Thursday, October 27, 2011

Effects of Hormone Stimulation on Brain Scans for Cushing's Disease

This study is currently recruiting participants.
Verified on August 2011 by National Institutes of Health Clinical Center (CC)

First Received on October 21, 2011.   No Changes Posted

Sponsor: National Institute of Neurological Disorders and Stroke (NINDS)
Information provided by: National Institutes of Health Clinical Center (CC) Identifier: NCT01459237



  • Cushing's disease can be caused by a tumor of the pituitary gland, a small gland about the size of a pea located at the base of the brain. These tumors produce high levels of hormones, which cause obesity, diabetes, and growth problems. The cure for this type of Cushing's disease is to have surgery that removes the tumor but leaves the pituitary gland alone. Currently, magnetic resonance imaging scans are the best way to find these tumors. However, many of these tumors do not show up on the scan.
  • Positron emission tomography (PET) scans use radioactive chemicals to light up parts of the body that are more active, such as tumors. Researchers want to try to make the small Cushing's disease tumors more active to help them show up on the scans. A special hormone will be given before the scan to make the tumors more active.


- To test the use of hormone stimulation to improve brain scans for Cushing's disease tumors.


- Individuals at least 8 years of age who will be having surgery to remove Cushing's disease tumors.


  • Participants will be screened with a medical history, physical exam, blood and urine tests, and imaging studies.
  • They will have three brain scans before surgery. The first scan is a magnetic resonance imaging scan to show a full picture of the brain. The second and third scans are PET scans.
  • The first PET scan will be given without the special hormone. The second PET scan will be done more than 24 hours but less than 14 days after the first PET scan. The second PET scan will be given with the special hormone.
  • Participants will have tumor removal surgery through another study protocol....

Pituitary Neoplasm

Study Type: Observational
Official Title: Prospective Evaluation of the Effect of Corticotropin-Releasing Hormone Stimulation on 18F-Fludeoxyglucose High-Resolution Positron-Emission Tomography in Cushing's Disease

Resource links provided by NLM:

Further study details as provided by National Institutes of Health Clinical Center (CC):

Estimated Enrollment: 30
Study Start Date: October 2011

Detailed Description:


Preoperative imaging identification and localization of adrenocorticotropin hormone (ACTH)-secreting pituitary adenomas is critical for the accurate diagnosis and the successful surgical treatment of Cushing's disease (CD). Unfortunately, over 40 percent of CD patients do not have a visible pituitary adenoma on magnetic resonance (MR)-imaging (the most sensitive imaging modality for ACTH-positive adenoma detection and localization). Lack of MR-imaging for diagnosis and to guide surgical resection results in significantly higher rates of surgical failure compared to cases associated with adenomas visible on MR-imaging. Because ACTH-adenomas are metabolically active compared to the surrounding pituitary gland, (18)F-fludeoxyglucose ((18)F-FDG) positron emission tomography (PET)-imaging in CD patients could be used to detect adenomas not detectable on MR-imaging. Moreover, corticotropin-releasing hormone (CRH) can be given to selectively increase the metabolic activity of ACTH-secreting pituitary adenomas to increase the likelihood of their detection and localization by (18)F -FDG PET-imaging. To determine the effect of CRH stimulation on (18)F-FDG uptake using PET-imaging in CD, we will perform (18)F-FDG high-resolution PET-imaging (with and without CRH stimulation) in CD patients.

Study Population

Thirty male and female CD patients 8 years and older will participate in this study.

Study Design

This is a single center trial to determine the effect of CRH stimulation on (18)F-FDG uptake in high-resolution PET-imaging of ACTH-adenomas in CD patients. CD patients will undergo (18)F-FDG high-resolution PET-imaging without CRH stimulation and (18)F-FDG high-resolution PET-imaging with intravenous CRH stimulation. The order of the PET scans will be randomized and the second PET scan will occur greater than 24 hours but less than 14 days after initial PET-imaging. For (18)F-FDG PET-imaging with CRH stimulation, intravenous (18)F-FDG will be given just before CRH administration. The PET images will be read by radiologists who are blinded to the administration of CRH. Within 12 weeks after completion of the last (18)F-FDG high-resolution PET-imaging scan, patients will undergo surgical resection of the pituitary adenoma. Surgical and histological confirmation of adenoma location will be used to assess the diagnostic and localization accuracy of PET-imaging and to compare to preoperative MR-imaging results in CD patients. Inferior petrosal sinus sampling (IPSS) results will be compared with imaging results and with surgical and histological findings.

Outcome Measures

The primary objective of this study is to determine the effect of CRH stimulation on (18)F-FDG uptake in high-resolution PET-imaging for CD. To assess and compare (18)F-FDG uptake without and with CRH stimulation, we will compare (18)F-FDG standardized uptake values (SUVs) in the region of interest (pituitary gland and pituitary adenoma). Secondary objectives include determining if CRH stimulation enhances detection of ACTH-adenomas as demonstrated on (18)F-FDG high-resolution PET-imaging and assessing the accuracy and sensitivity of (18)F-FDG high-resolution PET-imaging detection of ACTH-adenomas compared to MR-imaging. Measures to assess for these secondary objectives include comparing (18)F-FDG high-resolution PET-imaging (with and without CRH stimulation) detection to (1) MR-imaging detection of adenomas, (2) IPSS results, and (3) actual tumor location confirmed by histological findings to location predicted by PET- and MR-imaging within patients.


Ages Eligible for Study:   8 Years and older
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No


To be eligible for entry into the study, patients must meet all the following criteria:

  1. Be 8 years of age or older and able to undergo PET-imaging without needing general anesthesia.
  2. Able to provide informed consent (or guardian is able to provide consent in case of minor).
  3. Clinical diagnosis of CD based on medical records.
  4. Medically able to undergo resection of pituitary adenoma and planning to undergo surgical resection of adenoma within 12 weeks of PET-imaging.
  5. Normal liver enzymes: tests should be completed within 14 days before injection of the radiopharmaceutical; SGOT, SGPT less than or equal to 5 times ULN; bilirubin less than or equal to 2 times ULN.


Candidates will be excluded if they meet any of the following criteria:

  1. Pregnant or nursing women.
  2. Contraindication to MR-scanning, including pacemakers or other implanted electrical devices, brain stimulators, some types of dental implants, aneurysm clips (metal clips on the wall of a large artery), metallic prostheses (including metal pins and rods, heart valves, and cochlear implants), permanent eyeliner, implanted delivery pump, or shrapnel fragments
  3. Severe chronic renal insufficiency (glomerular filtration rate < 30 mL/min/1.73 m(2)), hepatorenal syndrome or post-liver transplantation.
  4. Elevated blood glucose level above 200 mg/dL on the day of the scan prior to (18)F-FDG administration.
  Contacts and Locations
Please refer to this study by its identifier: NCT01459237


Contact: Patient Recruitment and Public Liaison Office (800) 411-1222
Contact: TTY 1-866-411-1010


United States, Maryland
National Institutes of Health Clinical Center, 9000 Rockville Pike Recruiting
Bethesda, Maryland, United States, 20892

Thursday, October 20, 2011

PNA Webinar: "Growth Hormone Deficiency: Just the Facts!"

Title: Growth Hormone Deficiency: Just the Facts!
Date: Monday, October 24, 2011
Time: 10:00 AM - 11:00 AM PDT
After registering you will receive a confirmation email containing information about joining the webinar.

Presented by: Lewis Blevins, Jr, MD, Medical Director, Center for Pituitary Disorders, University of California, San Francisco

Dr. Blevins will discuss growth hormone deficiency, its diagnosis, the selection of patients for treatment, and expected outcomes of therapy.

Dr. Blevins has particular medical interest and specializes in pituitary tumors, Cushing's syndrome, acromegaly, hypopituitarism, craniopharynginoma, growth hormone deficiency, adrenal insufficiency, diabetes insipidus, and hypothalmic tumors. He attended medical school at East Tennessee State University, did his internship and medical residency at the University of Alabama Hospitals and fellowship at John Hopkins.

Reserve your webinar seat now at:

System Requirements
PC-based attendees Required: Windows® 7, Vista, XP or 2003 Server
Macintosh®-based attendeesRequired: Mac OS® X 10.5 or newer

Can Anyone Help Jutta?

Jutta writes:
I am a resident of Ontario Canada and have reason to belive I have cyclic Cushings with the last rapid weight gain and high cortisol about 6 years ago Serum cortisol was about 750 each time with high pm saliva cortisol identified last year. My gyneacologist discovered it 6 years ago and want a test done not covered by OHIP with a hopeful contact with a Boston specialist that he knows. I am scared I cannot afford the costs of diagnosos and treatment. Any suggestions?

Archived Interview With Andrea L, Pituitary Success Story, October 19, 2011

Andrea was interviewed on the BlogTalkRadio Cushing's Program on Wednesday, October 19, 2011

Listen live at

This interview is archived at and iTunes podcasts at

Listen to internet radio with CushingsHelp on Blog Talk Radio


Thursday, October 6, 2011

Andrea L, Pituitary Success Story, October 19, 6:00PM Eastern

Andrea will be interviewed on the BlogTalkRadio Cushing's Program on Wednesday, October 19 at 6:00PM

Listen live at

The Call-in number with questions or comments is (646) 200-0162

This interview will be archived at and iTunes podcasts at


From Andrea's bio: I first noticed something abnormal about my health in the summer of 2009, at age 23. I suddenly developed severe acne when I had had clear skin since I was a teenager, and I noticed more hair on my face and body than I was used to. In retrospect I realize that I’d also had bouts of weight gain, a buffalo hump and excessive sweating during my adolescent years, but I didn’t think anything of it at the time.

Around the same time I noticed the acne and hair growth, I also started putting on weight. I’d been on the thicker side for my height since childhood, so I decided to join Weight Watchers. Even though I was hungry a lot of the time, I stuck to the plan religiously and lost about a half pound per week. It was slow, but I was moving in the right direction so I stuck with it. I had bouts of fatigue throughout the process, but I would just assume that I needed to tinker with my diet – more protein, less protein, more fruit, less fruit, whatever. I tried a lot of different things, always focusing on getting adequate nutrition, but never had the energy that my Weight Watchers buddies seemed to have.

About six months later I finally went to my mom’s endocrinologist when I was visiting my parents in Texas. I was concerned that the acne and hair growth meant I had PCOS. All those tests came back normal, so the doctor gave me a 24 hour UFC just in case. It came back elevated, and she said I ought to follow up with an endocrinologist in New York where I live.

My next menstrual period didn’t come until 4 months later, and then they stopped completely.

My new endocrinologist in New York ordered more tests (you all know the drill). Over the next six months or so the 24 hour UFCs kept coming back high, salivary cortisols were normal or high, and one dexamethasone suppression test was kind of ambiguous. The doctor said that my urine volume was really high and might be screwing up the results, so I retested after limiting my fluid intake. That UFC came back normal, so I was instructed to follow up in six months.

As if on cue, the months following my normal UFC were great. For some reason I finally felt like I was bursting with energy. Beyond that, I had lost weight and even landed my dream job. At the time I assumed that the energy was from finally finding the right balance in my diet. The acne and hair growth were still there, but as far as I was concerned it was nothing that couldn’t be solved with some tweezers and makeup. Later I noticed in photos that even though I had lost weight, my face was much rounder than it had been before.

The nightmare began in January of 2011. I started feeling more anxious than usual. I began to cut more and more things out of my schedule because I didn’t feel like I had the mental energy to handle my normal workload. I had to take a Benadryl most nights to sleep. I started suffering from regular constipation for the first time in my life. My appetite increased markedly; I kept feeling less and less satisfied with my normal diet. I gave in and started rapidly gaining weight again.

After a particularly stressful week in February, I asked my mother to stay with me in New York for a little while, admitting that I had been feeling out of sorts. I figured I’d take a week off from work and just do fun stuff and I would be right back to normal.


The bouts of fatigue returned, this time so crushing that I didn’t even have the energy to make my own meals. I’ll never forget the day I attempted to go out for my morning jog, trying to convince myself that it was all “in my head,” and despite having plenty of cardiovascular and muscular strength, I could barely take a single step. I felt like the world had gotten bigger somehow, like I drank the shrinking potion from Alice in Wonderland.

At the same time, my appetite became so ravenous that I felt like I could gnaw my arm off 24/7. I also started feeling scatterbrained and having difficulty focusing. These were the beginnings of the cognitive symptoms that would prove to be the most debilitating of all.

My mother, god bless her eternally, suggested that the odd change in my mental state might have something to do with all those abnormal hormone levels from the prior year’s tests. I followed up with the endocrinologist again and had a very high 24 hour UFC. He ordered an MRI. My symptoms were getting worse, but my mom fatefully broke her foot and had to return to her home in Texas.

By the time March arrived I was so scatterbrained that I constantly felt drunk. Going to work was petrifying. My appetite was still insatiable.

Finally, the mood swings came. By “mood swings,” I don’t mean irritability. I mean that I became an ultra-ultra-rapidly cycling manic depressive. I would wake up at 3:30 in the morning giddy with energy, writing long, rambling e-mails to everyone I know, trying to go for a jog only to have to stop and dance to the music on my MP3 player in the middle of the Bronx. Then I would feel horrendously depressed mere hours later.

I could spend a lifetime attempting to describe the pain of bipolar depression. It is beyond despair. Take the icky feeling you might get with a cold or a flu and multiply it by a thousand. I was so distressed I felt like my brain was on fire. Like I had been poisoned. It would get so bad that I couldn’t speak. I vomited just from the discomfort. Once I went to the ER, desperate for relief. All my vitals were normal. They just let me ride it out, like I was having a bad drug trip. Later, I described these feelings to my roommate, who said she felt that exact feeling while going through narcotics withdrawal.

One of the most interesting aspects of this experience was that every time I got a migraine headache (which I've had periodically for most of my life), my depression would lift or I would get more manic. Note that if I had a choice, I would take a migraine every day of my life over the pain of severe depression.

I went to a psychiatrist, and much to my dismay, he told me I was not crazy. He gave me totally ineffective herbal mood-lifters and told me to go back to the endocrinologist. I started taking huge doses of caffeine in an attempt to take the edge off the low moods. It worked temporarily, but the feeling always returned. I ended up back in the ER after experiencing a lovely phenomenon called “sleep paralysis” (Google it) for two hours straight, which understandably gave me a panic attack. I was put on benzodiazepines, which prevented another panic attack but did nothing to make me more comfortable.

Some interminable time later, my endocrinologist called to inform me that I had a 5mm adenoma on my pituitary gland. I wept with relief and my family made immediate arrangements to take me to MD Anderson for surgery.

Maybe if I had read some of the bios on this site I would have anticipated what was to come. Cushing’s patients never have it that easy. In my scatter-brained, benzo-doped, manic-depressive stupor, I showed up at MD Anderson for…more tests. There, both a 24 hour UFC and dex/CRH test came back normal. A few things about the dex/CRH test were not administered as planned, but the in-house testing results combined with my still-normal bodyweight convinced MD Anderson that I did not have Cushing’s, and was simply a total nut case. They sent me on my way.

Finally I returned to my mom’s endocrinologist, the same woman who had had the foresight to give me my first 24 hour UFC. She ordered another round of tests and sent me to a wonderful psychiatrist who promised to do her best to make me feel better while we waited for a diagnosis. A litany of psychiatric medicines (mood stabilizers, sleeping pills, stimulants, antidepressants) would each work for a few days or a week and then wear off. Eventually the mood swings turned into a persistent, mind-numbing depression.

In retrospect, the benefit of having my mood fluctuate so violently earlier in my illness was that the depression didn’t have time to take hold of my thoughts. It was painful, yes, but I was able to fight the feelings of hopelessness and self-hatred with logic and positive self-talk. Later on I was not only completely miserable, but also came to believe that my misery would never end. I’m amazed I lived to tell the tale.

By midsummer I had a few more elevated 24 hour UFCs under my belt and had gained enough weight to look more “cushingoid.” This time I went to Methodist Hospital in Houston. The surgeon there agreed with my endocrinologists that I had pituitary Cushing’s, but disagreed that my MRI showed a defined adenoma. Again, Cushing’s patients never have it that easy. Luckily this surgeon was caring and proactive enough to order an IPSS and schedule me for surgery, though he warned me that it may not cure my depression. I asked for the surgeon to remove my entire pituitary gland in the event that he didn’t find a tumor.

August 23rd, 2011 was the day of my rebirth. I can attribute my euphoria in the week after the surgery to the strong pain meds I was on for the CSF drain, but by the time they were out of my system I was astounded to find that my mood and thinking were absolutely 100% normal. I can once again think, laugh, smile, sleep, taste, and enjoy the company of others. Within three weeks I had enough mental energy to resume working from home.

No tumor was found, so my entire gland was removed. No amount of hormone replacement in my future can dampen the joy of having my self back, permanently, with no fear of relapse. I’m not even fully recovered from surgery and I’m feeling better than I have in quite a long time. Even the constipation and acne are gone!

It's disorienting and traumatic to have essentially lived with a temporary form of bipolar disorder, only to be cured of it as suddenly as it began. I fancied myself knowledgeable about mental illness before this, but I know now that you just do not fully understand it until you feel it first-hand. Luckily it all feels like a distant memory now. There must be a natural sort of psychological distancing that occurs with a traumatic experience like that.

As I posted on the forums shortly after my surgery, for those of you who may have given up hope, keep fighting! Take it from me that there are better times ahead.


Putting pituitary disease on the radar in Irish healthcare

'The greatest part of our workload in the pituitary unit in Beaumont is pituitary tumours which have been referred for multidisciplinary work-up and consideration of neurosurgical intervention'

To mark National Pituitary Awareness Week, Prof Chris Thompson looks at this underdiagnosed and underfunded illness and the need to raise awareness of its complications.


The commencement of National Pituitary Awareness Week in Ireland provides a useful backdrop against which to write an article to highlight pituitary disease in this country.  To many doctors, pituitary disease is relegated to the status of a side show of the greater endocrinology speciality.

In Ireland, where, uniquely, endocrinology and diabetes are regarded as the same speciality — in most other Western countries they are entirely separate entities in large teaching hospitals — the development of services for patients with pituitary disease has been regarded as secondary to the provision of services to diabetes and other branches of ‘endocrinology’.

To a certain extent, this reflects the perception that pituitary disease is rare, whereas diabetes is common, affecting approximately 5 per cent of the population. But a patient with pituitary disease is not interested in the prevalence of their disease; they are, however, keenly enthusiastic that their condition is managed with services and expertise of an equivalent level of excellence to those provided by other European states.

With the information overload of the internet easily accessible, our well-educated patient population are quickly aware when services fall short.

In this article I will describe some of the more common pituitary conditions, broach the topic of diseases newly-recognised to cause pituitary dysfunction and address the need for well-supported, specialised units to provide effective management of pituitary conditions.

Presentation of pituitary disease
Pituitary disease is one of the greater mimickers of modern medicine with a multitude of presentations, which can make early detection difficult. The range of symptoms associated with hypopituitarism is so varied that there are very few ‘red flag’ symptoms that are pathognomonic of pituitary disease.
Diagnosis is dependent upon a high level of awareness of pituitary disease and a knowledge of conditions associated with hormone dysfunction.

Children with pituitary disease are often picked up early; the combination of headaches and excess growth, for instance, is almost pathognomonic of gigantism due to growth hormone excess, while failure to grow or progress through puberty will usually prompt early specialist referral. In adults, however, the wide variety of symptoms and slow nature of disease progression dictate that pituitary patients present to neurologists, neurosurgeons, ENT, ophthalmology, gynaecology and psychiatry, as well as to endocrinologists.

The greatest part of our workload in the pituitary unit in Beaumont is pituitary tumours which have been referred for multidisciplinary work-up and consideration of neurosurgical intervention.  We have approximately 1,400 patients with pituitary tumours on our books and many of these patients have deficiencies of all pituitary hormones.  Accurate diagnosis of the deficiencies and careful monitoring of treatment is at the complex end of the spectrum of pituitary disturbances.

The consensus document of the Royal Colleges of Physicians and Surgeons in the UK stresses that pituitary disease should not only be managed in units with multidisciplinary aspects with input from endocrinology, neurosurgery, neuroradiology, radiation therapy, neuro-ophthalmology and neuropathology, but that follow-up should be lifelong in view of the disease’s complexity.

The requirement for the new:return ratios demanded by the HSE are difficult to balance with the quality care recommendations of our professional bodies. Data from our own unit support the view of the consensus document.  There are well established data which show that survival in acromegaly is related directly to plasma growth hormone (GH) measurements.

In 2004, retrospective analyses of 92 patients previously operated on in Beaumont showed that 3 per cent of patients followed up in our own multidisciplinary unit had GH levels in the range associated with excessive mortality; the figure for patients followed up in non-pituitary units was close to 50 per cent.  Since then, we have provided follow-up care for all patients who have had their operations performed in Beaumont, unless geographical or other extenuating circumstances dictate otherwise.

Conditions newly associated with pituitary disease
Traumatic brain injury.  Following the observation that our register contained patients with hypopituitarism, our unit developed a research interest in pituitary dysfunction following brain injury, in conjunction with the Department of Neurosurgery. Our data showed that the prevalence of pituitary dysfunction in survivors of brain injury was 30 per cent.  The research programme has developed — with collaborative links with the University of Montpellier and Beaumont — and has become a key opinion leader and world leader in this field.  The research has translated seamlessly into patient care and we have now successfully treated many patients with this newly-recognised association.

Cranial irradiation. Our unit, in association with the Departments of Neurosurgery and Radiotherapy, published the index paper on pituitary disease following cranial irradiation for non-pituitary tumours; up to 50 per cent of patients showed abnormal function. This has led to a surveillance programme in conjunction with the radiotherapists, which has unearthed many patients who require hormonal treatment, with consequent improvement in quality of life. Our hope is that the surveillance programme provides further data on the natural history of the development of hypopituitarism after irradiation.

Sultan Kosen holds the Guinness World Record for being the tallest man in the world. His growth has resulted from a tumour affecting his pituitary gland.

Subarachnoid haemorrhage. Our current research programme is devoted to the quantification of the incidence and predictors of hypopituitarism following subarachnoid haemorrhage and the hormonal determinants of post-subarachnoid haemorrhage hyponatraemia. Preliminary data reveal significant pituitary abnormalities and the translational aim of the research is the identification of clinical, radiological and biochemical features that predict hypopituitarism in this condition.

Haemochromatosis. Dr Howell Walsh, recently retired from the South Infirmary, Cork, was at the forefront of the international drive to quantify the prevalence of hypopituitarism in the important condition of hereditary haemochromatosis.  His work is another example of the dynamism of the pituitary research programme in Ireland and its ability to directly affect patient care and subsequent quality of life.

Organisation of pituitary services
Having worked in endocrinology in Ireland, Scotland, England and the USA, I have no hesitation in declaring that our doctors and nurses compare favourably with anywhere in the world. With the research dynamism that matches the quality of the consultant staff, we have the raw material to provide outstanding pituitary care. The greatest threat to our ability to do so lies in the absence of an infrastructure to deliver such care.

Current government policy is aimed at concentrating clinical care into centres of excellence; this is entirely in line with the recommendations of the UK consensus document, which is directly applicable to Irish practice.  However, although the multidisciplinary pituitary units in Cork University Hospital and Beaumont Hospital provide a de facto national service, neither are recognised units for this work. Seventy per cent of my patients come from outside of my hospital’s catchment area and 40 per cent are referred from other endocrine specialists.  The Cork unit — with which we work in close collaborative collegiality — would have a similar experience.  However, the lack of recognition of the de facto national nature of the work of the two units leaves them vulnerable to bed closures in the current economic climate.

Recent bed closures in Beaumont include the unit in which the pituitary investigation beds were sited. Over a year on, the unit has not been re-established, with significant detriment to staff morale and our ability to deliver our part of the national pituitary workload.  Loss of either the Cork or the Beaumont units would significantly compromise our ability as a nation to deliver the high-quality care for pituitary patients that our people deserve, and to which the HSE should aspire.

The Irish Endocrine Society has written on four occasions to the HSE to seek the establishment of a Clinical Care Programme for Endocrinology, similar to those in existence for other specialities, in order to plan a National Strategy for pituitary care and other endocrine issues, but at the time of writing this article, the Irish Endocrine Society has yet to receive the courtesy of a response.

The establishment of a National Pituitary Unit on two sites — Beaumont and Cork — is entirely in keeping with the Government and the HSE’s commitment to concentrating care in high-quality, specialised units and would be almost cost neutral in terms of provision of infrastructure.
The high quality professionals are raring to go. The intellectual dynamism is waiting to be unleashed. Is the political will and the funding?

  • Professor Thompson is Professor of Endocrinology at Beaumont Hospital/RCSI and Secretary of the Irish Endocrine Society.  He is chairman of the European Hyponatraemia Network, a member of the international TBI/hypopituitarism working group and the European Endocrine Society delegate to the American Endocrine Society Hyponatraemia Guidelines Committee. He is also doctor to the Dublin senior Hurling Team.


Monday, October 3, 2011

Pituitary apoplexy in non-functioning pituitary adenomas: long term follow up is important because of significant numbers of tumour recurrences

Authors: Pal, A.1; Capatina, C.1; Tenreiro, A.P.1; Guardiola, P.D.1; Byrne, J.V.2; Cudlip, S.3; Karavitaki, N.1; Wass, J.A.H.1

Source: Clinical Endocrinology, Volume 75, Number 4, 1 October 2011, pp. 501-504(4)

Publisher: Wiley-Blackwell


Pal A et al. – Patients with classical pituitary apoplexy may show recurrent pituitary tumour growth and therefore these patients need continued post–operative surveillance if they have not had post–operative radiotherapy.

Objectives  The frequency of pituitary tumour regrowth after an episode of classical pituitary apoplexy is unknown. It is thus unclear whether regrowth, if it occurs, does so less frequently than with non-apoplectic non-functioning pituitary macroadenomas that have undergone surgery without postoperative irradiation. This has important repercussions on follow up protocols for these patients.


Design  Retrospective cohort study of patients diagnosed with classical pituitary apoplexy in Oxford in the last 24 years.


Measurements  MRI/CT scans of the pituitary were performed post-operatively and in those patients who did not receive pituitary irradiation, this was repeated yearly for 5 years and 2 yearly thereafter.


Results  Thirty-two patients with non-functioning pituitary adenomas who presented with classical pituitary apoplexy were studied. There were 23 men and the mean age was 56·6 years (range 29-85). The mean follow up period was 81 months (range 6-248). Five patients received adjuvant radiotherapy within 6 months of surgery and were excluded from further analysis. In this group, there were no recurrences during a mean follow up of 83 months (range 20-150). In the remaining 27 cases there were 3 recurrences, with a mean of 79 months follow up (range 6-248) occurring 12, 51 and 86 months after surgery. This gives a recurrence rate of 11·1% at a mean follow up of 6·6 years post surgery. All recurrences had residual tumour on the post operative scan.


Conclusions  Patients with classical pituitary apoplexy may show recurrent pituitary tumour growth and therefore these patients need continued post-operative surveillance if they have not had post-operative radiotherapy.

Document Type: Research article

DOI: 10.1111/j.1365-2265.2011.04068.x



Sunday, October 2, 2011

No scars after new surgery removes brain tumours through the nose


Last updated at 2:08 AM on 2nd October 2011

Retired company director Ron Jones has undergone a remarkable new form of surgery that allows brain tumours to be removed through the nose.

Traditionally, such operations involved surgeons opening  the skull – a procedure known  as a craniotomy – and delving downwards. 

Alternatively, parts of the brain were reached via large incisions in the side of the face or inside the mouth, all options that leave major scars. 

Revolutionary: Traditionally, such operations involved surgeons opening the skull

Revolutionary: Traditionally, such operations involved surgeons opening the skull


But pioneering brain surgeons at Sheffield’s Hallamshire Hospital have adopted a  US-developed technique to reach deep-set tumours using  an endoscope that is fed  through the nose. 

Ron, 83, a former grain salesman who lives in Market Rasen, Lincolnshire, with his wife Sylvia, a former teacher, was diagnosed with a tumour  on his pituitary gland, which  sits at the base of the skull, in October last year. 



These growths  are ideally suited for nasal endoscopy because the gland is close to the back of the nasal cavity and relatively easy to reach. Ron’s tumour was the size of a small egg. 

Surgeons now hope the success of this operation will pave the way for other types of brain tumour to be removed without making a single incision. 

The tumour is reached by  working through one nostril and making a hole in the back of the nasal cavity into the bottom of the skull. Through this hole, the surgeon can see the bottom of the pituitary gland and the tumour. 

Pioneering: The tumour is reached by working through one nostril and making a hole in the back of the nasal cavity into the bottom of the skull

Pioneering: The tumour is reached by working through one nostril and making a hole in the back of the nasal cavity into the bottom of the skull


Cutting instruments, also mounted on flexible or telescopic arms, are used to remove the growth in pieces. 
The new procedure reduces the operating time by up to  two hours, reduces the risk  of infection, and allows for  a quicker recovery compared  to the older techniques. 

Neurosurgeon Saurabh Sinha, who operated on Ron, says: ‘The endoscope provides a close-up view of the pituitary which means we can get all of the tumour out in one go. 

‘Because of Ron’s age, he might not have been considered for open brain surgery, as older patients don’t always recover from such a major procedure. And patients who have weaker hearts will benefit from this innovation. The beauty of the procedure is that there is less danger of brain damage or stroke, and the patient makes  a quicker recovery. 

Before, they may have been in hospital for a week. Now I can discharge some patients within three days.’

‘I first noticed something last year,’ says Ron. ‘I saw a tide mark in my vision. Later, I started having blinding headaches and seeing double.’

Scans showed Ron had a growth on his pituitary gland. About 2,000 people a year require surgery to remove tumours on the pituitary. 

Oval in shape, the gland measures an inch in length and it secretes eight hormones that control vital functions, such as body growth, general health and energy levels. In men it is responsible  for producing the sex hormone testosterone. Ten to 20 per cent of people have a benign pituitary tumour, but only a small  proportion of these cause symptoms, with a tiny fraction needing surgery. Most people are likely to live a normal life without knowing they have a tumour. But Ron’s growth was so large it was pressing on the nerves around the eyes, affecting his vision. 

‘I was also suffering pain in my joints, and having trouble going to the loo which doctors explained wasn’t just my age, but because the tumour was stopping my body from releasing the right hormones,’ says Ron. When he came round from the surgery there wasn’t  a single external mark.

‘When I was told I had a tumour in my head I had visions of my skull being sliced open to remove it,’ he says. ‘Now my sight is back to normal and I have been in no pain at all. I was walking around straight away, and back to playing golf in  two months. My memory isn’t what it was, and I have to write things down or I forget them, but I suppose that could just be my age. Physically, though, I feel better than ever.’

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