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trs

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About trs

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  • Birthday 10/07/1965

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    Hi my name is Trish. I joined the boards originally in 2004. Took time off after doctors convinced me I was just fat and dieted and exercised my way to really poor health. I was diagnosed in 2008 and had surgery in Nov. of that year. I don't think I was cured and I am currently testing again.

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  1. Haven't been around much just stopped by to see the new boards. Wow what a change. It will take me a while to learn to navigate them but, the site looks good Mary. Thanks for taking your time to update it.

  2. My first thought was at least he isn't from Transylvania. LOL. Good for your family.
  3. Maybe we are all just body builders in disquise. We should start a contest to see who is strongest with all of our "big muscles" showing off. I agree with the moron assessment you should've ask him which ways more a pound of feathers or a pound of lead. I betcha he would say the lead. A pound is a pound. I really doubt that medical school is as hard as they say.
  4. http://www.springerlink.com/content/u8361471j4484302/ Hypercoagulability in Cushing?s syndrome: the role of specific haemostatic and fibrinolytic markers Journal Endocrine Publisher Humana Press Inc. ISSN 0969-711X (Print) 1559-0100 (Online) Category Original Article DOI 10.1007/s12020-009-9186-y Subject Collection Medicine SpringerLink Date Tuesday, April 21, 2009 Add to marked items Add to shopping cart Add to saved items Permissions & Reprints Recommend this article PDF (194.0 KB)HTMLFree Preview Original Article Hypercoagulability in Cushing?s syndrome: the role of specific haemostatic and fibrinolytic markers Darko Kastelan1 , Tina Dusek1, Ivana Kraljevic1, Ozren Polasek2, Zlatko Giljevic1, Mirsala Solak3, Silva Zupancic Salek4, Jozo Jelcic1, Izet Aganovic1 and Mirko Korsic1 (1) Division of Endocrinology, Department of Internal Medicine, University Hospital Zagreb, Kispaticeva 12, 10000 Zagreb, Croatia (2) Department of Medical Statistics, Epidemiology and Medical Informatics, Andrija Stampar School of Public Health, Zagreb University School of Medicine, Zagreb, Croatia (3) University Hospital for Pulmonary Diseases, Zagreb, Croatia (4) Division of Haematology, Department of Internal Medicine, University Hospital Zagreb, Zagreb, Croatia Received: 14 January 2009 Accepted: 26 March 2009 Published online: 21 April 2009 Abstract Objective Hypercoagulability is a commonly described complication in patients with Cushing?s syndrome. Recent clinical studies have indicated various abnormalities of coagulation and fibrinolysis parameters which may be related to that phenomenon. The aim of this study was to investigate the mechanisms underlying the hypercoagulable state in patients with Cushing?s syndrome. Research methods and procedures A wide range of serum markers involved in the processes of blood coagulation and fibrinolysis was measured in a group of 33 patients with Cushing?s syndrome and 31 healthy controls. No participant was taking medication which could influence the result or had known diseases, except hypertension and diabetes, which could affect blood coagulation or fibrinolysis parameters. Results Patients with Cushing?s syndrome had higher levels of clotting factors II (P = 0.003), V (P < 0.001), VIII (P < 0.001), IX (P < 0.001), XI (P < 0.001) and XII (P = 0.019), protein C (P < 0.001), protein S (P < 0.001), C1-inhibitor (P < 0.001) and plasminogen activator inhibitor-1 (PAI-1) (P = 0.004). The activity of fibrinolytic markers, plasminogen (P < 0.001), antithrombin (P < 0.001) and antithrombin antigen (P = 0.001) was also increased in the patient group. Conclusion The study has demonstrated hypercoagulability in patients with Cushing?s syndrome manifest as increased prothrombotic activity and compensatory activation of the fibrinolytic system. We propose the introduction of thromboprophylaxis in the preoperative and early postoperative periods, combined with a close follow-up in order to prevent possible thromboembolic events in patients with Cushing?s syndrome.
  5. My mom has been struggling with her weight for years. She has been seeing this heart doctor that is one of the best in our state for over a decade. She just had two heart stints put in last week for a 80% blocked main artery and a 70% blocked secondary. She sees this doctor at least once a year. The first time I met him almost 8 or 9 years ago I told her to find a new doctor he was only focused on her weight being her only problem. If she had had heart problems during a colonoscopy and lucked out by her doctor being out of town who knows when the blockage would have been found. My guess would be have been on autopsy. I totally agree weight is a symptom. It takes 3,500 calories to make on pound of fat. 3,500 calories x 30 days=105,000 calories divided by 20lbs =5,250 calories a day. If I did the math right. I am not mathematician. That is how many calories you would need to consume (on top of any other calories need to just maintain your everyday physcial needs) to gain 20 lbs in one month. That means for the average woman who needs 1,500 calories a day for normal every day existience would have to be eating 6,750 calories a day to gain that much weight. How many of us have gained that kind of weight in a month and how many of us have eaten that many calories every day. There were many weeks that I wouldn't consume 5,250 calories all week while going to the gym working out hard. I didn't loose I gained. The math just doesn't add up does it. To consume 6,750 calories a day you would need to eat: 16 c (gal) 2%milk @120 calories/c=1,920 12 large eggs x 78 calories/egg=936 16 oz bacon (1 lb) x 145 calories/oz=2,320 16 oz bread(loaf)x74 calories/oz=1,184 3.5 choco. chip cookies 128/ea =320 35 cups of coffee x 2 calories/c=70 total 6,750 Please feel free to check my math I won't be offended.LOL. As long as you get the point. We should all make a chart like that to keep handy and give it to every doctor that tells us the standard crapola of eat less and exercise more. It breakfast time my fat butt better get cookin.
  6. LoriJane, the trip to Torrance is worth every single cent. I wish I had gone there on my first trip to LA. Hindsight is 20/20 as they say.
  7. Saw him on the news this morning. First thought endocrine.
  8. Ok this is what I have so far. What do you guys think. I just cut and pasted it so try to ignore the highlights etc. I fix those before I print. I am trying to make it easy on the attorney so they can get a quick overview of Cushings. I didn't know to use hypercortisolism to late now. Cushing?s disease Definition Cushing?s disease is a pituitary tumor that releases excessive amounts of cortisol (a steriod). Cortisol is a hormone that controls the sleep/wake cycle, metabolism, immunity, and the relative composition of body between fat/bone and muscle. Cortisol is the hormone that the body produces in response to stress. Cortisol, a very potent glucocorticoid?a group of adrenocortical hormones that protects the body from stress and affect protein and carbohydrate metabolism? is involved in regulating the functioning of nearly every type of organ and tissue in the body, and is considered to be one of the few hormones absolutely necessary for life. Cortisol is normally released during stressful situations. It controls the body's use of carbohydrates, fats, and proteins and also helps reduce the immune system's response to swelling (inflammation). Cortisol is involved in:  complex processing and utilization of many nutrients, including sugars (carbohydrates), fats, and proteins  normal functioning of the circulatory system and the heart  functioning of muscles  normal kidney function  production of blood cells  normal processes involved in maintaining the skeletal system  proper functioning of the brain and nerves  normal responses of the immune system Causes Cushing's disease is caused by a tumor or excess growth ( hyperplasia) of the pituitary gland. This gland is located at the base of the brain. People with Cushing's disease have too much ACTH. ACTH stimulates the production and release of cortisol, a stress hormone. Too much ACTH means too much cortisol. The adrenal glands are located on top of each kidney, and are responsible for releasing cortisol. The site of cortisol production is in the outer layer of the adrenal gland called the adrenal cortex. Release of cortisol is stimulated by ACTH, which is produced by the pituitary gland. The pituitary is juxtaposed to the base of the brain and serves as a type of control center for many other glands in the body. ACTH production occurs only when there is a low concentration of cortisol in the blood. Therefore, cortisol production can be abnormal due to abnormalities in the function of the adrenal gland or the pituitary gland. It can also be overproduced by abnormal regulation of ACTH Symptoms  Abdomen that sticks out and thin arms and legs (central obesity)  Acne or skin infections  Collection of fat on the back of the neck (buffalo hump)  Depression  Diabetes  Easy bruising  Excessive facial hair growth in females  Headache  Impotence  Increased urination  Moon face (round, red, and full)  Osteoporosis  Purple stretch marks on the abdomen, thighs, and breasts  Stopping of menstruation  Weakness  Weight gain Other clinical manifestations resulting from excessive cortisol production can be quite serious. Myopathy, or wasting away of the muscles often occurs. Due to the abnormal blood cell development that results from cortisol overproduction, the skin bruises more frequently and wounds do not heal as quickly. Skin tends to be fragile and thin. People with Cushing syndrome are susceptible to developing fractures, especially in the pelvic and spinal regions. Women are at a higher risk for developing osteoporosis or brittle bones. For all affected individuals, difficulty with activities such as lifting objects or getting up from a sitting position can lead to back pain and fractures. Because cortisol is also important for regulating insulin, patients with Cushing syndrome are at risk for developing diabetes. The function of cortisol is to regulate blood pressure, act as an anti-inflammatory mediator, and to regulate insulin metabolism. Cortisol plays a role during the metabolic activities associated with fat, protein, and carbohydrate metabolism. High levels of cortisol can cause sodium and water retention. Therefore, overproduction of cortisol can have medically important health-related implications that affect muscle contractions, heartbeat, and blood cell function. Possible Complications  Compression fractures  Diabetes  High blood pressure  Infections  Kidney stones  Anxiety, cognitive dysfunction, psychosis Most people have severe fatigue, weak muscles, high blood pressure and high blood sugar. Irritability, anxiety and depression are common. An individual with HPA-axis suppression cannot increase steroid production appropriately during a medical illness or other stress and would need to receive stress doses of steroids to avoid adrenal crisis. Thus, in an emergency, the potential for relative adrenal insufficiency should be considered in any patient with Cushing syndrome. Morbidity and Mortality Morbidity and mortality associated with Cushing syndrome are related primarily to the effects of excess glucocorticoids. However, a large primary pituitary tumor may cause panhypopituitarism and visual loss.  Two catastrophic medical crises that occur in glucocorticoid excess states are perforated viscera and opportunistic fungal infections.  Exposure to excess glucocorticoids results in multiple medical problems, including hypertension, obesity, osteoporosis, fractures, impaired immune function, impaired wound healing, glucose intolerance, and depression, emotional lability psychosis. The higher mortality rate observed in CS seems to be mainly caused by cardiovascular complications. Chronic hypercortisolism is associated with an increased incidence of cardiovascular risk factors such as systemic arterial hypertension, impaired glucose tolerance or diabetes, central obesity, hyperlipidemia, and hypercoagulability. Hypercortisolism promotes the development of hyperglycemia and decreased carbohydrate tolerance by increasing hepatic glycogen and glucose production and decreasing glucose uptake and utilization by peripheral tissues Increased body weight is one of the earliest signs of CS, with a characteristic redistribution of fat from peripheral to central parts of the body, mainly in the abdominal region. Glucocorticoids play a central role in the abdominal accumulation of body fat. An increased local generation of cortisol may take place in visceral adipose tissue because of high activity of 11?-hydroxysteroid dehydrogenase type I, resulting in high local concentrations of cortisol, by converting inactive cortisone into active cortisol. Visceral obesity is an independent risk factor for reduced life expectancy and also correlates with increased risk for disorders such as insulin resistance and diabetes, hyperlipidemia, hypertension, and atherosclerosis of coronary, cerebral, and peripheral vessels In hypercortisolism, there is an increase in circulating very low-density lipoprotein and low-density lipoprotein, but not high-density lipoprotein, with consequent elevation of total triglycerides and cholesterol levels. The insulin resistance state induced by glucocorticoid excess is likely to play a key role in the determination of lipid abnormalities. A complex derangement of the hemostatic system, characterized by both hypercoagulability and impaired fibrinolysis, is responsible for the thrombophilic state observed in patients with CS. Increased cortisol levels stimulate the synthesis of several clotting factors, such as fibrinogen by the liver, and von Willebrand factor by endothelial cells. Glucocorticoids also up-regulate the synthesis of plasminogen activator inhibitor type 1, the main inhibitor of the fibrinolytic system. This hypercoagulability state is a crucial factor predisposing CS patients to thromboembolic events, mostly after surgery and during IPS sampling. Therefore, patients with active CS should be treated as having a prothrombotic disorder, and antithrombotic prophylaxis should be considered. Glucocorticoids affect behavior, mood, neural activity, and a number of specific biochemical processes in the central nervous system. A number of psychiatric and psychological disturbances may be associated with CS, regardless of its etiology. Depending on the series, 50?80% of patients with CS meet Diagnostic and Statistical Manual of Mental Disorders IV criteria for major depression. A minority of patients have other psychopathological manifestations including mania, anxiety, and cognitive dysfunction. If psychotic symptoms occur, they are likely to be a complication of mania or severe depression. Suicidal tendency also has been reported in patients with CS. The somatotropic axis is negatively affected by exogenous or endogenous hypercortisolism, which reduces spontaneous GH secretion as well as the GH response to various stimuli, although with apparently minor changes in circulating IGF-I. Patients with CS develop the manifestations of the metabolic syndrome or syndrome X, including insulin resistance, visceral adiposity, dyslipidemia, carbohydrate intolerance, and/or diabetes mellitus type 2, coagulopathy, and hypertension as a direct or indirect consequence of concurrent and chronic cortisol excess. The abnormalities enhance the global cardiovascular risk that is responsible for the increased mortality of these patients. Prognosis The prognosis for individuals who receive treatment for Cushing syndrome is good with a high likelihood of being cured. However, in affected individuals that are not treated, the prognosis can be poor, with death eventually resulting from complications from hypertension, diabetes, or heart disease Despite cure of hypercortisolism, many patients exhibit residual symptoms in the first postoperative year or even longer, including problems with social and interpersonal relationships, anxiety, irritability, and demoralization. Adults with hypercortisolism have also impaired cognitive function associated with reversible apparent loss of brain volume. Cognitive deficits are often specific to the medial temporal lobe declarative memory system. Adult patients studied 1 yr after surgical cure show improvement in mood but no change in cognitive function, with a concomitant increased, but not normalization, of brain volume. Treatment Treatment depends on the specific reason for cortisol excess and may include surgery, radiation, chemotherapy or the use of cortisol-inhibiting drugs. If the cause is long-term use of glucocorticoid hormones to treat another disorder, the doctor will gradually reduce the dosage to the lowest dose adequate for control of that disorder. Once control is established, the daily dose of glucocorticoid hormones may be doubled and given on alternate days to lessen side effects. Pituitary Adenomas Several therapies are available to treat the ACTH-secreting pituitary adenomas of Cushing's disease. The most widely used treatment is surgical removal of the tumor, known as transsphenoidal adenomectomy. Using a special microscope and very fine instruments, the surgeon approaches the pituitary gland through a nostril or an opening made below the upper lip. Because this is an extremely delicate procedure, patients are often referred to centers specializing in this type of surgery. The success, or cure, rate of this procedure is over 80 percent when performed by a surgeon with extensive experience. If surgery fails, or only produces a temporary cure, surgery can be repeated, often with good results. After curative pituitary surgery, the production of ACTH drops two levels below normal. This is a natural, but temporary, drop in ACTH production, and patients are given a synthetic form of cortisol (such as hydrocortisone or prednisone). Most patients can stop this replacement therapy in less than a year. For patients in whom transsphenoidal surgery has failed or who are not suitable candidates for surgery, radiotherapy is another possible treatment. Radiation to the pituitary gland is given over a 6-week period, with improvement occurring in 40 to 50 percent of adults and up to 80 percent of children. It may take several months or years before patients feel better from radiation treatment alone. However, the combination of radiation and the drug mitotane (Lysodren?) can help speed recovery. Mitotane suppresses cortisol production and lowers plasma and urine hormone levels. Treatment with mitotane alone can be successful in 30 to 40 percent of patients. Other drugs used alone or in combination to control the production of excess cortisol are aminoglutethimide, metyrapone, trilostane and ketoconazole. Each has its own side effects that doctors consider when prescribing therapy for individual patients. Surgical Care  Cushing disease  Treatment of choice for classic Cushing disease is transsphenoidal surgery by an experienced neurosurgeon. The goal of surgery is to remove the adenoma, preserving as much pituitary function as possible.  The more extensive the mass and the resulting resection, the greater the risk for loss of pituitary function. Successful amelioration of hypercortisolism occurs in 60-80% of cases. Both open and laparoscopic techniques are possible. If unsuccessful, MRI-guided pituitary surgery, a new procedure, may be indicated. Lateralization of ACTH secretion via IPS catheterization and sampling is sometimes helpful in difficult cases.  Pituitary irradiation is employed when transsphenoidal surgery is not successful or not possible. The procedure is less successful than surgery in adults, with a 45% cure rate in adults and 85% cure rate in children. Late-onset adverse effects include hypopituitarism.  Bilateral adrenalectomy is an option if transsphenoidal surgery, pituitary irradiation, and medical therapy fail or if rapid normalization of cortisol levels is required. The patient then requires lifelong glucocorticoid and mineralocorticoid therapy.  In individuals who undergo bilateral adrenalectomy, Nelson syndrome, that is symptomatic enlargement of the pituitary gland and adenoma, may occur in one quarter to one half of adults not treated with pituitary irradiation and in as many as one quarter of patients pretreated with radiation therapy. Outlook (Prognosis) If the tumor can be surgically removed, the outlook is fair to good, depending upon whether the entire tumor is removed. Possible Complications The most serious complication is blindness, which can occur if the optic nerve is seriously damaged. Permanent hormonal imbalances may be caused by the tumor or its removal. This may require replacement of the affected hormones. (I have diagrams for this part but they would not paste) The pituitary gland is one of the body?s endocrine glands. It is sometimes called the ?master gland,? because it controls the functions of other endocrine glands. Endocrine glands release chemical messengers (hormones) into the bloodstream to be carried to organs and tissues throughout the body. The pituitary is located at the base of the brain. It is small and is divided into three parts: anterior lobe, intermediate lobe and posterior lobe. The anterior lobe is largest, making up about 80 percent of the gland. The anterior lobe produces the following hormones:  Growth hormone, which affects many other glands  Prolactin, which stimulates milk production in women after giving birth  Adrenocorticotropic hormone, which stimulates the adrenal glands  Thyroid-stimulating hormone, which stimulates the thyroid gland  Luteinizing hormone , which stimulates the ovaries or testes  Follicle-stimulating hormone, which stimulates ovaries or testes The intermediate lobe produces melanocyte, a hormone that controls skin pigmentation. The posterior lobe of the pituitary stores and releases an antidiuretic hormone that increases the absorption of water by the kidneys. This lobe also stores and releases oxytocin, a hormone that causes the uterus to contract , helps to slow blood flow during the birthing process and causes milk to flow when a woman breast-feeds. The pituitary is intimately involved in growth, development, maintenance and reproduction. The pituitary supplies growth hormone, which is responsible for growth from before birth to the end of growth at the end of puberty. The pituitary determines the timing for the onset of puberty and the cycling of the female menstrual cycle. It regulates the production of thyroid hormones that govern the overall metabolism of the body. It also controls the production of corticosteroids, which help govern such functions as electrolyte maintenance, blood pressure, inflammatory response and response to stress. Sources NIH Medline Plus The Hormone Foundation The Pituitary Society Mayo Clinic The Journal of Clinical Endocrinology and Metabolism Thanks everyone for your help.
  9. Well I kept telling the man filling out the intial form that I thought Cushings was my trouble but, there is not a category or whatever it is they call that. So he listed obesity and heart problems. I didn't have the Cushings diagnosis then I do now. Since obesity is a major symptom of Cushings along with cognitive problems (short term memory loss per their psychologist) and heart problems I would think a good lawyer could put that together. I hope anyway.
  10. I am trying to compile a few short to the point Cushings articles for a disability appeal. I have decided to use an attorney and would like to take some information on Cushings with me to the appt. I have Vs. article and some others for what Cushings is I really need some that tell the damage it causes in more detail than the basic heart problems, diabetes and infection. I have some that are really long and detailed with various aspects of symptoms but, I think these would be a little to long for the intial appeal. The attorney won't have much time to file the appeal.
  11. Were were you a few days ago when I was trying to find simple articles like that for disability attorney. Thanks for the find.
  12. Excellent interview you did a really good job.
  13. I took it a few years back. I didn't loose any weight with it. I am sure it was Cushings gain looking back now. I joined the class action lawsuit a few years ago and was reimbursed my cost of prescreptions all of about $400. or so. I couldn't find all of my reciepts and my doc didn't keep good notes (or he wouldn't give them to me). I do have heart trouble now and I often wonder if the Fen-Phen made it worse.
  14. Y'all now I will testify to the miraculous benefits of vitamin D3. Shelley I have seen them advertise for it helping seasonal affective disorder which, IMO, is a vitamin D3 deficiency.
  15. Thats the way I read it, also. Both rat groups with cortisol gained but, the sed. rats gained the most. The cortisol exercising rats didn't gain any more fat than the control group. It is saying that we should exercise to keep the high cortisol from turning to fat. I will sign up for there human control group because I know that the opposite is true in me. The more I exercised the fatter I got. Didn't need any lab rat to tell me so either.
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