Common Asthma Steroids Linked to Side Effects in Adrenal Glands

(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.

Day Eleven, Cushing’s Awareness Challenge 2015

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

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

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

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

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.

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

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