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Cushing’s Syndrome Subtype Affects Postoperative Time to Adrenal Recovery

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Berr CM. J Clin Endocrinol Metab. 2014;doi:10.1210/jc.2014-3632.

January 16, 2015

In patients undergoing curative surgical tumor resection for Cushing’s syndrome, the time to recovery of adrenal function is contingent upon the underlying etiology of the disease, according to recent findings.

In the retrospective study, researchers reviewed case records of 230 patients with Cushing’s syndrome. All patients were seen at a tertiary care center in Munich between 1983 and 2014, whose cases were documented in the German Cushing’s Registry. Patients were divided into three subgroups of Cushing’s syndrome: Cushing’s disease, adrenal Cushing’s syndrome and ectopic Cushing’s syndrome.

After applying various exclusion criteria, the researchers identified 91 patients of the three subgroups who were undergoing curative surgery at the hospital. The patients were followed for a median of 6 years. The researchers defined adrenal insufficiency as the need for hydrocortisone replacement therapy, and collected this information from patient records and laboratory results.

The duration of adrenal insufficiency was calculated as the interval between successful surgery and the completion of hydrocortisone replacement therapy. Cushing’s syndrome recurrence was defined as biochemical and clinical signs of hypercortisolism.

The researchers found a significant difference between Cushing’s syndrome subtypes in the likelihood of regaining adrenal function within 5 years of follow-up: The probability was 82% in ectopic Cushing’s syndrome, 58% in Cushing’s disease and 38% in adrenal Cushing’s syndrome (P=.001). Among the 52 participants who recovered adrenal function, the median type to recovery also differed between subtypes and was 0.6 years in ectopic Cushing’s syndrome, 1.4 years in Cushing’s disease and 2.5 years in adrenal Cushing’s syndrome (P=.002).

An association also was found between younger age and adrenal recovery in the Cushing’s disease participants (P=.012).

This association was independent of sex, BMI, symptom duration, basal adrenocorticotropic hormone and cortisol levels. No association was seen between adrenal recovery and length of hypercortisolism or postoperative glucocorticoid replacement dosage.

“It is the main finding of this series that the median duration of tertiary adrenal insufficiency was dependent on the etiology of [Cushing’s syndrome]: It was shortest in the ectopic [Cushing’s syndrome], intermediate in [Cushing’s disease] and longest in adrenal [Cushing’s syndrome] caused by unilateral cortisol producing adenoma,” the researchers wrote. “The significant difference to [Cushing’s disease] is an unexpected finding since by biochemical means cortisol excess is generally less severe in adrenal [Cushing’s syndrome]. If confirmed by others, our data have clinical impact for the follow-up of patients after curative surgery: Patients should be informed that adrenocortical function may remain impaired in benign conditions such as cortisol-producing adenoma.”

Disclosure: The study was funded in part by the Else Kröner-Fresenius Stiftung.

The original article is here: Healio



Beta-O2’s ßAir Bio-artificial Adrenal Device Shows Potential to Treat Adrenocortical Insufficiency and Other Stress-related Disorders

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ROSH HAAYIN, Israel, February 19, 2015 /PRNewswire/ —

Beta-O2 announced today the results of a series of pre-clinical studies demonstrating that the company’s ßAir Bio-artificial Adrenal device could offer a treatment for adrenocortical insufficiency and other stress-related disorders. The results are published in the current issue of the Proceedings of the National Academy of Sciences of the United States of America (PNAS). PNAS is one of the world’s most-cited and comprehensive multidisciplinary scientific journals, publishing more than 3,800 research papers annually.

The article, titled “Transplantation of bovine adrenocortical encapsulated in alginate can be viewed here .

The studies cited in the article were led by Professor Stefan Bornstein and Dr. Mariya Balyura at University Hospital Carl Gustav Carus Dresden.

Professor Bornstein said, “The Bio-artificial Adrenal supersedes an immunosuppression completely. The donor cells will be protected against the immune system responses of the patient. The system lets hormones pass the half-permeable walls into the body of the receiver. Our vision is that people in the future may even receive adrenal cells from another species, as, for example, from the pig. The device creates the biotechnical conditions for it.”

Professor Bornstein continued, “I am convinced that Beta-O2’s ßAir Bio-artificial Adrenal device will revolutionize the therapy of adrenocortical insufficiency. Many more patients could benefit from transplantation because the recipients wouldn’t need any immunosuppressive drugs, at all.”

ßAir is an implantable device that provides immune protection and optimal living conditions for cells implanted within it. It has thus far proven successful in providing a viable environment for islets of Langerhans or beta cells, to thrive and naturally produce insulin on demand, a necessary function missing in people with type 1 diabetes. The product for type 1 diabetes is called the ‘ßAir Bio-artificial Pancreas’. Three patients are currently implanted with the ßAir Bio-artificial Pancreas as part of an ongoing clinical study in Sweden.

“The news today indicates that the same immune protection system being used to treat type 1 diabetes patients in the clinical trial in Sweden, also appears to work well for other types of functional cells, such as adrenal cells. We found that when placed in the ßAir, the life span of the adrenal cells significantly increased. The capacity of the adrenal cells for stable, long-term basal hormone release significantly improved as well, as did their response to various stimulating hormones. Additionally, as described in the PNAS article, we learned that ßAir has xeno transplantation or cross species capabilities. For example, using the ßAir, pig adrenal cells can be transplanted into a living being other than a pig and still remain healthy and function properly,” said Dr. Dan J. Gelvan, chairman of the board of Beta-O2.

Dr. Gelvan continued, “What all this means is that transplantation of a ‘ßAir Bio-artificial Adrenal’ with cells from another species could prove to be a treatment option for patients with adrenocortical insufficiency and other stress-related disorders. This is important because current treatment options for adrenal insufficiency are limited and have unpleasant side effects. The study findings reported in the PNAS article are also significant as they offer a sneak preview of the huge potential of ßAIR. If it can provide a viable environment for many different types of cells, then ultimately it may be prove to afford an effective treatment, if not a cure, for a long list of illnesses.”

About Beta-O2 Technologies Ltd.

Beta-O2 Technologies Ltd. is a biomedical company developing a proprietary implantable bioreactor, the ßAir. The company’s flagship product is called the ßAir Bio-artificial Pancreas. It is in development as a treatment and potential cure for type 1 diabetes (T1D). ßAir was first designed to address the main problems of the otherwise successful procedures in which islets of Langerhans (i.e. pancreatic endocrine cells) are transplanted in diabetic patients, such as the need for life-long immunosuppressive pharmacological treatment and limited functionality of the transplanted islets over time due to an insufficient oxygen supply. The company’s second pipeline product is the ßAir Bio-artificial Adrenal for the treatment of adrenocortical insufficiency and other stress-related disorders. This product is currently at the pre-clinical stage of development. Beta-O2 investors include Aurum Ventures, Sherpa Innoventures, SCP Vitalife Partners, Pitango Venture Capital and Saints Capital.

For more information, please visit http://www.beta-o2.com .

Press contact:
Marjie Hadad
MH Communications
+972-54-536-5220
marjie@netvision.net.il

 

SOURCE Beta-O2 Technologies Ltd


Time to Recovery of Adrenal Function After Curative Surgery for Cushing’s Syndrome Depends on Etiology

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Address all correspondence and requests for reprints to: Martin Reincke, MD, Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Ziemssenstr. 1, D-80336 Munich, Germany. E-mail: .

Successful tumor resection in endogenous Cushing’s syndrome (CS) results in tertiary adrenal insufficiency requiring hydrocortisone replacement therapy.

The aim was to analyze the postsurgical duration of adrenal insufficiency of patients with Cushing’s disease (CD), adrenal CS, and ectopic CS.

We performed a retrospective analysis based on the case records of 230 patients with CS in our tertiary referral center treated from 1983–2014. The mean follow-up time was 8 years.

We included 91 patients of the three subtypes of CS undergoing curative intended surgery and documented followup after excluding cases with persistent disease, pituitary radiation, concurrent adrenostatic or somatostatin analog treatment, and malignant adrenal disease.

The probability of recovering adrenal function within a 5 years followup differed significantly between subtypes (P = .001). It was 82% in ectopic CS, 58% in CD and 38% in adrenal CS. In the total cohort with restored adrenal function (n = 52) the median time to recovery differed between subtypes: 0.6 years (interquartile range [IQR], 0.03–1.1 y) in ectopic CS, 1.4 years (IQR, 0.9–3.4 y) in CD, and 2.5 years (IQR, 1.6–5.4 y) in adrenal CS (P = .002). In CD the Cox proportional-hazards model showed that the probability of recovery was associated with younger age (hazard ratio, 0.896; 95% confidence interval, 0.822–0.976; P = .012), independently of sex, body mass index, duration of symptoms, and basal ACTH and cortisol levels. There was no correlation with length and extend of hypercortisolism or postoperative glucocorticoid replacement doses.

Time to recovery of adrenal function is dependent on the underlying etiology of CS.


Higher Cortisol Levels Found in Hair of Patients With Adrenal Insufficiency Using Hydrocortisone

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Patients on hydrocortisone replacement for adrenal insufficiency appear to have elevated cortisol concentrations in their scalp hair, according to recent findings.

In the cross-sectional study, Nienke R. Biermasz, MD, PhD, of Leiden University Medical Center in the Netherlands, and colleagues evaluated patients treated at the outpatient clinical of the medical center between July 2012 and January 2014. Participants included 132 adults with primary or secondary adrenal insufficiency being treated with hydrocortisone (group 1) and 42 controls with a pituitary disease receiving hydrocortisone (group 2). A third group of 195 healthy controls were also included in the analysis.

The researchers collected locks of roughly 150 hairs cut as close to the scalp as possible. The most proximal 3 cm of hair were used in the analysis to correlate with the most recent 3 months. The researchers extracted cortisol from the hair and used ELISA to measure cortisol concentration.

The researchers found that compared with healthy controls and group 2, group 1 had a higher hair cortisol concentration (P < .001) and hair cortisol concentration was associated with hydrocortisone dose (P = .04).

Male participants in group 1 had higher hair cortisol concentrations compared with women in the group (P < .001).

Compared with healthy controls, group 1 had a higher mean BMI (P < .001) and BMI was associated with hair cortisol concentration in the overall sample. The association between hair cortisol concentration and BMI was especially strong in men.

According to the researchers, further studies are needed to better understand the sex-specific associations between hair cortisol concentrations and hydrocortisone use in this population.

“Intriguingly, this gender effect seems to be specific for hydrocortisone use, since it is not present in controls with an intact [hyptothalamic-pituitary-adrenal axis],” the researchers wrote. “In female patients, higher self-reported hydrocortisone intake was associated with higher [hair cortisol concentration], whereas this association was not found in male patients who demonstrated on average higher [hair cortisol concentration] even in the lower dose range.” – by Jennifer Byrne

Disclosure: The researchers report no relevant financial disclosures.

From http://www.healio.com/endocrinology/adrenal/news/online/%7B1d2660eb-3f68-4302-94b2-321f73a4ee89%7D/higher-cortisol-levels-found-in-hair-of-patients-with-adrenal-insufficiency-using-hydrocortisone


Day Eleven, Cushing’s Awareness Challenge 2015

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UVA 2004
Cushing’s Conventions have always been special times for me – we learn a lot, get to meet other Cushies, even get referrals to endos!

As early as 2001 (or before) my pituitary function was dropping.  My former endo tested annually but did nothing to help me with the symptoms.

In the fall of 2002 my endo refused to discuss my fatigue or anything at all with me until I lost 10 pounds. He said I wasn’t worth treating in my overweight condition and that I was setting myself up for a heart attack. He gave me 3 months to lose this weight. Those 3 months included Thanksgiving, Christmas and New Years.  Needless to say, I left his office in tears, again.

Fast forward 2 years to 2004.  I had tried for awhile to get my records from this endo. He wouldn’t send them, even at doctors’ or my requests.

I wanted to go see Dr. Vance at UVa but I had no records so she would’t see me until I could get them.

Finally, my husband went to the former endo’s office and threatened him with a court order. The office manager managed to come up with about 13 pages of records. For going to him from 1986 to 2001 including weeks and weeks at NIH and pituitary surgery, that didn’t seem like enough records to me.

In April of 2004, many of us from the message boards went to the UVa Pituitary Days Convention. That’s where the picture above comes in.  Other pictures from that convention are here.

By chance, we met a wonderful woman named

Read Barbara Craven. She sat at our table for lunch on the last day and, after we learned that she was a dietitian who had had Cushing’s, one of us jokingly asked her if she’d do a guest chat for us. I didn’t follow through on this until she emailed me later. In the email, she asked how I was doing. Usually I say “fine” or “ok” but for some reason, I told her exactly how awful I was feeling.

Barbara emailed me back and said I should see a doctor at Johns Hopkins. I said I didn’t think I could get a recommendation to there, so SHE referred me. The doctor got right back to me, set up an appointment. Between his vacation and mine, that first appointment turned out to be Tuesday, Sept 14, 2004.

Just getting through the maze at Johns Hopkins was amazing. They have the whole system down to a science, moving from one place to another to sign in, then go here, then window 6, then… But it was very efficient.

My new doctor was wonderful. Understanding, knowledgeable. He never once said that I was “too fat” or “depressed” or that all this was my own fault. I feel so validated, finally.

He looked through my records, especially at my 2 previous Insulin Tolerance Tests. From those, he determined that my growth hormone has been low since at least August 2001 and I’ve been adrenal insufficient since at least Fall, 1999 – possibly as much as 10 years! I was amazed to hear all this, and astounded that my former endo not only didn’t tell me any of this, he did nothing. He had known both of these things – they were in the past records that I took with me. Perhaps that was why he had been so reluctant to share copies of those records. He had given me Cortef in the fall of 1999 to take just in case I had “stress” and that was it.

The new endo took a lot of blood (no urine!) for cortisol and thyroid stuff. I went back on Sept. 28, 2004 for arginine, cortrosyn and IGF testing.

He said that I would end up on daily cortisone – a “sprinkling” – and some form of GH, based on the testing the 28th.

For those who are interested, my new endo is Roberto Salvatori, M.D.
Assistant Professor of Medicine at Johns Hopkins

Medical School: Catholic University School of Medicine, Rome, Italy
Residency: Montefiore Medical Center
Fellowship: Cornell University, Johns Hopkins University
Board Certification: Endocrinology and Metabolism, Internal Medicine

Clinical Interests: Neuroendocrinology, pituitary disorders, adrenal disorders

Research Interests: Control of growth hormone secretion, genetic causes of growth hormone deficiency, consequences of growth hormone deficiency.

Although I have this wonderful doctor, a specialist in growth hormone deficiency at Johns Hopkins, in November, 2004, my insurance company saw fit to over-ride his opinions and his test results based on my past pharmaceutical history! Hello??? How could I have a history of taking GH when I’ve never taken it before?

Of course, I found out late on a Friday afternoon. By then it was too late to call my case worker at the drug company, so we had to appeal on Monday. My local insurance person also worked on an appeal, but the whole thing was  just another long ordeal of finding paperwork, calling people, FedExing stuff, too much work when I just wanted to start feeling better by Thanksgiving.

As it turned out the insurance company rejected the brand of hGH that was prescribed for me. They gave me the ok for a growth hormone was just FDA-approved for adults on 11/4/04. The day this medication was approved for adults was the day after my insurance said that’s what is preferred for me. In the past, this form of hGH was only approved for children with height issues. Was I going to be a ginuea pig again?

The new GH company assigned a rep for me, submitted info to pharmacy, and waited for insurance approval, again.

I finally started the Growth Hormone December 7, 2004.

Was the hassle and 3 year wait worth it?

Stay tuned for tomorrow, April 12, 2015 when all will be revealed.

Read

Read Dr. Barbara Craven’s Guest Chat, October 27, 2004

Thanks for reading :)

MaryO


Common Asthma Steroids Linked to Side Effects in Adrenal Glands

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(Reuters Health) – After stopping steroids commonly prescribed for asthma and allergies, a significant number of people may experience signs of malfunctioning in the adrenal glands, a European study finds.

So-called adrenal insufficiency can be dangerous, especially if the person’s body has to cope with a stress like surgery, injury or a serious illness, the study authors say.

“The takeaway message of the study is that in corticosteroid use there is a substantial risk of adrenal insufficiency,” senior author Dr. Olaf Dekkers, an endocrinologist at Aarhus University in Denmark, said by email. “Patients should be aware of this risk and be informed about potential symptoms.”

Those symptoms can include fatigue, dizziness, weight loss and salt cravings, the authors write in the Journal of Clinical Endocrinology and Metabolism.

Corticosteroids are man-made drugs designed to mimic the hormone cortisol, which the adrenal glands produce naturally. The drugs are usually used to counter inflammation in a wide range of conditions, including asthma, psoriasis, rheumatoid arthritis, lupus, blood cancers and organ transplants.

People with adrenal insufficiency do not make enough of two hormones, cortisol and aldosterone. Cortisol helps the body respond to stress, recover from infections and regulate blood pressure and metabolism. Aldosterone helps maintain the right amounts of salt, potassium and water in the body.

While on steroids, the body often produces less of these hormones naturally, and after coming off the drugs it can take a while for natural production to ramp back up. The result is adrenal insufficiency, which can be treated with medication to replace cortisol or aldosterone.

Dekkers and colleagues analyzed 74 research articles published from 1975 to 2014, covering a total of 3753 study participants, to see how different doses and types of corticosteroid treatment might impact the likelihood of developing adrenal insufficiency after treatment.

Researchers found the risk of adrenal insufficiency was highest when corticosteroids were taken orally or injected, and lower with inhaled, nasal or topical treatment.

When they looked just at patients using steroids for asthma, the researchers found that the risk of adrenal insufficiency was about 7 percent with inhaled corticosteroids, but about 44 percent with other formulations including oral medication.

Only about 2 percent of asthma patients on the lowest dose of steroids experienced adrenal insufficiency, compared with about 22 percent on the highest doses.

Similarly, slightly more than 1 percent of asthma patients on short-term steroids developed adrenal insufficiency, compared with about 27 percent on long-term treatment.

There is no way to safely halt treatment with corticosteroids that can rule out the potential for adrenal insufficiency, Dekkers said.

The side effect is more likely when patients take higher doses of steroids or remain on treatment for longer than three weeks, said Dr. Roberto Salvatori, medical director of the pituitary center at Johns Hopkins Hospital in Baltimore.

“It’s likely, and it’s often overlooked because most often the people who prescribe corticosteroids aren’t endocrinologists; they are in other specialities and they don’t recognize the symptoms of adrenal insufficiency,” said Salvatori, who wasn’t involved in the study.

He gives his patients on corticosteroids medical identification bracelets or necklaces to wear so they can be identified as at risk for adrenal insufficiency in an emergency. “This is a very important issue that’s not on the radar screen,” he said.

To be sure, more physicians are aware of the risk now than in the 1970s, and the standard doses and durations of corticosteroid treatment have been reduced in part because of this risk, said Dr. Douglas Coursin, a professor at the University of Wisconsin School of Medicine and Public Health in Madison. He, too, advises medical alert bracelets for patients on long-term or high-dose treatment.

“In the past, patients with asthma, certain immune diseases, those receiving some cancer therapies and those who had a solid organ transplant received higher doses for longer periods of time,” Coursin, who wasn’t involved in the study, said by email. “Overall, I think the risk may be lower than outlined in the study because of practice changes.”

SOURCE: bit.ly/1PjRHYw Journal of Clinical Endocrinology and Metabolism, online April 6, 2015.


Adrenal insufficiency – how to spot this rare disease and how to treat it

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adrenal-glandsAddison’s disease, or adrenal insufficiency, is a rare hormonal disorder of the adrenal glands that affects around 8,400 people in the UK.

The adrenal glands are about the size of a pea and perched on top of the kidneys, and affect the body’s production of the hormones cortisol and sometimes aldosterone.

When someone suffers from adrenal insufficiency, those glands aren’t producing a sufficient amount of these hormones. This can have a detrimental effect on someone’s health and well-being. But because the symptoms are similar to a host of other conditions, Addison’s disease can prove tough to isolate.

What to look out for

According to advice provided by the NHS, the symptoms in the early stages of Addison’s disease, which affects both men and women, are gradual and easy to misread as they’re similar to many other conditions.

People can experience severe fatigue, muscle weakness, low moods, loss of appetite, unintentional weight loss, low blood pressure, nausea, vomiting and salt craving.

“Symptoms are often misread or ignored until a relatively minor infection leads to an abnormally long convalescence, which prompts an investigation,” says Professor Wiebke Arlt from the Centre for Endocrinology, Diabetes & Metabolism at the University of Birmingham.

Life-threatening condition

If Addison’s disease is left untreated, the level of hormones produced by the adrenal gland will gradually decrease in the body. This will cause symptoms to get progressively worse and eventually lead to a potentially life-threatening situation called an adrenal, or Addisonian, crisis. Signs include severe dehydration; pale, cold, clammy skin; rapid, shallow breathing; extreme sleepiness; severe vomiting and diarrhoea. If left untreated, it can prove fatal, so the patient should be admitted to hospital as an emergency.

Back to basics

To understand the disorder, it’s important to get to grips with the basics and that means understanding what the adrenal glands are – and so to the science.

“Adrenal glands have an inner core (known as the medulla) surrounded by an outer shell (known as the cortex) ,” explains Arlt.
The inner medulla produces adrenaline, the ‘fight or flight’ stress hormone. While the absence of this does not cause the disease, the cortex is more critical.

“It produces the steroid hormones that are essential for life: cortisol and aldosterone,” he adds.

“Cortisol mobilises nutrients, enables the body to fight inflammation, stimulates the liver to produce blood sugar and also helps control the amount of water in the body. Aldosterone, meanwhile, regulates the salt and water levels, which can affect blood volume and pressure.”

Why does it happen?

The disorder occurs if the adrenal glands are destroyed, absent or unable to function and failure of the glands themselves is known as primary adrenal insufficiency.

“It’s most often caused by autoimmune disease where the body’s immune system mounts an attack against its own adrenal glands,” explains Arlt.

“However it can also be caused by infection, most importantly by tuberculosis and sometimes by both adrenal glands being surgically removed.”

The pituitary effect

Another important cause is any disease affecting the pituitary gland, which is located behind the nose at the bottom of the brain.
“The pituitary is the master gland that tells the other glands in the body what to do,” continues Arlt.

“The pituitary gland produces a hormone called ACTH (adrenocorticotropic hormone to give it its full name), which travels in the blood stream to the adrenal glands.

“Here it acts as a signal, causing the adrenal glands to produce more cortisol. If the pituitary gland stops making ACTH, [then] cortisol production by the adrenals is no longer controlled properly and a condition called secondary adrenal insufficiency arises.”

But in most cases, aldosterone is still produced, which means that people suffering from secondary adrenal insufficiency have fewer problems than those with primary adrenal insufficiency.

Determining a diagnosis

Due to the ambiguous nature of the symptoms, a Short Synacthen Test (SST) needs to be performed in order to diagnose adrenal insufficiency.

“This measures the ability of the adrenal glands to produce cortisol in response to (the pituitary hormone) ACTH,” says Arlt. “When carrying out this test, a baseline blood sample is drawn before injecting a dose of ACTH, followed by drawing a second blood sample 30 to 60 minutes later. Failing adrenal glands will not be able to produce a certain level of cortisol.”

Getting treatment

If someone has been conclusively diagnosed with adrenal insufficiency, they should receive adrenal hormone replacement therapy as advised by an endocrinologist, a doctor specialising in hormone-related diseases.

“A normal adrenal gland does not need supplements to function properly and there is no recognised medical condition called ‘adrenal fatigue’,” warns Arlt.

“Either the adrenal gland is fine and needs no treatment or there is adrenal insufficiency due to adrenal or pituitary failure.”

So if in doubt, don’t self-diagnose but book an appointment with your GP.

For more information, visit Addison’s Disease Self-Help Group (www.addisons.org.uk) or Pituitary Foundation.

From https://home.bt.com/lifestyle/wellbeing/adrenal-insufficiency-how-to-spot-this-rare-disease-and-how-to-treat-it-11363985141306


Myth: “Vitamins and Natural Remedies can cure/heal Cushing’s”

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myth-busted

 

More from Dr. Karen Thames:

Myth: “Vitamins and Natural Remedies can cure/heal Cushing’s”

Fact: Do you know how many people have told me that if I just “juice”, I will be cured from Cushing’s or Adrenal Insufficiency?! I appreciate the sentiment, but the sad reality is that no amount of juicing and no vitamin will cure Cushing’s. Some Cushing’s patients do take vitamins, some do eat raw food or paleo diets, and some even juice. However, this is just a lifestyle choice and not an attempt to cure Cushing’s. I must admit that when you have such a dreadful disease, you do sometimes take desperate measures to heal yourself. Perhaps, doing acupuncture or some other form of natural healing technique seems attractive at times. Take it from a person who has had acupuncture, seen many natural doctors, juiced, took vitamins, ate a raw food diet, and yes, I EVEN did a series of colonics! If you have ever had colonics, you know that it brings new meaning to the phrase, “no pain, no gain!”

Seriously, this is all before I knew I had Cushing’s. I watched as every person who administered the different kinds of treatment scratched their heads as I continued to gain weight, eventually at a rate of 5 pounds per week! They couldn’t believe that I was actually still gaining weight. Their natural and not surprising response, of course, was to project blame onto me. “Karen, there is NO way you are following protocol! You MUST be lying on your food log!” What we all didn’t realize is that I was suffering from a life-threatening illness called Cushing’s Disease that caused morbid obesity in me and that none of those “remedies” would EVER work!

Now, I have already been in Twitter wars over this topic. Someone tried to tell me that a raw food diet will “cure Cushing’s” and then she told me that I am “ignorant and in denial”! She proceeded to tell me that her daughter, though she had surgery to treat Cushing’s, was REALLY cured because of changing her diet. She also told me that the daughter, who had her Adrenal Glands removed, didn’t need steroids. Listen folks, this is VERY dangerous! I have no adrenal glands and I NEED steroids! Cortisol is life sustaining and you will die without it! I fully expect that someone will argue this point until the cows come home. It doesn’t matter. It won’t change the facts. Cushing’s is caused by excess cortisol in the body. The ONLY treatment is to target the source of the excess cortisol (i.e.brain tumor, adrenal tumor, ectopic tumor, or prolonged steroid use for another disease). Targeting the source is the first line of treatment. Cushing’s Syndrome/Disease will lead to death if not treated properly! #BattlegroundDiagnosis

Disclaimer: I am not a medical doctor. Please seek the advice of a medical professional if you have questions or need further assistance.

If you want to follow our documentary, please go to http://www.Facebook.com/Hug.A.Cushie



BLA Instead of Second Pituitary Surgery

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One of the problems that can arise with a BLA (bilateral adrenalectomy) instead of a repeat pituitary surgery for Cushing’s recurrence is Adrenal Insufficiency.  Another is Nelson’s Syndrome.

Nelson’s syndrome is a rare disorder that occurs in some patients with Cushing’s disease patients as a result of removing both adrenal glands. In Nelson’s syndrome, the pituitary tumor continues to grow and release the hormone ACTH.

This invasive tumor enlarges, often causing visual loss, pituitary failure and headaches. One key characteristic of Nelson’s disease is dark skin pigmentation, resulting from the skin pigment cells responding to the release of ACTH.


AnchorNelson’s Syndrome: Physiology

Nelson’s syndrome can develop as a result of a specific treatment (bilateral adrenalecomy) for the pituitary disease called Cushing’s disease. The harmful effects of Cushing’s disease are due to the excessive amount of the hormone cortisol produced by the adrenal glands.

To treat Cushing’s disease, your doctor may recommend removing the adrenal glands, during a procedure called a bilateral adrenalectomy. The procedure will stop cortisol production and provide relief. However, the procedure does not treat the actual tumor. Rapid growth of the pituitary tumor can occur.

In about 15-25 percent of patients who had a bilateral adrenalectomy, Nelson’ syndrome develops within one to four years.


Darkening of Skin Color - Nelson's Syndrome SymptomAnchor

Nelson’s Syndrome: Symptoms

The most obvious symptom of Nelson’s syndrome is the darkening of the skin color (hyperpigmentation).

Macroadenomas

Macroadenomas are large pituitary tumors. Large tumors can compress surrounding structures, primarily the normal pituitary gland and optic (visual) pathways, causing symptoms. The symptoms that result from the compression are independent of the effects of excess growth hormone secretion.
This may result in vision problems:

  • Vision loss. This occurs when macroadenomas grow upward into the brain cavity, compressing the optic chiasm.
  • A loss of the outer peripheral vision, called a bitemporal hemianopsia Bitemporal Hemianopsia - Symptom of Nelson's Syndrome
    • When severe, a patient can only see what is directly in front of them.
    • Many patients do not become aware of their visual loss until it is quite severe.
  • Other visual problems can include:
    • Loss of visual acuity (blurry vision), especially if the macroadenoma grows forward and compresses an optic nerve.
    • Colors not perceived as bright as usual

Pituitary Failure or Hypopituitarism

Increased compression of the normal gland can cause hormone insufficiency, called hypopituitarism. The symptoms depend upon which hormone is involved.


AnchorNelson’s Syndrome: Diagnosis

Most patients with Nelson’s syndrome have undergone a bilateral adrenalectomy for the treatment of Cushing’s disease

Diagnostic testing includes:

  • Hormone testing. Typically, the blood ACTH levels are very elevated. Learn more about hormone testing at the UCLA Pituitary Tumor Program.
  • MRI imaging. Magnetic resonance imaging (MRI) scan of the pituitary gland can detect the presence of an adenoma, a pituitary tumor.

AnchorNelson’s Syndrome: Treatment Options

Surgery for Nelson's Syndrome

Treating Nelson’s syndrome effectively requires an experienced team of experts. Specialists at the UCLA’s Pituitary Tumor Program have years of experience managing the complex coordination and care for treatment of Nelsons’ syndrome.

Treatment options include:

AnchorSurgery for Nelson’s Syndrome

Surgical removal of the pituitary adenoma is the ideal treatment; however, it is not always possible. Surgical removal requires advanced surgical approaches, including delicate procedures involving the cavernous sinus.

If surgery is required, typically the best procedure is through a nasal approach. Our neurosurgeons who specialize in pituitary tumor surgery are experts in the minimally invasive expanded endoscopic endonasal technique. This procedure removes the tumor while minimizing complications, hospital time and discomfort. This advanced technique requires specialized training and equipment.

Very large tumors that extend into the brain cavity may require opening the skull (craniotomy) to access the tumor. Our surgeons are also experts in the minimally invasive “key-hole” craniotomy, utilizing a small incision hidden in the eyebrow.

AnchorRadiation Therapy for Nelson’s Syndrome

Radiation Therapy for Nelson's SyndromeRadiation therapy can be effective in controlling the growth of the tumor. However, if you received radiation therapy in the past, additional radiation may not be safe.

Our Pituitary Tumor Program offers the latest in radiation therapy, including stereotactic radiosurgery. This approach delivers a highly focused dose of radiation to the tumor while leaving the surrounding brain structures unharmed (with the exception of the normal pituitary gland).

One consequence of radiation treatment is that it can cause delayed pituitary failure. This typically occurs several years after treatment, and continued long-term follow-up with an endocrinologist is important. You may require hormone replacement therapy.

Medical Therapy for Nelson’s Syndrome

Medication for Nelson's SyndromeMedical therapies for the treatment of Nelson’s syndrome are currently limited, but include:

  • Somatostatin-analogs (SSAs). These medications are typically used to treat acromegaly. A small number of Nelson’s syndrome patients may respond.
  • Cabergoline. This medication is typically used to treat prolactinomas; you may require a very high dose.
  • Temozolomide. This is a type of chemotherapy used to treat primary brain tumors called glioblastoma.

If you require medication to treat Nelson’s syndrome, our endocrinologists will monitor you closely.

From http://pituitary.ucla.edu/body.cfm?id=53

 


Roundup may cause potentially fatal ‘adrenal insufficiency’

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IMPORTANT!  A new study finds that the Roundup herbicide disrupts the hormonal system of rats at low levels at which it’s meant to produce no adverse effects. By the same mechanism It may be causing the potentially fatal condition of ‘adrenal insufficiency’ in humans.

Monsanto’s glyphosate-based herbicide Roundup is an endocrine (hormone) disruptor in adult male rats, a new study shows.

The lowest dose tested of 10 mg/kg bw/d (bodyweight per day) was found to reduce levels of corticosterone, a steroid hormone produced in the adrenal glands. This was only one manifestation of a widespread disruption of adrenal function.

No other toxic effects were seen at that dose, so if endocrine disruption were not being specifically looked for, there would be no other signs that the dose was toxic. However a 2012 study detected a 35% testosterone down-regulation in rats at a concentration of 1 part per million.

In both studies endocrine disruption was detected at the lowest level tested for, so we don’t know if, when it comes to endocrine disruption, there are ‘safe’ lower doses of Roundup. In technical parlance, this means that no NOAEL (no observed adverse effect level), was found.

Significantly, the authors believe that the hormonal disruption could lead to the potentially fatal condition know as ‘adrenal insufficiency’ in humans, which causes fatigue, anorexia, sweating, anxiety, shaking, nausea, heart palpitations and weight loss.

“A progressive increase in its prevalence has been observed in humans, while a very few studies relating to xenobiotic exposure and adrenal insufficiency development have been reported”, they write. The increasing levels of Roundup in the environment and food could be “one of the possible mechanisms of adrenal insufficiency.”

How does this level relate to safety limits set by regulators?

One problem with trying to work out how the endocrine disruptive level of 10 mg/kg bw/d relates to how ‘safe’ levels are set by regulators.

The experiment looked at Roundup, the complete herbicide formulation as sold and used, but regulators only look at the long-term safety of glyphosate alone, the supposed active ingredient of Roundup.

Safe levels for chronic exposure to the Roundup herbicide product have never been tested or assessed for regulatory processes. This is a serious omission because Roundup has been shown in many tests to be more disruptive to hormones than glyphosate alone, thanks to the numerous other ingredients it contains to enhance its weed-killing properties.

Given this yawning data gap, let’s for a moment assume that the regulatory limits set for glyphosate alone can be used as a guide for the safe level of Roundup.

The endocrine disruptive level of Roundup found in the experiment, of 10 mg/kg bw/d, is is well above the acceptable daily intake (ADI) set for glyphosate in Europe (0.3 mg/kg bw/d) and the US (1.75 mg/kg bw/d). But this isn’t a reason to feel reassured, since with endocrine effects, low doses can be more disruptive than higher doses.

Another worrying factor is that 10 mg/kg bw/d is well below the NOAEL (no observed adverse effect level) for chronic toxicity of glyphosate: 500 mg/kg bw/d for chronic toxicity, according to the US EPA.

In other words, the level of 500 mg/kg bw/d – a massive 50 times higher than the level of Roundup found to be endocrine disruptive in the experiment – is deemed by US regulators not to cause chronic toxicity.

This experiment shows they are wrong by a long shot. They failed to see toxicity below that level because they failed to take endocrine disruptive effects from low doses into account and industry does not test for them.

Hormone disruption take place at or below ‘no adverse effects’ levels

Interestingly, the NOAEL for glyphosate in industry’s three-generation reproductive studies in rats was much lower than that for chronic toxicity – 30 mg/kg bw/day for adults and 10 mg/kg bw/day for offspring.

However the latter figures – at which no adverse effects should be apparent from glyphosate – are at the same as or higher level than the level of Roundup found to be endocrine disruptive in the new study.

These results therefore show that the reproductive processes of the rats are sensitive to low doses that are apparently not overtly toxic. This in turn suggests that the reproductive toxicity findings are due to endocrine disruptive effects.

Regulatory tests still do not include tests for endocrine disruption from low doses, in spite of the fact that scientists have known about the syndrome since the 1990s.

In the final section of the new study, the researchers discuss its implications. They note that the effects seen in the Roundup-treated rats to the Adrenocorticotropic hormone receptor (ACTH) were similar to adrenal insufficiency in humans:

“The findings that Roundup treatment down regulates endogenous ACTH, is similar to the condition known as adrenal insufficiency in humans. This condition manifests as fatigue, anorexia, sweating, anxiety, shaking, nausea, heart palpitations and weight loss. Chronic adrenal insufficiency could be fatal, if untreated.

“A progressive increase in its prevalence has been observed in humans, while a very few studies relating to xenobiotic exposure and adrenal insufficiency development have been reported. The present study describes one of the possible mechanisms of adrenal insufficiency due to Roundup and suggests more systematic studies, to investigate the area further. “

Claire Robinson of GMWatch commented: “Since no safe dose has been established for Roundup with regard to endocrine disrupting effects, it should be banned.”

 


 

The study:Analysis of endocrine disruption effect of Roundup in adrenal gland of male rats‘ is by Aparamita Pandey and Medhamurthy Rudraiah, and published in Toxicology Reports 2 (2015) pp.1075-1085 on open access.

This article was originally published by GMWatch. This version has been subject to some edits and additions by The Ecologist.

From http://www.theecologist.org/News/news_round_up/2985058/roundup_may_cause_potentially_fatal_adrenal_insufficiency.html


In Production: Quick and Cheap Bedside Test for Cortisol Uses Smartphone

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An innovative method of measuring the stress hormone cortisol is being developed by researchers in Utah. Requiring just a simple kit and a smartphone to read results, this new approach should allow quick, affordable, and accurate testing of cortisol levels, enabling rapid diagnosis of adrenal diseases, the investigators say.

“A lab charges about $25 to $50 for a quantitative salivary cortisol test and has a turnaround time of days to a week,” said lead researcher Joel Ehrenkranz, MD, director of diabetes and endocrinology at Intermountain Medical Center, Murray, Utah. “This test, taken in a medical office or at home, will cost less than $5 and take less than 10 minutes,” he noted.

Dr. Ehrenkranz reported the details of the new test kit, developed at his institution, at ICE/ENDO 2014 week. He said he and his fellow researchers are now collating clinical data for a Food and Drug Administration (FDA) submission and hope to gain approval of the test as a class 2 medical device in the United States in 2015.

Chair of the session, Jeremy Tomlinson, MD, of University of Birmingham, United Kingdom, said the new approach employs “great technology and is an interesting innovation, but there are a few concerns. For example, how well will it perform against the state-of-the-art technique for measuring salivary cortisol, which is mass spectrometry — is it as sensitive?”

Also there is a possibility the immunoassay in the new test will cross react with another steroid hormone, prednisolone, that people might be taking for a whole range of inflammatory conditions, so “you would want to make sure it’s measuring what you want it to,” he noted.

And finally, there is the question of exactly how this would be used.

Cortisol levels are needed when conditions are suspected where too much or too little cortisol is produced, but the diagnosis for most of these doesn’t really need to be immediate, Dr. Tomlinson explained to Medscape Medical News. However, he conceded there might be a role for the assay in patients presenting to the emergency room or in developing nations.

No More Presumptive Treatment of Adrenal Insufficiency

At the meeting, Dr. Ehrenkranz said that adrenal diseases are commonly overlooked because current methods of measuring salivary cortisol require instrumentation and technical personnel and so are costly and unable to deliver timely results.

He noted also that a stint in the developing world convinced him that a simpler test was needed, so he and his colleagues set about developing an assay that would be inexpensive and easy to perform — they came up with disposable cortisol immunoassay strips containing a glass fiber element with colloidal gold-labeled murine anticortisol antibodies and a saliva collection pad.

The person being tested inserts a strawlike saliva collector under the tongue, which wicks the saliva to the immunoassay test strip housed in a cassette, which is then inserted into a reader in the device.

“The device…includes a case, a light pipe, and a lens and costs about a dollar to make. There is no battery power, and it’s unbreakable, passive, and reusable,” Dr Ehrenkranz said.

Because of the physical properties of the gold nanoparticles, a smartphone flash can illuminate and camera-image the color generated by the colloidal gold-labeled anticortisol antibodies, he explained.

The color subsequently generated is “read” by an app on the smartphone to give a cortisol reading, based on an algorithm derived from observed vs reference salivary cortisol values. The R value of this curve was 0.996 for salivary cortisol in the range of 0.012-3.0 µg/dL, Dr Ehrenkranz noted.

The new technology can therefore measure cortisol in a range sufficient to diagnose adrenal insufficiency and hypercortisolism and monitor physiologic variations in cortisol concentration, he said.

And the software is “operating-system agnostic,” he added, meaning the device can be used on all platforms, including iOS, Android, Windows, and BlackBerry, and it has a universal form factor that works with all smartphones.

“Measuring salivary cortisol at the point of care in 5 minutes using an inexpensive immunochromatographic assay, reader, and smartphone may obviate the need to presumptively treat patients for adrenal insufficiency and makes cortisol assays available to regions of the world that currently lack access to this diagnostic test,” he concluded.

Test of Use in Emergency Room, in Developing Countries

Dr. Tomlinson explained that diagnosis of Cushing’s syndrome — caused either by tumors of the pituitary gland producing too much ACTH or tumors of the adrenal gland producing too much cortisol — or alternatively, diagnosis of conditions where it’s thought too little cortisol is being secreted, such as Addison’s disease — an autoimmune process whereby the adrenal gland is destroyed — are not conditions “you necessarily have to diagnose in a few minutes by the bedside,” and therefore it is better to use the “gold standard” of diagnosis, mass spectrometry, in these cases.

But the new test “might be of use in determining whether people have enough of their own natural corticosteroid, in terms of deciding whether you need to give supplemental cortisol to people in an emergency situation,” he explained.

This could include patients presenting with suspected or underlying pituitary or adrenal disease or in people who have been on large doses of steroids who have then stopped taking them, so there will be a resulting suppression of their natural steroid production, he noted.

“That’s not an uncommon situation that we see in the emergency room. At the moment, if there’s suspicion, we might take a test but it takes a day or 2 to come back from the laboratory, and in the meantime we will give patients [presumptive] steroids. But you could do this test by the bedside,” he acknowledged.

And in developing countries, use of this test “is feasible, where cost comes into the equation and you might not have access to mass spectrometry; this could be an alternative and would help you to exclude or make these diagnoses,” he concluded.

This study was privately funded. Dr. Ehrenkranz and colleagues report no relevant financial relationships.

Joint Meeting of the International Society of Endocrinology and the Endocrine Society: ICE/ENDO 2014; June 24, 2014. Abstract OR48-2

From http://www.medscape.com/viewarticle/827580


Unilateral andrenalectomy may be valid first-line treatment for Cushing’s syndrome

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Debillon E, et al. J Clin Endocrinol Metab. 2015;doi:10.1210/jc.2015-2662.

In patients with evident Cushing’s syndrome related to primary bilateral macronodular adrenal hyperplasia, unilateral adrenalectomy of the large gland appears to be a suitable alternative to bilateral adrenalectomy as a first-line treatment, according to recent findings.

Unilateral adrenalectomy yielded normalized urinary free cortisol and improved Cushing’s syndrome, according to the researchers.

Olivier Chabre , MD, PhD, of the Service d’Endocrinologie-Diabétologie-Nutrition in France, and colleagues evaluated all patients (n = 15) with overt Cushing’s syndrome related to primary bilateral macronodular adrenal hyperplasia who underwent unilateral laparoscopic adrenalectomy of the larger gland between 2001 and 2015. Patients were seen for clinical and biological follow-up assessments at 1, 3 and 6 months postoperatively, 5 years after surgery and at the time of the last available urinary free cortisol measurement.

The study’s primary outcome measures were pre- and postoperative levels of urinary free cortisol, plasma cortisol, adrenocorticotropic hormone (ACTH), BMI, blood pressure, plasma glucose and lipids and measurements of these values on follow-up assessments. Patients were followed for a median of 60 months.

The researchers found that in early postoperative measurements, all 15 patients who underwent unilateral adrenalectomy achieved normal or low urinary free cortisol. Between 7 days and 1 month, there was a decrease in median urinary free cortisol from 2.19 times the upper limit of normal (ULN) at baseline to 0.27 ULN (P = .001). At 1 month, only one patient had elevated urinary free cortisol, and this patient went into remission by month 3 and continued to be in remission after 12 years of follow-up.

Forty percent of the patients developed adrenal insufficiency after unilateral adrenalectomy and latent adrenal insufficiency could not be excluded in two of the other patients. No predictors of postoperative adrenal insufficiency were identified.

Six of the patients had diabetes before unilateral adrenalectomy surgery; four of those were treated with antidiabetes drugs. At 12 months, only two of these patients had a continued need for antidiabetes drugs and had reductions in HbA1c despite decreases in their treatment. Recurrence occurred in two patients, demonstrating urinary free cortisol above the ULN at 7 years postoperatively and 8 years postoperatively. Both cases required treatment with mitotane, and in one of the patients, adrenalectomy of the second gland was required 9 years after the initial adrenalectomy.

According to the researchers, postoperative management and vigilant follow-up is needed in order to monitor patients for the risk for adrenal insufficiency.

“Further prospective studies are needed to better evaluate the long-term benefits of [unilateral adrenalectomy], which has one major benefit over [bilateral adrenalectomy]: if needed, [unilateral adrenalectomy] can be transformed in [bilateral adrenalectomy], while the opposite is obviously not true,” the researchers wrote. “One could propose that in further prospective studies [bilateral adrenalectomy] could be performed only if [unilateral adrenalectomy] fails to normalize [urinary free cortisol] at 1 month postoperatively.” – by Jennifer Byrne

Disclosure: The researchers report no relevant financial disclosures.

From Healio


Addison’s disease may cause psychosis, say researchers

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adrenal-glands

 

Research suggests that chronic adrenal insufficiency, more commonly known as Addison’s disease, may be responsible for psychiatric symptoms in those who suffer with it. Unfortunately, these symptoms are poorly understood and inadequately studied. In one case, a 41-year-old construction worker was admitted to a psychiatric clinic complaining of depression. He had trouble sleeping and concentrating and had lost 6 pounds due to a loss of appetite. He was placed on 20mg of fluoxetine but returned 2 weeks later complaining that the therapy did not work, and even reported hallucinating his ex-wife, who had recently died in a car accident. He returned again later 4 months later and was found to have a weak pulse, major hypotension, and hyponatremia and hyperkalemia. It was at this point that he was diagnosed with Addison’s disease.

The disease was first described by Thomas Addison in the mddle of the 19th century. It involves inadequate secretion from the adrenal glands, leading to lower secretion of glucocorticoids. Its usual symptom pigmentation involves fatigue, weight loss, nausea, vomiting, weakness and abdominal pain. Among its psychiatric symptoms are psychosis and delirium.


Adrenal Insufficiency Patients Require More Education on Adrenal Crisis

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adrenalcrisispathway

Greater efforts to educate patients with adrenal insufficiency and their families about prevention of adrenal crisis may be necessary, according to data presented at the American Association of Clinical Endocrinologists (AACE) 24th Annual Scientific & Clinical Congress.

Additionally, the researchers, who looked at patients treated for adrenal insufficiency, found that many are not being adequately trained or equipped to deal with an adrenal crisis.

“These patients can crash and we are not doing enough to help prevent problems,” study investigator Nitika Malhotra, MD, endocrinologist in Lansing, Michigan, said. “We did this study because we think this is a big problem.”

Malhotra, who presented the study findings at the meeting, explained that patients with adrenal insufficiency are at risk for developing adrenal crisis, and it is now estimated that 8% of patients with adrenal insufficiency are hospitalized for adrenal crisis each year.

The problem, according to Malhotra, is that far too many patients are failing to receive crises prevention education. Moreover, they are not receiving emergency glucocorticoid kits.

“All of the families need to be taught and that is not happening,” Malhotra said in an interview with Endocrinology Advisor. “It will reduce the morbidity and mortality and the hospitalization, and it may improve the quality of life of patients too.”

For their study, Malhotra and her colleagues collected data from patients with adrenal insufficiency who were seen at a single institution between March 2009 and March 2014.

The investigators conducted a retrospective chart review and examined age, gender, causes of adrenal insufficiency, glucocorticoid dose, and monitoring for hyponatremia and hyperkalemia. They also looked at postural blood pressure, crises prevention education for glucocorticoid dose adjustments during stress, and whether patients had a Medic Alert ID or a parenteral glucocorticoid kit.

The researchers identified 85 patients (29 males and 56 females) with adrenal insufficiency. Of these patients, 33 patients had primary adrenal insufficiency (38.8%) and 52 had secondary adrenal insufficiency (61.2%). The mean age of the patients was 55.8 years.

Among the 85 patients, 23 (27%) had postural blood pressures checked — five of whom were positive (21.7%). Seventy-seven patients (90.6%) were monitored for electrolytes, and 41 patients (48.2%) were on steroid doses above 20 mg per day.

However, the researchers found that only 57 patients (67.1%) had received steroid dose adjustment instructions. In addition, only 29 patients (34.1%) had a Medic Alert ID, and only 17 patients (20%) were setup with emergency parenteral glucocorticoid kits.

Even though this study has many inherent limitations, Malhotra said, it appears that the preventive strategies for adrenal crisis in patients with adrenal insufficiency are not being consistently followed.

Patient education is paramount for achieving a successful prevention strategy for adrenal crisis, and endocrinologists have a responsibility to make sure that all patients with adrenal insufficiency have a Medic Alert ID and access to emergency glucocorticoid kits, according to Malhotra.

Furthermore, she said families should receive adequate education about parenteral steroid administration and steroid dose adjustments in stressful situations.

At her institution, Malhotra said, endocrinologists are introducing an automated electronic alert in their electronic medical records to determine if this electronic prompt will improve adherence.

Reference

  1. Malhotra N et al. Abstract #102. Presented at: American Association of Clinical Endocrinologists (AACE) 24th Annual Scientific & Clinical Congress; May 13-17, 2015; Nashville, Tenn.

 

From http://www.endocrinologyadvisor.com/aace-2015/adrenal-crisis-in-adrenal-insufficiency/article/415123/


Action For Adrenal Disease

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Watch online Saturday April 16 at 1:00 PM eastern at https://plus.google.com/events/cpjbd8celcbfgngp8und662s198?hl=en
Secondary Adrenal Insufficiency and Addison’s Disease can be deadly, mostly because of the lack of education and awareness. We have lost too many and need to be proactive in preventing unnecessary deaths! Join us as we educate on what these diseases are, how easily they can become deadly and preventive measures we can all take to help this community. Brought to you by the National Adrenal Disease Foundation, with speakers who have personal experience with these diseases.

Our program will include:

Senior Administrator Nichole Klute Rushton••• of the Addison’s Disease Support Group (https://www.facebook.com/groups/addisons.support/) on Facebook, will speak in detail about the unfortunate adrenal insufficient patients who have tragically passed, reminding us that the danger of loss of life is a reality for every person with adrenal insufficiency who doesn’t receive the vital hormones they need

Administrator Debby Hunter ••• of the Living With Addison’s Disease Support on Facebook (https://www.facebook.com/groups/LivingWithAddisonsDisease/) who will give us tips on how we can approach our local emergency facilities and hospitals with information about adrenal insufficiency and its care in a crisis situation. She will also share her own personal experience with going through an adrenal crisis.

Deputy Sheriff Chris Spires••• who will speak on life as the husband of an Addison’s disease patient, and share with us how the law enforcement community views adrenal insufficient patients

Melanie Wong ••• National Adrenal Disease Foundation (http://www.NADF.us) Executive Director, who will speak about the recent tragic losses, and the vital importance of reminding the medical community about adrenal insufficiency, as well as NADF’s latest project to get NADF Adrenal Crisis Care posters displayed in every emergency room facility in the United States.



Morning Cortisol Rules Out Adrenal Insufficiency

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endo2016

 

Key clinical point: Skip ACTH stimulation if morning serum cortisol is above 11.1 mcg/dL.

Major finding: A morning serum cortisol above 11.1 mcg/dL is a test of adrenal function with 99% sensitivity.

Data source: Review of 3,300 adrenal insufficiency work-ups.

Disclosures: There was no outside funding for the work, and the investigators had no disclosures.

BOSTON – A random morning serum cortisol above 11.1 mcg/dL safely rules out adrenal insufficiency in both inpatients and outpatients, according to a review of 3,300 adrenal insufficiency work-ups at the Edinburgh Centre for Endocrinology and Diabetes.

The finding could help eliminate the cost and hassle of unnecessary adrenocorticotropic hormone (ACTH) stimulation tests; the investigators estimated that the cut point would eliminate almost half of them without any ill effects. “You can be very confident that patients aren’t insufficient if they are above that line,” with more than 99% sensitivity. If they are below it, “they may be normal, and they may be abnormal.” Below 1.8 mcg/dL, adrenal insufficiency is almost certain, but between the cutoffs, ACTH stimulation is necessary, said lead investigator Dr. Scott Mackenzie, a trainee at the center.

In short, “basal serum cortisol as a screening test … offers a convenient and accessible means of identifying patients who require further assessment,” he said at the annual meeting of the Endocrine Society.

Similar cut points have been suggested by previous studies, but the Scottish investigation is the first to validate its findings both inside and outside of the hospital.

The team arrived at the 11.1 mcg/dL morning cortisol cut point by comparing basal cortisol levels and synacthen results in 1,628 outpatients. They predefined a sensitivity of more than 99% for adrenal sufficiency to avoid missing anyone with true disease. The cut point’s predictive power was then validated in 875 outpatients and 797 inpatients. Morning basal cortisol levels proved superior to afternoon levels.

The investigators were thinking about cost-effectiveness, but they also wanted to increase screening. “We may be able to reduce the number of adrenal insufficiency cases we are missing because [primary care is] reluctant to send people to the clinic for synacthen tests” due to the cost and inconvenience. As with many locations in the United States, “our practice is to do [ACTH on] everyone.” If there was “a quick and easy 9 a.m. blood test” instead, it would help, Dr. Mackenzie said.

Adrenal insufficiency was on the differential for a wide variety of reasons, including hypogonadism, pituitary issues, prolactinemia, fatigue, hypoglycemia, postural hypotension, and hyponatremia. Most of the patients were middle aged, and they were about evenly split between men and women.

There was no outside funding for the work, and the investigators had no disclosures.

aotto@frontlinemedcom.com

From http://www.clinicalendocrinologynews.com/specialty-focus/pituitary-thyroid-adrenal-disorders/single-article-page/morning-cortisol-rules-out-adrenal-insufficiency/af59bab2bb014ca9d352c792f9d41653.html


Day 13, Cushing’s Awareness Challenge 2016

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UVA 2004
Cushing’s Conventions have always been special times for me – we learn a lot, get to meet other Cushies, even get referrals to endos!

As early as 2001 (or before) my pituitary function was dropping.  My former endo tested annually but did nothing to help me with the symptoms.

In the fall of 2002 my endo refused to discuss my fatigue or anything at all with me until I lost 10 pounds. He said I wasn’t worth treating in my overweight condition and that I was setting myself up for a heart attack. He gave me 3 months to lose this weight. Those 3 months included Thanksgiving, Christmas and New Years.  Needless to say, I left his office in tears, again.

Fast forward 2 years to 2004.  I had tried for a while to get my records from this endo. He wouldn’t send them, even at doctors’ or my requests.

I wanted to go see Dr. Vance at UVa but I had no records so she wouldn’t see me until I could get them.

Finally, my husband went to the former endo’s office and threatened him with a court order. The office manager managed to come up with about 13 pages of records. For going to him from 1986 to 2001 including weeks and weeks at NIH and pituitary surgery, that didn’t seem like enough records to me.

In April of 2004, many of us from the message boards went to the UVa Pituitary Days Convention. That’s where the picture above comes in.  Other pictures from that convention are here.

By chance, we met a wonderful woman named Barbara Craven. She sat at our table for lunch on the last day and, after we learned that she was a dietitian who had had Cushing’s, one of us jokingly asked her if she’d do a guest chat for us. I didn’t follow through on this until she emailed me later. In the email, she asked how I was doing. Usually I say “fine” or “ok” but for some reason, I told her exactly how awful I was feeling.

Barbara emailed me back and said I should see a doctor at Johns Hopkins. I said I didn’t think I could get a recommendation to there, so SHE referred me. The doctor got right back to me, set up an appointment. Between his vacation and mine, that first appointment turned out to be Tuesday, Sept 14, 2004.

Just getting through the maze at Johns Hopkins was amazing. They have the whole system down to a science, moving from one place to another to sign in, then go here, then window 6, then… But it was very efficient.

My new doctor was wonderful. Understanding, knowledgeable. He never once said that I was “too fat” or “depressed” or that all this was my own fault. I feel so validated, finally.

He looked through my records, especially at my 2 previous Insulin Tolerance Tests (ITT). From those, he determined that my growth hormone has been low since at least August 2001 and I’ve been adrenal insufficient since at least Fall, 1999 – possibly as much as 17 years! I was amazed to hear all this, and astounded that my former endo not only didn’t tell me any of this, he did nothing. He had known both of these things – they were in the past records that I took with me. Perhaps that was why he had been so reluctant to share copies of those records. He had given me Cortef in the fall of 1999 to take just in case I had “stress” and that was it.

The new endo took a lot of blood (no urine!) for cortisol and thyroid stuff. I went back on Sept. 28, 2004 for arginine, cortrosyn and IGF testing.

He said that I would end up on daily cortisone – a “sprinkling” – and some form of GH, based on the testing the 28th.

For those who are interested, my new endo is Roberto Salvatori, M.D.
Assistant Professor of Medicine at Johns Hopkins

Medical School: Catholic University School of Medicine, Rome, Italy
Residency: Montefiore Medical Center
Fellowship: Cornell University, Johns Hopkins University
Board Certification: Endocrinology and Metabolism, Internal Medicine

Clinical Interests: Neuroendocrinology, pituitary disorders, adrenal disorders

Research Interests: Control of growth hormone secretion, genetic causes of growth hormone deficiency, consequences of growth hormone deficiency.

Although I have this wonderful doctor, a specialist in growth hormone deficiency at Johns Hopkins, in November, 2004, my insurance company saw fit to over-ride his opinions and his test results based on my past pharmaceutical history! Hello??? How could I have a history of taking GH when I’ve never taken it before?

Of course, I found out late on a Friday afternoon. By then it was too late to call my case worker at the drug company, so we had to appeal on Monday. My local insurance person also worked on an appeal, but the whole thing was  just another long ordeal of finding paperwork, calling people, FedExing stuff, too much work when I just wanted to start feeling better by Thanksgiving.

As it turned out the insurance company rejected the brand of hGH that was prescribed for me. They gave me the ok for a growth hormone was just FDA-approved for adults on 11/4/04. The day this medication was approved for adults was the day after my insurance said that’s what is preferred for me. In the past, this form of hGH was only approved for children with height issues. Was I going to be a ginuea pig again?

The new GH company assigned a rep for me, submitted info to pharmacy, and waited for insurance approval, again.

I finally started the Growth Hormone December 7, 2004.

Was the hassle and 3 year wait worth it?

Stay tuned for April 15, 2016 when all will be revealed.

Read

Read Dr. Barbara Craven’s Guest Chat, October 27, 2004

Thanks for reading :)

MaryO


‘Adrenal Fatigue’ Not Always Used Accurately

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Dear Dr. Roach: I had apoplexy, a ruptured pituitary tumor, developed panhypopituitarism, then adrenal insufficiency. I am doing fairly well with cortisol replacement, thyroid supplement and oral diabetic medicine.

My problem is exhaustion that comes on very easily. I have other ailments to blame, too — chronic pain from fibromyalgia and tendinitis. I am 67. I am still able to work. Is adrenal fatigue a real issue, and if so, what can be done about it? — S.M.

Answer: The term “adrenal fatigue” is increasingly used, and not always correctly — or, at least, it is used in cases where it’s not clear if that is actually the case. But let me start by discussing what has happened to you. Pituitary apoplexy is bleeding into the pituitary gland, usually into a pituitary tumor, as in your case. This may cause severe headaches and vision changes, and often it prevents the pituitary from making the many important hormones that control the endocrine glands and regulate the body.

For example, without TSH from the pituitary gland, the thyroid won’t release thyroid hormone, and importantly, the adrenal gland can’t make cortisol without the influence of ACTH from the pituitary.

Rather than trying to replace TSH, ACTH and the other pituitary hormones, it is easier to directly replace the hormones made by the adrenal, thyroid and gonads. That’s why you are taking cortisol and thyroid hormone, and why younger women take estrogen and men testosterone. Although there is nothing wrong with your thyroid and adrenal glands, they simply won’t work unless stimulated.

Inadequate adrenal function from any cause leads to profound fatigue, and in the presence of severe stress, such as surgery or major infection, the body’s need for cortisol increases dramatically. Unless enough adrenal hormone is given in response, the result can be an immediate life-threatening condition called an Addisonian crisis.

Readers may email questions to ToYourGoodHealth@med.cornell.edu.

From http://www.vnews.com/To-Your-Good-Health–Adrenal-Fatigue–not-Always-Used-Accurately-1802516


Addison’s disease: Primary adrenal insufficiency

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Abstract

Adrenal insufficiency, a rare disorder which is characterized by the inadequate production or absence of adrenal hormones, may be classified as primary adrenal insufficiency in case of direct affection of the adrenal glands or secondary adrenal insufficiency, which is mostly due to pituitary or hypothalamic disease.

Primary adrenal insufficiency affects 11 of 100,000 individuals. Clinical symptoms are mainly nonspecific and include fatigue, weight loss, and hypotension. The diagnostic test of choice is dynamic testing with synthetic ACTH.

Patients suffering from chronic adrenal insufficiency require lifelong hormone supplementation. Education in dose adaption during physical and mental stress or emergency situations is essential to prevent life-threatening adrenal crises.

Patients with adrenal insufficiency should carry an emergency card and emergency kit with them.

From http://www.ncbi.nlm.nih.gov/pubmed/27129928


Six controversial issues on subclinical Cushing’s syndrome

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Abstract

Subclinical Cushing’s syndrome is a condition of hypercortisolism in the absence of signs specific of overt cortisol excess, and it is associated with an increased risk of diabetes, hypertension, fragility fractures, cardiovascular events and mortality.

The subclinical Cushing’s syndrome is not rare, being estimated to be between 0.2–2 % in the adult population. Despite the huge number of studies that have been published in the recent years, several issues remain controversial for the subclinical Cushing’s syndrome screening, diagnosis and treatment.

The Altogether to Beat Cushing’s syndrome Group was founded in 2012 for bringing together the leading Italian experts in the hypercortisolism-related diseases. This document represents the Altogether to Beat Cushing’s syndrome viewpoint regarding the following controversial issues on Subclinical Cushing’s syndrome (SCS):

(1) Who has to be screened for subclinical Cushing’s syndrome?
(2) How to screen the populations at risk?
(3) How to diagnose subclinical Cushing’s syndrome in patients with an adrenal incidentaloma?
(4) Which consequence of subclinical Cushing’s syndrome has to be searched for?
(5) How to address the therapy of choice in AI patients with subclinical Cushing’s syndrome?
(6) How to follow-up adrenal incidentaloma patients with subclinical Cushing’s syndrome surgically or conservatively treated?

Notwithstanding the fact that most studies that faced these points may have several biases (e.g., retrospective design, small sample size, different criteria for the subclinical Cushing’s syndrome diagnosis), we believe that the literature evidence is sufficient to affirm that the subclinical Cushing’s syndrome condition is not harmless and that the currently available diagnostic tools are reliable for identifying the majority of individuals with subclinical Cushing’s syndrome.

Keywords

Subclinical hypercortisolism, Adrenal incidentalomas, Hypertension, Diabetes, Osteoporosis


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