NSF…what is it?

Nephrogenic Systemic Fibrosis (NSF), also known as nephrogenic fibrosing dermopathy (NFD), is a condition that, so far, has occurred only in people with kidney disease. There is no convincing evidence that NSF is caused by a medication, a microorganism, or by dialysis. There have been no cases identified prior to early 1997. At this point it appears NSF is a systemic disorder with its most prominent and visible effects in the skin. For this reason, Nephrogenic Systemic Fibrosis has been suggested as an equivalent terminology in those previously diagnosed with NFD, and is preferred in that it more accurately reflects our current understanding of the disorder.

Neither the duration of kidney disease nor its underlying cause are related to the development of NSF. Some patients with NSF develop skin tightening in the earliest stages of kidney disease, and others may have had kidney disease for years. Specific triggers for the development of NSF are still being investigated. Recent reports have strongly correlated the development of NSF with exposure to gadolinium-containing MRI contrast agents. Further information from the US Food and Drug Administration regarding this observation can be found here: (http://www.fda.gov/cder/drug/advisory/gadolinium_agents.htm).

GE healthcare, one manufacturer of gadolinium-containing MRI contrast, has issued an informational announcement at: (http://www.amershamhealth-us.com/omniscan/safety/index.html).

NSF appears to affect males and females in approximately equal numbers. NSF has been confirmed in children and the elderly, but tends to affect the middle-aged most commonly. It has been identified in patients from a variety of ethnic backgrounds and from North America, Europe, and Asia.

Besides kidney disease, conditions that may be associated with NSF include coagulation abnormalities and deep venous thrombosis, recent surgery (particularly vascular surgery), recent failure of a transplanted kidney, and sudden onset kidney disease with severe swelling of the extremities. It is very common for the NSF patient to have undergone a vascular surgical procedure (such as revision of an AV fistula, or angioplasty of a blood vessel) or to have experienced a thrombotic episode (thrombotic loss of a transplant or deep venous thrombosis) approximately two weeks before the onset of the skin changes.

The associated conditions enumerated in the preceding paragraph frequently justify the use of gadolinium-enhanced MRI or MRA studies. Whether the recently announced association of NSF with gadolinium exposure is the common denominator of all NSF cases is still under investigation. A verifiable cause and effect relationship has not yet been established, but active efforts to prove or refute this relationship are underway. Two recent papers have verified the presence of gadolinium in the tissue of some patients with NSF, however, the study designs do not allow for determining whether the gadolinium caused the NSF (free article download #1)(free article download #2).

Symptoms and Signs

Patients with NSF describe swelling and tightening of the skin, usually limited to the extremities (images), but sometimes involving the trunk. The condition may develop over a period of days to several weeks. In many cases, the skin thickening inhibits the flexion and extension of joints, resulting in contractures. Severely affected patients may be unable to walk, or fully extend the joints of their arms, hands, legs, and feet. Complaints of muscle weakness are common. Approximately 5% of patients have a rapidly progressive (fulminant) course.

The skin changes may start as reddened or darkened patches, papules, or plaques. In time, the skin may feel “woody” and the surface may resemble the texture of the peel of an orange. Patients may experience burning, itching, or severe sharp pains in areas of involvement. Radiography may reveal calcifications of the soft tissue. Deep "bone pain" has been described in the hips and in the ribs.

The skin lesions are commonly symmetrical, with zones between the ankles and thighs most commonly involved, followed by involvement between the wrist and upper arms. Hand and foot swelling with blister-like lesions has also been reported. Some patients have reported yellow papules or plaques on or near the eyes. Rapid, new onset fluctuating hypertension of unknown cause has been described prior to the onset of the skin lesions.

Treatment options

While there is no consistently successful treatment for NSF, improving renal function (due to any modality) seems to slow or arrest NSF (and in many cases allows for gradual reversal of the process over time).

Critical assessment of the effects of any investigational therapy requires careful attention *and reporting* of the patient's renal function during therapy. Investigational therapies that show objective improvement in the setting of worsening or stable chronic renal failure should be targeted for further investigation. Therapies that show improvement of NSF while renal function is improving may or may not be contributing to the observed improvement. Given the recent association of NSF with gadolinium administration, any reports of investigational therapies should also clearly indicate whether gadolinium was administered during the therapeutic evaluation, and whether there was an identifiable clinical change in the patient's disease.

Treatments that have been tried and continue to be investigated include:

Oral steroids (prednisone): Has had some efficacy in doses of 1 mg/kg po qd. Patients with concurrent diabetes should be aware of the risks of hyperglycemia while taking this medication. All patients should be aware of the possibility of gastrointestinal ulceration while taking prednisone. In addition, osteoporosis is often accelerated while taking this medication, sometimes creating a rapid calcium-wasting state. It is not clear whether the prednisone is affecting the cutaneous disease, or the renal disease, but it does seem to work in a subset of patients.

Topical Dovonex (under occlusion): So far, responses have been anecdotal and largely subjective. Some patients report improvement in localized disease. The combination of occluded dovonex and clobetasol with vascular compression stockings has reportedly been of benefit.

Extracorporeal photopheresis (ECP): A recent article describes three patients in Europe who responded with softening of plaques after several courses of ECP. Each of these patients had no improvement in renal function during the treatment. All three of these patients had had NSF for less than one year. This report corroborates other anecdotal reports in the US that photopheresis is helpful in a subset of patients. Experience at Yale suggests that patients with longstanding NSF (arbitrarily set at one year) may not respond to this modality. This treatment is currently under investigation, although no formal trials are yet offered. Some insurance carriers are receptive to covering a trial of therapy, but in the event coverage cannot be secured, be advised that therapy is exceedingly expensive. Many patients and providers have reported that Medicare has provided coverage for ECP in recent cases.

Plasmapheresis: One study from Loma Linda University (ref 12) reported improvement in three patients with liver/kidney transplant. Two of these patients were noted to have concurrent improving renal function. It is unclear what contribution improving renal function may have had in the overall clinical improvement. Nevertheless, anecdotally, some persons have reported slight improvement following plasmapheresis. Several others have been reported who noted no improvement at all.

Cytoxan: Anecdotally, this medication has shown no improvement in a number of NSF patients.

Thalidomide: There are no formal reports on the success of this medication in NSF. However, some patients have reported subjective improvement. Long term tolerance of the drug may be an issue, however. There have been two reports among Registry patients of development of NSF in patients already taking thalidomide for other medical problems.

Ultraviolet therapy: I am aware of anecdotal use of PUVA, but have heard no reports of success. Article 38 discusses the use of UVA-1, evidently beneficial in the single case in this report. PUVA in combination with Soriatane and prednisone has been anecdotally helpful in two patients.

Physical therapy (PT): Some patients have reported that physical therapy, in particular, swimming, may be helpful in slowing the progression of joint contractures. There is no contraindication to PT, and the definite potential up-side suggests that PT should be pursued whenever possible. Deep massage has been reported to be of benefit.

Pentoxifylline (PXF): A recent report describes two NSF patients who received 1200 mg per day of oral pentoxifylline (ref 57). Both patients stabilized, and the one with less severe disease improved somewhat. The use of PXF is theoretically justified as it has known antifibrotic activity (thought to be at least partially related to TNF alpha antagonism). In addition, PXF is known to improve red blood cell flexibility, and therefore to improve circulation. As thrombosis seems to be an inciting event for many NSF patients, this mechanism could also be partially responsible for the improvements noted clinically. Many more patients will need to be treated to further evaluate the efficacy of this drug.

High Dose Intravenous Ig Therapy: Reference number 25 describes a patient who showed objective improvements with one cycle of therapy with this medication. Further improvement with additional cycles was not observed. No comment was made regarding the renal status of the patient while receiving this therapy. I have heard anecdotal information suggesting this therapy has been helpful in one other patient with NSF. Additional anecdotal data have been less promising.

Renal transplantation: Several patients have improved significantly with a return to normal kidney function (either as a result of transplantation or medical therapy). In other cases, kidney transplant has resulted in no obvious improvement of the lesions, even with a fully functioning, successfully transplanted organ. I am aware of no reason--at this time--that NSF patients should be excluded from receiving a renal transplant. There are many potential benefits to receiving a transplanted kidney, however, and further elaboration about this decision in the setting of NSF is discussed in reference 52. As many NSF patients have underlying hypercoagulable states, careful testing for coagulation disorders is recommended prior to transplantation to help reduce the incidence of unexpected and detrimental coagulopathies. Magnetic resononce angiography with gadolinium-containing agents should be avoided in NSF.

Prognosis

As NSF is a rare, relatively recent diagnosis, the natural history of the disease is not well understood. Some patients report a gradual improvement in mobility and slight softening of the skin over time. Complete spontaneous healing in a patient with ongoing kidney disease has not yet been reported.

Several patients with NSF have died as a result of complications of their kidney disease or transplant surgery. One patient, who elected to discontinue dialysis, had widespread fibrosis involving the diaphragm, psoas muscles, proximal esophagus and intimal areas of vessels of the kidney and lungs.

As mentioned above, some patients with NSF (estimated at 5% or less) have an exceedingly rapid and fulminant disease course that may result in death. NSF, by itself, is not a cause of death, but may contribute to death by restricting effective ventilation, or by restricting mobility to the point of causing an accidental fall that may be further exacerbated by fractures and clotting complications.

Suspected pathogenesis

Recent investigations suggest the cell responsible for the fibrosis seen in NSF is a recently characterized cell involved in wound healing and tissue remodeling. This cell--a circulating fibrocyte (CF)--is distinct from a fibroblast in that it has a CD34/procollagen dual positive profile and is blood-borne. In NSF, CFs are thought to leave the circulation (possibly aberrantly, or as a result of passive diffusion in fluid overload states) and differentiate in the dermis into cells that functionally and histologically resemble normal dermal fibroblasts. Because of the presence of these circulating cells, NSF can be considered a systemic disorder. Several reports have verified the presence of fibrosis in other organs in NSF, but whether the fibrosis is more likely in these patients than in the general population has not been formally verified.

The factors responsible for differentiation of CFs into terminal fibroblast-like cells are not clear, but are likely directly related to the underlying function of the kidneys. Because of the close association of surgery and thrombosis in most cases of NSF, thrombosis and/or endothelial damage may be partially responsible for the initiation of a series of events that culminates in NSF.

Noting the common preceding events of vascular surgery and thrombosis (as well as brain tumors in a small number of NSF patients--ref 17), we have been actively investigating the possibility that radiographic contrast agents might be a trigger in some NSF patients. One common denominator in all of these recognized comorbidities is the frequent use of contrast agents for angiography (detecting clots, planning surgery, and evaluating the vascularity of brain neoplasms). We had noted that contrast agents had been used (and sometimes had been temporally related to disease onset) in several patients. We elaborated upon the possibility that peripherally deposited radiographic contrast might be a target for circulating fibrocytes in a recent publication (ref 62).

Interestingly, a group in Austria working along similar lines simultaneously published a report (ref 57) that the MRI angiographic contrast agent known as "Gadolinium" had been used in all NSF patients in their study group. Those patients who had renal disease and were also exposed to Gadolinium but did not develop NSF were not acidotic at the time of their studies (those who developed NSF were, in fact, acidotic). A comparison of medications revealed no single medication could account for the findings in all patients (including the use of angiotensin converting enzyme inhibitors).

Another recent and larger scale study from Denmark (ref 74) also associated the use of gadolinium-containing contrast agents with NSF onset, although the acidosis suspected as being a facilitator in the Austrian study (above) was not observed. At this time it is not clear whether systemic acidosis is an independent risk factor for NSF, or whether it is etiopathogenic in any sense.

Given these data, it would be most prudent to recommend that the use of gadolinium-containing contrast agents be excluded to the greatest extent possible in patients with renal disease until these observations can be confirmed and clarified. A formal announcement from the FDA is present at: (http://www.fda.gov/cder/drug/advisory/gadolinium_agents.htm).

Links/Support

1. NFD Support Group at Yahoo.com This site is a point of communication about the disease as well as an electronic forum to share ideas and possible treatment measures. It is not organized or run by Yale, however, I try to keep abreast of comments made and interject thoughts when I feel they are helpful to the understanding of the disorder.
2. NFD Support.com "Developed to help those diagnosed with Nephrogenic Fibrosing Dermopathy and their families."
3. Nephrogenic Fibrosing Dermopathy at Emedicine.com This site is also a freely available information source on NFD/NSF. Registration is free.
4. Photopheresis center locater This site is maintained by Therakos (maker of photopheresis kits). In the past, the site has only functioned with Internet Explorer.
5. FDA reports on NSF and Gadolinium (June 8, 2006)
6. GE Healthcare comments about their gadolinium containing product (June 6, 2006)

Gifts of Support for NSF Research

Gifts of support are gratefully accepted, and are a special way to remember a friend or family member stricken with this disorder. Your cash donation is tax-deductible and forwarded immediately to the NSF research effort. Gifts should be addressed to Dr. Richard Edelson, Chairman of the Department of Dermatology at Yale University. A sample template letter is available here. Please feel free to modify it to suit your needs. Dr. Edelson's address, and instructions for completing the check, are present in the letter. [Please make the check payable to Yale University, not to Dr. Cowper!] If there are any questions, please contact our office. Thank you!

The International Center for NFD/NSF Research (ICNFDR)

The ICNFDR is a new appellation for a collaborating group of researchers based at Yale University who are involved with NSF research. The team consists of physicians and basic science researchers from several disciplines who have committed to working together in the search for the cause, treatment, and eventual eradication of NSF. The heart of the project is the NSF Registry (see below) a direct offshoot of the original CDC investigation that began in California several years ago. Until recently, the Centers for Disease Control have not been involved in NSF investigation for several years. However, the CDC has recently completed a site investigation, and when the data are released, new information will be posted. For now, continue to contact us as noted below. In addition, cases reported to the Food and Drug Administration are not necessarily fully reported to the ICNFDR, and vice versa (due to privacy constraints in both institutions and differing missions). Ideally, all cases should be reported to both organizations.

The goals of the ICNFDR are as follows:
1) Identification and diagnosis of individual cases of NSF (contacts via physicians and patients)
2) Informing the public and physicians about NSF (website, publication, lectures)
3) Researching the pathophysiology of NSF (lab studies, clinical studies, collaboration)
4) Clinical trials of promising therapies

In the next few months, this website will transition into the new ICNFDR website at Yale University. The official web address for the site is currently http://www.icnfdr.org . This new address is valid now, and will remain valid after the move to the Yale server.

The NSF Registry

Since NSF is a rare condition (with over 215 cases identified in the Registry so far) it is difficult to make generalizations about the disease. The Centers for Disease Control and Prevention (CDC) co-investigated cases of NFD/NSF with doctors from the University of California in San Francisco when the disorder was first identified. Since then, the investigative effort has moved to Yale University. Dr. Shawn Cowper is currently in charge of confirming and investigating cases of NSF.

The NSF Registry is a project that collects and organizes information about patients with NSF from all over the world. The goal of the project is to identify factors that may be related to or causative of NSF. In addition, information about treatment successes and failures will be collected in order to try to find effective therapies and design future medication/therapy trials. The summary of information you see on this website is the result of contributions of data to the NSF registry so far. The Registry is funded through several mechanisms (internally, through donations, and through grant monies provided by the General Clinical Research Center at Yale University).

In order to ensure that the data collected in the registry are accurate, it is important to first confirm the diagnosis. Several conditions resemble NSF, and these must be excluded from the data collection effort. If you suspect you or a loved one may have NSF, please have your physician contact Dr. Cowper as noted below.

If you have questions about NSF not answered by this information sheet, please forward them to Dr. Cowper at the e-mail address below. As you could imagine, the effort is quite complex and time consuming. Please be patient, your questions will be answered.


Citing this webpage

The information contained on this web page is copyrighted by Shawn E. Cowper, MD. The author grants permission to authors, educators, and physicians to use the information contained on this website if an appropriate citation is made. The format of the citation should be as follows:

Cowper SE. Nephrogenic Fibrosing Dermopathy [NFD/NSF Website]. 2001-2006. Available at http://www.icnfdr.org. Accessed mm/dd/yyyy.

Questions should be directed to the author at the email address below.

Contact Information

e-mail (preferred): registermc@juno.com
telephone: (203) 785-3524
fax: (203) 785-6869

Address to send microscope slides:

Carol Hribko
Yale Dermatopathology Service
PO Box 208059
15 York Street, LMP 5031
New Haven, CT. 06520-8059

Please do not send slides unless first instructed to do so by Dr. Cowper or Carol Hribko.

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From http://journals.endocrinology.org/joe/fca/JOE00103.htm

Glucocorticoid Feedback Control of Corticotropin (ACTH) in the Hypoxic Neonatal Rat
Hershel Raff¹ and Lauren Jacobson²

¹Endocrine Research Laboratory, Aurora St Luke's Medical Center, Medical College of Wisconsin Milwaukee, WI. 53215

²Center for Neuropharmacology and Neurosciences, Albany Medical College, Albany, New York, 12208

 
(Requests for offprints should be addressed to H Raff)

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Abstract

The objective of this study was to determine the effects of manipulating glucocorticoid negative feedback on acute ACTH and corticosterone responses to corticotrophin-releasing hormone (CRH) injection in 7-day old rats exposed to normoxia or hypoxia from birth. Chemical adrenalectomy was achieved with aminoglutethimide, and glucocorticoids were replaced with a low dose of dexamethasone. Hypoxia per se increased basal plasma corticosterone and attenuated the plasma ACTH response to CRH. Aminoglutethimide per se decreased plasma corticosterone and strongly increased basal plasma ACTH and anterior pituitary POMC gene expression. Dexamethasone partially attenuated elevations in basal plasma ACTH due to aminoglutethimide in both normoxic and hypoxic pups, but inhibited anterior pituitary POMC expression and CRH-induced plasma ACTH only in hypoxic pups. Despite this inhibition, hypoxic pups treated with both dexamethasone and aminoglutethimide still exhibited a significant CRH-induced increment in plasma ACTH that was lacking in hypoxic pups not treated with either dexamethasone or aminoglutethimide. We conclude that ACTH responses to acute stimuli in hypoxic neonatal rats are prevented by ACTH-independent increases in corticosterone rather than by intrinsic hypothalamic-pituitary hypoactivity.

Journal of Endocrinology

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General Health:

Robin posted a link to this PDF file: Hypothyroidism Can Cause Secondary Hyperlipidemia, (High cholesterol)
http://www.jstage.jst.go.jp/article/endocrj/advpub/0/0609250041/_pdf

From my email

NIH ANNOUNCES AWARDS IN CHRONIC FATIGUE SYNDROME RESEARCH

U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH
NIH News
NIH Office of the Director (OD) <http://www.nih.gov/icd/od/>
Office of Research on Women's Health (ORWH)
<http://orwh.od.nih.gov/>

FOR IMMEDIATE RELEASE: Monday, October 30, 2006

CONTACT: Marsha Love, 301-496-9472 <lovem@od.nih.gov>

NIH ANNOUNCES AWARDS IN CHRONIC FATIGUE SYNDROME RESEARCH

The Office of Research on Women's Health (ORWH) and the Trans-NIH Working Group for Research in Chronic Fatigue Syndrome (CFSWG) of the National Institutes of Health (NIH) are pleased to announce seven (7) awards in Chronic Fatigue Syndrome (CFS) research. The proposed studies will help researchers understand how the diverse symptoms in CFS are related to the interactions between the immune and neurological systems -- an important step towards developing effective treatments for a disabling condition.

The awards were funded by ORWH, Office of the Director, and four member institutes: The National Institute on Alcohol Abuse and Alcoholism (NIAAA), the National Institute of Environmental Health Sciences (NIEHS), the National Institute of Arthritis Musculoskeletal and Skin Diseases (NIAMS), and the National Institute of Neurological Disorders and Stroke (NINDS).

Katherine Light, Ph.D., University of Utah, St. Lake City, Utah, plans to first explore in humans the suggested mechanisms for the perception of pain and fatigue in CFS by assessing repeated patterns in the immune and neurological systems that are present before, during and immediately after mental and physical exertion. There is a possibility that findings will lead to the development of a biomarker for CFS. Her second pilot study will focus on identifying family risk patterns in CFS using the Utah Family Data Base (large genealogy data base) to explore the familial/genetic component of CFS. Identifying a genetic predisposition to CFS will assist in the development of more effective medications.

Theoharis Theoharides, M.D.,Ph.D., Tufts University, Boston, Massachusetts, will explore the relationship of human mast cells (molecules released in stress) in the brain, not only in explaining the
development of CFS but also in explaining the effects of antidepressants in relieving symptoms in CFS patients. Dr. Theoharides will examine the cellular changes that explain CFS symptoms using three different classes of antidepressants: tricyclic, serotonin uptake inhibitors and bupropion. Future studies will build on these findings to develop clinical trials of select antidepressants or other molecules that inhibit CFS.

Mary Ann Fletcher, Ph.D., University of Miami, Miami, Florida, plans to study the role of specific peptides: neuropeptide Y (NPY) and dipeptidyl-peptidase (CD26) in the development of CFS. These peptides, formed from amino acids (the basic building blocks of the body that are essential in combating illness), regulate many physiological and disease processes in the cardiorespiratory, immune, nervous and endocrine systems. This study will also examine aspects of the relationship
between different levels of peptides and the severity of CFS symptoms and may lead to the development of biomarkers.

Dianne Lorton, Ph.D. at the Sun Health Research Institute in Sun City, Arizona, will establish a tissue bank to make brain and spinal cord tissue available to study CFS/FM (fibromyalga). She has gathered an interdisciplinary research team that will determine the extent to which chronic pain in these patients is associated with glial (support cells of the nervous system) activation and resulting cytokine production (compounds essential to engage the immune response). While studies in rodents have shown this activation leads to inflammation and chronic pain, Dr. Lorton will test the extent that this process is involved in humans in order to target mechanisms to treat the chronic pain associated with CFS.

James Baraniuk, M.D., Georgetown University, Washington D.C., has found that despite its diverse clinical syndromes, the CFS proteome (the entire group of proteins in an organism or system) is the same, suggesting a strong relationship with malfunctioning of the central nervous system. Dr. Baraniuk developed the first predictive model of CFS based solely on objective data and he now proposes to recruit a new group of CFS and Healthy Control subjects to determine if the proteins
in their cerebrospinal fluid will be a predictive marker of the spectrum of CFS symptoms. There is a high probability that these methods and markers will be of diagnostic value and will be useful for assessing changes over time in disease severity and treatment effects.

Michael Antoni, Ph.D., at the University of Miami, Miami, Florida, has demonstrated the positive effects of participation in group cognitive behavioral stress management (CBSM) on quality of life, perceived stress, fatigue, memory, muscle pain and post-exertional malaise for CFS patients compared to those in a control condition. Many CFS patients are too debilitated to attend regular therapy sessions. Therefore, in the present study, he will test the physiological effects of a
telephone-based cognitive behavioral stress management intervention to illuminate CFS patients' neuroimmune mechanisms in relation to stress and stress management. The correlation of the neuroimmune parameters and the behavioral components promises to identify a biologically useful
marker for CFS.

Italo Biaggioni, M.D. at Vanderbilt University in Nashville, Tennessee, will explicate the role of the sympathetic nervous system (SNS) in the cardiovascular and inflammatory abnormalities in the subset of patients with postural tachycardia (POTS) -- increase in heart rate and often decrease in blood pressure on standing. Preliminary studies indicate a relationship between the mechanisms underlying POTS and CFS symptoms. Dr. Baggioni will test these hypotheses in a comprehensive set of experiments with appropriate controls.

"These innovative, interdisciplinary studies to help us better understand the role of the central nervous system in the origin and development of CFS; represent efforts of the Trans-NIH Working Group for Research on Chronic Fatigue Syndrome, chaired by the ORWH, to expand interest in CFS research. I am excited that these efforts could lead to major advances in understanding the disease processes of CFS and that they may also provide diagnostic biomarkers that can be used to measure
treatment effects. These studies may also help us understand why some of the known treatments are effective and lead to the development of newer and more targeted remedies," stated Dr. Vivian W. Pinn, M.D., Director of the ORWH.

The Office of Research on Women's Health (ORWH), Office of the Director, National Institutes of Health (NIH) serves as a focal point for women's health research at the NIH. For more information about NIH's Office of Research on Women's Health, visit <http://orwh.od.nih.gov/>.

The National Institutes of Health (NIH) - The Nation's Medical Research Agency - is comprised of 27 Institutes and Centers and is a component of the U. S. Department of Health and Human Services. It is the primary Federal agency for conducting and supporting basic, clinical, and translational medical research, and investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit <www.nih.gov>.
 
##

This NIH News Release is available online at: http://www.nih.gov/news/pr/oct2006/od-30.htm.

To subscribe (or unsubscribe) from this list, go to http://list.nih.gov/cgi-bin/wa?SUBED1=nihpress&A=1.

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New Feature! Add your Helpful Hints for Dealing with Cushing's to the website and the email Newsletters.

Newest Bios:
To add or edit your bio, http://cushings-info.com/tinc?key=ryQTnONX&formname=Bio
Adrenal Patients
Dan	Dan was diagnosed with Cushing's about 2 years ago and had pituitary surgery. No tumors were found, so it has now been decided he has Bilateral Adrenal Hypoplasty and needs an adrenalectomy of one or both of the glands.	Pittsburgh, PA
Not Yet Diagnosed Patients
Susan G (casag)	Susan G is not yet diagnosed but started experiencing symptoms in 1997. She is in the long and frustrating process of testing.	Colorado Springs/San Diego
Tammy (waiting)	Tammy is not yet diagnosed but has many symptoms. Her husband saw about Cushing's on TV so the doctors are running more tests.	Indiana
Pituitary Patients
Jessica W (pajessicaj)	It has now been 2 years since Jessica was diagnosed and had transsphenoidal surgery.  She wrote her Masters Thesis for her P.A. degree about the psychological aspects of this disease, and how this is often overlooked. She has now gone back to school to be a Doctor and believes she will specialize in Endocrinology.	Florida
Kaydee	Kaydee was diagnosed with Cushing's Disease 1999. She has had two surgeries and radiotherapy.	near Bristol, UK
Michelle	Michelle had an 8mm pituitary tumor. Michelle updated her bio after her pituitary surgery at University of Alabama in Birmingham January 25, 2006. She describes her post-op experiences.	Panama City, Florida
To add or edit your bio, http://cushings-info.com/tinc?key=ryQTnONX&formname=Bio
Newest Helpful Doctors:
To add your doctor, http://cushings-info.com/tinc?key=ryQTnONX&formname=Doctors

• If you've been diagnosed with Cushing's, please participate in the Cushing's Register

The information you provide will be used to create a register and will be shared with the medical world. It would not be used for other purposes without your expressed permission. Note: This information will not be sold or shared with other companies.

Lynne Clemens, President of CUSH Org is be the person responsible for the creation of this register.  You do not have to be a member of CUSH to fill out this questionnaire, as long as you are a Cushing’s patient. We do not believe that the world has an accurate accounting of Cushing’s patients. The only way to authenticate accuracy is with actual numbers. Your help will be appreciated. Thank you.

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Fundraising:

The Cushing's Store

for all kinds of Cushing's Labeled clothing, US Postage Stamps, coffee mugs, totebags and much more. Great for your endo or Secret Someone. Order Cushing's Awareness Wrist Bands here.

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Remember iGive.com...

... all year round. iGive.com allows online stores to donate a percentage of their profit to running these Cushing's Support sites: the message boards at http://cushings.invisionzone.com/index.php, http://www.cushings-help.com, http://www.cushings-info.com, http://www.cushings-support.com and http://www.cushingsonline.com. See the list of participating merchants ===>  FREE $5 DONATIONS!  <===     Each new member who joins iGive and shops will earn an additional $5 for the Cushing's Support sites! That's on top of the standard donations from shopping (up to 26% of each purchase benefits Cushing's Help and Support!). Only one hitch: supporters must shop within 45 days of joining to get the bonus. With over 600 stores now at iGive.com, we have something for everyone! Thank you so much for your support.

Upcoming Conventions, Meetings and Seminars:

December 7-10, 2006, "December in the Desert 2006" Conference, Rancho Mirage, California.
More info here 

December Dec 13, 2006, Pittsburg, PA, More info on the message boards.
Click for map and directions.

December Dec 13, 2006, UCLA (CA) Bi-monthly Pituitary Patient Support Group, more info and directions here

TBA, Washington, DC metro area, More info on the message boards.

February 9 to 11, 2007, MAGIC Foundation (Growth Hormone) Adult Educational Convention, Las Vegas, NV, More info.

February TBA, San Diego, CA.  More info on the message boards.

February 9 to 11, 2007, MAGIC Foundation (Growth Hormone) Adult Educational Convention, Las Vegas, NV, More info.

June 2-5, 2007, ENDO 2007, Toronto, Canada, Metro Toronto Center. More info as it becomes available.

More upcoming local meetings are listed here

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Online Chats:

Please join us in the Chat Room TONIGHT at 9 PM Eastern. Click to access through the message boards

If you are not yet a member of the message boards, please use this page: http://cushings.invisionzone.com/chatroom.htm

This room is always open, and has convenient links so that you can get needed information while you're chatting.

I hope to see you tonight!