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mertie

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  1. I was normal weight, but my sister was 5 pounds and she has some suspected pit problems. Interesting!
  2. While talking to another member recently who was feeling suicidal, I told her I thought we all felt that way at one time or another. I agree with Jo, the frustration and hopelessness we develop as a result of being dismissed and even ridiculed by some doctors has to contribute to our feeling this way. I don't believe I've ever discussed suicide with another Cushing's patient who hadn't at least thought about it as a way out of the misery. It's good to know this is part of the disease and that others feel this way as that may be what a suicidal patient needs to know. It helps to know it is a symptom and that we are not alone. And it helps to know we can live through it and get better and that the suicidal feelings can be a thing of the past.
  3. Thanks Mary. That confirms again what I keep telling myself...Get up and MOVE and be as healthy as possible. It all starts with the first walk!
  4. One small step for man.... A giant leap for those of us with this disease!
  5. http://www.pcworld.com/article/id,138082-c...es/article.html New Microsoft Service Stores Health Records Online HealthVault gives people a place to keep, research, and share medical informmation. Grant Gross, IDG News Service Saturday, October 06, 2007 10:00 AM PDT Microsoft Corp. has launched an online health-care service designed to help patients take control of their health records and monitor their medical conditions. Microsoft's HealthVault, announced Thursday in Washington, D.C., will allow users to store and share health records online, to collect and manage health data on a variety of home devices, and to search for health information. "We all know health is incredibly complex, it has lots of information, and we make it harder than it needs to be," said Peter Neupert, corporate vice president of Microsoft's Health Solutions Group. "By making it harder than it needs to be, bad things happen." Patients want tools to simplify their interactions with the health-care system, Neupert added. "They want an information system ... that puts them at the center, that makes it easy for them to manage their health, and their family, and their activities when they interact with the health system," he said. "It's hard, but it's not that hard. It's possible, and it's possible today." The HealthVault applications, available for free on the HealthVault Web site, are designed to allow patients to share their information safely and easily with health-care providers and manage their health issues, such as weight loss and long-term diseases, Microsoft said. The three pieces of HealthVault include: -- HealthVault Search, a specialized search engine designed to give the most relevant online health content and connect results with HealthVault-compatible products. -- The HealthVault repository account, an encrypted online e-health record that users and their families can share with doctors. -- The HealthVault Connection Center, a place where users can find "plug-and-play" drivers for health monitoring devices such as diabetes meters and heart-rate monitors to connect to the HealthVault accounts. "We need to make information reusable," Neupert said. "We're all frustrated ... by the simple, stupid things, like having to fill out the clipboard [at a doctor's office] all the time." The HealthVault was developed in cooperation with privacy advocates, including the bipartisan Coalition for Patient Privacy, Microsoft said. Dr. Deborah Peel, founder of the Patient Privacy Rights Foundation, praised the company for privacy controls on the service, including the prohibition of data transfer without "explicit" informed consent. "Consumers finally have a trusted place to store their personal health information that will not be data-mined, because they alone control it," Peel said. Microsoft's new e-health platform will probably be the largest not affiliated with an insurance provider or specific employer, said Lynne Dunbrack, program director at Health Industry Insights, a market research and advisory services firm. But the effort faces several challenges, Dunbrack said. Microsoft is banking on its relationships with outside software developers to create programs that work with HealthVault, she said. In addition, less than 30 percent of doctor's offices and hospitals now use electronic health records, so it will be a challenge for many users to find data to populate the HealthVault records, she said. Only about 1 percent to 3 percent of U.S. consumers have adopted personal e-health records, she said, despite a major push from U.S. President George Bush's administration and several private groups. One of the issues is privacy concerns. "Consumers are quite wary of having their personal health information available and accessible over the Internet," Dunbrack said. Microsoft said more than 40 applications and devices will work with HealthVault now or in the near future. Partners offering applications or devices that will work with HealthVault include: American Diabetes Association; American Heart Association; American Lung Association; Diet.com; Eclipsys Corp.; Healthphone Solutions Ltd.; LifeScan Inc.; Medifast Inc.; NewYork-Presbyterian Hospital; NoMoreClipboard.com; Texas Instruments Inc.; US Wellness Inc.; and Vital Data Technology. Developers interested in building their own HealthVault-based products can download the HealthVault software development kit.
  6. This article brought to mind Sandy and Martin and what they've gone through. Could their difficulty be SWS?
  7. I thought this was interesting and might be helpful for some of our members: http://www.eje-online.org/cgi/content/full/153/2/207?ck=nck Steroid withdrawal syndrome after successful treatment of Cushing?s syndrome: a reminder A Bhattacharyya, K Kaushal, D J Tymms1 and J R E Davis Department of Endocrinology, Manchester Royal Infirmary, Manchester, UK and 1 Department of Endocrinology, Royal Albert Edward Infirmary, Wigan, Lancashire, UK (Correspondence should be addressed to J R E Davis, Department of Endocrinology, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, UK; Email: julian.davis@man.ac.uk) Abstract Steroid withdrawal syndrome (SWS) usually refers to relapse of the disease being treated after withdrawal of glucocorticoid therapy, or the symptoms of adrenal insufficiency which occur when glucocorticoids are rapidly reduced or stopped. A less well-recognised form of SWS is that which develops when patients experience a symptom complex similar to that of adrenal insufficiency despite acceptable cortisol levels. We describe three patients who presented with this form of SWS following surgical treatment for endogenous Cushing?s syndrome. All responded well to a short-term increase in the dose of glucocorticoid replacement therapy, with the median duration of the syndrome being 10 months (range 6?10 months). Trough serum cortisol levels above 100 nmol/l, with peaks between 460 and 750 nmol/l were documented in the first two patients at presentation with SWS. It is thought that the syndrome may result from development of tolerance to glucocorticoids, and mediators considered to be important in its development include interleukin-6, corticotrophin-releasing hormone, vasopressin, and central noradrenergic and dopaminergic systems. The exact underlying mechanism for SWS remains unclear. However, with increasing recommendations for use of lower doses of replacement glucocorticoids, its incidence may increase. Physicians need to be aware of this condition, which is self-limiting and easily treated by a temporary increase in the dose of glucocorticoid replacement therapy. It is possible that a slower glucocorticoid tapering regimen than that used in the standard postoperative management of patients undergoing pituitary surgery may reduce the risk of development of SWS. Introduction Glucocorticoids are used to control the activity of inflammatory, autoimmune, allergic and neoplastic conditions. The term steroid withdrawal syndrome (SWS) has traditionally been used to describe the relapse of the disease being treated following withdrawal of glucocorticoid therapy (1?3). An ill-defined symptom complex with fever, anorexia, mood swings, generalised body aching, and weight loss is also recognised, occurring when supraphysiological doses of glucocorticoids are reduced rapidly to a low maintenance dose (1, 3, 4). This is due to suppression of the hypothalamo?pituitary?adrenal (HPA) axis by the glucocorticoid therapy, and with rapid reduction or cessation of treatment patients experience symptoms of hypocortisolism particularly at times of intercurrent illness or stress (5). However, an alternative form of SWS can occur where patients experience symptoms of adrenal insufficiency despite acceptable serum cortisol levels (1, 3). We describe three patients with endogenous Cushing?s syndrome who experienced this latter form of SWS post-operatively (Table 1). All three patients responded well to a short-term increase in the dose of glucocorticoid replacement therapy. View this table: [in this window] [in a new window] Table 1 Patient characteristics. Case 1 A 26-year-old male presented to our unit with a twelvemonth history of marked obesity, high blood pressure, proximal muscle weakness and pink abdominal striae. Investigations revealed a high midnight cortisol value of 523 nmol/l (normal 50?250 nmol/l) and high urinary free cortisol (UFC: 2317 and 2084 nmol/24 h, normal Within four weeks of surgery he presented with depression, fatigue, generalised myalgia and insomnia. On examination, his blood pressure showed a postural drop of 20 mm Hg (from 115/80 mm Hg). Full blood count and biochemistry were normal, as were thyroid function tests. A cortisol day curve on 10, 5 and 5 mg hydrocortisone was satisfactory, with inter-dose daytime nadir levels of cortisol above 100 nmol/l (Fig. 1; sample taken before each dose and 2 h after the morning and midday doses). The symptoms failed to respond to anti-depressants and tranquilizers. With a presumptive diagnosis of SWS, the dose of hydrocortisone was increased to 15, 10 and 5 mg and later to 20, 10 and 10 mg daily. His symptoms improved over the next few weeks. An attempt to reduce the dose of hydrocortisone four months after surgery was unsuccessful. A further attempt was made ten months after surgery when hydrocortisone was reduced slowly from 40 to 30 mg daily and after a further three months he successfully tolerated a dose reduction to 10, 5 and 5 mg. At present, three years after the initial diagnosis, he remains well on this dose. The source of ectopic ACTH secretion remains unidentified but is presumed to be a small benign carcinoid tumour. View larger version (15K): [in this window] [in a new window] Figure 1 Cortisol day curves in patient 1 (dashed line) and patient 2 (solid line) while taking 10, 5, and 5 mg hydrocortisone. Samples were taken before each dose and 2 h after the mid-day and evening doses, showing satisfactory nadir levels of serum cortisol at a time when patients had marked SWS symptoms. Case 2 A 25-year-old female was referred for investigation of infertility. She complained of weight gain, hirsutism and oligomenorrhoea, and UFC was 274 nmol/24 h. Her midnight cortisol value was raised at 522 nmol/l and serum ACTH levels varied between 8 and 16 pg/ml. Serum cortisol was suppressed by high-dose but not low-dose dexamethasone. A pituitary MR scan showed a normal sized pituitary gland with no evidence of an adenoma. On inferior petrosal sinus sampling, the central-to-peripheral gradient of ACTH increased from 11.5 at baseline to >25 on the left side following administration of corticotrophin-releasing hormone (CRH). She underwent transsphenoidal surgery a year after diagnosis. Histology confirmed the removal of a corticotroph adenoma with some normal anterior pituitary tissue. She was started on 150 mg hydrocortisone in three divided doses, which was titrated down to 10, 5 and 5 mg daily within seven days of surgery. Initially she felt well, but about 3 weeks after surgery she started to feel lethargic, and experienced insomnia, restlessness and tremor. Baseline haematology, biochemical profile, and thyroid function were normal. An insulin tolerance test showed a normal growth hormone response to hypoglycaemia but no serum cortisol response (peak 55 nmol/l), so hydrocortisone replacement was continued. A cortisol day curve on 10, 5 and 5 mg hydrocortisone was satisfactory (Fig. 1), and daytime nadir serum cortisol levels were 205 and 155 nmol/l. Considering the possibility of SWS, her dose was increased to 20, 10 and 10 mg daily and within two weeks she felt much better. Over the next six months we slowly reduced the dose of hydrocortisone without any relapse of her symptoms. Case 3 A 48-year-old female presented with a six-month history of weight gain, proximal muscle weakness, generalised fatigue, facial plethora and multiple bruises. Her clinical appearance was suggestive of Cushing?s syndrome, UFC was 1510 nmol/24 h, and morning serum cortisol was 788 nmol/l, with a midnight value of 479 nmol/l. Plasma ACTH was Discussion Four aspects of glucocorticoid withdrawal are important, whether occurring after cessation of therapeutic doses of glucocorticoids or after successful treatment of endogenous glucocorticoid excess, namely: (i) relapse of the disease for which the drug was originally prescribed, (ii) suppression of the HPA axis, which can occur for a variable length of time (iii) psychological dependence, and (iv) a non-specific withdrawal syndrome occurring in the setting of adequate circulating cortisol levels (3), as occurred in our three patients. Although the symptomatology of SWS is similar to that of adrenal insufficiency, it is not identical, since a mixed picture occurs consisting of both hormone deficiency as well as a generic withdrawal syndrome (3). Howlett, in discussing hydrocortisone replacement for adrenal insufficiency, advocated that the UFC and 0900 h serum cortisol values should be within the reference range for the normal population (to avoid over-replacement) and 1230 h and 1730 h serum cortisol values should be above 50 nmol/l, preferably above 100 nmol/l (to avoid under-replacement) (6). In our first two patients we have clearly documented serum cortisol levels above this cut-off at the time of presentation with SWS (Fig. 1). A therapeutic trial of a higher dose of hydrocortisone was beneficial and in the first case symptoms relapsed when we tried to taper the dose of hydrocortisone too rapidly. We believe all 3 patients had developed SWS following successful surgical treatment of prolonged endogenous hypercortisolism (Table 1). The form of SWS that we have described, characterised by anorexia, nausea, lethargy, fever, arthralgia, skin desquamation, weakness, postural hypotension, vomiting and weight loss, was recognised as early as 1960, although the exact mechanism of action is not clear, nor is its prevalence (3, 4, 7, 8). Suppression of the HPA axis by the hypercortisolaemic state, whether endogenous or exogenous, was initially thought to be responsible, until the axis was shown to be normal in these patients, with normal baseline cortisol levels (7). Subsequently, Amatruda et al. demonstrated some suppression of the HPA axis in these patients but, importantly, serial plasma and urine steroid levels were within normal limits, and there was no correlation between the status of the HPA axis and the severity or duration of SWS (4). Hence the condition was attributed to a state of ?relative adrenal insufficiency? as tissues had been exposed to high levels of steroids for a prolonged period. It is thought that these individuals develop tolerance to glucocorticoids, such that the replacement doses used are inadequate to allow correct functioning of the central nervous system and other organs (3). Tyrrell describes the possibility of a relative state of glucocorticoid resistance in these patients, effectively rendering them hypoadrenal (8). In more recent studies, a rise in the level of interleukin-6 (IL-6) has been linked with the acute form of SWS occurring immediately after surgery for Cushing?s syndrome in patients who were hypocortisolaemic, and a similar symptom complex was noted after infusion of IL-6 (9, 10). Papanicolaou et al. found that even by day 9 or 10 postoperatively, when these patients were on glucocorticoid replacement, IL-6 levels decreased but were not back to normal (9). Alterations in the concentrations of a number of other mediators have been hypothesised to play a role in the development of the SWS, notably CRH and central noradrenergic and dopaminergic systems, reviewed in more detail by Hochberg et al. (3). There are few specific recommendations in standard endocrinology textbooks and the medical literature regarding the rate at which glucocorticoid therapy should be reduced following successful surgical treatment of Cushing?s syndrome. Orth and Kovaks recommend that 200 mg hydrocortisone should be given over the first 24 h after surgery, then ?100 mg, 75 mg, 50 mg and maintenance hydrocortisone (10 to 25 mg each morning) on successive days thereafter? (11). Miller and Tyrrell state that postoperative hydrocortisone replacement is ?reduced to maintenance doses (30 mg per day) by the seventh to tenth day? (12). However, in a Cushing?s Newsletter, Cook (13) has suggested the administration of 60?80 mg hydrocortisone for 2 weeks, followed by a reduction of 10?20 mg every 10?14 days until a maintenance dose is reached. There is, therefore, considerable variation amongst endocrinologists regarding recommendations for the tapering of glucocorticoids. The patients we have described, particularly the first two cases, provide a useful reminder of the need for more gradual tapering of glucocorticoid doses to a maintenance level in the setting of successfully treated Cushing?s syndrome, in order to reduce the risk of development of SWS postoperatively. Concerned about potential long-term side effects of glucocorticoids, endocrinologists increasingly recommend lower doses of replacement glucocorticoids (6, 14), and consequently the risk of SWS is increased. Furthermore, hypoadrenalism is the most potent stimulus to recovery of ACTH secretion postoperatively in pituitary-dependent Cushing?s syndrome (15), thus most physicians will aim to decrease the steroid dose to the lowest tolerated maintenance level as quickly as possible. However, patients with Cushing?s syndrome have usually been hypercortisolaemic for a prolonged period prior to surgery; a few additional weeks of high serum cortisol levels secondary to ?over-treatment? with replacement hydrocortisone postoperatively may therefore be preferable to the morbidity associated with SWS. In our third patient, however, despite a gradual tapering of glucocorticoid therapy to maintenance levels over a two-month period following unilateral adrenalectomy, SWS still occurred. In conclusion, although the exact mechanism of SWS is not clear, physicians involved in the management of endogenous or exogenous steroid excess need to be aware of this condition. Caution must be exercised by endocrinologists regarding the rate at which they initially reduce replacement glucocorticoid therapy following successful surgery for Cushing?s syndrome. It is possible that a slower tapering regimen than that used in the standard postoperative management of patients undergoing pituitary surgery may reduce the chances of SWS. Pre-operative normalisation of cortisol secretion using gradually increasing doses of medical therapy to suppress steroidogenesis may also be beneficial in preventing later SWS. However, it is important to remember that SWS is a self-limiting state, and should it occur, its management should include a temporary increase in the dose of glucocorticoids, followed by slow tapering to a maintenance dose. References Dixon RB & Christy NP. On the various forms of corticosteroid withdrawal syndrome. American Journal of Medicine 1980 68 224?230.[CrossRef][iSI][Medline] George CF & Robertson D. Clinical consequences of abrupt drug withdrawal. Medical Toxicology and Adverse Drug Experience 1987 2 367?382.[iSI][Medline] Hochberg Z, Pacak K & Chrousos GP. Endocrine withdrawal syndromes. Endocrine Reviews 2003 24 523?538.[Abstract/Free Full Text] Amatruda TT Jr, Hurst MM & D?Esopo ND. Certain endocrine and metabolic facets of the steroid withdrawal syndrome. Journal of Clinical Endocrinology and Metabolism 1965 25 1207?1217.[iSI][Medline] Swartz SL & Dluhy RG. Corticosteroids: clinical pharmacology and therapeutic use. Drugs 1978 16 238?255.[iSI][Medline] Howlett TA. An assessment of optimal hydrocortisone replacement therapy. Clinical Endocrinology 1997 46 263?268.[CrossRef][Medline] Amatruda TT Jr, Hollingsworth DR, D?Esopo ND, Upton GV & Bondy PK. A study of the mechanism of the steroid withdrawal syndrome. Evidence for integrity of the hypothalamic?pituitary?adrenal system. Journal of Clinical Endocrinology and Metabolism 1960 20 339?354. Tyrrell JB. Glucocorticoid therapy. In Endocrinology and Metabolism, edn 3, ch. 15, pp 855?882. Eds P Felig, JD Baxter & LA Frohman. New York: McGraw-Hill, Inc., 1995. Papanicolaou DA, Tsigos C, Oldfield EH & Chrousos GP. Acute glucocorticoid deficiency is associated with plasma elevations of interleukin-6: does the latter participate in the symptomatology of the steroid withdrawal syndrome and adrenal insufficiency? Journal of Clinical Endocrinology and Metabolism 1996 81 2303?2306.[Abstract] Papanicolaou DA, Wilder RL, Manolagas SC & Chrousos GP. The pathophysiologic roles of interleukin-6 in human disease. Annals of Internal Medicine 1998 128 127?137.[Abstract/Free Full Text] Orth DN & Kovaks WJ. The Adrenal Cortex. In Williams Textbook of Endocrinology, edn 9, ch. 12, pp 517?664. Eds JD Wilson, DW Foster, HM Kronenberg & PR Larsen. Philadelphia: WB Saunders Company, 1998. Miller WL & Tyrrell JB. The adrenal cortex. In Endocrinology and Metabolism, edn 3, ch. 12, pp 555?711. Eds P Felig, JD Baxter & LA Frohman. New York: McGraw-Hill, Inc., 1995. Cook D. The Cushing?s Newsletter. February 1999. Peacey SR, Guo CY, Robinson AM, Price A, Giles MA, Eastell R & Weetman AP. Glucocorticoid replacement therapy: are patients over treated and does it matter? Clinical Endocrinology 1997 46 255?261.[CrossRef][Medline] Trainer P, Newell-Price J & Besser M. Cushing?s syndrome. In Endocrinology and Diabetes, edn 1, ch. 5.9, pp 817?829. Eds JAH Wass & SM Shalet. Oxford: Oxford University Press, 2002.
  8. I received my ribbon magnet this week and love it! I hope it will help someone along the way.
  9. This is great news! I hope it is effective. And if it isn't, at least the pharmaceutical companies will put money into making people more aware of Cushing's. At least that's the way I see it. Thanks, Mary!
  10. I want a ribbon magnet, Mary. Where do I order?
  11. How about: CUSHING's. It's all in your head. And then the website address?
  12. This is great information, Mary. Thanks for sharing it. I'm going to pass it along to one of my diabetic friends who has a huge hump!
  13. Miss you so much Dawn! I hope you are doing well. Love ya!

  14. Mary & Robin, you are both amazing! WOO HOO indeed! Thanks so much!
  15. Yes, thanks for sharing this Robin! It is so cool. I've been reading tons of stuff from your flakes! There's so much good information there.
  16. Dawn, You are such a good friend, I appreciate you so much. Thanks for all your help. Love ya!

  17. It appears to be the senator from Connecticut. Here's his website: http://dodd.senate.gov/
  18. I sent the author an email. I hope many of us will. This is terribly misleading and could hurt people! And that doctor needs to find out the truth, too. I'm surprised he sees 2 patients a year if he thinks 10 to 20 pounds is the average weight gain!
  19. Thinking of you and sending good thoughts your way, Mary. We love you and miss you. You have made a difference in so many lives, including mine. I am forever grateful.

  20. You're a beautiful person and have been a source of inspiration and hope to me, as well as a good friend.

  21. Here's the letter I received back from my representative this morning. So looks like I have more writing to do! Dear Ms. Loper, Thank you for contacting me concerning raising awareness about Cushing’s Syndrome. I appreciate your sentiments and suggestions. Pursuant to your e-mail, I preformed some additional research on this disease. As you are more then well aware, Cushing's Syndrome is a relatively rare disease that commonly affects adults aged 20 to 50. Most researches estimate that between 10 to 15 of every million people are affected each year with this disease. It is largely caused by an excess of cortisol production, a normal hormone produced in adrenal glands located above each kidney. Prior to you e-mail, I was not aware of this disease. From time to time, the Michigan Legislature will pass Resolutions which raise awareness about different subject matters related to such things as health related issues, Michigan History and state leaders. While these Resolutions do not expend tax dollars on research or educational services for a particular cause or purpose, they do help increase public awareness when media outlets cover the passage of such Resolutions. Considering your request, I would like look into composing such a Resolution on the subject matter of this disease. In doing so, it would prove to be most helpful if I could have you do a couple things which would assist me in formulating such a Resolution. First, I would like to ask you to document and explain your personal story, detailing how you were diagnosed and perhaps specific information from your doctor detailing the time, place, and medical conditions which helped him diagnose this disease. In addition, if you know any other individuals that have been diagnosed with Cushing’s Syndrome from northern Michigan, the more information and personal stories that I could gather to use and incorporate into such a Resolution would prove to be most helpful. While I cannot guarantee that such a Resolution would pass, I would be happy to have something drafted which would help you and others promote and increase public awareness of this disease. Thank you again for bringing this matter to my attention. If you have any specific questions or comments about my request, please be sure to contact my staff direct. I have made Mr. Dan Dundas in my Lansing Office aware of our communications and he would be more than happy to follow up with any inquiries you might have. Sincerely, Kevin A. Elsenheimer It's a start!
  22. Just a reminder that we all need to get letters out to our representatives and senators in each state to encourage the passing of Cushing's Awareness Day 2007. This can generate a lot of media attention for us, but we all need to write the letters! There is a template here on the site that we can use and personalize, or you can write your own letter, but please remember we need to keep doing this until our presence is noticed! This is something we can all participate in and make a difference! Oops! sorry for the double post!
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