Monday, April 22, 2013

Cushing’s syndrome increased risk for coronary arterial atherosclerosis

Ok. Here is a new article describing cardiovascular damage that Cushing's causes.

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Cushing's syndrome increased risk for coronary arterial atherosclerosis

Neary NM. J Clin Endocrinol Metab. 2013;doi:10.1210/jc.2012-3754.

  • April 19, 2013

In a recent study supported by the NIH, researchers determined that patients with Cushing's syndrome have a greater risk for developing coronary arterial atherosclerosis, increasing their rate of cardiovascular morbidity. These findings were published in theJournal of Clinical Endocrinology & Metabolism.

The researchers conducted a prospective case-control study of 15 consecutive patients with adrenocorticotropic hormone (ACTH)-dependent Cushing's syndrome who were matched with 15 controls (aged 32 to 66 years) with at least one risk factor for cardiac disease (ie, diabetes, hypertension, hyperlipidemia, family history of early-onset coronary artery disease and previous or current smoking).

Researchers used a multidetector CT (MDCT) coronary angiogram scan to measure calcified and noncalcified coronary plaque volume and Agatston scores. Additional variables included fasting lipids, BP, history of hypertension or diabetes and 24-hour urine free cortisol excretion.

According to data, patients with Cushing's syndrome had significantly greater noncalcified plaque volume and Agatston scores compared with controls (noncalcified plaque volume median [interquartile ranges]: 49.5 vs. 17.9, P<.001; Agatston score: 70.6 vs. 0, P<.05).

Patients with Cushing's syndrome also demonstrated higher systolic (143 mm Hg) and diastolic (86 mm Hg) BP compared with controls (systolic: 134 mm Hg, diastolic: 76 mm Hg).

The limitations of the study include the small cohort of patients and potential selection bias due to ectopic ACTH secretion. However, the researchers wrote that these findings demonstrate a significant difference between the two groups included in the study.

"Overall, the findings point to the possible causes of cardiovascular morbidity in patients treated with exogenous steroids and indicate the need for further studies of that population," they wrote.

Disclosure: The researchers report no relevant financial disclosures.

PERSPECTIVE
Alice C. Levine, MD

Alice C. Levine

  • It has long been recognized that endogenous hypercortisolism (Cushing's syndrome) and administration of supraphysiologic doses of glucocorticoids are associated with increased mortality, primarily due to cardiovascular disease. Excess glucocorticoids induce all of the features of the metabolic syndrome including obesity with central weight gain, hypertension, impaired glucose tolerance/diabetes mellitus and dyslipidemia, all of which increase cardiovascular risk. In this small but well-designed study, the authors attempt to determine whether excess glucocorticoids have a direct adverse effect on the coronary vasculature. Utilizing multidetector computerized tomographic (MDCT) coronary angiography, a validated noninvasive method of assessing calcified and noncalcified coronary plaques, they compared measurements of coronary plaques (Agatston score) in 15 patients with ACTH-dependent Cushing's syndrome (CS) vs. 15 age-, sex- and body weight-matched controls with at least one risk factor for cardiac disease. They found significantly greater coronary calcifications and noncalcified coronary plaque volumes in patients with active or previous hypercortisolism.

    There are obvious limitations to the study; most notably the small sample size, the predominance of patients with CS due to ectopic ACTH (14/15) and significantly more hypertension in the CS vs. the control group. However, other than the HTN, the groups were well-matched and there was no statistical difference in the Framingham risk scores between groups. This is the first study to demonstrate direct effects of CS on coronary plaque burden.

    The findings, while unsurprising, underscore several important features of CS which endocrinologists need to consider. Firstly, as there were no statistical differences in plaque burden in patients with CS who were eucortisolemic (4/15) vs. those who were hypercortisolemic (11/15) at the time of study, the effects of CS on the coronary vasculature may persist even after biochemical cure. Many previous studies in larger cohorts have similarly demonstrated that the adverse effects of high glucocorticoids on cardiovascular, metabolic, psychiatric and neurocognitive function may be only partially reversible with disease remission. Secondly, even adjusting for all the confounding variables, hypercortisolism seems to be an independent risk factor for the development of coronary artery disease. The possible mechanisms underlying this observation are discussed and include increases in prothrombotic factors, circulating levels of vascular endothelial growth factor (VEGF) and angiogenesis. It is also plausible that cortisol increases atherosclerosis through the mineralocorticoid rather than the glucocorticoid receptor, suggesting the possibility of treating this particular deleterious effect of hypercortisolism with a mineralocorticoid-receptor blocker such as spironolactone.

    Within the CS group, no significant correlations were observed between the coronary plaque volumes and the duration of CS or urinary free cortisol (UFC) either at presentation or at the time of MDCT. Although this lack of correlation may also be attributable to the small sample size, it is well known that the onset of Cushing's syndrome is often insidious and it is impossible to pinpoint the exact duration of the abnormality in most patients. This study's finding of direct, adverse and possibly irreversible effects of hypercortisolism on the coronary vasculature should make endocrinologists even more vigilant in diagnosing and treating the disease as early as possible in its course.

    • Alice C. Levine, MD
    • Professor of medicine, division of endocrinology, diabetes and bone diseases
      Co-Director of The Adrenal Center
      Icahn School of Medicine
      Mount Sinai, New York, NY
  • Disclosures: Levine reports no relevant financial disclosures.
http://www.healio.com/endocrinology/adrenal/news/online/%7B23128043-7B9B-4EDC-85E1-3D98F0BD48E5%7D/Cushings-syndrome-increased-risk-for-coronary-arterial-atherosclerosis-

Long-term elevated cortisol may be important cardiovascular risk factor

Not about Cushing's exactly, but this article does underscore cardiovascular risk that Cushies face, particularly why diagnosis is critically important to prevent associated diseases.

******************

Diabetes / Endocrinology News

  • Hair Analysis Can Show Elevated Cortisol Levels

    Hair analysis reveals longer-term cortisol levels; may be helpful in CV risk assessment



    Elevated levels of the stress hormone cortisol, detectable in hair samples, is associated with increased risk of cardiovascular disease, according to a study published online April 17 in the Journal of Clinical Endocrinology & Metabolism.

FRIDAY, April 19 (HealthDay News) -- Elevated levels of the stress hormone cortisol, detectable in hair samples, is associated with increased risk of cardiovascular disease, according to a study published online April 17 in the Journal of Clinical Endocrinology & Metabolism.

Laura Manenschijn, M.D., from the Erasmus Medical Center in the Netherlands, and colleagues randomly selected 283 community-dwelling elderly participants (median age, 75 years) from a population-based cohort. Three centimeter hair segments were used to measure cortisol.

The researchers found that hair cortisol levels were significantly lower in women than in men (21.0 pg/mg hair versus 26.3 pg/mg hair). There was a significantly increased cardiovascular risk associated with high hair cortisol levels (odds ratio, 2.7) as well as a significantly increased risk of type 2 diabetes mellitus (odds ratio, 3.2). Hair cortisol levels were not found to be associated with non-cardiovascular diseases.

"The increased cardiovascular risk we found is equivalent to the effect of traditional cardiovascular risk factors, suggesting that long-term elevated cortisol may be an important cardiovascular risk factor," the authors write.


http://www.pri-med.com/pmo/MedicalNewsDetail.aspx?id=9128&topic=mc-topic::KA8A584VY&printview=true&tabIndex=



High Long-Term Cortisol Levels, Measured in Scalp Hair, Are Associated With a History of Cardiovascular Disease


 Authors
  1. E. F. C. van Rossum
  1. Department of Internal Medicine (L.M., J.W.K., E.F.C.v.R.), Erasmus MC, 3000 CA Rotterdam, The Netherlands; Department of Epidemiology and Biostatistics (L.S., N.M.v.S., S.v.d.P., G.M.E.E.P., P.L.), EMGO Institute for Health and Care Research, VU University Medical Center, 1081 HZ Amsterdam, The Netherlands; University of Queensland (G.M.E.E.P.), Schools of Human Movement Studies and Population Health, Brisbane 4029, Queensland, Australia; and Department of Endocrinology (P.L.), VU University Medical Center, 1081 HZ Amsterdam, The Netherlands
  1. Address all correspondence and requests for reprints to: Laura Manenschijn, Erasmus MC, Department of Internal Medicine, Room Ee-542, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. E-mail: l.manenschijn@erasmusmc.nl.

Abstract

Background: Stress is associated with an increased incidence of cardiovascular disease. The impact of chronic stress on cardiovascular risk has been studied by measuring cortisol in serum and saliva, which are measurements of only 1 time point. These studies yielded inconclusive results. The measurement of cortisol in scalp hair is a novel method that provides the opportunity to measure long-term cortisol exposure. Our aim was to study whether long-term cortisol levels, measured in scalp hair, are associated with cardiovascular diseases.

Methods: A group of 283 community-dwelling elderly participants were randomly selected from a large population-based cohort study (median age, 75 y; range, 65–85 y). Cortisol was measured in 3-cm hair segments, corresponding roughly with a period of 3 months. Self-reported data concerning coronary heart disease, stroke, peripheral arterial disease, diabetes mellitus, and other chronic noncardiovascular diseases were collected.

Results: Hair cortisol levels were significantly lower in women than in men (21.0 vs 26.3 pg/mg hair; P < .001). High hair cortisol levels were associated with an increased cardiovascular risk (odds ratio, 2.7; P = .01) and an increased risk of type 2 diabetes mellitus (odds ratio, 3.2; P = .04). There were no associations between hair cortisol levels and noncardiovascular diseases.

Conclusions: Elevated long-term cortisol levels are associated with a history of cardiovascular disease. The increased cardiovascular risk we found is equivalent to the effect of traditional cardiovascular risk factors, suggesting that long-term elevated cortisol may be an important cardiovascular risk factor.

  • Received October 19, 2012.
  • Accepted February 22, 2013.

Thursday, April 11, 2013

Ending an "out of date practice" proves critically damaging for a under-diagnosed patient community

One in five people are identified to have a pituitary tumor when studied at autopsies. How will we know anything about the pituitary now?


And grisly?! Unless the coroner cracks the skull open on a stone like a coconut, I feel confident in saying that actually LIVING with pituitary tumors and dysfunction is really what makes life grisly.

* * * * *


Colorado coroner update signed into law

| April 4, 2013 | Updated: April 4, 2013 5:39pm

DENVER (AP) — An update to Colorado antiquated coroner system has been signed into law. Gov. John Hickenlooper signed the update Thursday.
The law updates death-investigation protocol. Changes include a requirement that law enforcement must call coroners as soon as a body is discovered — not after a potential crime scene investigation is complete.
The coroner law also eliminates the grisly but out-of-date practice of removing pituitary glands in autopsies.
The coroner update comes two years after Colorado set new standards for when the state's mostly elected coroners must order autopsies.
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Coroner law: http://bit.ly/16tMTrh

Wednesday, April 3, 2013

Stress can hurt your bones, too

Cortisol weakens bones and leads to osteoporosis. 

How? Why? 

Finally, after being diagnosed with osteopenia three years ago, I found the information I wanted to know.

*****

In the article, "Stress can hurt your bones, too", "Stress plays a critical role in slowly, but steadily, bringing about the onset of osteoporosis. When your bone tissue is constantly remodelled within the body, the show is run by two cell types: osteoblasts that help in depositing new bone tissue and osteoclasts that break down old bone tissue. Dr Bhonsle says, "Your bone density is determined by the rate at which these cells work. Under stress, our adrenal glands increase the production of cortisol. Cortisol, known as the 'stress hormone' as it's released by the body in response to stress, can decrease bone density by inhibiting the bone-building osteoblasts." With decreased osteoblast activity, the body ends up with more broken down bone tissue than deposited, causing low bone density and eventually osteoporosis. Interestingly, America which figures among the countries with the highest calcium intake, also has one of the highest rates of osteoporosis. The solution, health experts say, doesn't lie in getting more calcium, but excreting less of it. When you face stress, you lose calcium through urine. Dr Bhonsle adds, "More cortisol leads to a dip in calcium absorption and a spike in its excretion."

Read more here:
http://m.timesofindia.com/life-style/health-fitness/health/Stress-can-hurt-your-bones-too/articleshow/19145909.cms


Also, take a look at this article, entitled, Are You Concerned with Bone Loss?
http://livingwellnessblog.wordpress.com/tag/osteopenia/

BLOGGER NOTE: On April 22, 2013, I underwent a second bone density test. It has been over three years since my last and first test.  Although my Cushing's and cortisol haven't stopped misbehaving, I am still hopeful that I will remain in the osteopenia category. I do not want to join my 71-year old mother in the osteoporosis line. Results expected in 7-10 days.

Cushing's Awareness: A few days late and so many dollars short

I'm two days late, but I do plan to blog in April. In honor of Harvey Cushing, whose birthday is April 7, I will blog 30 entries in 30 days. Hopefully, our group of friends and family will get the support we deserve, all because someone posted an article during blog month.

What are you doing to spread the word about Cushing's? You have all month to dream big and get started. Tell me all about it in the comments, and I'll repost! When we work together and encourage each other, the Cushie community brightens and new Cushies can self-diagnose. This will be so worth it!

Melissa

Sunday, March 31, 2013

Endoscopic v. Microscopic pituitary surgery

I am learning new things about Cushing's even six years after first seeing the word in print. I did not fully understand the surgical difference and thus possible benefits of endoscopic surgery. For the life of me, I can't remember which I had on my two surgeries, and not much slips by me. I feel like neurosurgeons and even endocrinologists don't emphasize this difference. This made other patients and me believe we were getting the same surgery while at different facilities, but we are not. 

As I continue to determine my next step for treatment after two failed pituitary surgeries and six long years seeking diagnosis and treatment, my mind gets tangled in all the unknowns. I wonder what small change could have led to cure. It might not be helpful, but it does keep me researching and sharing what I find here.
 

Patient's Symptoms Of Cushing's Disease 
Beginning To Abate After 
Endoscopic Pituitary Cure

Sunday, March 24, 2013

How chronic pain has made me happier

The difficulty in recovering from Cushing's is that for some, it fails to leave us -- despite multiple surgeries or even cortisol-lowering drug therapies. I have room for improvement in this area.

In the article below, Rob Heaton offers an insightful look into chronic pain, and he captures the feelings and emotions surrounding those issues well and turns them into happiness.





When Rob Heaton say chronic pain is like mental illness, I want to add the uncured Cushing's often causes chronic pain and mental illness.

I'll share this short excerpt with you, then please read the entire piece regarding how Rob got happy with chronic pain.

"Chronic pain is like mental illness. It is a squeamish, taboo class of affliction that few people know how to deal with, so you and others dance around the issue and you don't have to admit to any fragility."


How chronic pain has made me happier | Robert Heaton


Saturday, March 16, 2013

Cortisol and Tinnitus



I had my second pituitary tumor resection surgery done at MD Anderson Cancer Center on April 20, 2011. My ears have been ringing with tinnitus ever since. My first evening I awoke after being in recovery, I asked my husband to close the curtains to block out the light and try to be quiet. All sound was bothering me. I woke a little later to see my mother and two sisters whispering in the room. They had come to see me after surgery and my husband relayed my requests. When i returned home, my husband hammered blankets across our bedroom windows to block out sunlight and noise. It was nearly blacked out, and it was my favorite part of the house and vital to my recovery after surgery.

Even today though, I don't like a lot of noise or light in the house. My windows are covered with different blankets but still blacked out. While my husband is at work, I keep the TV off. I hate all the chattering and noise from commercials. I don't listen to music in the car anymore. It's too noisy. I hate it. Yes, this classically-trained-vehicle-singer no longer likes it or does it. My radio is off while on the road.

Since my surgery, for nearly two years, I
have faced tinnitus on a daily basis--loud nonstop buzzing. It is not pulsatile with my heart beat (like another cause of tinnitus). It is not localized in my ears. It is difficult to describe, but I feel like I am wearing a headband that buzzes. I hear the buzzing in both ears, around the top of my head and through my brain. Tonight it is so loud, it sounds like a bug zapper.

I have mentioned my tinnitus to several endocrinologists and neurosurgeons. None have asked follow up questions and none have related it to my fluctuating adrenal hormones. Last week, one stated it was unrelated to the pituitary.

Then I find this article below which states:

"Tinnitus is a frequent, debilitating hearing disorder associated with severe emotional and psychological suffering. Although a link between stress and tinnitus has been widely recognized, the empirical evidence is scant."

Why can't my doctors help me?  Why don't they know what I stumble across on the Internet as medical fact?  Why must I continue to put the pieces together for them to see the diagnostic picture? The Art of Diagnosis is not only exhausting me; it is draining my life light right out of me.

When will someone sweep me off my crippled feet and discover the treatment that will return me to my vibrant self?

************

BMC Ear, Nose and Throat Disorders 2012, 12:4 doi:10.1186/1472-6815-12-4

Cortisol suppression and hearing thresholds in tinnitus after low-dose dexamethasone challenge

Veerle L Simoens1,2,3 and Sylvie Hébert3,4,5*


Background

Tinnitus is a frequent, debilitating hearing disorder associated with severe emotional and psychological suffering. Although a link between stress and tinnitus has been widely recognized, the empirical evidence is scant. Our aims were to test for dysregulation of the stress-related hypothalamus-pituitary adrenal (HPA) axis in tinnitus and to examine ear sensitivity variations with cortisol manipulation.

Methods

Twenty-one tinnitus participants and 21 controls comparable in age, education, and overall health status but without tinnitus underwent basal cortisol assessments on three non-consecutive days and took 0.5 mg of dexamethasone (DEX) at 23:00 on the first day. Cortisol levels were measured hourly the next morning. Detection and discomfort hearing thresholds were measured before and after dexamethasone suppression test.

Results

Both groups displayed similar basal cortisol levels, but tinnitus participants showed stronger and longer-lasting cortisol suppression after DEX administration. Suppression was unrelated to hearing loss. Discomfort threshold was lower after cortisol suppression in tinnitus ears.

Conclusions

Our findings suggest heightened glucocorticoid sensitivity in tinnitus in terms of an abnormally strong glucocorticoid receptor (GR)-mediated HPA-axis feedback (despite a normal mineralocorticoid receptor (MR)-mediated tone) and lower tolerance for sound loudness with suppressed cortisol levels. Long-term stress exposure and its deleterious effects therefore constitute an important predisposing factor for, or a significant pathological consequence of, this debilitating hearing disorder.


******

FREE:  The electronic version of this article is the complete one and can be found at:

http://www.biomedcentral.com/1472-6815/12/4

Monday, March 4, 2013

Reoccurrence: A Cushie's Worst Nightmare

Hooray. You somehow heard the word
Cushing's. Someone finally ran the right tests at the right time. You finally got some highs in cortisol and low ACTH (adrenal tumor) or high ACTH (pituitary tumor). A little spot doesn't light up on your mri ("hypointensity") and it is suspicious for a tumor. Ah ha. This is your surgical target.You finally found a genius neurosurgeon but s/he is three states away from you. You organize coverage for the house and kids while your parents and spouse go off to surgery with you. You are finally getting a surgery. You can believe it is finally happening. You wonder if you will every make it out alive and in what condition, what cortisol condition. 

Within a week or a few months, you start suspecting a reoccurrence. This is so unfair. You had surgery yet you still have Cushing's. Returning symptoms don't lie. Lab values don't lie. Doctors even neurosurgeons don't often know what to do with you-- they said they got all the tumor out, so... ?  They don't understand why the labwork shows high cortisol and high ACTH, I mean, they removed pituitary tumor out of your head!

This is one of many moments of true despair in a Cushie's life.

Every Cushing's patient worries about it, and most doctors deny it even is possible. "One surgery will remove the tumor and you'll be back to normal. No problem."  

Yeah, we wish.

This article gives some parameters for
post op ACTH levels - not just cortisol -  that may indicate a cure versus the dreaded reoccurrence. 

All Cushies study articles like this, hoping that their post op numbers fall within the magical range of cured Cushies. We are looking for hope even when there is none to be found.

Note: this is a small study with only 55 patients. Not a large sample size, but hey. Maybe they are on to something.

------------------


Recurrences of ACTH-Secreting Adenomas After Pituitary Adenomectomy Can Be Accurately Predicted by Perioperative Measurements of Plasma ACTH Levels


  • Received November 15, 2012.
  • Accepted February 4, 2013.
 Authors
  1. Baha M. Arafah
  1. Division of Clinical and Molecular Endocrinology, Department of Neurological Surgery, University Hospitals Case Medical Center, Louis Stokes Cleveland Veterans Medical Center And Case Western Reserve University, Cleveland, Ohio 44106
  1. Address all correspondence and requests for reprints to: Baha M. Arafah, MD, Division of Clinical and Molecular Endocrinology, University Hospitals Case Medical Center, 11100 Euclid Avenue, Cleveland, Ohio 44106. E-mail:baha.arafah@case.edu.

Abstract

Background: Adenomectomy is the treatment of choice for ACTH-secreting adenomas. Although the development of ACTH deficiency immediately after adenomectomy suggests surgical success, disease recurrence was reported in patients who developed hypocortisolism postoperatively. In the current study, we examined the value of measuring perioperative plasma ACTH and cortisol levels in predicting disease recurrence of patients with ACTH-secreting adenomas.

Methods: Consecutive patients (n = 55; 41 females, 14 males) with clinical, biochemical, and histological documentation of ACTH-secreting adenomas were investigated after pituitary adenomectomy. All patients were followed with clinical monitoring and frequent measurements of plasma ACTH and serum cortisol levels, and none received glucocorticoids unless or until they developed symptoms of adrenal insufficiency or when their serum cortisol levels were ≤3 μg/dL.

Results: Postoperative serum cortisol levels reached ≤3 μg/dL in 46 of 55 and were ≥4 μg/dL in the remaining 9. Simultaneously measured plasma ACTH levels in the latter 9 patients were >40 ng/L when the serum cortisol reached its nadir. In contrast, among the 46 patients who had serum cortisol levels of ≤3 μg/dL, plasma ACTH levels measured simultaneously were ≤20 ng/L in 38 of 46 and >20 ng/L in the remaining 8. During a mean follow-up period of nearly 7 years, patients who had a nadir plasma ACTH of >20 ng/L developed recurrences even though their postoperative serum cortisol levels were ≤3 μg/dL.

Conclusions: Despite profound hypocortisolemia after adenomectomy, a simultaneously measured plasma ACTH level of >20 ng/L in the perioperative period is highly predictive of future recurrence of ACTH-secreting adenomas.

  • Received November 15, 2012.
  • Accepted February 4, 2013.

Tuesday, February 12, 2013

Persistent Cushing's

Treatment of Cushing's Disease if Surgery Fails

"Bilateral adrenalectomy is usually reserved and employed as a last resort when all else has failed and the patient is in grave danger due to the consequences of high cortisol levels. However, the success and relatively low risk of complications of laparoscopic bilateral adrenalectomy prompts us to reconsider our attitudes towards adrenalectomy in patients with residual and recurrent Cushing's disease. Perhaps adrenalectomy should be employed earlier in the course of treatment of patients with refractory Cushing's disease."


Guidelines for Doctors and their Patients who have Residual Cushing's Disease

Lewis S. Blevins, Jr. MD and Gwen Stanhope, PA-C

California Center for Pituitary Disorders at University of California, San Francisco 

http://ccpd.ucsf.edu/Patient%20guide%20re%20residual%20Cushing's%20Syndrome.pdf

Monday, February 11, 2013

Patient's Symptoms Of Cushing's Disease Beginning To Abate After Endoscopic Pituitary Cure

Another patient's tale of ofd symptoms, misdiagnosis, and surgical path in hopes for a cure.

Thanks for sharing your story, Kathie.

http://www.medicalnewstoday.com/releases/90154.php

Extrapituitary Parasellar Microadenoma in Cushing’s Disease

These articles about pituitary tumor tissue located outside the pituitary really make me suspicious about what could be source of my uncured Cushing's.

Extrapituitary Parasellar Microadenoma in Cushing's Disease


Tuesday, February 5, 2013

The Science of Stress

This Oprah article could easily be entitled: 

The Science of Stress:
5 Things Cortisol is Doing to Your Body


It is all here, in black and white. 

Yet we Cushies suffer in a waiting game for treatment--whether it is our first, second, third, or FOURTH (mine) line of treatment. 

Our bodies are breaking down. 

We are literally losing our minds -- cognitively and emotionally -- as we live each day in a broken body with no end date to look forward to, no time limit to endure. The struggling and suffering is endless. It is heartbreaking.

*****************

The Science of Stress: 5 Things Worrying Is Doing to Your Body
http://www.oprah.com/spirit/Science-of-Stress-What-Stress-Does-to-Your-Body


Thursday, January 31, 2013

Loneliness impacts the human body like physical stress

Many Cushies long for a unflinching, strong, support structure that won't let us fall down while we are sick. I believe, actually, that any person facing medical hardships and uncertainty in health revert to a scared person whose best chance to thrive is with many hands to hold. 

Cushies know that many of us do not have these support systems in place. We cry and wish it were different. We reach out for help, and help is not given. Everyone has their own life to live, even parents, siblings, and friends, and maybe that makes stopping to really help and get involved with a sick person difficult. Time has run out for all families.

I just learned that:

 "Loneliness impacts the human body 
      like physical stress."

I was shocked. I often feel forgotten, lonely, isolated, due to hormonal
imbalances but all the lack of community
support. I cried. How will we ever win? 

The Cushing's destroys every aspect of our lives, and people around us get compassion fatigue. After six years with little patient improvement ( prognosis: negative, for the Seinfeld fans), it is difficult for most to stay involved. Their compassion fatigues and their care can runs out of gas.

After reading this article, I'd like to take a moment to say:

It is not my fault I am sick.

It is not my fault I have reoccurring  tumors in my brain and that I am now facing a third surgery in hopes of beating Cushing's.

It is not my fault that I am no longer the worker, friend, wife, daughter, cousin, sister or aunt that I once was, and that you all still want me to be. I have mourned the loss of my self and my spirit every day since from March 2007, when I first discovered my Cushing's diagnosis. That has been 2,160 days of loneliness.  I also mourn my loss of being about to be the kind of friend and family I had been previously. That guilt creeps in, too. In the end, though, I remain lonely and forgotten.

-- Loneliness impacts the body like physical stress. 

-- Cushing's patients have excess cortisol, which hampers all efforts to control and regulate stress.

-- Lack of emotional support leaves Cushies lonely.

-- Loneliness becomes another source of stress that a Cushie's bodies can not process.

Poor support systems actually lower a Cushie quality of life when Cushies feel isolated, lonely, and forgotten.

*-*-*-*

I'll be blunt. If you are not involved in the support or care of your Cushie loved one, you are contributing to their loneliness, and hastening their deaths. 

On the Cushie's death certificate, it could say "primary cause is Cushing's; secondary cause of death is loneliness."

Now what steps will you take to make sure your Cushie doesn't feel forgotten, isolated, and lonely?

Call and ask. Call and care.



Sunday, December 23, 2012

New Orphan Drug Approved for Cushing's




FDA NEWS RELEASE

For Immediate Release: Dec. 14, 2012
Media Inquiries: Morgan Liscinsky, 301-796-0397; morgan.liscinsky@fda.hhs.gov 
Consumer Inquiries: 888-INFO-FDA

FDA approves Signifor, a new orphan drug for Cushing's disease

The U.S. Food and Drug Administration today approved Signifor (pasireotide diaspartate) injection for the treatment of Cushing's disease patients who cannot be helped through surgery.

Cushing's disease is caused by over-production of cortisol, a hormone made by the adrenal glands. A tumor in the pituitary gland leads to overstimulation of the adrenal gland, which results in excess cortisol production. Cortisol regulates many important functions in the body, including response to stress and injury. Patients with Cushing's disease may have increased weight, glucose intolerance or diabetes, high blood pressure, easy bruising, and increased risk for infections.
 
"Although surgery tends to be first line therapy to treat Cushing's disease, Signifor is a new treatment option for patients when surgery hasn't worked or isn't an option," said Mary Parks, M.D., director of the Division of Metabolism and Endocrinology Products in the FDA's Center for Drug Evaluation and Research.

The safety and effectiveness of Signifor were evaluated in a clinical trial of 162 Cushing's disease patients. Trial participants were randomly chosen to receive one of two dose levels of Signifor over a six-month treatment period. Some patients who safely responded to the medication where allowed to continue treatment. Signifor resulted in decreased cortisol levels as measured in urine collected over a 24-hour period. This reduction was seen as early as one month after starting treatment. About 20 percent of patients in the clinical trial were able to reduce urine cortisol levels into the normal range.

Signifor caused increases in blood sugar levels, which could be detected as early as two weeks after starting treatment. Continued treatment caused or worsened diabetes in some patients; therefore, patients need to be carefully monitored for this side effect and be treated appropriately with anti-diabetic therapies, including insulin.

The FDA is requiring three postmarketing studies for Signifor: a clinical trial to assess high blood sugar (hyperglycemia) management; a long-term prospective observational cohort study (registry) of patients with Cushing's disease treated with Signifor; and focused safety monitoring for reports of serious hyperglycemia, acute liver injury, and adrenal insufficiency.

Signifor is administered under the skin (subcutaneously) twice daily, and will be dispensed with a Medication Guide, including instructions for patients and caregivers that describe the risks and adverse reactions people should be mindful of when using the product.

The most common adverse reactions observed in the clinical trial included hyperglycemia, diarrhea, nausea, abdominal pain, and gallstones.

Signifor is manufactured by Novartis Pharma Stein AG, Stein, Switzerland.

For more information:

The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nation's food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products.

#


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See http://www.signifor.us/index.jsp for more information.