Includes: Adult Growth Hormone Deficiency, Panhypopituitarism, Cushings and Acromegaly
July 19-22, 2012
Westin- Lombard
Chicago, Illinois
For immediate information please email or call our office: ContactUs@magicfoundation.org or (708) 383-0808.)
Speakers include:
Today's Cushing's Awareness Challenge post is about kidney cancer (renal cell carcinoma). You might wonder how in the world this is related to Cushing's. I think it is, either directly or indirectly.
I alluded to this in Day Nine when I said:
I finally started the Growth Hormone December 7, 2004.
Was the hassle and 3 year wait worth it?
Stay tuned for Day 12, April 12, 2012 when all will be revealed.
So, as I said, I started Growth Hormone for my panhypopituitarism on December 7, 2004. I took it for a while but never really felt any better, no more energy, no weight loss. Sigh.
April 14 2006 I went back to the endo and found out that the argenine test that was done in 2004 was done incorrectly. The directions were written unclearly and the test run incorrectly, not just for me but for everyone who had this test done there for a couple years. My endo discovered this when he was writing up a research paper and went to the lab to check on something.
So, I went off GH again for 2 weeks, then was retested. The "good news" was that the argenine test is only 90 minutes now instead of 3 hours.
Wow, what a nightmare my argenine retest started! I went back for that Thursday, April 27, 2006. Although the test was shorter, I got back to my hotel and just slept and slept. I was so glad that I hadn't decided to go home after the test.
Friday I felt fine and drove back home, no problem. I picked up my husband for a biopsy and took him to an outpatient surgical center. While I was there waiting for the biopsy to be completed, I started noticing blood in my urine and major abdominal cramps. I left messages for several of my doctors on what I should do. I finally decided to see my PCP after I got my husband home.
When Tom was done with his testing, his doctor took one look at me and asked if I wanted an ambulance. I said no, that I thought I could make it to the emergency room ok - Tom couldn't drive because of the anaesthetic they had given him. I barely made it to the ER and left the car with Tom to park. Tom's doctor followed us to the ER and became my new doctor.
They took me in pretty fast since I was in so much pain, and had the blood in my urine. They thought it was a kidney stone. After a CT scan, my new doctor said that, yes, I had a kidney stone but it wasn't the worst of my problems, that I had kidney cancer. Wow, what a surprise that was! I was admitted to that hospital, had more CT scans, MRIs, bone scans, they looked everywhere.
My open radical nephrectomy was May 9, 2006 in another hospital from the one where the initial diagnosis was made. My surgeon felt that he needed a specialist from that hospital because he believed preop that my tumor had invaded into the vena cava because of its appearance on the various scans. Luckily, that was not the case.
My entire left kidney and the encapsulated cancer (10 pounds worth!) were removed, along with my left adrenal gland and some lymph nodes. Although the cancer (renal cell carcinoma AKA RCC) was very close to hemorrhaging, the surgeon believes he got it all. He said I was so lucky. If the surgery had been delayed any longer, the outcome would have been much different. I will be repeating the CT scans every 3 months, just to be sure that there is no cancer hiding anywhere. As it turns out, I can never say I'm cured, just NED (no evidence of disease). This thing can recur at any time, anywhere in my body.
I credit the argenine re-test with somehow aggravating my kidneys and revealing this cancer. Before the test, I had no clue that there was any problem. The argenine test showed that my IGF is still low but due to the kidney cancer I couldn't take my growth hormone for another 5 years - so the test was useless anyway, except to hasten this newest diagnosis.
So... either Growth Hormone helped my cancer grow or testing for it revealed a cancer I might not have learned about until later.
My five years are up now. My kidney surgeon *thinks* it would be ok to try the growth hormone again. I'm still a little leery about this, especially where I didn't notice that much improvement.
By Liz Meszaros
PHILADELPHIA -- May 5, 2010 -- Gamma-knife radiosurgery may effectively achieve tumour control in patients who have recurrent residual pituitary adenoma, researchers stated here at the 2010 Annual Meeting of the American Association of Neurological Surgeons (AANS).
"Radiosurgery is an excellent treatment option for patients with recurrent or residual pituitary tumours," noted investigator Jason P. Sheehan, MD, PhD, University of Virginia, Charlottesville, Virginia, speaking here on May 3. "It offers a high rate of tumour and endocrine control. As such, it allows most patients to avoid repeat open surgery or lifelong, expensive medical management."
Dr. Sheehan and colleagues conducted a single-centre retrospective study of the largest group of radiosurgery patients with a pituitary adenoma to date. In all, 418 patients who had undergone gamma-knife radiosurgery were followed for a minimum of 6 months (median 31 months). Factors related to endocrine remission, control of tumour growth, and development of pituitary deficiency were analysed.
Tumour control was achieved in 90.3% of patients, and higher radiation doses significantly resulted in tumour shrinkage. In patients with secretory pituitary adenoma, such as seen in Cushing's disease or acromegaly, median time to endocrine remission was 48.9 months.
Tumour-margin radiation dose was inversely correlated with time to achievement of endocrine remission (P < .05). Smaller adenoma size correlated with improved endocrine response in patients with secretory adenomas.
"Smaller tumour size improves the chances of endocrine control and lowers the risk of new pituitary hormone deficiency following stereotactic radiosurgery. A higher radiosurgical dose offers a greater chance of endocrine and tumour control," Dr. Sheehan noted.
New-onset pituitary hormone deficiency following surgery was seen in 24.4% of patients. There were no cases of panhypopituitarism, and 1 case of posterior pituitary insufficiency. Treatment with pituitary-hormone suppressive medication at the time of surgery was related to a loss of pituitary function (P < .05).
"Radiosurgery has become an increasingly important technique for the treatment of recurrent or residual pituitary adenomas. It affords effective growth control, hormonal normalisation, and an acceptable risk of delayed endocrinopathy," concluded Dr. Sheehan.
Dr. Sheehan was presented with the Synthes Skull Base Award for this research.
[Presentation title: Gamma Knife Radiosurgery for Pituitary Adenomas: Factors Related to Radiologic and Endocrine Outcomes in a Series of 400+ Patients.]
Yesterday was my 4-year surgery anniversary. Amazing how time flies. If anyone had told me then that I’d have four years to live, it wouldn’t have seemed like “enough”, though.
Four years ago yesterday was also the first (and only!) Cushie Cruise, leaving for Bermuda on Mother’s Day. I wasn’t able to go due to financial reasons, but a very kind Cushie Angel made it possible. I got new clothes, and was very excited. I’d never been to Bermuda.
So, along comes this surprise cancer. I told my surgeon-to-be while still in the ER about this cruise and he said no way could I go.
I ended up getting out of the hospital the day before the cruise, the day before Mother’s Day, and the doctor was right. There would have been no way I could have gone and enjoyed this cruise. It was a few weeks before I could even walk, and several days before I could consider getting off pain meds.
Another lucky Cushie got to go in my place, so all was not lost. I got to use my new clothes on a “second chance” cruise and I’m now 4 years cancer free!
Happy endings all around!
Here’s a review of the cruise by other non-Cushies with lots of pictures: http://www.cruisereviews.com/RoyalCaribbean/ExploreroftheSeas115.htm
If you’re a member of the Cushing’s Help message boards, you can see cute pictures of “Penelopee Cruise” at http://cushings.invisionzone.com/index.php?showtopic=16494. Penelopee was made from someone’s 24-hour UFC jug. The pictures and captures are a real hoot.
At four years post-op, I have no signs of my cancer returning or showing up in another organ. (Hooray!) I do have an enlarged lymph node between my lungs but that seems stable at this time.
Energy levels are still very low thanks to the combination of post-pituitary surgery panhypopituitarism, the removal of one adrenal during kidney surgery and low-functioning remaining adrenal. Beats the alternative, though!
Daily (l-o-n-g) naps are a must and, I guess, will always be. Doctors haven’t seem to come up with any ideas for extra energy for me.
I don’t have any lingering symptoms from my bout with cancer, so it’s all good.
As I learned to say in church yesterday, despite my illnesses, “I am blessed!”
Free Abstract Article (Fulltext) Article (PDF 148 KB)
Original Paper
Magnetic Resonance Imaging and Pituitary Function in Children with Panhypopituitarism
Guimei Li, Peng Shao, Xiaojun Sun, Qian Wang, Lijuan Zhang
Provincial Hospital Affiliated to Shandong University, Shandong, PR China
Address of Corresponding Author
Horm Res Paediatr 2010;73:205-209 (DOI: 10.1159/000284363)
Key Words
Abstract
Background: To explore the relationship between magnetic resonance imaging (MRI) findings and multiple pituitary-target hormones in patients with panhypopituitarism or multiple pituitary hormone deficiency (MPHD).
Methods: 125 patients with MPHD (102 boys, MPHD group) and 90 age-, sex- and Tanner stage-matched normal children (control group) were enrolled. 96 of the patients with MPHD underwent MRI scans of the hypothalamic-pituitary area. The patients were subdivided into five stages according to their MRI findings. The serum concentrations of GH, IGF-1, FT4, TSH, ACTH, cortisol, FSH, LH, prolactin, testosterone and estradiol were measured in patients and in controls.
Results: MRI stage was significantly positively correlated with the number of pituitary hormone deficiencies (r = 0.9, p < 0.001). MRI stage was negatively correlated with peak GH, IGF-1, FT4, cortisol and anterior pituitary height (r = –0.43, –0.47, –0.67, –0.54, and –0.49, respectively, p < 0.01). Diabetes insipidus patients could be stratified according to their MRI stage; diabetes insipidus was found mainly in patients with absence of the posterior pituitary bright spot or small ectopic posterior pituitary bright spot on MRI.
Conclusion: An abnormal MRI finding is evidence of MPHD and, correspondingly, there is a noteworthy correlation between MRI and pituitary function.
Copyright © 2010 S. Karger AG, Basel
INTRODUCTION
Adrenal insufficiency can be caused by diseases of the adrenal gland (primary), interference with corticotropin (ACTH) secretion by the pituitary gland (secondary), or interference with corticotropin-releasing hormone (CRH) secretion by the hypothalamus (tertiary). This topic will review the major causes of the latter two disorders; the causes of primary adrenal insufficiency, and the clinical manifestations and approach to diagnosis are discussed separately. (See "Causes of primary adrenal insufficiency (Addison's disease)" and "Clinical manifestations of adrenal insufficiency in adults" and "Diagnosis of adrenal insufficiency in adults".)
SECONDARY ADRENAL INSUFFICIENCY
Any process that involves the pituitary and interferes with ACTH secretion can cause secondary adrenal insufficiency. The ACTH deficiency may be isolated, or occur in conjunction with other pituitary hormone deficiencies (panhypopituitarism).
Panhypopituitarism — Pituitary tissue can be destroyed and hormone secretion reduced by large pituitary tumors or craniopharyngiomas, infectious diseases such as tuberculosis or histoplasmosis, infiltrative diseases, lymphocytic hypophysitis, head trauma, and large intracranial artery aneurysms. Pituitary infarction can occur at the time of delivery if excessive blood is lost and hypotension occurs (Sheehan's syndrome), and hemorrhage may occur into a pituitary tumor (pituitary apoplexy). Pituitary metastases are frequently (about 5 percent) found in patients with disseminated cancer at autopsy; however, these metastases rarely reduce hormone secretion [1]. (See "Causes of hypopituitarism".)
ACTH deficiency due to genetic pituitary abnormalities is rare. ACTH and cortisol deficiency have been described in patients with multiple pituitary hormone deficiencies due to mutations in the PROP-1 (Prophet of Pit-1) gene, even though PROP-1 is not expressed in corticotropes. The onset of cortisol deficiency, which may be severe, ranges from childhood to late adulthood [2-5]. Mutations in other transcription factors involved in early pituitary development (HESX1, LHX4) also can result in variable degrees of hypopituitarism that include ACTH deficiency [6,7]. (See "Causes of hypopituitarism".)
Isolated ACTH deficiency — Isolated ACTH deficiency is a rare disorder [8]. The defect is probably at the pituitary level because there is no ACTH secretory response to CRH or vasopressin, as there usually is in hypothalamic disorders [9-11]. Occasional patients may have hypothyroxinemia and hyperprolactinemia that are corrected with glucocorticoid replacement [12,13].
The only difference was my pain was in the front. I have never in my life had such excruciating pain. Mine came across suddenly. Pain in afternoon, diagnosed with cancer in ER three hours later. No pesky going from doctor to doctor, testing and more testing with this cancer. Bang - instant diagnosis.
More info in this old post.
I loved this quote at the end and need to remember it and quote it each day: “This is living with cancer. But you’re living.”
My version will be “This is living with post-Cushing's, panhypopituitarisim, low growth hormone, low adrenal function and cancer. But you’re living.”
From http://www.curetoday.com/index.cfm/fuseaction/article.show/id/2/article_id/1131
BY KAREN PATTERSON
As new therapies stack up, controlling advanced kidney cancer is becoming a reality.
Tattooed in Chinese lettering over the former location of Marc Benner’s right kidney are the words “Kidney Cancer Survivor”—emblems of his year-and-a-half-long journey battling stage 4 renal cell carcinoma.
Benner, of Jackson, New Jersey, was 42 in 2007 when he began feeling excruciating pain in his back and noticed blood in his urine. “Like most guys, back then you couldn’t get me to the hospital,” he says. “I thought I was just passing a stone, to be honest.” In December that year, surgeons at Thomas Jefferson University Hospital in Philadelphia removed his kidney using minimally invasive robotic surgery. At the same time they excised a lung mass. He was back at work 10 days later.
But his battle was only beginning. His first set of scans in early 2008 showed masses in his liver and lung. That’s when his doctors prescribed Sutent (sunitinib), one of several relatively new drugs for advanced kidney cancer. Benner took Sutent for about a year, in cycles where he was on the drug for four weeks and off for two. Although he still has nodules in his lung—and a tumor just above his hip—the spots on his liver have disappeared. “I think it helped buy me time,” he says of the drug. And the self-described “gym rat” has been lifting more weight than ever in his workouts.
When his cancer progressed on Sutent, he switched to Nexavar (sorafenib). “I’ve heard a lot of good things about Nexavar,” he says, three weeks after beginning the drug. Ultimately, he hopes that this drug, too, will buy him time until other treatments are available. “There’s some new stuff out there that might work better,” he says.
Benner is typical not just because his cancer is a type known as clear cell, which accounts for the vast majority of the almost 55,000 renal cancers diagnosed in the United States yearly, but also in his mix of hope for the future and anticipation of what’s coming next through the pharmaceutical pipeline.
Robert Figlin, MD, interim director of City of Hope Comprehensive Cancer Center in Duarte, California, and director of the center’s kidney cancer program, says that more treatments are available for metastatic renal cell carcinoma (RCC) than ever. In addition to the current arsenal of Sutent, Nexavar, and Torisel (temsirolimus), and the newly approved Afinitor (everolimus), all green-lighted by the Food and Drug Administration since December 2005, one additional product is likely to receive approval for kidney cancer this year—Avastin (bevacizumab). While they don’t promise a cure, collectively the five drugs have the potential to extend patients’ lives considerably.
Before the new agents came on the market, “there was no progress and few options,” says Robert Motzer, MD, who oversees the clinical trials program for advanced kidney cancer at Memorial Sloan-Kettering Cancer Center in New York City. “Now it’s changed dramatically. … You can see it in the faces of the patients.”
“This is a waterfall time for patients,” adds Figlin, who is also chair of medical oncology and therapeutics research at City of Hope. “The challenges for both doctors and patients are now how to choose the proper drugs, in what sequence, and whether or not to use them in combination.”
These new, so-called targeted, drugs vary in their mechanism of action in the body. Sutent, Nexavar, and Avastin disrupt a process known as angiogenesis—the formation of blood vessels that feed tumors. In a phase III trial to demonstrate Avastin’s potential benefit, a combination of the drug and an older treatment, interferon, nearly doubled the window of time in which patients’ metastatic RCC failed to progress, compared with placebo plus interferon.
Torisel and Afinitor are in a class of drugs called mTOR inhibitors, which means they target a cell protein that is part of a biochemical pathway implicated in the growth of tumor cells as well as blood vessels. While phase III trials have shown, for instance, that Sutent versus interferon can more than double the time before progression for many advanced kidney cancers, the mTOR inhibitors might be able to extend that period further.
In addition, Torisel, which is given intravenously weekly, has been studied in the treatment of patients with poor prognosis RCC—“those with the most symptoms, most extensive disease, who would otherwise have a short survival,” says Motzer. “It was the first of the targeted agents to show a survival benefit in that very poor prognosis population.” That population, he adds, accounts for up to one-quarter of people who are first diagnosed with metastatic kidney cancer.
The eagerly anticipated approval of Afinitor occurred in late March. That drug is administered orally, and updated results from a phase III trial examining people whose cancers had progressed on Sutent, Nexavar, or both found that Afinitor delayed the cancer’s progression by a median period of almost five months, compared with just less than two months in patients receiving a placebo. Afinitor also compared favorably to the other drugs in terms of quality of life and safety profile, with mouth ulcers and anemia among the side effects.
“The sense we have is that if a cancer cell builds up resistance to one medicine with one mechanism of action, switching over to another mechanism is attractive,” Motzer says.
A Chronic Disease?
Figlin says evidence most strongly supports using the new agents in sequence, with the antiangiogenic agents first, followed by an mTOR inhibitor if the cancer progresses. “That’s not to say other drugs can’t be interwoven, but the data are not as robust.”
Research into combinations of the targeted agents has, meanwhile, been disappointing. “Our early studies showed there seemed to be more toxicity in the combinations,” Motzer says. “So I’m more firmly behind the sequential use of these agents.”
The new drugs also appear beneficial for the approximately 20 percent of RCC patients whose tumors are not clear-cell type. While the benefits might not be as dramatic, “these targeted agents should still be used,” Figlin says.
For advanced clear-cell RCC, the medicines have made a dramatic difference in physicians’ conversations with patients. Figlin says he can tell newly diagnosed patients and their families that there’s a high chance of benefit from the treatment, with the potential to improve symptoms and extend life. “Although they are not curative treatments, they can turn this disease into more of a chronic management disease,” he says. “We were not able to have that conversation just five years ago.”
Coming down the pipeline are other promising new agents currently being tested in large phase III trials. “We are already embarking on next-generation drugs,” Figlin says, including the angiogenesis inhibitors pazopanib and axitinib, which have a mechanism of action similar to Sutent and Nexavar. “Both of these may have more activity than our currently available drugs.” They might also have a better side effect profile, he says. “That’s what we’re looking for—better tolerance and more effectiveness.”
The AXIS trial, a phase III study still recruiting patients, will test how axitinib measures up to Nexavar as second-line treatment for metastatic RCC. Results of the study are expected in mid-2010. Also going head-to-head in a phase III study are pazopanib and Sutent in locally advanced or metastatic RCC.
Experts agree there’s room to improve the targeting of known biochemical pathways related to kidney cancer as well as other pathways that may be important but aren’t as clearly understood.
The Old Kid on the Block
Before the targeted agents arrived on the scene, treatments known as biological or immune therapies, which enlist the body’s immune system to fight the cancer, were the standard of care. One such treatment, interferon, available since the 1980s, prompted a response in just a fraction of patients, and most would later see their disease progress. Interferon, Figlin notes, is the agent to which the new drugs have been compared in many of the clinical trials, but it no longer has much of a role as a treatment by itself.
Interleukin-2, or IL-2, an immune therapy on the market since 1992 but rarely used, has had checkered success. Administered to a small, sturdy subset of patients by experienced treatment teams in high (and very toxic) doses, IL-2, also referred to as Proleukin, has the potential to provide a cure in a very small number of patients—5 to 10 percent—with advanced RCC. Researchers, however, are still trying to figure out exactly how it works. “Unfortunately, with decades of experience, we still do not understand why some people benefit tremendously and some don’t benefit at all,” Figlin says.
Sue Guenther, 60, of Mesa, Arizona, has experienced high-dose IL-2 firsthand as part of a clinical trial in 2006. “I call it flu in a bag. It makes you sick as a dog,” says Guenther, who is also a survivor of thyroid cancer and sarcoma.
Like many people with kidney cancer, her malignancy was discovered by happenstance—a misstep on some marble stairs, she says, literally saved her life. Guenther stepped down hard, and subsequent pain in her right kidney sent her to the doctor for scans.
That was in 2004, when she underwent a radical nephrectomy at Northwestern Memorial Hospital in Chicago for a large, stage 3 tumor near her liver. By early 2006, doctors found a 9-millimeter metastatic tumor in her lung, reduced to 2 millimeters after combination therapy, including IL-2, in the clinical trial.
Michael Atkins, MD, deputy director of the division of hematology-oncology at Beth Israel Deaconess Medical Center in Boston, believes high-dose IL-2 should remain an important first-line therapy because it is the only one shown to even occasionally cause complete and lasting responses—but it may be rendered less effective and more toxic after treatments such as Sutent. He acknowledges the issue is controversial.
“My view is there is a select group of patients and tumors, yet to be completely defined, that are best initially treated with IL-2, with the antiangiogenic or targeted agents reserved for those patients whose disease fails to respond to IL-2,” says Atkins, who is also leader of the Kidney Cancer Program at Dana-Farber/Harvard Cancer Center and a professor of medicine at Harvard Medical School.
Although hard data are pending on factors that can predict responsiveness to IL-2, Atkins notes that researchers do have some idea of the clinical and biochemical characteristics that may mark patients most likely to benefit. The new therapies are a trade-off, he says. “While the new therapies help the average patient in a major way, without Proleukin, the cure of advanced kidney cancer is likely to become an even rarer event.”
Motzer, on the other hand, sees little role for IL-2, saying the current progress and excitement in the treatment of kidney cancer is based on the discovery and implementation of the targeted agents in the past five years.
The Ups and Downs
One disadvantage of the new drugs is a variety of toxic side effects. Another is price: They can cost tens of thousands of dollars a year. And the drugs require ongoing outpatient management, including monitoring for cardiovascular side effects in patients who received Sutent and/or Nexavar.
On Sutent, Benner had acid reflex, diarrhea, and fatigue, and had to drop his 50 mg daily dose to 37.5 mg. (Researchers are continuing to evaluate dosing strategies for the drug.) Everything, except chocolate, tasted like metal. On Nexavar, at an 800 mg daily dose, Benner developed a rash starting on his head and face, which moved to his chest and arms. “It almost was like second-degree burns,” he says, noting that his dose was reduced, then re-escalated. He takes special care of his feet, using ointments to avoid blisters that might arise from redness he has there. “I’m a pretty resilient person,” Benner says. “You can’t let a disease beat you.”
Guenther’s treatment odyssey, meanwhile, continued in 2007 and 2008, when she twice underwent cryoablation to treat tumors on her remaining kidney, which is functioning at about 70 percent. She, too, ended up on Sutent.
The first month, starting with a 50 mg daily dose that was later reduced to 37.5 mg, she found the fatigue devastating. The second month she also had a foul taste in her mouth and was living basically on just a few crackers a day. “I thought, ‘At least I’ll lose weight on Sutent,’ ” she says. But her doctor said no, people tend to gain weight on the drug. “It was then that I remembered God had a sense of humor.”
As of her last scans, her two major lung metastases were significantly reduced, and smaller lung spots were gone. “It looked like the Sutent was working,” she says. “This is living with cancer. But you’re living.”
From http://jcem.endojournals.org/cgi/content/abstract/94/6/1966
Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2008-2636
Right arrow Cardiovascular Endocrinology
The Journal of Clinical Endocrinology & Metabolism Vol. 94, No. 6 1966-1972
Copyright © 2009 by The Endocrine Society
Effects of Dehydroepiandrosterone Replacement on Vascular Function in Primary and Secondary Adrenal Insufficiency: A Randomized Crossover Trial
Sam P. L. Rice, Neera Agarwal, Hemanth Bolusani, Robert Newcombe, Maurice F. Scanlon, Marian Ludgate and D. Aled Rees
Centre for Endocrine and Diabetes (S.P.L.R., N.A., H.B., M.F.S., M.L., D.A.R.) and Department of Primary Care and Public Health (R.N.), School of Medicine, Cardiff University, Cardiff CF14 4XN, United Kingdom
Address all correspondence and requests for reprints to: Dr. D. Aled Rees, Centre for Endocrine and Diabetes Sciences, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, United Kingdom. E-mail: reesda@cf.ac.uk.
Context: Patients with Addison’s disease and hypopituitarism have increased mortality, chiefly related to vascular disease. Both diseases are characterized by dehydroepiandrosterone (DHEA) deficiency, yet this is not usually corrected. It is unclear whether treatment of these conditions with DHEA improves cardiovascular risk.
Objective: The aim of the study was to evaluate the effects of DHEA on arterial stiffness and endothelial function in subjects with Addison’s disease and hypopituitarism.
Design and Intervention: Forty subjects (20 with Addison’s disease, 20 with panhypopituitarism) were assigned to consecutive 12-wk treatment periods of DHEA 50 mg or placebo in a randomized, double-blind, crossover design separated by an 8-wk washout.
Main Outcome Measures: Primary outcome parameters were measures of arterial stiffness [augmentation index, central blood pressure, brachial and aortic pulse wave velocity (PWV)] and endothelial function. Serum androgens, anthropometry, and metabolic biochemistry (lipids, homeostasis model of assessment for insulin resistance, high sensitivity C-reactive protein, adiponectin, plasminogen activator inhibitor-1) were also assessed.
Results: Despite normalization of DHEA sulfate, androstenedione, and testosterone (females), DHEA replacement did not affect augmentation index, aortic PWV, brachial PWV, central blood pressure, or endothelial function. DHEA did not affect any anthropometric or metabolic measures, apart from a small reduction in high-density lipoprotein cholesterol (–0.08 mmol/liter; P = 0.007; 95% confidence interval for the difference, –0.13 to –0.02 mmol/liter).
Conclusions: Short-term DHEA supplementation does not significantly affect measures of arterial stiffness or endothelial function in patients with adrenal insufficiency.
MaryO'Note: Since these are blogs, I have no idea how accurate any of this info may be...
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survive the journey: The Cardiovascular Risks of Growth Hormone Deficient Adults: "I have growth hormone deficiency (GHD) and other pituitary hormone deficiencies due to a pituitary tumor. My surgery to remove the tumor did not help any, and when I had the Arginine GH stimulation test this past spring, I did not produce nearly enough GH. GH is pulsatile and needs stimulation in order to be tested correctly. IGF-1 is not a reliable marker of GH production."
An interview with Kate (Fairley).
Kate (Fairley) has had symptoms since 1991. She has had two pituitary surgeries and another recurrence. She is not yet cured and her current diagnoses are Idiopathic Intracranial Hypertension, panhypopituiarism and a CSF leak. Kate writes in her message board signature:
Pituitary Cushings: Kate and Dr. Ted Friedman on National Geographic TV were featured on the National Geographic channel. The show, called the Science of Obesity, has a segment on Cushing's syndrome.
Today, 127 million adult Americans are considered overweight, but few reach the extreme proportions of the exceptionally obese. What are the physical stresses of weighing more than 500 pounds and what steps can reverse it? NGC provides an understanding of what happens inside the bodies of these massive people & why a person can pack on hundreds more pounds than those with typical weight challenges. The show explores the genetics behind weight gain & medical advances available to help prevent it.
I hope that all of you can watch this. Please consider contacting your local media about doing your story! There is still much work to do to increase Cushing's awareness.
Read Kate's articles:
First off, I'd like to thank you all for your good wishes, support and prayers. I could do the Sally Field thing and say "...and I can't deny the fact that you like me, right now, you like me!" but I won't.
I plan to print everything out and take it with me to the hospital as a cheery-upper.
Alice has been such a wonderful friend through all this, calling, checking up on me, keeping all of you updated on things as they are known right now. Her support and love has been such a wonderful blessing in my life, especially now.
As it is, I'm currently feeling "normal" whatever that is. If I didn't know I had a problem, I would think that I was just fine.
I am fortunate that I found this out before the tumor could grow any larger. I am fortunate that I was close to the ER, not driving home from Baltimore, or in Baltimore, Oklahoma or on the cruise.
I know that the tumor has been growing for quite a while - it's very large. I saw the MRI images and even I can tell that it's not normal. As far as I know now, all the other scans have been fine. I had an abdomen CT, chest CT, brain MRI, chest/abdomen MRI and a full body bone scan.
When I was in the ER Friday, they assumed that it was a kidney stone and did the first abdominal CT scan looking to see where that was. They came back with the news that yes, I had a kidney stone but that it was the least of my worries at them moment. So, I was admitted to the hospital and had all the other scans except the bone scan. Knowing what I know now, it would have been better and easier for me to have had the bone scan as an inpatient. As soon as I checked out and was out of the system, it was harder to get an "emergency" (not scheduled weeks in advance) bone scan. Oh, well.
My surgery will be next Tuesday, May 9, at 9:30AM at Fairfax Hospital ( http://www.inova.org/inovapublic.srt/ifh/index.jsp ). I'm expected to stay there for 3-5 days post op and they don't anticipate any pesky complications like chemo or radiation at this time.
For now, I'm keeping my normal schedule, avoiding reading horror stories online, eating, sleeping - even napping! - as usual. Sometimes I even forget that I have this little medical appointment next week.
For a non-phone person I've talked with so many people these last few days, it's mind-boggling.
I'm happy to report that all is not lost on the cruise. Someone will replace me - and there will be another cruise later in the year. YEA! My main "concern" on that now is that I'll lose weight (finally!) post-op and my cruisewear will no longer fit. Yeah, right.
In thinking back, I think it's a good thing that my arginine test was messed up in Sept of 05. If it hadn't been, I wouldn't have redone it on Thursday. I believe that having that stuff in my body was what made my kidneys rebel and act up on Friday. So, without the lab screw-up I might not have known anything for a long time.
So, it's all good.
Thanks to everyone who has called and posted such wonderful things. I cannot begin to imagine what my email looks like...
June 12, 2006 post-op:
Thank you all for your prayers, good wishes, cards, phone calls, gifts, general "cheery-uppers". They all really helped me on my road to recovery.
I do have a ton of thank you cards to send out to lots of people - I'm very slow at that sad.gif Under normal circumstances my handwriting is terrible. Now, post-op kidney cancer, I can no longer take my arthritis meds or any NSAIDs and my writing will probably be even worse.
I am very nearly better, not much pain anymore, a nasty big scar and my energy levels aren't so great. Of course, they were awful before. I can no longer take the GH even though I'm deficient. In 5 years (if I survive!) I can take the GH again, supposedly.
I've had a lot of time to do a lot of thinking over the last 6 weeks. I know I was extraordinarily lucky to have my tumor discovered before it was too late. The lab reports and my surgeon reported that it would only have been a week or so before the tumor had hemorrhaged and caused major problems. Thank goodness the argenine retest for GH had caused me to bleed - at least I think that's what set it off. If I hadn't had all the blood and pain for one day only, I'd have had no clue that I had this cancer and who knows what would have happened in that next week.
I will be getting CT scans every 3 months for awhile to be sure that there is no cancer hiding out.
Update October 26, 2006
I went to see my Johns Hopkins endo again last week. He doesn't "think" that my cancer was caused by the growth hormone although it may well have encouraged the tumor to grow faster than it would have.
He was happy to see that I had lost 22 pounds since my last 6 month visit. Not all of that was from surgery! He reminded me that I can take more cortisone, but I hate to do that because I gain weight so fast when I take more.
He thought that my blood pressure was low - for me, not for "normal" people. He took my pressure several times, lying down, getting up quickly. But I never got dizzy. Maybe my pressure increase was temporary when the cancer started. All these mysteries I have that no one can answer.
My energy levels are lower than when I was on GH, and they're lower again because I had the adrenal removed, because of my panhypopit, because of my cancer (even though currently NED, it can come back at any time, because of my GH deficiency...
Every day is a challenge getting up, doing something useful, doing something without arthritic pain and weakness, having the energy to finish even something "easy". I'm starting to get very depressed over all this.
If this is the way the rest of my life is going to be, why bother?
