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MaryO

~Chief Cushie~
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Everything posted by MaryO

  1. Thank you so much for sharing your dad's story, Andy. What a sad, difficult one it is. I know when Dr. Cushing was originally testing people for Cushing's disease, he found some of his early patients in the circus (bearded woman, etc) and other patients have been in mental wards before their diagnosis. This disease, especially untreated, can really cause havoc in all aspects of a person's life. I hope you and your family have been able to find some peace since the original article.
  2. Dexamethasone, a cheap and widely used steroid, has become the first drug shown to be able to save lives among Covid-19 patients in what scientists hailed as a “major breakthrough”. Results of trials announced on Tuesday showed dexamethasone, which is used to reduce inflammation in other diseases, reduced death rates by around a third among the most severely ill Covid-19 patients admitted to hospital. The results suggest the drug should immediately become standard care in patients with severe cases of the pandemic disease, said the researchers who led the trials. “This is a result that shows that if patients who have Covid-19 and are on ventilators or are on oxygen are given dexamethasone, it will save lives, and it will do so at a remarkably low cost,” said Martin Landray, an Oxford University professor co-leading the trial, known as the RECOVERY trial. “It’s going to be very hard for any drug really to replace this, given that for less than 50 pounds ($63.26), you can treat eight patients and save a life,” he told reporters in an online briefing. His co-lead investigator, Peter Horby, said dexamethasone was “the only drug that’s so far shown to reduce mortality - and it reduces it significantly.” “It is a major breakthrough,” he said. “Dexamethasone is inexpensive, on the shelf, and can be used immediately to save lives worldwide.” There are currently no approved treatments or vaccines for Covid-19, the disease caused by the new coronavirus which has killed more than 431,000 globally. Saving ‘countless lives’ The RECOVERY trial compared outcomes of around 2,100 patients who were randomly assigned to get the steroid, with those of around 4,300 patients who did not get it. The results suggest that one death would be prevented by treatment with dexamethasone among every eight ventilated Covid-19 patients, Landray said, and one death would be prevented among every 25 Covid-19 patients that received the drug and are on oxygen. Among patients with Covid-19 who did not require respiratory support, there was no benefit from treatment with dexamethasone. “The survival benefit is clear and large in those patients who are sick enough to require oxygen treatment, so dexamethasone should now become standard of care in these patients,” Horby said. Nick Cammack, a expert on Covid-19 at the Wellcome Trust global health charity, said the findings would “transform the impact of the Covid-19 pandemic on lives and economies across the world”. “Countless lives will be saved globally,” he said in a statement responding to the results. The RECOVERY trial was launched in April as a randomised clinical trial to test a range of potential treatments for Covid-19, including low-dose dexamethasone and the malaria drug hydoxycholoroquine. The hydroxychloroquine arm was halted earlier this month after Horby and Landray said results showed it was “useless” at treating Covid-19 patients. Global cases of infection with the novel coronavirus have reached over 8 million, according to a Reuters tally, and more than 434,000 people have died after contracting the virus, the first case if which was reported in China in early January. From https://www.cnbc.com/2020/06/16/steroid-dexamethasone-reduces-deaths-from-severe-covid-19-trial.html
  3. Presented by Georgios A. Zenonos, MD Assistant Professor of Neurological Surgery Associate Director, Center for Skull Base Surgery University of Pittsburgh Medical Center 200 Lothrop Street, Pittsburgh PA, 15217 Presbyterian Hospital, Suite B400 Register Now! After registering you will receive a confirmation email containing information about joining the Webinar. Date: Wednesday July 1, 2020 Time: 3:00 PM Pacific Daylight Time, 6:00 PM Eastern Daylight Time
  4. Presented by Georgios A. Zenonos, MD Assistant Professor of Neurological Surgery Associate Director, Center for Skull Base Surgery University of Pittsburgh Medical Center 200 Lothrop Street, Pittsburgh PA, 15217 Presbyterian Hospital, Suite B400 Register Now! After registering you will receive a confirmation email containing information about joining the Webinar. Date: Wednesday July 1, 2020 Time: 3:00 PM Pacific Daylight Time, 6:00 PM Eastern Daylight Time
  5. https://doi.org/10.1016/S2213-8587(20)30215-1 Over the past few months, COVID-19, the pandemic disease caused by severe acute respiratory syndrome coronavirus 2, has been associated with a high rate of infection and lethality, especially in patients with comorbidities such as obesity, hypertension, diabetes, and immunodeficiency syndromes.1 These cardiometabolic and immune impairments are common comorbidities of Cushing's syndrome, a condition characterised by excessive exposure to endogenous glucocorticoids. In patients with Cushing's syndrome, the increased cardiovascular risk factors, amplified by the increased thromboembolic risk, and the increased susceptibility to severe infections, are the two leading causes of death.2 In healthy individuals in the early phase of infection, at the physiological level, glucocorticoids exert immunoenhancing effects, priming danger sensor and cytokine receptor expression, thereby sensitising the immune system to external agents.3 However, over time and with sustained high concentrations, the principal effects of glucocorticoids are to produce profound immunosuppression, with depression of innate and adaptive immune responses. Therefore, chronic excessive glucocorticoids might hamper the initial response to external agents and the consequent activation of adaptive responses. Subsequently, a decrease in the number of B-lymphocytes and T-lymphocytes, as well as a reduction in T-helper cell activation might favour opportunistic and intracellular infection. As a result, an increased risk of infection is seen, with an estimated prevalence of 21–51% in patients with Cushing's syndrome.4 Therefore, despite the absence of data on the effects of COVID-19 in patients with Cushing's syndrome, one can make observations related to the compromised immune state in patients with Cushing's syndrome and provide expert advice for patients with a current or past history of Cushing's syndrome. Fever is one of the hallmarks of severe infections and is present in up to around 90% of patients with COVID-19, in addition to cough and dyspnoea.1 However, in active Cushing's syndrome, the low-grade chronic inflammation and the poor immune response might limit febrile response in the early phase of infection.2 Conversely, different symptoms might be enhanced in patients with Cushing's syndrome; for instance, dyspnoea might occur because of a combination of cardiac insufficiency or weakness of respiratory muscles.2 Therefore, during active Cushing's syndrome, physicians should seek different signs and symptoms when suspecting COVID-19, such as cough, together with dysgeusia, anosmia, and diarrhoea, and should be suspicious of any change in health status of their patients with Cushing's syndrome, rather than relying on fever and dyspnoea as typical features. The clinical course of COVID-19 might also be difficult to predict in patients with active Cushing's syndrome. Generally, patients with COVID-19 and a history of obesity, hypertension, or diabetes have a more severe course, leading to increased morbidity and mortality.1 Because these conditions are observed in most patients with active Cushing's syndrome,2 these patients might be at an increased risk of severe course, with progression to acute respiratory distress syndrome (ARDS), when developing COVID-19. However, a key element in the development of ARDS during COVID-19 is the exaggerated cellular response induced by the cytokine increase, leading to massive alveolar–capillary wall damage and a decline in gas exchange.5 Because patients with Cushing's syndrome might not mount a normal cytokine response,4 these patients might parodoxically be less prone to develop severe ARDS with COVID-19. Moreover, Cushing's syndrome and severe COVID-19 are associated with hypercoagulability, such that patients with active Cushing's syndrome might present an increased risk of thromboembolism with COVID-19. Consequently, because low molecular weight heparin seems to be associated with lower mortality and disease severity in patients with COVID-19,6 and because anticoagulation is also recommended in specific conditions in patients with active Cushing's syndrome,7 this treatment is strongly advised in hospitalised patients with Cushing's syndrome who have COVID-19. Furthermore, patients with active Cushing's syndrome are at increased risk of prolonged duration of viral infections, as well as opportunistic infections, particularly atypical bacterial and invasive fungal infections, leading to sepsis and an increased mortality risk,2 and COVID-19 patients are also at increased risk of secondary bacterial or fungal infections during hospitalisation.1 Therefore, in cases of COVID-19 during active Cushing's syndrome, prolonged antiviral treatment and empirical prophylaxis with broad-spectrum antibiotics1, 4 should be considered, especially for hospitalised patients (panel). Panel Risk factors and clinical suggestions for patients with Cushing's syndrome who have COVID-19 Reduction of febrile response and enhancement of dyspnoea Rely on different symptoms and signs suggestive of COVID-19, such as cough, dysgeusia, anosmia, and diarrhoea. Prolonged duration of viral infections and susceptibility to superimposed bacterial and fungal infections Consider prolonged antiviral and broad-spectrum antibiotic treatment. Impairment of glucose metabolism (negative prognostic factor) Optimise glycaemic control and select cortisol-lowering drugs that improve glucose metabolism. Hypertension (negative prognostic factor) Optimise blood pressure control and select cortisol-lowering drugs that improve blood pressure. Thrombosis diathesis (negative prognostic factor) Start antithrombotic prophylaxis, preferably with low-molecular-weight heparin treatment. Surgery represents the first-line treatment for all causes of Cushing's syndrome,8, 9 but during the pandemic a delay might be appropriate to reduce the hospital-associated risk of COVID-19, any post-surgical immunodepression, and thromboembolic risks.10 Because immunosuppression and thromboembolic diathesis are common Cushing's syndrome features,2, 4 during the COVID-19 pandemic, cortisol-lowering medical therapy, including the oral drugs ketoconazole, metyrapone, and the novel osilodrostat, which are usually effective within hours or days, or the parenteral drug etomidate when immediate cortisol control is required, should be temporarily used.9 Nevertheless, an expeditious definitive diagnosis and proper surgical resolution of hypercortisolism should be ensured in patients with malignant forms of Cushing's syndrome, not only to avoid disease progression risk but also for rapidly ameliorating hypercoagulability and immunospuppression;9 however, if diagnostic procedures cannot be easily secured or surgery cannot be done for limitations of hospital resources due to the pandemic, medical therapy should be preferred. Concomitantly, the optimisation of medical treatment for pre-existing comorbidities as well as the choice of cortisol-lowering drugs with potentially positive effects on obesity, hypertension, or diabates are crucial to improve the eventual clinical course of COVID-19. Once patients with Cushing's syndrome are in remission, the risk of infection is substantially decreased, but the comorbidities related to excess glucocorticoids might persist, including obesity, hypertension, and diabetes, together with thromboembolic diathesis.2 Because these are features associated with an increased death risk in patients with COVID-19,1 patients with Cushing's syndrome in remission should be considered a high-risk population and consequently adopt adequate self-protection strategies to minimise contagion risk. In conclusion, COVID-19 might have specific clinical presentation, clinical course, and clinical complications in patients who also have Cushing's syndrome during the active hypercortisolaemic phase, and therefore careful monitoring and specific consideration should be given to this special, susceptible population. Moreover, the use of medical therapy as a bridge treatment while waiting for the pandemic to abate should be considered. RP reports grants and personal fees from Novartis, Strongbridge, HRA Pharma, Ipsen, Shire, and Pfizer; grants from Corcept Therapeutics and IBSA Farmaceutici; and personal fees from Ferring and Italfarmaco. AMI reports non-financial support from Takeda and Ipsen; grants and non-financial support from Shire, Pfizer, and Corcept Therapeutics. BMKB reports grants from Novartis, Strongbridge, and Millendo; and personal fees from Novartis and Strongbridge. AC reports grants and personal fees from Novartis, Ipsen, Shire, and Pfizer; personal fees from Italfarmaco; and grants from Lilly, Merck, and Novo Nordisk. All other authors declare no competing interests. References 1 P Kakodkar, N Kaka, MN Baig A comprehensive literature review on the clinical presentation, and management of the pandemic coronavirus disease 2019 (COVID-19) Cureus, 12 (2020), Article e7560 View Record in ScopusGoogle Scholar 2 R Pivonello, AM Isidori, MC De Martino, J Newell-Price, BMK Biller, A Colao Complications of Cushing's syndrome: state of the art Lancet Diabetes Endocrinol, 4 (2016), pp. 611-629 ArticleDownload PDFView Record in ScopusGoogle Scholar 3 DW Cain, JA Cidlowski Immune regulation by glucocorticoids Nat Rev Immunol, 17 (2017), pp. 233-247 CrossRefView Record in ScopusGoogle Scholar 4 V Hasenmajer, E Sbardella, F Sciarra, M Minnetti, AM Isidori, MA Venneri The immune system in Cushing's syndrome Trends Endocrinol Metab (2020) published online May 6, 2020. DOI:10.1016/j.tem.2020.04.004 Google Scholar 5 Q Ye, B Wang, J Mao The pathogenesis and treatment of the ‘Cytokine Storm’ in COVID-19 J Infect, 80 (2020), pp. 607-613 ArticleDownload PDFView Record in ScopusGoogle Scholar 6 N Tang, H Bai, X Chen, J Gong, D Li, Z Sun Anticoagulant treatment is associated with decreased mortality in severe coronavirus disease 2019 patients with coagulopathy J Thromb Haemost, 18 (2020), pp. 1094-1099 CrossRefView Record in ScopusGoogle Scholar 7 AM Isidori, M Minnetti, E Sbardella, C Graziadio, AB Grossman Mechanisms in endocrinology: the spectrum of haemostatic abnormalities in glucocorticoid excess and defect Eur J Endocrinol, 173 (2015), pp. R101-R113 View Record in ScopusGoogle Scholar 8 LK Nieman, BM Biller, JW Findling, et al.Treatment of Cushing's syndrome: an endocrine society clinical practice guideline J Clin Endocrinol Metab, 100 (2015), pp. 2807-2831 CrossRefView Record in ScopusGoogle Scholar 9 R Pivonello, M De Leo, A Cozzolino, A Colao The treatment of Cushing's disease Endocr Rev, 36 (2015), pp. 385-486 CrossRefView Record in ScopusGoogle Scholar 10 J Newell-Price, L Nieman, M Reincke, A Tabarin Endocrinology in the time of COVID-19: management of Cushing's syndrome Eur J Endocrinol (2020) published online April 1. DOI:10.1530/EJE-20-0352 Google Scholar View Abstract From https://www.thelancet.com/journals/landia/article/PIIS2213-8587(20)30215-1/fulltext
  6. MaryO

    Anxious

    Welcome, Ellie. I can't image how hard it would be to get a diagnosis (or not!) during these COVID times. Unfortunately, results from blood tests aren't going to be the answer - just a part of an answer. You need to get UFCs (urine free cortisol) Do you need to get a referral to an endo? They are the best to diagnose Cushing's - if you get one who is familar with testing. That's the important part. Not all endos "believe in Cushing's" which is incredible to me. Unfortunately, there's no real way of speeding a Cushing's diagnosis along. And, I don't think you'd want to (although I did when I was in the diagnosis phase!) You want to be absolutely sure that this is what you have AND the source - pituitary, adrenal, ectopic, steroid-induced... Best of luck to you and please keep us posted.
  7. J Clin Endocrinol Metab . 2003 Apr;88(4):1554-8. doi: 10.1210/jc.2002-021518. Francesca Pecori Giraldi 1, Mirella Moro, Francesco Cavagnini, Study Group on the Hypothalamo-Pituitary-Adrenal Axis of the Italian Society of Endocrinology Affiliations PMID: 12679438 DOI: 10.1210/jc.2002-021518 Abstract Cushing's disease (CD) presents a marked female preponderance, but whether this skewed gender distribution has any relevance to the presentation and outcome of CD is not known. The aim of the present study was the comparison of clinical features, biochemical indices of hypercortisolism, and surgical outcome among male and female patients with CD. The study population comprised 280 patients with CD (233 females, 47 males) collected by the Italian multicentre study. Epidemiological data, frequency of clinical signs and symptoms, urinary free cortisol (UFC), plasma ACTH and cortisol levels, responses to dynamic testing, and surgical outcome were compared in female and male patients. Male patients with CD presented at a younger age, compared with females (30.5 +/- 1.93 vs. 37.1 +/- 0.86 yr, P < 0.01), with higher UFC and ACTH levels (434.1 +/- 51.96 vs. 342.1 +/- 21.01% upper limit of the normal range for UFC, P < 0.05; 163.9 +/- 22.92 vs. 117.7 +/- 9.59% upper limit of the normal range for ACTH, P < 0.05). No difference in ACTH and cortisol responses to CRH, gradient at inferior petrosal sinus sampling, and cortisol inhibition after low-dose dexamethasone was recorded between sexes. In contrast, the sensitivity of the high-dose dexamethasone test was significantly lower in male than in female patients. Of particular interest, symptoms indicative of hypercatabolic state were more frequent in male patients; indeed, males presented a higher prevalence of osteoporosis, muscle wasting, striae, and nephrolitiasis. Conversely, no symptom was more frequent in female patients with CD. Patients with myopathy, hypokalemia, and purple striae presented significantly higher UFC levels, compared with patients without these symptoms. Lastly, in male patients, pituitary imaging was more frequently negative and immediate and late surgical outcome less favorable. In conclusion, CD appeared at a younger age and with a more severe clinical presentation in males, compared with females, together with more pronounced elevation of cortisol and ACTH levels. Furthermore, high-dose dexamethasone suppression test and pituitary imaging were less reliable in detecting the adenoma in male patients, further burdening the differential diagnosis with ectopic ACTH secretion. Lastly, the postsurgical course of the disease carried a worse prognosis in males. Altogether, these findings depict a different pattern for CD in males and females. From https://pubmed.ncbi.nlm.nih.gov/12679438/
  8. Sherry passed away this afternoon, naturally and peacefully in her sleep. She loved her community and we know how grateful she was to every one of her friends on here for the genuine love and support she’s received over the years. We (her family) are processing, but will share details about her celebration of life when we’ve worked it out. Sherry's bio: I have been very ill for many years now, since 1999 that I know of. But it had always come and gone, until 2004 when it decided to stay. At first it was a mystery as to what was wrong. I was seeing a psychiatrist that felt very strong that what I was dealing with was endocrine related. He mentioned a few things that it could be and one was Cushing’s, so I looked it up on the internet and sure enough I had many of the symptoms of Cushing’s disease, moon face, buffalo hump, weight gain, big round belly, red face, very ruddy complexion, acne, nausea, depression, fatigue, hirsutism, depression, anxiety, hypertension, unusual bruising, and highs and lows of energy. I found this support group on the internet at Cushings-help.com and they helped me find Dr.William Ludlam at OHSU. He told me I had a suddle case of Cushing’s and had a pituitary tumor on the right side displacing the pituitary to the left. Although Dr.Ludlam originally saw tumors on both sides, I had a pituitary tumor that seemed to be cyclic. When it turned on I had major Cortisol energy, when it turned off I got very achy, nausea, and very tired. In March of 2006 I was officially diagnosed after 1 long year of testing, and went on to have my first unsuccessful Transphenoidal pituitary surgery 3/23/2006 with Dr. Johnny Delashaw at OHSU. I had a second unsuccessful pituitary surgery 10/12/06 and finally a BLA 11/7/06. I am now cured of Cushing’s disease 2 1/2 years out from my BLA and I am still very sick, I traded Cushing’s disease for Addison’s disease, and my body does not like it. Cushing’s did a lot more damage than ever thought; I have permanent nerve damage to my lower back, damage to soft tissues throughout my body, Diabetes, High lipids, Fatty liver, I have no usable veins, I have permanent port-a-cath in now so they can access my veins for blood draws and any IV stuff I may need in emergency’s. I had my period for 1 year straight so I had a full hysterectomy 8/20/08. I am permanently panhypopituitary now, no working hormones any more. I am on all replacement hormones, except DDAVP. I ended up with a new doctor that gave me a severe case of steroid induced Cushing’s. I am still dealing with this aftermath; the details are in my timeline. My timeline will update you as to where I am at now. I will try to keep the timeline updated so you know where I am at as far as getting better. Please don’t let this scare you, most people are cured and go on to live lives as best they can, and a lot of people are doing very well. Towards the end of my Cushing’s I went full blown, Dr.Ludlam told me this was a progressive disease and in me this was the case. So if you believe you have Cushing’s, get to a specialist that knows Cushing’s disease, don’t waste time on doctors that do not know the disease, it is so worth it in the end to get to the right doctor. This disease is one of the hardest endocrine diseases to diagnose. Cushings_help.com/ founder MaryO has been a lifesaver for me and still is, I have met people from all over the country, over the years I have made many friends that have, had or are still in the diagnostic phase. I live in a small town of around 10,000 people and I hear all the time, oh I know so and so that had or has a pituitary tumor. What I am finding out is there are a lot of people in this town that have this disease, it is suppose to be rare, one in a million, my next goal is to get my story out and have local people contact me, then start a support group. Maybe get some accurate numbers of actual pituitary/brain tumors and find out why this is happening in this small town. It will be a big adventure but if it saved even one life it will be worth it. I know of 3 definite pituitary Cushing’s cases so far. My Timeline of illness to diagnosis 3rd pregnancy 1994 pre-term labor again, stopped, gestational diabetes, son born 3 weeks early and I got toxemia after my son was born, was told this is very rare. I should have known RARE would be a word I would hear a lot in my future. 1995-Left breast discharge, surgical biopsy done, lump removal of marble size, this should have signaled a full hormonal work-up, but didn’t. No cancer. 1997-1999 Depression and severe anxiety with panic attacks…Diagnosis of Fibromyalgia. Weight 130# 1999- First occurrence of unknown mystery illness. Hypertension, fatigue, flushing, swelling of face, hives, and much more that lasted several months. Sick on and off with mystery illness. Tumor was turning on and off. April 1999-2004-Severe nausea and vomiting, extreme fatigue, weight gain of 50# in about 1 years time, headaches, dizziness, hypertension, tachycardia, muscle and bone pain, malor rash, other rashes, IBS, occasional unexplained low grade fevers, anxiety and depression much worse, increased hirsutism, almost constant mouth sores, memory loss, cognitive difficulties, loss of coordination, syncope, excessive energy spurts, insomnia. **Off work for 3 months April-June due to symptoms…Saw PCP, Gastroenterologist, Rheumatologist and Cardiologist… diagnosis Peptic ulcer/Chronis Gastritis and Chronic pain Syndrome and Tachycardia/Hypertension. Abdominal/Pelvic Cat scan done and fatty liver noted. High Cholesterol and Triglycerides discovered. Nov-2004 My Psychiatrist was the first to mention Cushing’s or a Pheochromocytoma; he felt all my symptoms where due to endocrinology. He did not want to see me again until I was seen at OHSU. I have never seen him again due to insurance change. I really need to thank him. Dec-2004 10# weight gain in 1 week with severe abdominal distention….another Cat scan done, lymph nodes around vena cava where enlarged. Jan-2005 Went to OHSU for diagnosis….First saw an endocrinologist that was not experienced with Cushing’s, she ordered 1 UFC and 2 midnight saliva tests, and told me to test when I felt my worst; Tests where low so she felt my symptoms where not due to my endocrine system. Boy was she wrong. I needed to test when I felt good, or high. Feb-2005 Went to the Pituitary Unit at OHSU and saw Dr.Ludlam, he believed that I had Cushing’s but we needed to prove it. MRI saw adenoma on right side displacing pituitary to the left. He originally thought he saw tumors on both sides, he was right. Lot’s of testing done. Testing did not prove it yet. Dr believes I am Cyclic. It took 1 year for diagnoses from Dr.Ludlam. April-2005 Peripheral vision test done by local optometrist, showed some peripheral loss in left eye. May 2005-Lot’s more Cushing’s testing, PICC line in all month. Major dizziness, passed out and fell this month. Diagnosed with Type 2 Diabetes but cannot treat due to extreme highs and lows, trying to control glucose with diet. I have very high and low Cortisol days. I am very cyclic at this point. June/July 2005-Three TIA like event’s… left sided weakness and numbness. Saw Neurologist that sent me to Neurologist at OHSU. Found three new white matter lesions seen on my brain MRI. Unknown cause. 5 in all now. August 2005-Had to leave my beloved job teaching Medical Assistants due to symptoms. I had one more TIA like event. Sep-2005 Neurologist at OHSU ran several tests and came to the conclusion that if in fact we could prove Cushing’s, all of my symptoms where due to this disease. I stopped all medications by choice. Nov-2005 I went back for extensive testing at OHSU with Dr.Ludlam and sure enough the numbers started proving my case. Very high midnight serum Cortisol’s among other high tests. Jan/Feb 2006-PICC line in and extensive Cushing’s testing done with CSS in Feb. CSS showed left sided gradient strongly. Cortisol numbers have proven my case, finally…. I had a midnight serum Cortisol of 34.1, the Midnight Salivaries, Midnight Serum Cortisol, UFC’s and CSS all positive for Cushing’s disease. March 23, 2006 I finally had Pituitary surgery at OHSU, they found the tumor on the left side bigger than originally though and removed the whole left half of my Pituitary gland. I was in the hospital for 6-days due to complications of Diabetes Insipitus and Adrenal Insuffiency. April-2006 Seen in the ER 3 times. Hospitalized for 4 days again due to complications, Blood cultures showed infection. I am on very high doses of Hydrocortisone and also taking DDAVP for the Diabetes Insipitus. April 2006- I am finally getting better somewhat…..This has been one heck of a roller coaster ride. I am now on Hydrocortisone 40/40/30. I am told we won’t know if I am cured for 3-6 month’s. June 5, 2006- Off Hydrocortisone stimulated my Cortisol to 24 on the ACTH stim test. August, 2006- Not cured, testing again!!! I had that gut feeling when I woke from the first surgery. I just knew… October 12, 2006- Second Pituitary surgery, more tumor on right side, most of my pituitary gland removed. Surgery unsuccessful, still have Cushing’s disease. November 7, 2006- BLA ...soon to be cured of Cushing's. Dec 2006/Jan 2007- Very sick due to another blood infection. Lot’s of adrenal crises due to infections. 3 blood infections to date. November 2008- 2 years out from my BLA and I am still very sick, I traded Cushing’s disease for Addison’s disease, and my body does not like it. Towards the end of my Cushing’s I went full blown, Dr.Ludlam told me this was a progressive disease and in me this was the case. Cushing’s did a lot more damage than ever thought; I have permanent nerve damage to my lower back requiring permanent narcotic pain relief through a pain center, damage to soft tissues throughout my body, diabetes, high lipids, fatty liver (NASH), Osteopenia, I have no usable veins, they are destroyed due to the high Cortisol, I have permanent port-a-cath in now so they can access my veins for blood draws and any IV stuff I may need, I had my period for 1 year straight because of lack of appropriate hormones after my surgeries so I had a full hysterectomy 8/20/08. I am permanently panhypopituitary now, no working pituitary hormones any more at all. I must replace all pituitary hormones, except DDAVP. Please don’t let this scare you, most people are cured and go on to live lives as best they can, and a lot of people are doing very well. June 21, 2009-Since writing in November I sat on the couch in severe AI until around September when I was put with a doctor that has been seeing Cushing’s patients for 38 years, he put me a on a very high dose of Dexamthasone and Florinef and forgot about me, he ended up with cancer and is no longer seeing patients. In the meantime, I got severe steroid induced Cushing’s and have had severe complications from it. I started falling from atrophied muscles and broke both hips, I ended up in a wheelchair, which I am happy to say I am out of now, had to have surgery on my left hip to pin it, it is still not healing, I am having absorption issues with calcium, iron, vitamins, minerals and meds. So I have to do my DEX by injections. We are now trying to find out why I am having absorption issues. I have a new endo at OHSU Dr.V and he is wonderful. He has brought my steroids down to a safe level and did it slow. He really seems to know his stuff as far as after care. I do not think he does the diagnosis process for Cushing’s. I would definitely go back to Dr.Ludlam if I had to go through it again. But I know there are many other great Cushing’s experts out there, this was just my experience. I know I will get better, but it may be a while. I am still at home handicapped, can barely go to the grocery store and I do not drive as I am on a high dose of Morphine. My goal is to get my pain under a 5 and be able to drive myself around. That is a good goal for now. Then on to finding out why my small town has so many tumors and starting a support group. I just need to get to a point where I feel I can be a good advocate for Cushing’s and right now I can’t. But that is the goal. Nov 16, 2009 I am still not well, I have broken my ankle, have no idea how, woke up one morning and it was broken. I am almost down to my 1/2 mg of DEX and am happy about that. had 2 surgeries in Sep and Oct on both elbows for ulnar nerve decompression. The first surgery got infected and a week later I had sepsis, which they think I had a small bowel preferation that healed itself. I was ambulanced up to OHSU and was in AI. It was a very rare bowel bacteria running through my blood stream, I was very sick. I just want to get well, but for some reason I am going through one thing after another. I am praying that 2010 will be my year of healing and I will have a good quaility of life then.That is what I am counting on. UPDATE January 23, 2016 2016: wow has the past few years have been a roller coaster. I don't know dates because I'm having memory issues at 47 years old. I have had 5 port-a-caths. I kept getting sepsis and every time they would take me to surgery and remove my port. Then place another when I was better. I have no veins that work. So I received IV port fluids 2-3x a week. I just recently had sepsis, when I get it I have a 50/50 % chance of survival. They removed my port and did not place another. So no more fluids which was for Pots. I had labs done through my port every 2 weeks. Now everything stopped. I am producing small amounts of cortisol. After a BLA. Intermittently. I am just now starting to feel good for 2 weeks now. I have started the exercise program called T-Tapp. I love it. No jumping or hard moves. 15 min and that's it. I am a grandma of 2 and one due any day. So for now I hope I'm on the road to recovery at least the best I can. HOME | Sitemap | Abbreviations | Adrenal Crisis! | Glossary | Forums | Bios | Add Your Bio | Add Your Doctor | MemberMap | CushieWiki
  9. Braun LT, Fazel J, Zopp S Journal of Bone and Mineral Research | May 22, 2020 This study was attempted to assess bone mineral density and fracture rates in 89 patients with confirmed Cushing's syndrome at the time of diagnosis and 2 years after successful tumor resection. Researchers ascertained five bone turnover markers at the time of diagnosis, 1 and 2 years postoperatively. Via chemiluminescent immunoassays, they assessed bone turnover markers osteocalcin, intact procollagen‐IN‐propeptide, alkaline bone phosphatase, CrossLaps, and TrAcP 5b in plasma or serum. For comparison, they studied 71 gender‐, age‐, and BMI‐matched patients in whom Cushing's syndrome had been excluded. The outcomes of this research exhibit that the phase immediately after surgical remission from endogenous CS is defined by a high rate of bone turnover resulting in a striking net increase in bone mineral density in the majority of patients. Read the full article on Journal of Bone and Mineral Research.
  10. Dr. Friedman will discuss topics including: Who should get an adrenalectomy? How do you optimally replace adrenal hormones? What laboratory tests are needed to monitor replacement? When and how do you stress dose? What about subcut cortisol versus cortisol pumps? Patient Melissa will lead a Q and A Sunday • May 17 • 6 PM PST Click here on start your meeting or https://axisconciergemeetings.webex.com/axisconciergemeetings/j.php?MTID=mb896b9ec88bc4e1163cf4194c55b248f OR Join by phone: (855) 797-9485 Meeting Number (Access Code): 802 841 537 Your phone/computer will be muted on entry. Slides will be available on the day of the talk here There will be plenty of time for questions using the chat button. Meeting Password: addison
  11. Thank you so much, Mayela - I'll definitely check this out. We need all the help we can get and I'm glad that Dr. Burton is trying to help Cushing's patients. 13 years is a long time to withhold a potentially helpful drug. I'm so sorry you're having a relapse Are you planning another pituitary surgery, BLA or something else?
  12. Those are all definitely symptoms of Cushing's...and excess cortisol. I think I had every one of them while I was being diagnosed. Have you taken steroids, especially often? They can cause these symptoms. Definitely mention these symptoms to your doctor. Please keep us posted.
  13. MaryO

    Naturopath

    Heidi, my first instinct was to say no but I did a search of the boards and found 177 posts on this topic so some people have actually gone this route. If you join the boards, you can read those responses. My reasoning for saying no was that if you have Cushing's, it is generally caused by a tumor and surgery is the only way to deal with the tumor. If Cushing's is caused by taking steroids, weaning off the steroids can sometimes help. Have you been diagnosed with Cushing's? If so, do you know what type? Best of luck to you!
  14. First published:03 May 2020 Read the entire article at https://doi.org/10.1002/alr.22540 Potential conflict of interest: None disclosed. Presented at the 65th Annual Meeting of the American Rhinologic Society, on September 14, 2019, in New Orleans, LA. Abstract Background Endoscopic transsphenoidal surgery (ETS) for the resection of pituitary adenoma has become more common throughout the past decade. Although most patients have a short postoperative hospitalization, others require a more prolonged stay. We aimed to identify predictors for prolonged hospitalization in the setting of ETS for pituitary adenomas. Methods A retrospective chart review as performed on 658 patients undergoing ETS for pituitary adenoma at a single tertiary care academic center from 2005 to 2019. Length of stay (LoS) was defined as date of surgery to date of discharge. Patients with LoS in the top 10th percentile (prolonged LoS [PLS] >4 days, N = 72) were compared with the remainder (standard LoS [SLS], N = 586). Results The average age was 54 years and 52.5% were male. The mean LoS was 2.1 days vs 7.5 days (SLS vs PLS). On univariate analysis, atrial fibrillation (p = 0.002), hypertension (p = 0.033), partial tumor resection (p < 0.001), apoplexy (p = 0.020), intraoperative cerebrospinal fluid (ioCSF) leak (p = 0.001), nasoseptal flap (p = 0.049), postoperative diabetes insipidus (DI) (p = 0.010), and readmission within 30 days (p = 0.025) were significantly associated with PLS. Preoperative continuous positive airway pressure (CPAP) (odds ratio, 15.144; 95% confidence interval, 2.596‐88.346; p = 0.003) and presence of an ioCSF leak (OR, 10.362; 95% CI, 2.143‐50.104; p = 0.004) remained significant on multivariable analysis. Conclusion For patients undergoing ETS for pituitary adenomas, an ioCSF leak or preoperative use of CPAP predicted PLS. Additional common reasons for PLS included postoperative CSF leak (10 of 72), management of DI or hypopituitarism (15 of 72), or reoperation due to surgical or medical complications (14 of 72). From https://onlinelibrary.wiley.com/doi/abs/10.1002/alr.22540?af=R
  15. Presented by Jamie J. Van Gompel, M.D., B.S., Professor in Neurosurgery and Otolaryngology specializing in endoscopic/open skull base focusing on Pituitary tumors as well as Epilepsy at the Mayo Clinic in Rochester, Minnesota, USA and Garret W. Choby, M.D., a fellowship-trained rhinologist and endoscopic skull base surgeon practicing at the Mayo Clinic. Objectives: - Understand the additional considerations that are key to performing endonasal surgery during the COVID pandemic - Identify the practice changes that are allowing pituitary surgery to proceed safely - Characterize the nasal cavity and nasopharynx as a reservoir for the coronavirus - Identify the risk of undergoing pituitary surgery during the Covid -19 pandemic Register Now! After registering you will receive a confirmation email containing information about joining the Webinar. Date: Monday, May 11, 2020 Time: 4:00 PM Pacific Daylight Time - 5:15 PM Pacific Daylight Time
  16. Presented by Jamie J. Van Gompel, M.D., B.S., Professor in Neurosurgery and Otolaryngology specializing in endoscopic/open skull base focusing on Pituitary tumors as well as Epilepsy at the Mayo Clinic in Rochester, Minnesota, USA and Garret W. Choby, M.D., a fellowship-trained rhinologist and endoscopic skull base surgeon practicing at the Mayo Clinic. Objectives: - Understand the additional considerations that are key to performing endonasal surgery during the COVID pandemic - Identify the practice changes that are allowing pituitary surgery to proceed safely - Characterize the nasal cavity and nasopharynx as a reservoir for the coronavirus - Identify the risk of undergoing pituitary surgery during the Covid -19 pandemic Register Now! After registering you will receive a confirmation email containing information about joining the Webinar. Date: Monday, May 11, 2020 Time: 4:00 PM Pacific Daylight Time - 5:15 PM Pacific Daylight Time
  17. Presented by Nelson M. Oyesiku, MD, PhD, FACS Professor of Neurosurgery and Medicine Vice-Chairman, Neurosurgery Residency Program Director Emory University School of Medicine Register Now! After registering you will receive a confirmation email containing information about joining the Webinar. Date: Sunday, May 10, 2020 Time: 11:00 AM Pacific Daylight Time to 12:15 PM Pacific Daylight Time/ 2:00 PM - 3:15 PM Eastern Daylight Time
  18. Presented by Nelson M. Oyesiku, MD, PhD, FACS Professor of Neurosurgery and Medicine Vice-Chairman, Neurosurgery Residency Program Director Emory University School of Medicine Register Now! After registering you will receive a confirmation email containing information about joining the Webinar. Date: Sunday, May 10, 2020 Time: 11:00 AM Pacific Daylight Time to 12:15 PM Pacific Daylight Time/ 2:00 PM - 3:15 PM Eastern Daylight Time
  19. Dr. Friedman will discuss topics including: Who should get an adrenalectomy? How do you optimally replace adrenal hormones? What laboratory tests are needed to monitor replacement? When and how do you stress dose? What about subcut cortisol versus cortisol pumps? Patient Melissa will lead a Q and A Sunday • May 17 • 6 PM PST Click here on start your meeting or https://axisconciergemeetings.webex.com/axisconciergemeetings/j.php?MTID=mb896b9ec88bc4e1163cf4194c55b248f OR Join by phone: (855) 797-9485 Meeting Number (Access Code): 802 841 537 Your phone/computer will be muted on entry. Slides will be available on the day of the talk here There will be plenty of time for questions using the chat button. Meeting Password: addison For more information, email us at mail@goodhormonehealth.com
  20. Dr. Friedman will discuss topics including: Who should get an adrenalectomy? How do you optimally replace adrenal hormones? What laboratory tests are needed to monitor replacement? When and how do you stress dose? What about subcut cortisol versus cortisol pumps? Patient Melissa will lead a Q and A Sunday • May 17 • 6 PM PST Click here on start your meeting or https://axisconciergemeetings.webex.com/axisconciergemeetings/j.php?MTID=mb896b9ec88bc4e1163cf4194c55b248f OR Join by phone: (855) 797-9485 Meeting Number (Access Code): 802 841 537 Your phone/computer will be muted on entry. Slides will be available on the day of the talk here There will be plenty of time for questions using the chat button. Meeting Password: addison For more information, email us at mail@goodhormonehealth.com
  21. MaryO

    Normal Cortisol tests

    More responses: And
  22. Cushing syndrome, a rare endocrine disorder caused by abnormally excessive amounts of the hormone cortisol, has a new pharmaceutical treatment to treat cortisol overproduction. Osilodrostat (Isturisa) is the first FDA approved drug who either can’t undergo pituitary gland surgery or have undergone the surgery but still have the disease. The oral tablet functions by blocking the enzyme responsible for cortisol synthesis, 11-beta-hydroxylase. “Until now, patients in need of medications…have had few approved options, either with limited efficacy or with too many adverse effects. With this demonstrated effective oral treatment, we have a therapeutic option that will help address patients' needs in this underserved patient population," said Maria Fleseriu, MD, FACE, professor of medicine and neurological surgery and director of the Pituitary Center at Oregon Health Sciences University. Cushing disease is caused by a pituitary tumor that releases too much of the hormone that stimulates cortisol production, adrenocorticotropin. This causes excessive levels of cortisol, a hormone responsible for helping to maintain blood sugar levels, regulate metabolism, help reduce inflammation, assist in memory formulation, and support fetus development during pregnancy. The condition is most common among adults aged 30-50 and affects women 3 times more than men. Cushing disease can lead to a number of medical issues including high blood pressure, obesity, type 2 diabetes, blood clots in the arms and legs, bone loss and fractures, a weakened immune system, and depression. Patients with Cushing disease may also have thin arms and legs, a round red full face, increased fat around the neck, easy bruising, striae (purple stretch marks), or weak muscles. Side effects of osilodrostat occurring in more than 20% of patients are adrenal insufficiency, headache, nausea, fatigue, and edema. Other side effects can include vomiting, hypocortisolism (low cortisol levels), QTc prolongation (heart rhythm condition), elevations in adrenal hormone precursors (inactive substance converted into hormone), and androgens (hormone that regulated male characteristics). Osilodrostat’s safety and effectiveness was evaluated in a study consisting of 137 patients, of which about 75% were women. After a 24-week period, about half of patients had achieved normal cortisol levels; 71 successful cases then entered an 8-week, double-blind, randomized withdrawal study where 86% of patients receiving osilodrostat maintained normal cortisol levels, compared with 30% who were taking a placebo. In January 2020, the European Commission also granted marketing authorization for osilodrostat. From https://www.ajmc.com/newsroom/patients-with-cushing-have-new-nonsurgical-treatment-option
  23. MaryO

    Normal Cortisol tests

    Has anyone suggested Cyclic Cushing's to you? That's where tests cycle normal/abnormal but no one knows how long a person's cycle could be. That's even harder to diagnose due to the constant fluctuations and some endos don't believe in it, although I don't understand how a doctor can't believe in a disease. Here are the bios of some Cushies with Cyclic Cushing's: https://cushingsbios.com/category/cyclic/
  24. MaryO

    Normal Cortisol tests

    Here's another answer I got:
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