Notes on the Magic Foundation Cushing’s Conference, 2012

Posted on July 23, 2012 by MaryO

Here are links to all the posts in order, although some still need to be edited.  I posted these directly from the meeting hall with no rereads or rewrites.  If anyone has anything to add, edit or delete, please let me know!

 

  • Magic Conference: Understanding your Pituitary Gland in Health and Disease

Dr. Frohman will present an overview of the pituitary gland. He will cover general aspects of pituitary function and testing and also review the types of pituitary disease that occur, including pituitary tumors and Sheehan’s Syndrome. Many people ask and wonder if Growth Hormone Deficiency can be inherited. Dr. Frohman will also briefly address that concern.

 

http://cushingshelp.blogspot.com/2012/07/magic-conference-understanding-your.html

 

  • Magic Conference: Testing and Diagnosis Process for Pituitary Disorders

Pituitary disorders can be difficult to diagnose in many cases. Dr. Salvatori will discuss the different testing and diagnostic procedures to determine the pituitary disorder. MAGIC receives many calls asking about diagnostic procedures. This segment will be helpful in understanding what procedures are used today to provide the best treatment available.

http://cushingshelp.blogspot.com/2012/07/magic-conference-testing-and-diagnosis.html

 

  • Magic Conference: Managing Medications and Aftercare of Treatments

It is crucial to monitor your treatments and aftercare of treatments when living with a pituitary disorder. Dr. Salvatori will discuss the importance of these issues so you will be aware of how to manage your pituitary disorder. A simple diagnosis does not mean that medications may be altered or changed in the future. This segment will assist you with information on how to manage your future.

http://cushingshelp.blogspot.com/2012/07/magic-conference-managing-medications.html

 

  • Magic Conference: Cushing’s Disease, Are We Closer to Medical Therapies?

A significant proportion of patients with Cushing’s Disease are not cured by primary surgical treatment, the disease is prone to relapse and significantly damages quality of life. Adjuvant radiotherapy is an increasingly unattractive option for clinicians who wish to spare their patients hypopituitarism and other potential complications. Some pharmacological options are currently available but tend to have dose-limiting side effects. New agents recently approved or under investigation will be discussed and strategies to select the optimal drug or drug combination for individual patients reviewed.

http://cushingshelp.blogspot.com/2012/07/magic-conference-cushings-disease-are.html

 

  • The Trip So Far…

MaryO’s personal experiences and thoughts

http://cushingshelp.blogspot.com/2012/07/the-trip-so-far.html

 

  • Cushing’s Help Turned Twelve During the Conference!

Twelve  years ago I was talking with my dear friend Alice, who runs a wonderful menopause site, Power Surge, wondering why there weren’t many support groups online (OR off!) for Cushing’s and I wondered if I could start one myself.  We decided that I could.

This website (http://www.cushings-help.com) first went “live” July 21, 2000 and the message boards September 30, 2000. Hopefully, with this site, I’ve made  some helpful differences in someone else’s life.

http://cushingshelp.blogspot.com/2012/07/today-we-twelve.html

 

  • Magic Conference: Treating Cushing’s Disease with Surgery: Ways of Achieving a Cure

Dr. McCutcheon will discuss the ways of treating Cushing’s disease from the surgical perspective, including the different ways of getting to the pituitary, the chances of success, and the potential complications. In addition, special nuances and pitfalls ofsurgery in Cushing’s (as opposed to other types of pituitary tumor) will be addressed.

http://cushingshelp.blogspot.com/2012/07/magic-conference-treating-cushings.html

 

  • Phil and the Zebra Undies

Dr. McCutcheon is a surprise participant in a gift to Phil.

http://cushingshelp.blogspot.com/2012/07/phil-and-zebra-undies.html

 

  • Real Talk: Psychological Process of Illness, part 1

This Segment will be broken into two sections. Part I will be provide an open opportunity for participants to ask relevant questions around the emotional/mental issues in living with a chronic illness. Participants will be able to openly talk about depression, anxiety, trauma, and other processes that occur when living illness.

 

Due to confidentiality issues, most of this segment is not shared.

http://cushingshelp.blogspot.com/2012/07/real-talk-psychological-process-of.html

 

  • Real Talk: Psychological Process of Illness, part 2

Part II will focus on seeing ourselves as survivors of illness and the process of staying empowered through illness that impacts us in such a powerful way. Principles of empowerment and how one can turn adversity into opportunity will be discussed. This segment should create an environment that is non judgmental and motivating.

 

Due to confidentiality issues, most of this segment is not shared.

http://cushingshelp.blogspot.com/2012/07/real-talk-psychological-process-of_21.html

 

  • The Rest Of The Trip

Wind-up and heading home

http://cushingshelp.blogspot.com/2012/07/the-rest-of-trip.html

Eventually, all these posts will be edited, cleaned up and typos corrected.;

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Clinicopathological Correlations in Pituitary Adenomas

Posted on June 16, 2012 by MaryO

Ozgur Mete, Sylvia L. Asa

Article first published online: 14 JUN 2012

DOI: 10.1111/j.1750-3639.2012.00599.x

Keywords:

corticotroph adenoma;gonadotroph adenoma;immunohistochemistry;lactotroph adenoma;pituitary adenoma;somatotroph adenoma;thyrotroph adenoma;transcription factors

Abstract

Pituitary adenomas are common neuroendocrine neoplasms arising from adenohypophysial cells. Recent progress in our understanding of pituitary tumorigenesis as well as pathways involved in molecular cytodifferentiation of the adenohypophysis has impacted on the classification of pituitary adenomas.

The detailed comprehensive classification of pituitary adenomas is now well recognized to reflect specific clinical features and genetic changes that predict targeted treatments, as well as prognostic information for patients with pituitary adenomas.

Therefore, the clinical responsibility of pathologists is not only limited to the distinction of pituitary adenomas from other sellar lesions, but also to provide a comprehensive subtype classification using appropriate ancillary tools. In this article, we highlight an approach to clinical diagnosis and pitfalls in the classification of these common neoplasms.

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Medical management of Cushing’s disease: what is the future?

Posted on June 14, 2012 by MaryO

Fleseriu M, Petersenn S.

Source

Departments of Medicine and Neurological Surgery, Northwest Pituitary Center, Oregon Health & Science University, Portland, OR, USA.

Abstract

Cushing’s disease (CD) is caused by a corticotroph, adrenocorticotropic-hormone (ACTH)-secreting pituitary adenoma resulting in significant morbidity and mortality. Transsphenoidal surgery is the initial treatment of choice in almost all cases.

Remission rates for microadenomas are good at 65-90 % (with an experienced neurosurgeon) but remission rates are much lower for macroadenomas. However, even after postoperative remission, recurrence rates are high and can be seen up to decades after an initial diagnosis. Repeat surgery or radiation can be useful in these cases, although both have clear limitations with respect to efficacy and/or side effects.

Hence, there is a clear unmet need for an effective medical treatment. Currently, most drugs act by inhibiting steroidogenesis in the adrenal glands. Most is known about the effects of ketoconazole and metyrapone. While effective, access to ketoconazole and metyrapone is limited in many countries, experience with long-term use is limited, and side effects can be significant. Recent studies have suggested a role for a pituitary-directed therapy with new multireceptor ligand somatostatin analogs (e.g., pasireotide, recently approved in Europe for treatment of CD), second-generation dopamine agonists, or a combination of both.

Mifepristone (a glucocorticoid receptor antagonist) is another promising drug, recently approved by the FDA for treatment of hyperglycemia associated with Cushing’s syndrome. We review available medical treatments for CD with a focus on the two most recent compounds referenced above.

Our aim is to expand awareness of current research, and the possibilities afforded by available medical treatments for this mesmerizing, but often frightful disease.

PMID: 22674211 [PubMed – as supplied by publisher]

From http://www.ncbi.nlm.nih.gov/pubmed/22674211

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Pasireotide in Cushing’s Disease

Posted on May 31, 2012 by MaryO

N Engl J Med 2012; 366:2134-2135 May 31, 2012

 

To the Editor:

In their study, Colao et al. (March 8 issue)1 examined the clinical efficacy and safety of two different doses of subcutaneous pasireotide in patients with newly diagnosed, persistent, or recurrent Cushing’s disease. Since alternative therapies (including bilateral adrenalectomy) are available for patients with persistent or recurrent Cushing’s disease, it would be important to consider all options before embarking on what might turn out to be many years of medication.

Giovanni Targher, M.D.
University of Verona, Verona, Italy 

No potential conflict of interest relevant to this letter was reported.

1 References

To the Editor:

The phase 3 trial by Colao et al. showed the efficacy of 12 months of treatment with subcutaneous pasireotide (600 or 900 μg twice daily) in patients with Cushing’s disease. We now report results after 7 years of treatment with pasireotide administered as part of a phase 2 study.1 In July 2004, a 43-year-old woman with Cushing’s disease, whose 24-hour urinary free cortisol level was 9.2 times the upper limit of normal, began 15 days of treatment with subcutaneous pasireotide (600 μg twice daily) that resulted in normalization of these levels (Figure 1AFIGURE 1Effects of Pasireotide Treatment on 24-Hour Urinary Free Cortisol Levels and on Adrenocorticotropin Hormone Levels during Desmopressin-Stimulation Testing.). When treatment was halted for 35 days, urinary free cortisol levels increased. In September 2004, she resumed treatment with pasireotide (600 μg twice daily), which led to clinical improvement (i.e., a weight loss of 13 kg, regular menstrual cycles, and reduced hirsutism). Hyperglycemia ensued (glycated hemoglobin, 5.7 to 7.7%), and weakness necessitated a temporary reduction in the dose to 450 μg twice daily (November 2004 to October 2005). Since November 2005, when the patient resumed taking the 600-μg dose twice daily, urinary free cortisol levels have remained in the normal range at most monthly assessments. Basal and desmopressin-stimulated adrenocorticotropin levels also decreased as a result of treatment with pasireotide (Figure 1B). To date, she has not had any serious adverse events. This case illustrates the long-term efficacy of pasireotide without the development of resistance to the drug’s effects.

Rossella Libé, M.D.
INSERM Unité 1016, Paris, France

Lionel Groussin, M.D., Ph.D.
Université Paris Descartes, Paris, France

Jérôme Bertherat, M.D., Ph.D.
Hôpital Cochin, Paris, France 

Drs. Libé and Bertherat report being investigators for studies of pasireotide in Cushing’s disease funded by Novartis. No other potential conflict of interest relevant to this letter was reported.

1 References

Author/Editor Response

We concur with Targher’s implication that the advantages and disadvantages of all management options should be considered for each patient before a specific treatment is advised.

Libé and colleagues present a very interesting case of a patient with Cushing’s disease in the extension of a phase 2 study of pasireotide. This patient was treated with pasireotide for a much longer duration than the 1 year reported in the phase 3 study.

Annamaria Colao, M.D., Ph.D.
University of Naples Federico II, Naples, Italy

Mario Maldonado, M.D.
Novartis Pharma, Basel, Switzerland

Since publication of their article, the authors report no further potential conflict of interest.

 

From http://www.nejm.org/doi/full/10.1056/NEJMc1204078

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Correlation Between Histological Subtypes and MRI Findings in Clinically Nonfunctioning Pituitary Adenomas

Posted on May 30, 2012 by MaryO

Hiroshi Nishioka, Naoko Inoshita, Toshiaki Sano, Noriaki Fukuhara and Shozo Yamada

Clinically nonfunctioning pituitary adenomas (CNFPAs) consist of several histological subtypes, including null cell adenoma (NCA), silent gonadotroph cell adenoma (SGA), silent corticotroph adenoma (SCA), and other silent adenomas (OSA) (i.e., GH, TSH, and prolactin adenomas).

To detect possible correlations between MRI findings and the subtypes, we retrospectively studied 390 consecutive patients with CNFPA who underwent surgery between 2008 and 2010. They were classified into three groups: NCA/SGA (313 cases), SCA (39 cases), and OSA (36 cases); in addition there were two unusual cases of plurihormonal adenoma.

Three MRI findings were less common in NCA/SGA than in the other groups (P < 0.0001): giant adenoma (>40 mm), marked cavernous sinus invasion (Knosp grade 4), and lobulated configuration of the suprasellar tumor. When these MRI findings were negative in patients older than 40 years old, 91.0 % (212/233) were NCA/SGA.

These MRI findings were frequently noted despite a low MIB-1 index in SCA. OSA showed a high MIB-1 index and a preponderance in younger patients. In conclusion, although SCA and OSA consisted of only 20 % of CNFPAs, their frequency significantly increased when the tumor was large, invasive, and lobulated, and the patient was younger than 40 years old.

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