Menopause, Obesity, and Diabetes Top ENDO 2015 Agenda

ENDO_2015

 

Menopause, obesity, and diabetes will top the clinical agenda at the Endocrine Society’s annual meeting, ENDO 2015, with a focus on personalized and precision approaches to disease management.

Endocrine-disrupting chemicals will also take the stage at the meeting, which runs from Thursday, March 5, through Sunday, March 8, in San Diego, California. New research to be presented includes an examination of the economic costs of exposure to these chemicals and their potential teratogenic effects.

Other topics on the agenda are the effects of male obesity on a couple’s fertility, a nasal spray that could cut calorie consumption, and a renewed look at the long-term safety of menopausal hormone therapy.

“The Endocrine Society is really known for cutting-edge research,” society president Richard J Santen, MD, from the University of Virginia School of Medicine, Charlottesville, told Medscape Medical News.

“For many of us in the field, it’s the premier meeting for both science and clinical reviews and new science presentations and networking,” added steering committee chair Matthew Ringel, MD, from Wexner Medical Center, Ohio State University, Columbus. “We’re excited about trying to increase the clinical-science part of the meeting and what would be relevant to clinical, basic, and translational-research attendees.”

As always, the meeting will feature bench science, bedside medicine, and the translation from one to the other, including plenary talks on both precision and personalized approaches to menopause, new genetic discoveries in obesity that could point to novel treatment targets, the link between antihyperglycemic therapy and cardiovascular disease, and fresh insights into the mechanisms of polycystic ovary syndrome.

The meeting begins the morning of Thursday, March 5, with two presidential plenary talks: “Genomics, Pharmacogenomics, and Functional Genomics in Menopausal Women: Implications for Precision Medicine,” by oncologist James N Ingle, MD, from the Mayo Clinic, Rochester, Minnesota, and “Personalized Menopause Management: Clinical and Biomarker Data That Inform Decision Making,” by JoAnn E Manson, MD, of Brigham and Women’s Hospital, Boston, Massachusetts.

“This issue of precision medicine has been such a hot topic, but people don’t really understand it. So the fact that we’re going to feature it in the very first talk is of interest,” Dr Santen said.

While this talk will offer a glimpse of the future, individualized approaches to menopause treatment are already here and will be featured in the session immediately following the plenary, when “Treatment of Symptoms of Menopause: An Endocrine Society Clinical-Practice Guideline” will be presented.

Wide Range of Endocrine Topics Will Be Addressed

Two other clinical-practice guidelines, on management of primary adrenal insufficiency and treatment of Cushing’s syndrome, will also be revealed during the meeting, on Saturday and Sunday, respectively.

And in a special scientific session on Friday, Janet Woodcock, MD, director of the US Food and Drug Administration’s Center for Drug Evaluation and Research, will speak on “Safety and Efficacy of Diabetes Drugs: Steering Between Scylla and Charybdis.”

Meanwhile, clinically focused “Meet the Professor” sessions will address obesity and diabetes, along with a wide range of other endocrine topics, including flushing and sweating disorders, vitamin D, thyroid, gynecomastia, endocrine tumors, testosterone therapy, and genetic counseling for endocrine patients. .

The meeting’s move — from June in previous years to March — means that it is no longer back-to-back with the annual scientific sessions of the American Diabetes Association (ADA).

“We’ve moved the meeting to March, which allows us some separation from the ADA to give us an opportunity to pull in some top diabetes topics and speakers. We’ve always done that over the years, but it allows a little more focus on that area,” Dr Ringel noted.

And, he hopes, more clinicians will be able to attend both meetings going forward. “Years ago, people tried to go to both, one after the other….It’s especially hard for clinicians to be away for that length of time,” he said.

There’s another new feature for ENDO 2015 that is likely to prove popular: “Endocrine Science Social” events will take place at 6:00 pm following the afternoon symposia each day, so attendees can discuss the topics over drinks.

“The philosophy is there’s synergy between scientists and clinicians,” Dr Santen explained.

“With more than 8000 attendees expected, the meeting overall is too big for networking, so we’re going to have a social gathering after the sessions each afternoon.”

Rare Diseases, Loud Voices

world-rare-disease-2015

 

This year, Novartis is adopting the theme, “Rare Diseases, Loud Voices,” is offering content aimed at helping to amplify the voices of patients, families and caregivers impacted by rare diseases including Cushing’s disease. We are providing educational materials and resources highlighting several rare diseases thorough a Rare Disease Day specific microsite on our website (http://www.novartisoncology.com/world-rare-disease-day-2015.jsp) and across our social media channels, including Twitter, YouTube, Facebook, Pinterest, LinkedIn and Instagram.

On the microsite you will see we have also just launched two new resources – a whiteboard animation video (also posted to the Novartis YouTube page) and an infographic (also posted to the Novartis Pinterest page (https://www.pinterest.com/pin/384002305703664913/).

As part of our Twitter activity, several Cushing’s disease-specific tweets have been issued this week, featuring the hashtags #GetLoud, #RDD2015 and #raredisease, as well as complementary visual content to try to help tie Cushing’s disease to the larger RDD discussion.

How to spot a monkey in a white coat

Tip #3:  If at first you see a monkey, get a second opinion.   If you see a monkey on the second try, get a third opinion.  To limit the number of monkeys you see, talk to other patients that are having the same problems as you.  If they managed to see a good doctor, try and see their doctor.

Why is it good to listen to other patients?  Because patients aren’t monkeys.  They have been in your shoes and have already done a lot of the hard work for you.  I learned this when I had Cushing’s.  After seeing a large number of monkeys, it was other patients that finally sent me to a really good doctor.  And he listened to me and did tests and took all the evidence into account when trying to get me better.  And he succeeded.

Read the entire post at How to spot a monkey in a white coat.

Myth: “Men1 and Men2 are the only genetic causes of Cushing’s”

Myth: “Men1 and Men2 are the only genetic causes of Cushing’s”

myth-busted

FACT: This is a Myth. More current research has explored multiple etiologies of Cushing’s. It was once thought that heredity had no influence on the development of Cushing’s Syndrome/Disease and our knowledge was once limited in this sense. Researchers have done more work in terms of exploring genetic factors in the onset of this disease. *~Robin Ess (Cushing’s educator and advocate)

The following causes for Cushing’s have all been explored:

1. Men 1

2. Men2

3. FIPA

4. CAH/BAH

5. PRKAR1A(protein kinase,cAMP-dependent, regulatory, type I, ? gene)

http://www.medscape.org/viewarticle/564106_2

6.(PDE11A)

http://www.medscape.org/viewarticle/564106_4

http://www.medscape.org/viewarticle/564106_6

7.PRKACA

http://www.nature.com/nrendo/journal/v10/n8/pdf/nrendo.2014.89.pdf?WT.ec_id=NRENDO-201408

http://www.ncbi.nlm.nih.gov/pubmed/24700472

http://www.nature.com/ng/journal/v46/n6/full/ng.2956.html

https://www.genomeweb.com/sequencing/exome-sequencing-study-narrows-new-cushings-syndrome-gene-culprit

8.ARMC5

http://www.sciencedaily.com/releases/2014/10/141013090455.htm

http://www.nejm.org/doi/full/10.1056/NEJMoa1304603

Genetics of adrenal diseases in 2014: Genetics improves understanding of adrenocortical tumours

2014 has seen advances in our understanding of benign and malignant tumours of the adrenal cortex, particularly in Cushing syndrome. Modern genetics has generated a flurry of data. The challenge is to give sense to them; however, the difficulties of collecting the clinical data must not be underestimated.

Download this information at http://www.nature.com/nrendo/journal/vaop/ncurrent/full/nrendo.2014.215.html

  • References
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  2. Goh, G. et al. Recurrent activating mutation in PRKACA in cortisol-producing adrenal tumors. Nat. Genet. 46, 613617 (2014).
  3. Sato, Y. et al. Recurrent somatic mutations underlie corticotropin-independent Cushing’s syndrome. Science 344, 917920 (2014).
  4. Cao, Y. et al. Activating hotspot L205R mutation in PRKACA and adrenal Cushing’s syndrome. Science 344, 913917 (2014).
  5. Assié, G. et al. ARMC5 mutations in macronodular adrenal hyperplasia with Cushing’s syndrome. N. Engl. J. Med. 369, 21052114 (2013).
  6. Assié, G. et al. Integrated genomic characterization of adrenocortical carcinoma. Nat. Genet. 46, 607612 (2014).
  7. Beuschlein, F. et al. Somatic mutations in ATP1A1 and ATP2B3 lead to aldosterone-producing adenomas and secondary hypertension. Nat. Genet. 45, 440444 (2013).
  8. Scholl, U. I. et al. Somatic and germline CACNA1D calcium channel mutations in aldosterone-producing adenomas and primary aldosteronism. Nat. Genet. 45,10501054 (2013).
  9. Azizan, E. A. et al. Somatic mutations in ATP1A1 and CACNA1D underlie a common subtype of adrenal hypertension. Nat. Genet. 45, 10551060 (2013).
  10. Fernandes-Rosa, F. L. et al. Genetic spectrum and clinical correlates of somatic mutations in aldosterone-producing adenoma. Hypertension 64, 354361 (2014).