilities. Because of that, you are way ahead of the doctor who has to figure out which patient, out of all the patients she’s seen that day, needs something special. That recognition is the start of diagnosis.

Read the article and comments at

Gastric inhibitory polypeptide-dependent cortisol hypersecretion--a new cause of Cushing's syndrome.

André Lacroix, M.D., Edouard Bolté, M.D., Johanne Tremblay, Ph.D., John Dupré, M.D., Pierre Poitras, M.D., Hélène Fournier, M.D., Jean Garon, M.D., Dominique Garrel, M.D., Francis Bayard, M.D., Ph.D., Raymond Taillefer, M.D., Richard J. Flanagan, Ph.D., and Pavel Hamet, M.D., Ph.D.

N Engl J Med 1992; 327:974-980October 1, 1992



Corticotropin-independent nodular adrenal hyperplasia is a rare cause of Cushing's syndrome, and the factors responsible for the adrenal hyperplasia are not known.


We studied a 48-year-old woman with Cushing's syndrome, nodular adrenal hyperplasia, and undetectable plasma corticotropin concentrations in whom food stimulated cortisol secretion.


Cortisol secretion had an inverse diurnal rhythm in this patient, with low-to-normal fasting plasma cortisol concentrations and elevated postprandial cortisol concentrations that could not be suppressed with dexamethasone. The cortisol concentrations increased in response to oral glucose (4-fold increase) and a lipid-rich meal (4.8-fold increase) or a protein-rich meal (2.6-fold increase), but not intravenous glucose. The infusion of somatostatin blunted the plasma cortisol response to oral glucose. Intravenous infusion of gastric inhibitory polypeptide (GIP) for one hour increased the plasma cortisol concentration in the patient but not in four normal subjects. Fasting plasma GIP concentrations in the patient were similar to those in the normal subjects; feeding the patient test meals induced increases in plasma GIP concentrations that paralleled those in plasma cortisol concentrations. Cell suspensions of adrenal tissue from the patient produced more cortisol when stimulated by GIP than when stimulated by corticotropin. In contrast, adrenal cells from normal adults and fetuses or patients with cortisol-producing or aldosterone-producing adenomas responded to corticotropin but not to GIP.


Nodular adrenal hyperplasia and Cushing's syndrome may be food-dependent as a result of abnormal responsiveness of adrenal cells to physiologic secretion of GIP. "Illicit" (ectopic) expression of GIP receptors on adrenal cells presumably underlies this disorder. (N Engl J Med 1992;327:974–80.)

Media in This Article

Figure 1Plasma Cortisol Concentrations in a Patient with Food-Induced Cushing's Syndrome during Fasting and after Eating.

Figure 2Plasma Cortisol and GIP Responses to Oral Glucose Administration (○), Intravenous Glucose Administration (●), and Protein-Rich (□) and Lipid-Rich () Meals in a Patient with Food-Induced

Tuesday, April 26, 2011

Doctors Perform Brain Surgery...Through The Nose


(COLUMBUS, Ohio) – Imagine your doctor telling you that you have a brain tumor at the base of your skull, and it could be removed without a single visible scar on your face.  It may sound like the plot of a sci-fi thriller, but it’s actually happening at Ohio State’s James Cancer Hospital.

How?   “We go through the nostril, without performing any incision in the patient’s face or in the head” said Dr. Daniel Prevedello, director of the minimally invasive cranial surgery program at Ohio State University Medical Center.  “It means we don’t have to cut through the flesh or remove large pieces of the skull, which avoids deformation of the patient’s face.”

The approach is known as an endoscopic endonasal approach, in which two surgeons work side by side to remove tumors and lesions at the base of the skull.  A neurosurgeon uses two tiny surgical instruments in one nostril, a head an neck surgeon does the same in the other nostril.  After accessing the base of the brain through the sinus cavity, the surgeons use highly sophisticated mappings of the brain, similar to GPS technology, to find and resect problem areas.  

Most of the tumors and lesions come out the same way the surgical instruments went in - through the nose.  “Some tumors we do have to remove them piecemeal through the nostril” said Dr. Bradley Otto, a head and neck surgeon at the Otolaryngology department at the Ohio State University Medical Center.  “We try not to do that as much as possible, but all of the lesion or the tumor we remove, is removed through the nostril without any incisions in the face.”

Normally, a patient’s face would be cut open or even peeled back to access the base of the skull, but not with this technique.  Going through the nose not only cuts down on recovery time from surgery, but it allows other treatments to take place sooner as well. “You have less normal tissue to heal and you can do radiation and other types of oncological treatment earlier” said Prevedello.

It was the perfect option for Tricia Wharton.  Tricia was eight months pregnant when doctors discovered a tumor at the base of her brain.  Treating the tumor was challenging enough, but doctors also had to consider the health of her unborn child.

“It wasn’t safe for the baby at that time to do radiation or chemo” said Wharton.  So, doctors had to come up with another plan.

Doctors gave Wharton steroid injections to help develop her baby’s lungs as much as possible, then, at 33 weeks, they delivered the baby early.
“I had the C-section on a Sunday and then my sinus surgery on a Friday” said Wharton.  “We were both in the hospital at the same time, in the same hall.  We were just a few floors away from each other so after my surgery I was able to visit her.”

Within a matter of days both mom and baby were cleared to go home, and because Tricia’s recovery time was dramatically reduced due to the endonasal technique, she could not only take care of herself, but her newborn baby.

“I was actually surprised at how fast it healed” she said.  “Three weeks after surgery our life was pretty much back to normal.  I could do almost everything I could before.”

While this type of surgery can prove to be remarkably effective, it is still fairly rare.  Prevedello says only a few medical centers around the world offer the two-surgeon, endoscopic endonasal approach.  In fact, several doctors from Europe spent several weeks in Columbus training in this technique with surgeons at Ohio State’s James Cancer Hospital.

“It’s not something you’ll find common place in a lot of hospitals across many cities” he said.  Dr. Otto agrees, and says because of the uniqueness of the procedure, they’re treating patients from all over the globe.

“Our patient population tends to be not just the Columbus area and the vicinity, but  really throughout the United States and we’ve actually had a few international patients come in as well.”


Calories & Cushing's Disease


Cushing's disease is a condition where the pituitary gland produces too much ATCH, or adrenocorticotropic hormone. The increased ATCH levels cause the adrenal glands to release additional cortisol, a hormone used to metabolize carbs, fats and proteins, as well as regulate the effects of insulin, which moves glucose from the bloodstream to the cells where it can be used for fuel. The changes in metabolism and insulin usage may lead to unintentional weight gain, specifically along the midsection and upper back.


While there's usually no way to avoid weight gain with Cushing's disease, you can often minimize it by limiting your caloric intake. The number of calories, however, varies greatly from person to person. This is at least partly why the Warren Grant Magnuson Clinical Center at the National Institutes of Health recommends talking to a dietitian to establish the appropriate caloric intake for you. Not only is your caloric need affected by the disease, but it's also based on your height, weight, gender, age and level of physical activity.


Besides limiting caloric intake, most medical professionals will tell you to balance your diet. It isn't enough to just cut calories; you should do so healthily. Draw from all food groups, including fruits, vegetables, whole grains, lean meats and low-fat dairy when changing your diet to minimize weight gain. Again, a dietitian is your best source for determining exactly what your body needs.


Weight gain isn't the only complication associated with Cushing's disease. Many people with this syndrome find that their bones are thinning, which may require an increased intake of calcium. Try to get at least 800 mg a day, unless you are between ages 11 and 24, which necessitates an intake of 1,200 mg. To help the body better absorb calcium, increase your intake of vitamin D, advises

Fat and Cholesterol

Watch your intake of total fat, saturated fat, trans fat and cholesterol. Along with weight gain and thinning bones, many people with Cushing's disease have difficulties managing their cholesterol levels.Keep your total fat intake to no more than 25 to 35 percent of your calories. Limit saturated fat intake to no more than 7 percent of your calories and trans fat to no more than 1 percent. Limit dietary cholesterol to less than 300 mg.

Dana George

About this Author

Dana George has been a freelance writer since 2005, penning numerous articles, Web content and marketing collateral for both print and online. His articles have appeared in "Healthy Knowledge" magazine, "Minneapolis Metro Mix" and "Meefers." George holds a Bachelor of Arts from the University of Wisconsin.

Article reviewed by Mary Branham

Last updated on: 04/23/11
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About this Author

Dana George has been a freelance writer since 2005, penning numerous articles, Web content and marketing collateral for both print and online. His articles have appeared in "Healthy Knowledge" magazine, "Minneapolis Metro Mix" and "Meefers." George holds a Bachelor of Arts from the University of Wisconsin.


Endocrine Society Releases Guidelines on Pituitary Incidentalomas

Wednesday, April 20, 2011 - Elsevier Global Medical News

Surgical treatment of a pituitary incidentaloma is recommended when the lesion is causing a visual field deficit or other visual abnormalities, such as ophthalmoplegia “or neurological compromise,” according to evidence-based clinical practice guidelines published by the Endocrine Society.

Surgery is also recommended when the lesion is abutting or compressing the optic nerves or chiasm on MRI, when a patient is experiencing pituitary apoplexy with visual disturbance, or if a patient has a hypersecreting tumor other than a prolactinoma, according to the guidelines, which appear in the society’s journal (J. Clin. Endocrinol. Metab. 2011;96:894-904).

The guidelines pertain to adults, as there are no available data on these lesions in the pediatric population.

A pituitary incidentaloma is defined as “a previously unsuspected pituitary lesion that is discovered on an imaging study performed for an unrelated reason.” That does not include a symptom such as visual loss that is related to the lesion, “but rather [a study done] for the evaluation of symptoms such as headache, or other head or neck neurological or CNS complaints or head trauma.”

Such surprise findings are not uncommon, according to a statement from the society, which noted that small incidentalomas were discovered in as many as 20% of adults who had head imaging with MRI or CT scans for unrelated reasons.

“Fortunately, incidentalomas are almost always benign and usually do not need surgery,” Dr. Pamela Freda, an endocrinologist at Columbia University in New York who chaired the task force that wrote the guidelines, said in the statement. The guidelines make recommendations about evaluating and treating such patients, “indicating when surgical therapy may be necessary,” she added.

Surgery may be considered for patients with pituitary incidentalomas if there is clinically significant growth of the lesion, loss of endocrinologic function, or an “unremitting headache,” or if a patient is planning a pregnancy and has a lesion close to the optic chiasm.

The guidelines include recommendations on the initial evaluation of patients, follow-up testing of patients who do not meet criteria for surgical removal of the lesion, and medical therapy. For example, after an incidentaloma is identified, a patient should undergo a complete history and physical examination “that includes evaluations for evidence of hypopituitarism and a hormone secretion syndrome,” as well as biochemical evaluations, if there is evidence for either of these conditions, the guidelines state.

None of the seven authors of the guidelines declared a “significant financial interest” or a “leadership position” within the pharmaceutical industry. Dr. Freda’s disclosure states that she has “financial, business or organization interests” in Novartis, Ipsen, and Pfizer. Other authors also disclosed financial, business, or organization interests in those three companies, and/or in Novo Nordisk, Tercica/Ipsen, or no relevant financial interests.

The guidelines are cosponsored by the European Society of Endocrinology.

The society’s patient-education affiliate, the Hormone Foundation, is publishing a related patient guide that can be found at


Friday, April 15, 2011

Corcept Therapeutics Submits NDA for Corlux in Cushing’s Syndrome


Getting in just under the wire on its second self-imposed deadline, Corcept Therapeutics (Nasdaq: CORT) finally announced submission of its NDA for Corlux (mifepristone) in Cushing’s Syndrome, a disease characterized by high levels of circulating cortisol resulting in glucose intolerance, hypertension, depression, and obesity. Corlux is a glucocorticoid receptor-II (GR-II) antagonist which can block the effects of the glucocorticosteroid cortisol. The company has Orphan Drug Designation for Corlux in Cushing’s Syndrome and is hoping to secure priority review if the FDA accepts their submission. There are currently no therapies approved in the United States exclusively for Cushing’s Syndrome, and care typically revolves around symptom management. Corcept believes (quite logically) that focusing on the underlying biochemical problem will be a better way of treating this disease.

Corcept announced positive Phase 3 data at the end of 2010 and beginning of 2011, with both primary and secondary endpoints being reached. The trial was conducted in two groups of Cushing’s patients who were either glucose-intolerant or hypertensive and who had failed, relapsed from, or were ineligible for surgery on cortisol-producing tumors.

The glucose intolerant group’s primary endpoint was a 25% or better improvement in glucose tolerance, and a response rate of 60% was achieved in this arm of patients. The primary endpoint for the hypertensive group was an improvement of 5mm or greater in diastolic blood pressure, and 43% of patients achieved this level. Both response rates are considered statistically significant (above the 20% “hurdle rate”), the drug was well tolerated in the trials, and no major side effects were reported. Furthermore, the secondary endpoint of “global clinical improvement” was met by 87% of patients in the study as analyzed by a data review board comprised of three academic physicians with clinical Cushing’s Syndrome experience.

Commonly observed side effects were adrenal insufficiency, endometrial thickening, and hypokalemia. The majority of serious adverse events were determined not to be drug-related, and any adverse effects that were drug-related were resolved with clinical management. It is worth noting that 88% of the patients involved in the study opted to enter into a long-term extension study, which can be seen as a vote of confidence by the patient population in Corlux’s efficacy and tolerability. Corcept plans to present detailed trial data at the Endocrine Society Annual Meeting in June which will likely allow a more comprehensive analysis of its approval odds. As of right now, Corlux’ chances look good.

Corcept originally announced plans to submit the NDA by the end of March; hopefully the two week extension needed to submit to the FDA means the company took extra care in finalizing its application. Stay tuned for updates on Corcept Therapeutics as the regulatory fate of their first clinical candidate unfolds.


Random postoperative day 3 cortisol as a predictor of hypothalamic-pituitary-adrenal axis integrity after transsphenoidal surgery


Endocrine Practice


American Association of Clinical Endocrinologists


1530-891X (Print) 1934-2403 (Online)


Health Services, Medical Sciences and Endocrinology






Maryam I. Khan, MD1, 2, Mouhammed A. Habra, MD, FACE1, Ian E. McCutcheon, MD3, Graciela M. Nogueras-González, MPH4, Jessica K. Devin, MD1, Naifa L. Busaidy, MD1, Nicholas B. Levine, MD3, Wayne Lindstrom, MD1, David Kagan, MD1, Camilo Jimenez, MD1, Steven G. Waguespack, MD, FAAP, FACE1

1Department of Endocrine Neoplasia and Hormonal Disorders, University of Texas M. D. Anderson Cancer Center, Houston, TX, USA
2Division of Diabetes, Endocrinology and Metabolism, Baylor College of Medicine, Houston, Texas, USA
3Department of Neurosurgery, University of Texas M.D. Anderson Cancer Center, Houston, TX, USA
4Division of Quantitative Sciences, University of Texas M.D. Anderson Cancer Center, Houston, TX, USA


Objective: To determine if a random postoperative day 3 (POD3) cortisol ≥10μg/dl is predictive of adrenal sufficiency (AS) at 3-10 weeks after transsphenoidal surgery (TSS) and during long-term clinical follow up.

Methods: We retrospectively reviewed the case records of 466 patients who underwent TSS at our institution between 1991 and 2008. Eighty-three patients met inclusion criteria for the study: random cortisol measured on the morning of POD3, adrenal dynamic testing performed 3-10 weeks after TSS, and clinical assessment of the hypothalamic-pituitary-adrenal (HPA) axis at least 6 months after TSS.

Results: The sensitivity of a random POD3 serum cortisol ≥10μg/dl for the prediction of AS at a median follow up of 42 days was 64.81% (95% CI: 50.6-77.32), with an odds ratio of 3.1 (95% CI: 1.08-8.58). The specificity was 62.1% (95% CI: 42.3-79.3). At a median follow up of 500 days, only 2 patients with a POD3 cortisol ≥10μg/dl required hydrocortisone replacement, both of whom had multiple anterior pituitary hormone deficiencies and evidence of pituitary dysfunction during the perioperative period.

Conclusions: In the appropriate clinical context, a POD3 cortisol ≥10μg/dl accurately predicts the integrity of the HPA axis. The final decision regarding corticosteroid replacement should be individualized, taking into consideration the POD3 cortisol level, the clinical context in which the measurement was obtained, and any evidence of concomitant pituitary dysfunction in the perioperative period.

transsphenoidal resection, adrenal insufficiency, pituitary adenoma, hydrocortisone replacement

Show References


Obesity is a Predictor of Morbidity in 1,629 Patients Who Underwent Adrenalectomy

DOI: 10.1007/s00268-011-1070-2

Hadiza S. Kazaure, Sanziana A. Roman and Julie A. Sosa



We examined the impact of obesity on 30-day outcomes of adrenalectomy using a multi-institutional database.


Patients who underwent adrenalectomy in 2005–2008 according to the American College of Surgeons-National Surgical Quality Improvement Project (ACS-NSQIP) data set were grouped by body mass index (BMI): normal weight (BMI = 18.5–24.9 kg/m2), overweight (BMI = 25.0–29.9 kg/m2), obese (BMI = 30.0–34.9 kg/m2), and morbidly obese (BMI ≥ 35 kg/m2). Outcomes of the higher BMI groups were compared to those of the normal BMI group using χ2, analysis of variance (ANOVA), and multivariate regression.


There were 1,629 patients in the study: 22% were normal weight, 31% overweight, 22.2% obese, and 24.7% morbidly obese. Compared to normal-weight patients, obese and morbidly obese patients had a 12.5 and 16.7% increase in operation times (129 vs. 145 and 150 min, respectively, p ≤ 0.01) and sustained more wound complications (0.2 vs. 0.4 and 1.2%, p < 0.001), including superficial and deep wound infections (p < 0.001 and p < 0.01, respectively). Morbid obesity independently predicted overall complications (odds ratio [OR] 2.9, 95% confidence interval [CI]: 1.7–5.7), wound complications (OR 6.1, 95% CI: 2.0–18.9), and septic complications (OR 3.1, 95% CI: 1.1–8.8). Obesity independently predicted longer total time in the operating room (p < 0.006). There were no differences in rates of reoperation and length of hospital stay by BMI category.


Obesity is an independent risk factor that needs to be considered in surgical decisions regarding adrenalectomy. Morbidly obese adrenalectomy patients are particularly at risk for wound and septic complications.

Presented in part at the 6th Annual Academic Surgical Congress, Huntington Beach, CA, 1 February 2011.

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Treatment Guidelines for Pituitary Incidentalomas Issued

Emma Hitt, PhD

April 12, 2011 — The Endocrine Society has issued clinical guidelines for the endocrine assessment and treatment of pituitary incidentaloma that indicates surgical therapy under some conditions.

Pamela U. Freda, MD, with the Columbia College of Physicians & Surgeons in New York, NY, led the panelists who developed the guidelines, which were reported in the April 2011 issue of the Journal of Clinical Endocrinology & Metabolism.

The 7-member panel sought to develop practice guidelines for the endocrine evaluation and treatment of pituitary incidentalomas through the evaluation of systematic reviews of evidence. They also participated in conference calls and email discussions to develop the guidelines.

The panel recommends that patients with a pituitary incidentaloma undergo a complete history and physical examination, laboratory evaluations screening for hormone hypersecretion and hypopituitarism, and a visual field examination if the lesion abuts the optic nerves or optic chiasm.

They also recommend that patients with incidentalomas who do not meet criteria for surgical removal be monitored with clinical assessments and neuroimaging, which should include a magnetic resonance imaging (MRI) scan at 6 months for macroincidentalomas, 1 year for a microincidentaloma, and thereafter progressively less frequently if the incidentaloma is unchanged in size.

Patients should also undergo visual field examinations if they have incidentalomas that abut or compress the optic nerve and optic chiasm (6 months and yearly), as well as endocrine testing in the case of macroincidentalomas (6 months and yearly) after initial evaluation.

According to the study authors, the evidence for or against a recommendation for surgery because of growth of a pituitary incidentaloma is limited. The panel suggests that surgery is indicated if patients have a visual field deficit resulting from the lesion; other visual abnormalities, such as ophthalmoplegia or neurologic compromise from compression by the lesion; a lesion abutting or compressing the optic nerves or optic chiasm on MRI; pituitary apoplexy with visual disturbance; or hypersecreting tumors other than prolactinomas as recommended by other Endocrine and Pituitary Society guidelines.

In addition, surgery should be considered in patients with a pituitary incidentaloma if there is clinically significant growth of the pituitary incidentaloma, if there is loss of endocrinologic function, if a patient is planning pregnancy with a lesion close to the optic chiasm, or if a patient has unremitting headache.

The study authors add that the "success of surgery for hormone secreting tumors is highly dependent on the expertise, skill, and case volume of a pituitary surgeon supported by an experienced team."

Medical therapy for pituitary incidentalomas has not been systematically studied, the authors note. "In patients with incidentalomas and hyperprolactinemia that may be due to tumoral compression of the hypothalamic-pituitary stalk, symptomatic hyperprolactinemia may be treated with a dopamine agonist," they write. However, they add that incidentalomas other than a prolactinoma are unlikely to shrink, and lesions should still be monitored regardless of changes in prolactin levels.

The study authors have disclosed various financial relationships with Novartis, Ipsen, Pfizer, Novo Nordisk, Tercica/Ipsen, and/or KER Unit (Mayo Clinic).

J Clin Endocrinol Metab. 2011;96:894-904. Abstract



Sunday, April 10, 2011

Pituitary hyperplasia secondary to acquired hypothyroidism: case report

Roberto Franceschi email, Umberto Rozzanigo email, Riccarda Failo email, Maria Bellizzi email and Annunziata Di palma email

Italian Journal of Pediatrics 2011, 37:15doi:10.1186/1824-7288-37-15

Published: 7 April 2011

Abstract (provisional)

Objective and Importance: despite recent progress in imaging, it is still difficult to distinguish between pituitary adenoma and hyperplasia, even using Magnetic Resonance Imaging (MRI) with gadolinium injection. We describe an example of reactive pituitary hyperplasia from primary hypothyroidism that mimicked a pituitary macroadenoma in a child.

Clinical Presentation: a 10 year old boy presented with headache and statural growth arrest. MRI revealed an intrasellar and suprasellar pituitary mass. Endocrine evaluation revealed primary hypothyroidism.

Intervention: the patient was started on levothyroxine with resolution of the mass effect.

Conclusion: primary hypothyroidism should be considered in the differential diagnosis of solid mass lesions of the pituitary gland. Examination of thyroid function in patients with sellar and suprasellar masses revealed by MRI may avoid unnecessary operations which can cause irreversible complications.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.


Saturday, April 9, 2011

Clinical Trial: Safety and Efficacy of LCI699 in Cushing's Disease Patients

This exploratory study is a proof of concept study to determine whether LCI699 can safely reduce the level of urinary free cortisol in patients with Cushing's disease...

Date First Received: April 6, 2011

Last Updated: April 6, 2011

Verified by: Novartis, April 2011

Clinical Trial Phase: Phase 2 | Start Date: March 2011

Overall Status: Recruiting

Estimated Enrollment: 12

Condition Keyword(s):

Additional Keyword(s) Provided by Clinical Trial Investigators:


Condition MeSH Term(s), Assigned with an Experimental Algorithm:

Intervention MeSH Term(s), Assigned with an Experimental Algorithm:

Brief Summary

Official Title: “A Proof of Concept, Open-label, Forced Titration, Multi-center Study to Assess the Safety/Tolerability and Efficacy of 10-weeks Treatment of LCI699 in Patients With Cushing's Disease”

This exploratory study is a proof of concept study to determine whether LCI699 can safely reduce the level of urinary free cortisol in patients with Cushing's disease.

Study Type: Interventional

Study Design: Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment

Study Primary Completion Date: December 2011

Intervention(s) in this Clinical Trial

  • Drug: LCI699

Arms, Groups and Cohorts in this Clinical Trial

  • Experimental: LCI699

Outcome Measures for this Clinical Trial

Primary Measures

  • Change in 24 hour urine free cortisol concentration
    • Time Frame: 10 weeks
      Safety Issue?: No

Secondary Measures

  • Changes in hormone levels, e.g. testosterone, estradiol
    • Time Frame: 10 weeks
      Safety Issue?: No
  • Changes in metabolic abnormalities, e.g. insulin, Hemoglobin A1C (HbA1C)
    • Time Frame: 10 weeks
      Safety Issue?: No

Criteria for Participation in this Clinical Trial

Inclusion Criteria:

  • Patients with confirmed Cushing's Disease with confirmation of pituitary origin of excess Adrenocorticotropic Hormone (ACTH)
  • Patients on medical treatment must complete a washout period prior to baseline

Exclusion Criteria:

  • Patients treated with mitotane 6 months prior to Visit 1
  • Patients with compression of the optic chiasm
  • Patients with a known inherited syndrome as the cause for hormone over secretion
  • Patients with Cushing's syndrome due to ectopic ACTH secretion or adrenal Cushing's syndrome
  • Patients with pseudo-Cushing's syndrome
  • Patients who are not biochemically euthyroid
  • Diabetic patients with poorly controlled diabetes (HbA1c >9%)
  • Other protocol-defined inclusion/exclusion criteria may apply

Gender Eligibility for this Clinical Trial: Both

Minimum Age for this Clinical Trial: 18 Years

Maximum Age for this Clinical Trial: 75 Years

Are Healthy Volunteers Accepted for this Clinical Trial?: No

Clinical Trial Investigator Information

Lead Investigator: Novartis Pharmaceuticals Industry

Overall Clinical Trial Officials and Contacts

Novartis Pharmaceuticals Study Director Novartis Pharmaceuticals  

Overall Contact: Novartis Pharmaceuticals 001-862-778-8300 

Additional Information

Information obtained from on April 07, 2011

Link to the current record.

Study ID Number: CLCI699C2201 Identifier: NCT01331239

Health Authority: France: Afssaps - French Health Products Safety Agency

Clinical Trials Authorship and Review

Clinical Trials content is provided directly by the U.S. National Institutes of Health via and is not reviewed separately by Every page of specific clinical trials information contains a unique identifier which can be used to find further details directly from the National Institutes of Health.


Low Incidence of Adrenal Insufficiency after Transsphenoidal Surgery in Patients with Acromegaly: A Long-Term Follow-Up Study

Anne Marij G. Burgers*, Nieke E. Kokshoorn*, Alberto M. Pereira, Ferdinand Roelfsema, Johannes W. A. Smit, Nienke R. Biermasz and Johannes A. Romijn

Department of Endocrinology and Metabolism, Leiden University Medical Center, 2300 RC Leiden, The Netherlands

Address all correspondence and requests for reprints to: N. R. Biermasz, Department of Endocrinology and Metabolic Diseases C4-R, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands. E-mail:

Context: The long-term prevalence of adrenal insufficiency after transsphenoidal surgery for GH-secreting pituitary adenomas is unknown. However, recently a single study reported a high prevalence of adrenal insufficiency in acromegalic patients after surgical and/or medical treatment without postoperative radiotherapy.

Objective: The objective of the study was to assess the prevalence and incidence rates of adrenal insufficiency in consecutive patients during long-term follow-up after successful transsphenoidal surgery for acromegaly.

Design: In 91 consecutive patients in remission after transsphenoidal surgery only, we retrospectively reviewed insulin tolerance tests, CRH stimulation tests, metyrapone tests, and ACTH stimulation tests used to assess corticotrope function.

Results: Early postoperatively, insufficient adrenal function was observed in 16 patients (18%), which was transient in eight and irreversible in eight other patients in the first year of postoperative follow-up. Therefore, after the first year, the prevalence of adrenal insufficiency was 9%. Late, new-onset adrenal insufficiency developed in only three patients 13, 18, and 24 yr after surgery. The incidence rate of late adrenal insufficiency after successful surgery was 2/1000 person-years. After long-term follow-up, a median of 8.1 (1–31 yr), the prevalence of secondary adrenal insufficiency was 12% in patients in remission after surgery for acromegaly.

Conclusion: The prevalence of adrenal insufficiency 1 yr after surgery was 9%, whereas during prolonged follow-up, the incidence rate of adrenal insufficiency was only 2/1000 person-years in patients in remission after surgery. Therefore, development of late-onset adrenal insufficiency is a very infrequent complication in patients with acromegaly in remission after transsphenoidal surgery only.


Pituitary tumor: Optician check-up `helped man discover cause of vision problems

By Alexa Kaczka

By paying a visit to an optician in Edinburgh, a man was able to rescue his sight thanks to the detection of a major health problem, it has been revealed.

The Edinburgh Evening News has reported on the experience of 62-year-old Blackhall man Scott Anderson, who found out that he had a pituitary brain tumour after an appointment he had with KD Wallace Optometry.

An appointment with a neurologist was made for Mr Anderson after he went to the optician, which revealed that a tumour was present.

Mr Anderson told the news provider that a number of years had elapsed since his previous trip to an optician.

He stated: "I am embarrassed to recognise that it has been about 15 years since I last went for an eye test."

When it comes to people's eye health, the Prevent Blindness America COO, Jeff Todd, recently encouraged sports players to wear adequate eye protection as the weather improves.


Cushie warriors: men, women & children who battle Cushing’s numerous times in hopes of winning the war

MelissaTX posted this on the message boards in honor of Cushing's Awareness Day, April 8:

Many of you only know one person with Cushing’s. It is difficult to understand or keep up with ‘your person’ as s/he seeks treatment. You have probably never known someone with Cushing’s before, right? You do know, however, that ‘your person’ talks about Cushing’s a lot or is pretty darned passionate about their Cushie friends. We lean on and help others even as we struggle to find our way through complicated testing, surgery (-ies), and hopefully, cures.

You see, for us, we know MANY people with Cushing’s through website. Cushing’s is a house guest who ruins our lives and won’t leave us alone. We Cushies all find it incredibly frustrating to have hit the many walls. We see it every day: patients insulted, dismissed, and defeated. When it happens to us, we are often rendered speechless. When we see our fellow Cushies meet the same poor medical treatment, we become incensed. Ultimately, we know our bodies best, and we are found to be correct. We know when we have a disease as devastating as Cushing’s.

For Cushing’s Awareness Day, we compiled this list of Cushing’s patients from all over the world who are fighting Cushing’s and seek treatment and a cure through multiple surgical procedures and even radiation. A glossary of terms is located at the bottom of the list.

Every patient wants to be understood, supported, and cared for. We want you to know that we are one of many who suffer from this ‘rare’ albeit rarely diagnosed disease.

Today, the Cushing community stands before you, asking you to recognize us for the struggles we face and for you to be the most supportive and caring friend or family member you can be to ‘your person.’

(NOTE: This is only a sample collected through a short time on the Cushing’s messages boards. There are many, many more patients like us).

  1. Melissa, Texas.
    Pituitary surgery #1: June 2009.
    Pituitary surgery # 2: soon in April 2011.
  2. Sarah, Oregon.
    Pituitary surgery #1: Nov 2009.
    Pituitary surgery #2: March 2010.
    Pituitary Surgery #3: Sept 2010.
    BLA: April 2011.
  3. Alex B, California
    Pituitary surgery March 2008
    BLA July 2009.
  4. Krystine T, Washington
    1st failed Pituitary surgery March 1996
    2nd failed Pituitary surgery Dec 2002
    BLA Dec 2004
    3rd failed Pituitary surgery Sept 2009
    MEGA ONE DAY Radiation ZAP Aug 2010
  5. Jill, Denver, Colorado
    left adrenalectomy Nov 2006
    right adrenalectomy Feb 2008
  6. Karen, Hinesburg,Vermont
    1st Pituitary surgery in Portland OR, January 9,2006. Not successful.
    2nd Pituitary surgery in Seattle Washington July 9, 2007.
    CSF leak July 13, 2007. I'm in remission.
  7. Christy, Oklahoma.
    Pituitary surgery 9-2004 Oklahoma City
    BLA 11-2004 Oklahoma City
    Rest Tissue PIT 9-2006 Pittsburgh
    CSF leak repair with titanium after the last pituitary surgery and it was removed 5-2009.
  8. Beth, Winnipeg, Manitoba, Canada.
    Gamma knife December 2006 and again December 2008. Still broken, and if the tumor grows more (it's been stable for a bit now), I'll likely be headed for a 3rd time!
  9. Justin K., Kansas
    Pituitary surgery, May 19, 2008.
    BLA, May 6, 2009.
  10. Jessica K., Kansas.
    Pituitary surgery, May 16, 2008.
    BLA, May 6, 2009.
  11. Bill K., Kansas.
    Pituitary surgery, August 14, 2009.
    BLA, June 2, 2010.
  12. Danielle, Massachusetts.
    Pituitary Surgery #1 Dec 16, 2009.
    Pituitary Surgery #2 February 11, 2010.
    BLA Sep 2, 2010
  13. Trisha T, Tampa FL
    Pituitary surgery 4/07
    Currently trying to avoid BLA with various meds.
  14. Cindy W, Kentucky.
    Pituitary Surgery 11-5-07
    BLA 03-07-08
    CSF Leak repair 10-28-08
  15. Lisa, Illinois.
    Pituitary Surgery 5-30-08
    BLA 11-4-09
    Still not cured.
  16. Susan G.
    Pituitary Surgery 7/07
    Cleared for 2nd pituitary surgery 10/10.
  17. Kimberly, Illinois.
    Pituitary Surgery 11-2-2009
    BLA 2-2-2011.
  18. Debra, Virginia
    Debra v. Gallbladder due to Cushings, 1/2005
    root canal due to broken tooth 8/2008
    Pituitary surgery 10/2008
    BLA 6/2010
    Sinus/leak repair 1/2011
    Surgeries offered and rejected == repair of foot muscles, lap band surgery; surgery for excess stomach acid
  19. Lisa O, Washington State
    3/25/2009-pituitary surgery
  20. April, KY.
    Unsuccessful pituitary surgery 1/15/10.
    Testing again.
  21. Elizabeth J, KY
    Pituitary Surgery 7-2-2009
    BLA Sept. 15, 2010
  22. Trisha S, Indiana
    Pituitary surgery 11/13/2008.
    Not cured - retesting.
  23. Lynne R, Oxford, England.
    Pituitary surgery April 2008
    CSF leak repairs: April 2008, May 2008, May 2008 (3 leaks in the space of 5 weeks), with meningitis as a result of the leaks.
    Issues due to pituitary gland removal: crohns disease, pernicious anaemia, life dependent on multiple medications [hydrocortisone, ddavp, thyroxine, hrt, growth hormone, colestyramine, Vit B12 injections etc, etc. ( oh, and it stole my life- and I'd quite like it back please)]
  24. Dara M, Limerick, Ireland.
    Pituitary surgery 29th June 2009
    got MRSA in sinus as a result, had surgery to remove scar tissue.
    MRSA is not for Christmas, for me it's for life xxx
  25. Philip B, New Jersey.
    Pituitary surgery at MD Anderson October 31, 2007.
    Testing for Recurrence since Jan. 2011.
    Replacing Growth hormone and Testosterone
  26. Donna, Winnipeg, Manitoba, Canada
    Pituitary surgery Aug2009.
    new tumor march 2010 but not told about it until sept2010 when it got to 9mm.
    had gamma knife nov. 2010.
    still waiting to be better. tumor has not shrunk yet
  27. Michelle, California.
    Pituitary surgery February 2009.
    BLA February 2010.
    Not cured. Testing. 2 tumors showed on MRI.
  28. Shauna N, Washougal, WA.
    Pituitary surgery 8/2/01
    BLA 2/5/02.
  29. Robin S, Salem, VA
    Pituitary surgery Dec. 14, 2006
    BLA June 16, 2010
  30. Lori, Great Neck, NY
    Diagnosed 12/1994.
    Pituitary surgery 3/1995
    Pituitary surgery 5/1997
    Pituitary surgery 7/1999
    Still sick. Possible Cyclical?
  31. Nan, New Jersey
    Pituitary Surgery, October 2010
  32. Dan, Delaware.
    Pituitary Surgery #1 August 2009.
    Pituitary Surgery #2 February 2011.
  33. Cyndie M, New Jersey
    Pituitary 1-09-2009
    Upcoming BLA 4-28-2011.
  34. Kim S., Pennsylvania
    Surgery #1 Jan 2010 positive for Acromegaly but was trying to find a cure for Cushings.
    Testing since Oct 2010 for Cushings.
  35. Kay, New Jersey
    1st & 2nd Pituitary surgery June 2008 - in remission
  36. Jenny, Iowa.
    Pituitary Surgery #1- May 2008.
    Pituitary Surgery #2- April 2009.
    Currently considering a BLA vs. pituitary surgery #3.
  37. Tanya, Buffalo, NY
    Pituitary surgery #1 - February 2010
    currently seeking re-diagnosis
  38. Denise P, Dallas,Oregon
    2003 Pituitary surgery Vanderbilt
    2004 canceled pituitary removal after screws were in (I was in pre-op) Vandy
    2004 Stereotactic Radiosurgery- Vanderbilt
    2005 Right half of Pit removed - OHSU
    2005 BLA - OHSU
  39. Cate, Georgia
    Pituitary surgery #1 and 2 -- August 2009.
    In remission.
  40. Kate, New Jersey
    Pituitary surgery #1 - Jan. 2007 (Failed)
    Pituitary surgery #2 - July 2007 (Total Pit Removal; Failed)
    CSF Leak Surgeries - Oct. 2007 (Failed; still have small leak)
    Open BLA with 18" incision - Sept. 11, 2008
    Gamma Knife Radiosurgery - Oct. 2009
    No pit, no adrenals, radiation damage to hypothalamus (cannot regulate body temp.)
  41. Pat, California
    Pituitary Surgery #1: August 2000.
    Pituitary Surgery #2 December 2007.
    Currently testing for surgery #3.
  42. Christy, New Mexico
    Pituitary surgery November 2010.
    Considering BLA
  43. Brenda, Alberta, Canada
    Pituitary surgery May, 2007
    BLA May, 2007
  44. Jamie, Washington State
    Pituitary surgery #1: March 2010.
    Pituitary surgery #2: April 2010.
  45. Melissa, Florida
    Pituitary surgery #1: March 2009.
    Pituitary surgery #2: December 2009.
    BLA to come?
  46. Vicki, Buffalo, NY
    Pituitary surgery #1: October 2009.
    Pituitary surgery # 2: April 2010.
    BLA soon to come.
  47. Gina, Georgia
    Pituitary surgery #1: March 2009.
    Bilateral Adrenalectomy: October 2009.
  48. Sherry C, Silverton OR
    1st pituitary surgery 3/2006
    2nd pit surgery 9/2006
    BLA 10/2006.
    Sick since 1999 but diagnosed in 2005.
    Tested for 1 year. Knew I had Cushing's since 2004.
    Still sick....but it's the aftermath of the damage the cortisol did to me and the steroids now.
  49. Melyssa, Colorado
    Pituitary Surgery # 1: August 2009.
    Currently testing again.
  50. Michaela, Toronto, Ontario, Canada.
    Pituitary surgery 1 -- June 2005
    Pituitary surgery 2 -- Jan 2008
    Pituitary surgery 3 -- July 2008
    BLA -- July 2009
  51. Gisella, California
    Pituitary surgery #1: October 2009.
    Pituitary surgery #2: August 2010.
    Pituitary surgery # 3 or BLA to come.
  52. (Additions to original list, 4/9/2011)
    Tonya, NW Indiana
    Pituitary Tumor: Transphenoidal Hypophgsectomy - May, 2000
    Gamma Knife - July 2003
    then developed two Anyeurisms and had Anyerism Clippings in Nov., 2007.
    Unfortunately, now th as t I have clips in my head, nobody will run an MRI so now I have no way of monitoring the tumor growth since.
  53. AnellH, Dominican Republic
    I'm cured 01 Dec 2009 total pituitary removed.

From Glossary:

Pituitary Adenomas
Several therapies are available to treat the ACTH-secreting pituitary adenomas of Cushing's disease. The most widely used treatment is surgical removal of the tumor, known as transsphenoidal adenomectomy. Using a special microscope and very fine instruments, the surgeon approaches the pituitary gland through a nostril or an opening made below the upper lip. Because this is an extremely delicate procedure, patients are often referred to centers specializing in this type of surgery. The success, or cure, rate of this procedure is over 80 percent when performed by a surgeon with extensive experience. If surgery fails, or only produces a temporary cure, surgery can be repeated, often with good results. After curative pituitary surgery, the production of ACTH drops two levels below normal. This is a natural, but temporary, drop in ACTH production, and patients are given a synthetic form of cortisol (such as hydrocortisone or prednisone). Most patients can stop this replacement therapy in less than a year.

For patients in whom transsphenoidal surgery has failed or who are not suitable candidates for surgery, radiotherapy is another possible treatment. Radiation to the pituitary gland is given over a 6-week period, with improvement occurring in 40 to 50 percent of adults and up to 80 percent of children. It may take several months or years before patients feel better from radiation treatment alone. However, the combination of radiation and the drug mitotane (Lysodren®) can help speed recovery. Mitotane suppresses cortisol production and lowers plasma and urine hormone levels. Treatment with mitotane alone can be successful in 30 to 40 percent of patients. Other drugs used alone or in combination to control the production of excess cortisol are aminoglutethimide, metyrapone, trilostane and ketoconazole. Each has its own side effects that doctors consider when prescribing therapy for individual patients.

CSF, Cerebrospinal fluid leak: A more rare, although sometimes expected, result of surgery is drainage from the nose of a clear, watery liquid called cerebrospinal fluid (CSF), which is a normal fluid that surrounds the brain. Large pituitary tumors lean up against a membrane that separates this fluid space from the nose, and a CSF leak may occur if this membrane is absent or opened during surgery. The surgeon will generally recognize a CSF leak when it occurs and will "repair" the leak by placing a small amount of abdominal fat over the leak. The patient may awake from surgery and find that it was necessary for the surgeon to place a small tube in the lower back to allow CSF to drain into a bag and help the leak to seal. The tube is placed while the patient is still under anesthesia, and it is not painful while in place. The tube (about 3 millimeters in diameter) will remain in the lower back for 3-5 days and the patient will be kept in the hospital during this period. After the tube is removed (a painless, approximately 15-second procedure), the patient usually will be able to leave the hospital later the same day with the leak sealed. In most cases, CSF leakage does not occur and the patient may expect to go home 2 to 4 days after surgery.

BLA, Bilateral Adrenalectomy: Surgical removal of both the adrenal glands.

Gamma Knife: This is a more focused radiation treatment than conventional radiation, which reduces the risk of hypopituitarism. It provides a large dose of radiation to a tumor so that when the tumor cells divide, they die. As this method depends on the rate of cell division, symptoms may persist long after the radiation treatment.

Radiotherapy, preferably with stereotactic radiation, is effective in controlling tumor growth in the majority of patients who have residual tumor after surgery.


MaryO'Note: Thanks for doing all this work, Melissa! You did a fantastic job and the numbers are really telling.

Since you said we could copy it, I'm going to put it on if you don't mind.

If anyone on this list has a bio on the website, and you'd give your permission, I'd like to link your bio to your stats on this list.


Friday, April 8, 2011

Sphenoid sinus pyocele after transsphenoidal approach for pituitary adenoma

Mario Giordano, Venelin M. Gerganov, Wolfgang Draf and Rudolf Fahlbusch


Transsphenoidal pituitary adenoma surgery is related to a low morbidity rate. The complications that can occur are classified as intra- and extracranial. The aim of the study is to discuss one group of these complications involving the sphenoid sinus: mucocele and its possible transformation into pyocele.

We evaluate clinical presentation, management strategy and the outcome after long-term follow-up presenting an explicative case and a review of the literature. A patient presented to our outpatient clinic 8 months after transsphenoidal surgery for selective removal of a pituitary adenoma because of an acute onset of frontal headache during an airplane travel, fever and pulsating sensation in left eye and ear. MRI revealed a contrast-enhancing lesion in the left inferior portion of the sphenoid sinus.

An endonasal endoscopic revision of the sphenoid sinus was performed. After opening of the scar to enter in the left sinus a pyocele was found and treated with drainage and marsupialisation. Development of sphenoid sinus pyocele is an extremely rare postoperative complication of transsphenoidal surgery. This lesion should be taken in consideration in patients presenting with retroorbital headache of acute onset and fever after pituitary surgery. Diagnosis can be suspected on the MRI studies and confirmed by a targeted flexible endoscope examination. Endoscopic drainage with wide opening of the sphenoid sinus and marsupialisation is the treatment of choice to avoid recurrences.

Keywords Pyocele – Transsphenoidal approach – Pituitary adenoma

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Expression and Roles of Pannexins in ATP Release in the Pituitary Gland

Shuo Li, Ivana Bjelobaba, Zonghe Yan, Marek Kucka, Melanija Tomic and Stanko S. Stojilkovic

Section on Cellular Signaling (S.L., Z.Y., M.K., M.T., S.S.S.), Program in Developmental Neuroscience, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-4510; and Department of Neurobiology (I.B.), Institute for Biological Research "Sinisa Stankovic," University of Belgrade, 11000 Belgrade, Republic of Serbia

Address correspondence and reprint requests to: Dr. Stanko Stojilkovic, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Building 49, Room 6A-36, 49 Convent Drive, Bethesda, Maryland 20892-4510. E-mail: or .

Pannexins are a newly discovered three-member family of proteins expressed in the brain and peripheral tissues that belong to the superfamily of gap junction proteins. However, in mammals pannexins do not form gap junctions, and their expression and function in the pituitary gland have not been studied. Here we show that the rat pituitary gland expresses mRNA and protein transcripts of pannexins 1 and 2 but not pannexin 3. Pannexin 1 was more abundantly expressed in the anterior lobe, whereas pannexin 2 was more abundantly expressed in the intermediate and posterior pituitary. Pannexin 1 was identified in corticotrophs and a fraction of somatotrophs, the S100-positive pituicytes of the posterior pituitary and AtT-20 (mouse pituitary adrenocorticotropin-secreting cells) and rat immortalized pituitary cells secreting prolactin, whereas pannexin 2 was detected in the S100-positive folliculostellate cells of the anterior pituitary, melanotrophs of the intermediate lobe, and vasopressin-containing axons and nerve endings in the posterior lobe. Overexpression of pannexins 1 and 2 in AtT-20 pituitary cells enhanced the release of ATP in the extracellular medium, which was blocked by the gap junction inhibitor carbenoxolone. Basal ATP release in At-T20 cells was also suppressed by down-regulating the expression of endogenous pannexin 1 but not pannexin 2 with their short interfering RNAs. These results indicate that pannexins may provide a pathway for delivery of ATP, which is a native agonist for numerous P2X cationic channels and G protein-coupled P2Y receptors endogenously expressed in the pituitary gland.