Birthday of the Message Boards

September 30, 2000 - Birth of the Message Boards

September 30, 2000 – Birth of the Message Boards

Today  is the birthday, or anniversary, of the boards starting September 30, 2000 (The rest of the site started earlier that year in July)

As of today, we have 12,043 members who have made 380,324 posts.

Find the message boards here: http://cushings.invisionzone.com/

Interview with Fabiana October 21

Fabiana had transsphenoidal surgery (pituitary) July 30th 2004.  She had a recurrence after seven years of being Cushing’s free.  A second pituitary surgery on 10/26/2011 was unsuccessful.

Another Golden Oldie, this bio was last updated 9/12/2015

interview

Fabiana will be our guest in an interview on BlogTalk Radio  Wednesday, October 21 at 6:00 PM eastern.  The Call-In number for questions or comments is (657) 383-0416.

The archived interview will be available after 7:00 PM Eastern through iTunes Podcasts (Cushie Chats) or BlogTalkRadio.  While you’re waiting, there are currently 88 other past interviews to listen to!

~~~

Well it has taken me a year to write this bio…and just to give some hope to those of you just going thru this process…I have to say that after surgery I have not felt better! I am back to who i always knew I was….the depression and anxiety is gone and I am living life like a 24 year old should!

I guess it all started when i was sixteen (hindsight is 20-20 i guess). My periods stopped i was tired all the time and the depression started. We all kind of just chalked it up to being sixteen. But my mom insisted something was not right. we talked with my gyno…who said nothing was wrong, I had a fungus on my head (my hair was getting really thin) and sometimes girls who had normal periods (in my case three years of normal periods) just go awry.

My mom wasnt hearing that and demanded a script for an endo. I went….he did blood work…and metioned cushings. But nothing came back definitive…so they put me on birthcontol and gave me some hormones and the chushings was never mentioned again because that all seemed to work.

As time went on my depression got worse, the shape of my body started to change-my face and stomach was the most noticeable- and my energy level kept going down. I kept going back to the doctors asking to be tested for mono..or something. I went to a psycologist….but i knew there was no reason for my depression. Two of them told me “i had very good insight” and that I didnt need them. I started getting more anxiety..especially about going out socially.

High school ended and my typical optimistic personality started to decline. I put on a good act to my friends but my family was seeing me break down all the time. I went away for college (all the while gaining weight). My sophmore year I had a break down..I called my family crying that i needed help. I couldnt beat my depression. I didnt drink in college because i knew that would mean instant weight gain, i barely went out…i exercised everyday..hard….i joined weight watchers…i stuck with it. I was at 103 lbs….that crept up to 110…that crept up to 117…each time my weight goal would be “ohh if i could just get back to 108..112…115” with each weight gain my original weight goal would get higher and higher.

Internally i felt like I was constantly under a black cloud..i knew there was no reason why i shoudl feel this way..i was doing great in school, i had a supportive family, an amazing boyfriend and great friends…why was i depressed? I was becoming emotionally draining to the people closest to me…I would go home a lot on the weekends…i was diagnosed with PMDS….like severe PMS..and was given an antidepresant…i hated it it made me feel like a zombie…i stopped taking it and just made it apoint to work on fighting the depression….and the weight gain.

When i was done college i was about 120 lbs. My face was getting rounder and rounder..i was noticing more hair on my face and arms…and a hump between my shoulder blades and the bottom of my neck. My mom saw a tv show about Polycystic ovarian syndrome and felt that maybe that was what was going on with me…i went to my PCP with this and she said it was possible and that i should to talk to my gyno….I am 4’8 and at the time weighing close to 125..i talked to my gyno and she said I was not heavy..that i was just “itailan” ..i told her my periods were getting abnormal again even w/the birthcontrol and that i was so tired all the time and my arms and legs ached. I also told her that i was bruising very easily…and that the weight gain would not stop despite my exercising and following the atikins diet very strickly for over 6 weeks. My boyfriend and I decided to try the diet together..he lost 35 llbs in 6 weeks..i lost NOTHING! I went back to my PCP who ordered an ultra sound of my ovaries…..NOTHING.(i kept thinking i was going crazy and that it was all in my head)….she also decided to do some blood work…and as i was walking out the door she said..”you know what..i am going to give you this 24hr urine test too. Just so that we cover everything”. I just kept thinking please let something come back ….please dont let this be all my fault…please dont let this be all in my head…..please dont let me be crazy. When i got the test results back it turned out that the 24hr urine test was the one test i needed to get on the right track to finding what was wrong. My cortisol level was 3x’s the normal.

I went to an endo…by the time i got to the endocronoligist i was up to 130…i could not work a full day without needing a full day of sleep and my body was aching beyond description. I was crying all the time…in my room…and was becoming more and more of a recluse…i would only hang out with my boyfriend in our houses. I looked my symptoms up on the internet and saw cushings…that was it! I went to the endo and told him..i think it is cushings….he said he had only saw it one other time and that he wanted to do more tests. I got CAT scans, x-rays, MRI’s….my adrenals my pituitary my lungs….he did a CRH stimulation test which was getting blood work done every fifteen minutes for 90minutes….it took weeks to get that test scheduled..no one had ever heard of it and therefore did not know how to do it…..finally after 3 months of tests my dr. felt he had enough evidence to diagnos me with cushings disease (tumor on my pituitary) I was diagnosed in March of 2004. By this time i was about 137 lbs i had to work part time (i am an occupational therapist for children..i do home visits….i could not make it thru a whole day)

In April i had to change to office work…i could not lift the children and i could barely get up off the floor. I have to say i was one of the lucky people who worked for people who were very supportive and accomidating…my boss was very willing to work with me and willing to hold my job for me.

July 30th 2004 i finally had transphenodial surgery to remove my tumor (they went thru my lip and nose because they felt my nose was too small). It is now over 1 year later….i am down to 108 lbs, i have so much energy…no depression….and i dont mind looking at myself in the mirror…i am enjoying my friends and my boyfriend…(who stayed with me thru it all) And my family. I feel healthy mentally, emptionally, and physically. And i just got back into my size 2 jeans!!!

It was a crappy time…(as i am sure you all can atest to) but i learned a lot…..most importantly i was bombarded by good wishes and prayers….friends requested masses for me…a nun in brazil prayed for me…people who i never thought i touched their lives…took the time to wish me well…send an email..or call….I got to experience the wonderful loving nature of human beings and i was lucky to be supported by my family (my mom, dad, and two younger brothers) and my boyfriend throughout this entire tough journey.

This experience taught me to realize the strength i have as well as to appreciate the good and the bad in life. I was on hydrocortizone for about 8 months…i was lucky that my tumor was in its own little sack so my pituitary gland was not touched. In the end in took about 7 years to diagnose me..i think that if the dr. at 16 would have pursued the cushings idea nothing would have been found because it took so long for my symptoms to really peak…needless to say i love my PCP and my endo ..and that i changed gyno’s…

I just want to let anyone out there going thru this disease to know..you are not alone….and to take each day is stride…when you need help ask for it….and that this road can lead to a happy ending. God Bless!

ps- it is ok to feel bad about what you are going thru…it is a tough thing to endure…and when the docotors tell you there is noting wrong…..follow your gut…and you keep searching for the doctor that will listen… If there is anyone in the philadelphis of south jersey area who needs someone to talk to please feel free to email me…fapadula@hotmail.com…i will help you out the best i can!

Update November 6, 2011

Well- here is an update, after seven years of being Cushings free it has returned.

With in those seven years I married my college boyfriend and we now have a son- Nicholas who will be 2 in Decemeber. It has been a blessed and wonderful seven years. However right around when my son was turning 1 I started to notice symptoms again. Increase facial hair, the whole “roundness” of my body, buffalo hump. I decided I was going to work out hard, eat right, and see – I didnt just want to jump to any conclusions. I stuck to it- and nothing…..my hair started thinning again and the acne was coming back and then the missed periods…..so I went to my PCP- told them i needed the 24hr urine and wouldnt you know…..427 cortisol level (on that 0-50 scale)……here we go again.

So back to endo- now at Penn Pituitary Center…..it was another journey b/c the tumor wasnt definative on MRI, and it seems to be cycling…..but I was diagnosed with Cushings again- with the option of 2nd pit surgery or BLA…….after some months of trying to make a decision I went with the 50/50 chance of the second pituitary surgery on 10/26/2011.

It didnt work- my levels never came down in the hospital and I went home w/ out of range cortisol levels and no need for medication……BLURG……Sooooo on to the next step…..after I recover from this surgery I will most likely have the BLA- with the hopes of not having to deal with Cushings ever again. This time around has been a little more difficult just with being a mom and feeling sick- but I still continue to be amazingly blessed with a supportive family and husband and we are surrounded by love and support and for that I am beyond greatful.

I keep all of you in my prayers for relief and health- as I ( we all) know this no easy journey.

Many Blessings!

Fabiana

Update September 12, 2015

So to bring this up to date. My second pituitary surgery in 2011 was unsuccessful. January of 2012 I had both of my adrenal glands removed. Going to adrenal insufficiency was a very difficult transition for me. It took me nearly 2 years before I felt functional. As time went on I felt more human, but I haven’t felt healthy since that day. I can and do function, but at a lower expectation of what I used to be capable of….my “new normal”.

My husband and I decided to try for a second child…my pituitary was damaged from the second surgery and we needed fertility…after 8 months of fertility I got pregnant and we had our second son January of 2015.

In April of 2015 we discovered that my ACTH was increasing exponentially. MRI revealed a macroadenoma invading my cavernous sinus. The tumor is sitting on my carotid artery and milimeterrs away from my optic chasim. I was not a candidate for another surgery due to the tumors proximity to.both of those vital structures.

So September 1st of this year I started daily radiation treatments. I spent my 34th birthday getting my brain zapped. I am receiving proton beam therapy at the Hospital of the University of Pennsylvania. I am so lucky to live so close to an institute that has some of the rarest treatment options.

Again Cushing’s is disrupting our life, my husband goes with me every night to radiation while family takes turns watching the kids….I am now on my 18th year of fighting this disease. I never imagined it would get to this point.

But here we all are making the best of each day, fighting each day and trying to keep things as “normal” as possible. Blessings to all of you fighting this disease…my new go to saying is” ‘effing Cushing’s”! For you newbies…Fight, Advocate for yourselves, and find a doc who doesn’t dismiss you and hang on to them for dear life.

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Cushing’s Disease – Quality of Life, Recurrence and Long-term Morbidity

European Endocrinology, 2015;11(1):34–8 DOI:10.17925/EE.2015.11.01.34

Abstract:

Cushing’s disease (CD) is a rare disorder caused by an adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma. Chronic exposure to hypercortisolism leads to significant morbidities, which may be only partially reversible after remission of the disease, as well as to impairment of the health-related quality of life (HRQoL) and an increase in mortality. Transsphenoidal surgery (TSS) is the treatment of choice, and recurrence rates vary widely, confirming the need for lifelong follow-up. This review summarises the studies performed on HRQoL, recurrence rates and morbidities in patients who have CD.

Keywords: Cushing’s disease, quality of life, recurrence, morbidity
Received: February 18, 2015 Accepted March 16, 2015 CitationEuropean Endocrinology, 2015;11(1):34–8 DOI:10.17925/EE.2015.11.01.34

Correspondence: Isabel Huguet, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Old Rd, Headington, Oxford, OX3 7LJ, UK. E: ihm.huguet@gmail.com

Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any non-commercial use, distribution, adaptation and reproduction provided the original author(s) and source are given appropriate credit.

Cushing’s disease (CD) is a rare condition caused by an adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma. Chronic hypercortisolism is associated with the development of several morbidities that impair health-related quality of life (HRQoL) and contribute to an increased mortality rate.1–5 Obesity and metabolic alterations, hypertension and cardio-/ cerebrovascular complications, neuropsychiatric, muscle/skeletal, hypercoagulability/thromboembolism and immune consequences remain the most challenging.

Despite successful treatment of CD, a number of adverse consequences may persist long after cure or may even be irreversible. Moreover, the remission/cure criteria of CD vary between different studies, making comparison of the results difficult.

This paper aims to review and summarise the studies performed on HRQoL, recurrence rates and morbidities during long-term follow-up in patients who have CD.

Materials and Methods
The available literature was evaluated to address questions on HRQoL, recurrence and morbidities in CD. The literature search was conducted in two stages: (1) identification, review and inclusion of all the most relevant articles published in PubMed having the keywords CD, remission, cure, HRQoL and morbidities and (2) additional hand research conducted on the basis of bibliographies of identified articles, with articles referring to paediatric population and case reports excluded and with papers referring to Cushing’s syndrome (CS) reviewed and included only if presenting data on CD.

Quality of LifeHRQoL was initially assessed in CD patients using such generic measures as the Short Form (SF)-366 and the SF-127and measures of specific symptoms associated with the disease, including the Hospital Anxiety and Depression Scale (HADS).8 More recently, two disease-specific measures, the CushingQoL9 and the Tuebingen CD-2510,11 have been developed. Tables 1 and 2 present studies evaluating QoL using various questionnaires in CD patients having active disease or in remission.

Quality of life is significantly impaired not only in patients with active CD,9 but also in those in long-term remission,12,13regardless of the presence of hormonal deficiencies9 or treatment strategies,14,15 and patients who have CS report more negative illness perceptions than do patients who have other acute or chronic conditions.16

Quality of Life Assessed by Generic Questionnaires
Lindholm et al. reported that patients in remission for more than 5 years after initial surgery scored significantly worse in all subscales of SF-36 except for mental health and bodily pain.17 van Aken et al. evaluated patients cured for a mean period of 13.6 years and showed that general perceived well-being was reduced compared with healthy controls for all subscales in SF-36 and the Nottingham Health Profile (NHP). Moreover, such patients scored worse in all subscales of fatigue (Multidimensional Fatigue Inventory [MFI]-20), anxiety and depression (HADS).18 In comparison with subjects having other pituitary adenomas, patients who had CD were the most severely affected in all parameters of the SF-36 questionnaire.8 Sonino et al. studied patients who had CS in remission (the majority of them had CD) for 1 to 3 years and found significantly higher scores in anxiety, depression, anger, hostility and psychotic symptoms in the Symptom Rating Test (SRT) questionnaire in comparison with healthy controls.19 When the Beck Depression Inventory (BDI), SF-36 and the multidimensional body-self relations questionnaire (MBSRQ) were used, patients who had CD demonstrated lower QoL, lower body image perception and higher levels of depression compared with healthy controls, particularly in cases of persistent disease.15

Quality of Life Assessed with Disease-specific Questionnaires
Since 2008, two disease-specific questionnaires have been developed: CushingQoL and Tuebingen CD-25. The CushingQoL questionnaire was evaluated by Webb et al. in a multicentre European study. Active CD was associated with worse scores, but the presence of hypopituitarism or prior pituitary radiotherapy did not determine differences in the scores.9 Similarly, Santos et al. found that active CD patients scored worse on the CushingQoL questionnaire than did cured subjects.20 Wagenmakers et al. found that CD patients in remission without hormonal deficiencies scored significantly better than those having hormone deficiencies but significantly worse thanthe control group on 50 % of the items of the questionnaires.14 The Tuebingen CD-25 also demonstrated significant differences in all subscales and the total score between active CD patients and healthy controls.10,11

The post-operative improvement in HRQoL could be predicted by the presence of pre-operative HRQoL impairment, andyounger patients were more likely to improve. Patients without post-operative pituitary deficiencies improved significantly in the cognition scale.21,22

QoL does not change after short-term biochemical remission induced by medical therapy but may improve after sustained control of the hypercortisolism.23,24

To summarise, most of the results on HRQoL in CD derive from generic questionnaires raising concerns about how appropriate these are for the reliable and accurate assessment of the HRQoL of patients with this rare condition. Interestingly, despite the use of the same type of questionnaire in some studies, the subscales mainly affected show variation among them, suggesting that either CD affects several dimensions in QoL in a heterogeneous way in different patient groups, or these questionnaires are not specific enough. The newly developed questionnaires focus on important disease-specific aspects of the QoL, and their sensitivity in detecting changes renders them a very promising and useful tool in clinical practice.

Recurrence
Transsphenoidal surgery is the treatment of choice in CD, with immediate post-operative remission rates ranging from 59 % to 94 % and recurrence rates from 3 % to 46 %, both depending upon the definition criteria, the duration of follow-up, the number of patients studied and the inclusion of macroadenomas (see Table 3).2,25–29A small number of studies have used undetectable or very low post-operative serum cortisol levels as a strict criterion of remission, but most have defined effective remission as the resolution of clinical features and the reversal of hypercortisolism (in serum or urine), along with the recovery of cortisol suppressibility on dexamethasone administration or a normal cortisol circadian rhythm. Predictors of remission in CD include age at diagnosis, presence of hypertension or diabetes,4,5 response to desmopressin testing,30 identification of tumour at surgery and an adenoma histology positive for ACTH.31–33

Out of concern about recurrence of CD after initial remission, several parameters have been evaluated and are still matter of debate. Factors that have been associated with a low (but not zero) risk of CD recurrence include undetectable or low early morning serum levels of cortisol,33 low plasma levels of ACTH and prolonged requirement for glucocorticoid replacement after pituitary surgery. The effects of serum cortisol levels in the early post-operative period on predicting relapse have been assessed in various studies. No recurrences were found by Trainer et al.34during a median follow-up of 40 months in patients with a postoperative serum cortisol of <50 nmol/l; similar results were reported after a median follow-up of 58 months by McCance et al.35 In contrast to these findings, several series have reported recurrence rates of 11.5 % and 15 % despite a serum cortisol <50 nmol/l post surgery.27,28 Another possible parameter is the length of adrenal insufficiency post-TSS. Thus it has been suggested that patients who have a shorter duration of adrenal insufficiency have a significantly higher risk of relapse.36

Accordingly, after successful treatment of CD, there is no accurate criterion that can ensure lifelong cure, and although the evidence shows a more optimal outcome in patients who achieve severe cortisol deficiency after TSS, lifelong follow-up is mandatory.

Morbidities
CD is associated with significant comorbidities – metabolic and vascular complications, osteoporosis, neuropsychiatric dysfunction and immunosuppression – that increase mortality and affect daily life. A number of these may persist long after cure or may even be permanent.37

Metabolic and Vascular Complications
It is well recognised that CD increases cardiovascular risk, with hypertension and obesity the most common associated risk factors. The cardiovascular complications are part of the metabolic syndrome, but hypertension related to endogenous hypercortisolism is not simply a component of the CS-related metabolic syndrome. The renin–angiotensin system, mineralocorticoid activity, the sympathetic nervous system and the vasoregulatory systems have been reported to be involved in the pathophysiology of hypertension, but the mechanisms are only partially understood.38

The adverse cardiovascular risk profile of patients who have CD39is attributed to metabolic and vascular aberrations, as well as to changes in cardiac structure and function. Patients who have CD have increased leptin,40,41 resistin42 and pro-inflammatory agents, such as tumour necrosis factor-α and interleukin-6, C-reactive protein and low ghrelin levels.40 Moreover, they are characterised by a prothrombotic phenotype attributed to various abnormalities of coagulation and fibrinolysis: these include shortened activated partial thromboplastin time,43 increased factor VIII, von Willebrand factor, fibrinogen and plasminogen activator inhibitor-1,43 decreased fibrinolytic capacity44 and increased α2-antiplasmin.45 Endothelium-dependent flow-mediated vasodilatation is impaired, and several humoral markers of endothelial dysfunction (such as endothelin, homocysteine, vascular endothelial growth factor, osteoprotegerin and cell adhesion molecules) are elevated. Cardiac echocardiograms demonstrate left ventricular hypertrophy, concentric remodelling and diastolic and systolic dysfunction.

Persistent clinical abnormalities have been documented in terms of cardiovascular complications, showing that remission of hypercortisolaemia reduces, but does not completely eliminate them. Colao et al. reported that 27 % of patients having CD in remission for 5 years had persistently atherosclerotic plaques, compared with only 3 % of gender-, age- and body mass index–matched controls.45 Faggiano et al. also found persistence of the metabolic syndrome, vascular damage and atherosclerotic plaques after disease remission.46

Thus it is likely that disease remission does not entirely reverse cardiovascular morbidities affecting long-term survival and that lifelong follow-up is needed, with particular emphasis on cardiovascular risk factors.

Bone
Bone loss is attributed to decreased osteoblastic activity, increased osteoclastic bone resorption and impaired enteral calcium absorption. In the ERCUSYN study, osteopenia at the spine and hip was reported in 40 % and 46 % of patients who had CD, respectively, and osteoporosis at the spine and hip in 22 % and 12 %, respectively.47,48 Bone mineral density (BMD) does not completely recover following remission,49,50 though normalisation in some skeletal sites has been reported in the long-term.51

Glucocorticoid-induced vertebral fractures may develop even in the presence of normal or slightly low BMD. The risk of fractures at comparable BMD values with controls suggests that components of bone strength, not assessed by routine densitometric approaches, are also affected by glucocorticoids (including bone architecture, geometry and remodelling). Methods of assessment other than measurement of BMD are required, because despite the improvement of BMD after correction of hypercortisolism, the quality of the bone likely remains compromised.

Immune System
Hypercortisolism induces reversible immunosuppression. During hypercortisolaemia, autoimmune disorders improve but may worsen during remission and new ones develop.52 There is a high risk of superficial fungal, opportunistic or bacterial infections.

Neuropsychiatric Manifestations
Glucocorticoids are known to influence many functions of the central nervous system. Hypercortisolaemia is associated with depression, disrupted sleep and a wide range of cognitive impairments (derangement of memory – especially short-term – irritability and decreased concentration). High anxiety levels and low externalising behaviour are common emotional disorders.53Smaller hippocampal volumes and generalised brain atrophy have been described.54 Functional magnetic resonance imaging studies in patients having CD have demonstrated emotion-processing difficulties and hyperactivity in the frontal and subcortical regions, similar to major depressive disorders. After remission, hippocampal volumes increase and emotional and cognitive functions improve,53–55 but profound structural alterations in the brain remain such as smaller volumes in the anterior cingulate cortex, a structure involved in cognitive–affective processes and behavioural adaptation.56

The new data on persistent changes in the central nervous system after cure of CD support the hypothesis that psychiatric symptoms and cognitive impairment could be related to structural changes, providing the basis for future research on the neurobiological background of psychological dysfunction in this complex condition.

Conclusions
CD is associated with significant adverse sequelae affecting longterm morbidity, mortality and quality of life. To some extent, the duration and severity of hypercortisolism determine the possibility of reversion of the morbidities, but a number of manifestations may persist long after cure – possibly permanently. Generic questionnaires and disease-specific measures have evaluated many aspects of the quality of life impaired, not only during the active state, but also when in remission.

Despite initial successful treatment, there is a risk of relapse, and post-operative hypocortisolism is the most significant predictor of remission. These long-term and persistent changes are challenging to our understanding of hypercortisolaemia but in a clinical context suggest that long-term follow-up is essential in all patients having CD, even those apparently cured.

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From http://www.touchendocrinology.com/articles/cushing-s-disease-quality-life-recurrence-and-long-term-morbidity/page/1/0

The New Molecular Landscape of Cushing’s Disease

Silviu Sbiera#Timo Deutschbein#Isabel Weigand, Martin Reincke, Martin FassnachtcorrespondenceBruno Allolio
#These authors contributed equally to this work.
A few days after acceptance of this manuscript, Bruno Allolio passed away.

Cushing’s disease (CD) is caused by corticotropin-secreting pituitary adenomas and results in substantial morbidity and mortality. Its molecular basis has remained poorly understood until the past few years, when several proteins and genes [such as testicular orphan nuclear receptor 4 (TR4) and heat shock protein 90 (HSP90)] were found to play key roles in the disease. Most recently, mutations in the gene of ubiquitin-specific peptidase 8 (USP8) increasing its deubiquination activity were discovered in a high percentage of corticotroph adenomas. Here, we will discuss emerging insights in the molecular alterations that finally result in CD. The therapeutic potential of these findings needs to be carefully evaluated in the near future, hopefully resulting in new treatment options for this devastating disorder.

Trends

Transsphenoidal surgery and radiotherapy are the treatment of choice in CD. However, despite high initial remission rates, a significant percentage of patients relapse.

Owing to the poor understanding of the pathophysiology of CD, drug therapy is still limited and often only ameliorates the clinical manifestations through blocking of ACTH release or adrenal cortisol synthesis.

Recent research has identified several important proteins (e.g., EGFR, HSP90, TR4, and AVPR1b) whose deregulation is associated with CD and may therefore represent potential therapeutic targets.

Frequent, novel mutations in the USP8 gene that are associated with corticotroph pituitary adenomas were recently discovered that result in reduced EGFR degradation and increased POMC activation in vitro.

Keywords:

Cushing’s disease, pituitary, gene expression, epidermal growth factor receptor, ubiquitin-specific peptidase 8, 14-3-3 proteins

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RARE Patient Advocacy Summit

 

I’m on my way to California today.  I was nominated for an award in the 2015 Tribute to Champions of Hope so I’ll be flying to Huntington Beach  for the 2-day  Fourth Annual RARE Patient Advocacy Summit. Follow along with LiveStream.

Saturday night will be the Gala.

Find my name on the list of nominees here: https://globalgenes.org/championsofhope/

One of the very best parts of this trip, though, is that I’m staying with a good friend from the Cushing’s Community.

WOOHOO

 

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