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Everything posted by MemberGone

  1. The Radiation Boom - Stereotactic Radiosurgery Overdoses Harm Patients
  2. Gina, this is excellent - thanks for posting! (and I too am wondering about the vascular disease and respiratory link...having had some issues with respiratory stuff in particular at times)
  3. Judy and Jess - this is very very cool. While I really feel so badly about what your family has gone through, god love you for using your expierences (and blood!) to help others in the future.
  4. An eye opener and worth reading: Generic Drug Safety - investigation by Self
  5. Thanks, Mary - I found this very interesting as well! Glad to see the recognition, too, about the dex test not being the gold standard after all...and that some of us don't get elevated 24 hour ufcs. I didn't see a mention of the late night serum cortisol test, which was unfortunate, though.
  6. It's a long story on how I came to find this information, but it is very interesting and a significant concern that I suspect is not generally understood. Growth hormone replacement is for more important than I realized....
  7. To view article on Medscape click here From Endocrine Practice Cardiovascular Risk in Patients with Growth Hormone Deficiency: Effects of Growth Hormone Substitution Posted 04/11/2007 Albert G. Burger, MD;1 John P. Monson, MD;2 Anna M. Colao, MD;3 Anne Klibanski, MD4 Author Information Abstract and Introduction Abstract Objective: To review the literature on the increased cardiovascular risk in patients with growth hormone (GH) deficiency and the positive effects of GH replacement. Methods: We analyze the factors that contribute to cardiovascular risk in GH deficiency, including body composition and lipid profile, and summarize GH treatment strategies and results described in the literature. Results: The prominent clinical finding in patients with GH deficiency is the increased abdominal fat, even in patients with normal weight. Cardiac ejection volume tends to be decreased, and arterial distensibility is diminished. The lipid status is also worsened, accompanied by increased inflammatory markers, such as highly sensitive C-reactive protein. Typically, GH treatment reduces visceral fat and increases muscle mass, changes that diminish cardiovascular risk. Because of direct effects as well as increased hemodynamic performance and increased blood volume, cardiac performance is improved. With GH therapy, total cholesterol and low-density lipoprotein levels decrease by 10% to 20%, and inflammatory markers such as C-reactive protein decline. Carbohydrate metabolism during moderate to long-term treatment is minimally affected, although obese patients with GH deficiency on rare occasion may have hyperglycemia or even diabetes. Conclusion: The relevance of the beneficial effects of GH on the cardiovascular system is strongly suggested but not fully proved. The results in a large cohort of GH-treated patients (the KIMS or Pharmacia and Upjohn International Metabolic Surveillance database) demonstrated no difference in cardiovascular risk in comparison with that in a control population after a mean of 3 years of treatment. Introduction Growth hormone (GH) deficiency in adults is frequently attributable to tumors affecting the hypothalamic-pituitary region. Deficiency of GH, however, is not only seen in this clinical context. GH is among the most sensitive pituitary hormones to irradiation, traumatic brain injury, and possibly chemotherapy. Clinically, GH deficiency may easily be missed. In a 5-year follow-up study of patients having received classic external radiotherapy for pituitary or other brain lesions, GH deficiency was noted in almost 100% of the cases.[1] Mainly gonadal function and, somewhat less frequently, thyroidal and adrenal function were also affected. Investigators have established that patients with panhypopituitarism have an increased cardiovascular (CV) risk.[2] Conventional therapy with thyroid hormones, cortisol, and sex hormones? particularly gonadal substitution in women?is certainly effective in decreasing the CV risks.[3] Nonetheless, it has been recognized that these patients, even though treated with thyroid and steroid hormones, continue to have a higher than normal CV risk, the risk in women exceeding that in men.[2,4-6] In addition, cerebrovascular disease was more frequent, particularly in women. In 1990, Rosen and Bengtsson[7] first reported that, despite classic substitution therapy (excluding GH replacement), patients with panhypopituitarism remained at increased CV risk and suggested that GH deficiency might have an etiologic role. Other investigators, however, have suggested that external irradiation or the underlying pituitary pathologic condition may have an etiologic role in cerebrovascular disease. Lean Body Mass Versus Adipose Tissue The increased CV risk in overweight patients is particularly dependent on a high proportion of abdominal (visceral) fat in comparison with total body fat.[8-12] Insulin resistance (IR), increased inflammatory markers, and microvascular and macrovascular disease are common complications. Patients with GH deficiency demonstrate a high prevalence of obesity and share most of the risk factors of those with simple obesity. Blood pressure, however, is not necessarily increased in patients with GH deficiency. Nonobese and even lean patients with GH deficiency have a high ratio of abdominal to total body fat.[5,11] They are at a higher CV risk than an age- and weight-matched population. It is recognized that these subjects have a lean body mass deficit of approximately 3 to 4 kg and an increase of 1 to 2 kg in abdominal fat. This pattern is frequently observed in women with panhypopituitarism but is also seen in men.[8] Vascular Motility and Plaque Formation The poor CV profile of patients with hypopituitarism and GH deficiency was further substantiated by observations of vascular mortality, plaque formation, increased intima-media thickness (IMT), decreased production of nitric oxide (NO), abnormal lipid profiles, inflammatory markers, and development of IR. The macrovascular abnormalities were first investigated by ultrasonography in 1992 and 1993.[13,14] These early studies documented that atheromatosis of the abdominal aorta and the femoral and carotid arteries was more pronounced in patients with GH deficiency than in the control population. In addition, the distensibility of these arteries, measured by ultrasonography, was appreciably reduced. Several studies have confirmed and extended these findings.[15-21] Apparently, there was no sex-related effect on the prevalence or severity of atherosclerosis in adult patients with GH deficiency.[21] The distensibility of the forearm arteries has been studied by using an ischemic-hyperemic stress or by applying pharmacologic dilatation of the vessels. All studies confirmed an increased stiffness of the arteries in comparison with that in the control population. The pathophysiologic basis for these findings has been documented by the remarkable work of Boger et al.[22] They were able to demonstrate that GH was responsible for endothelial NO production. NO is not only a potent vasodilator but also an inhibitor of low-density lipoprotein (LDL) oxidation in the arterial wall, superoxide radical elaboration, smooth muscle proliferation, and platelet aggregation and therefore has a potent antiatheromatous action. Most likely, many if not all of these effects are mediated by insulin-like growth factor-I (IGF-I). Cardiac Performance GH and IGF-I have a direct positive effect on cardiac morphologic findings and function, which are essential for cardiac performance. In experimental models, hypophysectomy induces a decrease in size of several organs, including the heart, which is reversed by administration of GH.[23] In human GH deficiency, this relationship is well documented in childhood-onset disease; in such patients, reduced systolic performance is responsible for the hypo-kinetic syndrome detected in some of these children.[24] In adult-onset GH deficiency, some studies have also described a decrease of left ventricular (LV) muscle mass and cardiac ejection volume[25-28] whereas others have not,[29,30] early adulthood-onset disease being more subject to these changes than onset in middle age or in elderly patients. GH treatment tends to improve cardiac function. This result has been documented by studies in childhood-onset and adult-onset GH deficiency[31,32] and confirmed by a large meta-analysis that included all the published randomized controlled trials on cardiac aspects of GH replacement.[10] That article reports a significant positive effect on LV mass, interventricular septum, LV posterior wall, LV end-diastolic diameter, and stroke volume after GH therapy in adults.[10] Lipids and Lipoproteins Meta-analysis of the lipid status of patients with GH deficiency clearly indicates the presence of an adverse lipid profile. Among elderly patients, a substantial proportion have elevated total cholesterol and LDL levels, and high-density lipoprotein cholesterol concentrations tend to be decreased. In some studies, the atherogenic apolipoprotein (apo) B-100 was evaluated and tended to be increased.[3,33,34] Triglyceride levels also tend to be increased.[5,10] This lipid profile is consistent with an increased risk of atherosclerosis and CV events. Inflammatory Markers Atherosclerosis is an inflammatory process, and markers such as highly sensitive C-reactive protein (hsCRP) or interleukin-6 (IL-6) are highly sensitive indicators if other sources of inflammation, such as infections, are excluded.[9,35-37] Examples of other less frequently used markers are serum myeloperoxidase, fibrinogen, sialic acid levels, cystatin C, and adhesion of monocytes.[38] In patients with GH deficiency, hsCRP values and myeloperoxidase are considerably increased, whereas fibrinogen has only a tendency to be increased.[39] Carbohydrate and Amino Acid Metabolism Despite normal blood glucose levels, patients with GH deficiency tend to have an increased serum insulin concentration and evidence of IR, consistent with the augmented abdominal (visceral) adiposity. IR has been documented by using various techniques, including glucose clamp studies.[8,40,41] Interestingly, patients with acromegaly also show a tendency for having IR and diabetes mellitus, despite a reduction in abdominal adiposity; this finding suggests that both an excess and a lack of GH result in IR. Elevated serum homocysteine levels are considered an independent risk factor for increased CV events. In placebo-controlled studies in men, GH treatment was found to decrease fasting homocysteine levels. These changes did not correlate with changes in C-reactive protein (CRP), IL-6, or insulin levels.[42-44] In summary, patients with hypopituitarism, despite adequate treatment of pituitary deficiencies other than GH deficiency, have the morphologic features and many of the biochemical findings that characterize patients with a high CV risk. Investigators have estimated that there are approximately a 2-fold increase in CV risk in men beyond the age of 50 years and a 3.5 to 4-fold increase in women of that age-group. Importantly, the increased CV risk also seems to be relevant for patients with GH deficiency who have a normal body mass index. The most important factors in GH deficiency and their changes with GH treatment are summarized in Table 1 . Biochemical Diagnosis of GH Deficiency in Adults The definition of partial degrees of GH deficiency remains controversial, although the diagnosis is rarely difficult or contentious in patients with structural pituitary disease. Despite the availability of highly sensitive assays that measure GH down to 0.02 ng/mL, the diagnosis cannot be based on basal GH values. Among the functional tests, the insulin tolerance test remains the "gold standard." It is commonly agreed that, after profound hypoglycemia (plasma glucose levels <2.2 mmol/L or 40 mg/dL), severe GH deficiency is confirmed if serum GH values do not exceed 3 ng/mL.[45,46] Criteria for patients with incomplete GH deficiency do exist but are beyond the scope of this review. The test has obvious limitations in elderly patients, in patients with diabetes mellitus, and in obese patients, and it is contraindicated in patients with epilepsy or ischemic heart disease. Other validated tests are the glucagon and the growth hormone-releasing hormone/arginine test.[47] Another well-tolerated test, the hexarelin test, which works through the ghrelin receptor, is not universally available.[48] Treatment Schedules Most specialists would propose an IGF-I value in the range of the mean value + 2 SD as a target for adequate treatment, taking into account the age-adjusted reference range. GH treatment should be initiated with use of a low dose (to prevent side effects) and then gradually increased. Maintenance doses differ for childhood-onset or adult-onset disease as well as age and sex of the patient. In men, dosages range from 0.3 to 0.6 mg daily; in premenopausal women or those receiving orally administered estrogens, a higher dosage?from 0.4 to 1 mg daily[49,50] ?is usually required. The dose cannot be strictly calculated on the basis of body weight or surface area but must be altered in accordance with the age- and sex-adjusted normalized serum IGF-I values. Thus, adjustment of treatment is necessary after onset of the menopause or after discontinuation of estrogen therapy. For achieving a full effect on many variables such as body composition, maintenance treatment must be continued for at least 6 months. For other end points such as bone density, a period of 18 months may be needed to demonstrate a significant effect, and improvement may continue beyond 18 months of treatment. Of note, the early trials of GH replacement used higher doses, which occasionally had to be reduced during the experimental protocol because of side effects. This factor can make the interpretation of results more difficult. Contraindications to GH treatment are active malignant disease, benign intracranial hypertension, and diabetic retinopathy. Patients with a past history of a cured malignant condition, other than skin cancer, should undergo thorough evaluation for the risks versus benefits of treatment. Concerns about GH treatment and malignant lesions stem from the positive association observed between IGF-I levels and risk of cancer, particularly prostate cancer, in the normal population. Men with the highest quartile of IGF-I values had a relative risk of prostate cancer of 4.3.[51] Despite these observations in normal populations, surveillance studies have thus far not been able to show any increased risk of malignant involvement in treated patients with GH deficiency in comparison with those not treated with GH. Effects of GH Treatment Clinically, the most striking change in CV risk factors with GH treatment is the improvement of body composition, a 1- to 3-kg decrease of abdominal or visceral fat and an increase in muscle mass, together with improved physical performance (Fig. 1).[10,12,52-55] These effects are also seen in elderly patients.[56] The increase of cardiac mass?in particular, LV mass?was noted in several studies, including in adult patients with childhood-onset GH deficiency. The increase of LV mass was within physiologic limits; pathologic cardiac hypertrophy attributable to GH substitution therapy has not been reported. After discontinuation of GH treatment, the positive effect does not persist, and within 6 months, LV mass returns to pretreatment values.[30,32,57-60] Figure 1. (click image to zoom) Effects of growth hormone (GH) treatment in patients with GH deficiency. + = favorable effects of GH; ? = slightly positive or neutral effects. The effect on cardiac mass is associated with enhanced cardiac performance. Improvement of both systolic and diastolic filling function has been observed. In addition to the changes in cardiac mass, hemodynamic improvements due to increased plasma volume and red blood cell mass also contribute to better cardiac performance.[22,25,61] The improvement of cardiac performance could be documented at rest, at peak exercise testing, and during sustained exercise.[31] Confirmation of these observations was obtained in a large meta-analysis of all the available published studies on cardiac aspects of GH replacement. After therapy with GH in adult patients, significant positive effects were noted on LV mass, interventricular septum, LV posterior wall, LV end-diastolic diameter, and stroke volume.[62] These results apply obviously to physiologic GH substitution because an excess of GH, as seen in patients with acromegaly, may induce pathologic cardiac hypertrophy, predisposing to arrhythmias and ultimately cardiac failure. An improvement in the lipid profile is often seen after GH replacement therapy. A meta-analysis of several studies documented the effects of GH therapy on total cholesterol: the changes are particularly prominent in elderly patients with increased serum cholesterol levels and are not clearly seen in young subjects with normal cholesterol levels. Apo B-100, the crucial protein for cholesterol metabolism and a known independent risk factor for CV disease,[63] has been shown to decrease after GH therapy.[64] LDL cholesterol concentrations decrease, although with the currently used lower substitution doses of GH the effect is more modest and not seen uniformly in randomized placebo-controlled trials. In comparison with statins, the effect of GH may be less impressive because the mean decrease in total cholesterol level is about 10% to 20% with GH. It is, however, not negligible because it is an additive effect.[33] The effects on serum triglycerides have been variable, some authors reporting a decrease and others not finding this result.[5,10] Arterial distensibility and plaque formation are also favorably affected by GH treatment. These findings have been documented by echo Doppler ultrasound investigations of the carotid arteries. IMT has also been measured. The IMT decreased significantly (approximately 0.1 to 0.2 mm) with GH treatment. Nonetheless, the effect was dependent on continuous treatment; stopping GH treatment for 6 to 12 months resulted in a recurrent increase of IMT. GH treatment is also associated with improved peripheral vasodilatation. This outcome can be documented by testing the flow-mediated vasodilatation of a brachial artery (see previous material). These results point to endothelium-derived NO and its crucial role in vasodilatation. Production of NO, judged from urinary nitrate and cyclic guanosine monophosphate production, shows a sustained improvement with GH treatment. In light of these effects, it is not surprising that systolic and diastolic blood pressure measurements decrease slightly but significantly in hypertensive and normotensive patients in response to GH replacement therapy. The role of inflammation is critical in the pathogenesis of atheromatosis. CRP, by interacting with endothelial receptors, accelerates vascular inflammation and the development of atheromas. Its effect is mediated mainly through IL-6, a proinflammatory cytokine. hsCRP values are good indicators of CV risk; values of less than 1 mg/L, 1 to 3 mg/L, or greater than 3 mg/L indicate low, average, and high risk, respectively. Most patients with GH deficiency have CRP values in the range of moderate to high risk.[65] By controlling for other risk factors, it can be estimated that the risk for an acute CV event is increased approximately 4-fold. Most, but not all, published studies[20] demonstrate a significant decrease of CRP values with GH replacement therapy. IL-6, myeloperoxidase, and fibrinogen are also inflammatory markers of vascular risk, although they have not been studied as extensively as CRP. It is noteworthy that only a few drugs have been shown to decrease CRP values, the best known being the statins. GH is also a cytokine, and its receptor belongs to the family of the cytokine receptors. Intracellular activation occurs through STAT4 (the signal-transducing activator of transcription protein 4), a well-known pathway for cytokines. It is tempting to speculate that by interfering with the action of proinflammatory cytokines, GH reduces or even reverses IMT and plaque formation. Caveats Although one might be impressed by the many favorable effects of GH substitution in patients with GH deficiency, it must be remembered that acromegaly is associated with an increased incidence of cardiac insufficiency and arrhythmias, development of IR, and overt type 2 diabetes. Interestingly, patients with severe GH deficiency also show signs of IR. During early GH treatment, glucose tolerance may even worsen before improving. Typically, it normalizes after several months of treatment, probably a consequence of decreasing abdominal adiposity. With long-term GH treatment in nonobese patients, serum insulin, glucose levels, and the homeostasis model assessment index (insulin/glucose ratio as an index of IR) tend to normalize. In obese patients with GH deficiency, however, an increase in blood glucose levels, in rare cases within the diabetic range, has been observed.[33] Thus, carbohydrate metabolism during long-term GH therapy should be monitored. Conclusion For clinicians, it is becoming clear that the substantially increased CV risk in patients with hypopituitarism and GH deficiency can be ameliorated by adequate treatment with GH. The effects of GH replacement have been carefully monitored in the KIMS (Pharmacia and Upjohn International Metabolic Surveillance) database, which includes approximately 10,000 patients. This database did not specifically address the question of CV risk; thus, the possibility exists of inadequate and potentially biased patient recruitment. In these GH-treated patients, the incidence of CV events did not differ from that in the control population after a mean of 3 years, a finding that suggests that GH replacement may be antiatherogenic. There was also no evidence of increased incidence of malignant disease.[66-69] For this reason, in many countries, GH substitution therapy is routinely accepted and reimbursed by medical insurance companies. Continued monitoring of GH-treated patients should also facilitate accumulation of evidence of the CV benefit of this treatment. In summary, there is no doubt that adult patients with hypopituitarism and GH deficiency have an increased CV risk (odds ratio of 2 for men and 3.5 to 4 for women). The risk is not only limited to overweight patients but also seen in those with normal body mass index. In the follow-up of these patients with GH treatment, body weight and abdominal adiposity, readily documented by recording the waist-to-hip ratio, are certainly useful in daily clinical practice. Among the biochemical factors, hsCRP, total cholesterol, LDL, and apo B levels can be monitored. Moreover, in patients with known CV disease, IMT may be a helpful marker. The effectiveness of GH treatment must be monitored carefully by measuring the age- and sex-adjusted IGF-I values, and the glucose status must be followed throughout the entire treatment period. Improvement of CV function should not be expected before at least 6 months of stable treatment.
  8. He's great, isn't he? I'm so excited that your story will be out there in the medical communicty, Cindy! It will help so many. Sorry about the continued csf leak issue, though! Hugs, Linda
  9. I got interrupted and didn't get to finish listening to the interview, but what I did hear was just great. I wanted to thank Robin and MaryO for setting this venue up, and Alicia for sharing her story tonight. (Alicia - glad you found us!!) It was great to put a "voice" to her posts! (and Robin, thanks too for explaining that all we have to do is click on the link you provided and that we don't have to download anything)
  10. I'm listening right now - this is so very cool! Robin - you are a born interviewer....and Mary, I am loving hearing your story!!
  11. Phil, I am so so so sorry that you are experiencing symptoms and feel like you still have Cushings. One thing I wanted to mention is that sometimes additional tumor can be lurking in places that are not visible during surgery. It is so frustrating, and I'm so sorry. Have you done any cortisol testing yet or gotten a post-op MRI? We're here to help as you face whatever may be next. Lots of hugs, Linda
  12. Petrosal sinus sampling for diagnosis of Cushing's disease : evidence of false negative results Titre du document / Document title Petrosal sinus sampling for diagnosis of Cushing's disease : evidence of false negative results Auteur(s) / Author(s) LOPEZ L. (1) ; BARCELO B. (1) ; LUCAS T. (1) ; SALAME F. (1) ; ALAMEDA C. (1) ; BORONAT M. (1) ; SALTO L. (1) ; ESTRADA J. (1) ; Affiliation(s) du ou des auteurs / Author(s) Affiliation(s) (1) Department of Endocrinology, Cl?nica Puerta de Hierro, Universidad Aut?noma de Madrid, Madrid, ESPAGNE R?sum? / Abstract OBJECTIVE While inferior petrosal sinus (IPS) sampling correctly diagnoses pituitary-dependent Cushing's syndrome if a significant ratio of plasma ACTH between the IPS and the peripheral blood is demonstrated, little has been said about the significance of a negative ratio in Cushing's disease (e.g. a false-negative result). This study evaluates the results of IPS sampling in patients with Cushing's disease, and compares them with both imaging findings and transsphenoidal examination. DESIGN The results of IPS sampling were retrospectively compared with both imaging findings and transsphenoidal examination. IPS samples were obtained before and 2, 5 and 10 minutes after intravenous administration of 100 μg of CRH. PATIENTS Thirty-two patients with Cushing's disease were evaluated. All subsequently underwent transsphenoidal examination of the pituitary gland. MEASUREMENTS The ratio of the ACTH concentrations at the IPS and in the peripheral blood (IPS : P ratio), and the ratio of the ACTH concentrations between the IPSs (interpetrosal ratio) were calculated. Radiographic evaluation of the pituitary gland was performed with magnetic resonance imaging (MRI, 29 cases) or computed tomography imaging (CT, 3 cases). RESULTS Transsphenoidal examination of the pituitary gland revealed a microadenoma in 27 cases. Radiological imaging showed a signal compatible with a microadenoma in 22 cases (68.8%), and correctly located the tumour at the side found at surgery In 14 of the 22 cases with positive transsphenoldal findings (MRI 13 cases, CT 1 case, overall 63.6%). Successful bilateral catheterization was accomplished in 30 patients (93.8%). Samples before and after CRH stimulation were drawn in 24 cases. No major complications were observed with the technique. IPS catheterization correctly predicted Cushing's disease (by means of a significant IPS : P ACTH ratio) in 27 of the 30 patients (90%) with basal sampling, and in 23 of the 24 cases with samples drawn before and after CRH administration (95.8%). Taking Into account the 12 patients with a lateral microadenoma shown at transsphenoidal examination, IP sinus ACTH ratio was in agreement with the side recorded by the neurosurgeon in 8/12 cases (66.7%). MRi correctly located the tumour in 8112 patients (66.7%). One patient showed no significant IPS : P ACTH ratio in any set of samples. His MRI showed no sign of a microadenoma. Two years later, another pituitary MRI evaluation showed a midline hypodense signal. The transsphenoidal examination revealed a microadenoma and the post-operative plasma cortisol and urinary free cortisol fell to 293 nmol/l and 100 nmol/24 h, respectively. CONCLUSIONS Only when a significant IPS : P ACTH ratio is present can Cushing's disease be established by IPS sampling. The absence of a significant IPS : P ACTH ratio does not necessarily imply ectopic secretion of ACTH, nor does it exclude Cushing's disease. The results of lateralization by IPS sampling do not remove the need for a thorough transsphenoidal examination of the contents of the sella turcica. Revue / Journal Title Clinical endocrinology (Clin. endocrinol.) ISSN 0300-0664 CODEN CLECAP Source / Source 1996, vol. 45, no2, pp. 147-156 (1 p.1/4)
  13. Hi, Shelley. I had the dex/crh test as well....and my results were considered "very abnormal", however not diagnostic, since the upward spike in cortisol didn't happen until after 30 minutes. I believe the "diagnostic" level for the test is 1.4 or higher at the 15 minute mark. My results were: at 15 minutes: 1 at 30 minutes: 1 at 45 minutes: 2 at 60 minutes: 4 Earlier that same week, I had two high midnight serum tests (two nights in a row), one elevated ACTH at midnight, one high salivary, and two absolutely normal 24 hour ufcs done on the same days as the late night blood draws. My surgical pathology confirmed Cushings. Linda
  14. You ARE a tech wizard, Robin! I love it!! But is it something us mere mortals can do? I particularly like the idea of organizing all my "stuff" in one area....right now I have links saved here and there, articles saved here and there, etc. And I love the idea of being able to share with each other, too. Very cool!!
  15. I have learned so much on this cushing's journey, much of it from all of you and this site. I wanted to share those learnings, in the event that it helps anyone else. Obviously - my own opinions here! My best wishes to everyone on their cushings journey. Linda ********************************************** 1. Trust your instincts. 2. Trust your instincts some more. 3. Do your research – read everything you can, talk to people, use this website and the message boards. Slog through research papers. Not all of it will make sense, but it is amazing how much you can learn, and how much it will help you on your diagnostic journey. 4. Not everyone will have every one of the "typically described" symptoms of the hump, moon face, straie, and central obesity. Some people get them all, some people get some, and others don't develop these signs. 5. While substantial weight gain is very common with Cushings, there are some people who have only mild or moderate weight gain. What seems to be the common thread, however, is the inability to lose it in spite of diet and exercise. 6. You don't need to test positive on every single test, or test positive on every type of test, to have Cushings. There is substantial variation in how we present with the disease, and in which tests will identify the excess cortisol in our bodies. Do not let a single negative result on any one test, or negative results on a particular type of test, prevent you from aggressively pursuing a Cushings diagnosis if there is strong suspicion. For example, it is possible for an individual to have proven Cushings without ever having a positive on a ufc or dex suppression test. 7. Do not waste time, energy and financial resources on unhelpful doctors. 8. Whenever possible, get to a true Cushings expert as soon as the disease is suspected. 9. When seeing a new endocrinologist, don't be afraid to ask: a. What is your opinion on cyclic or intermittent Cushings? b. When and how might you diagnose a mild or early case of Cushings? Do you recommend treatment in those cases? c. Do you believe it is possible for someone to have Cushings without all or some of the commonly associated stigmata (straie, hump, moon face, substantial weight gain)? d. What is your diagnostic criteria for Cushings? i. Lab tests ii. Physical symptoms iii. Imaging e. How many patients have you diagnosed with Cushings? f. What surgeon(s) do you recommend and work with for your patients with tumors that are causing Cushings? g. If Cushings is suspected, how can we work together to maximize testing to give us answers as quickly as possible? How can I most easily get my test results from your office? 10. Make sure your doctor is willing to support the amount of testing that may be necessary to allow you to begin to distinguish between high and low periods. Make sure your doctor is also willing to support multiple types of tests to appropriately rule in/out Cushings. 11. Create a binder and get copies of every single test. (Make additional copies of test results so that you have extra available to perhaps send in advance to a new doctor, or to be able to readily provide a copy during your appointment as necessary). Get copies of clinic notes as well. Organize them into the binder. My binder has the following tabs: a. Spreadsheet that summarizes most relevant test results b. Current medical history/summary of symptoms c. Imaging reports d. Cortisol test results (serum, salivary, ufcs) e. Other lab results (including EKGs and other relevant tests) f. Eyes (visual field tests, letter from eye doctor, etc) g. Clinic Notes 12. Research tests. It is not uncommon for a test to be ordered or interpreted incorrectly. 13. MRIs are only tools. They can be interpreted differently by different people and they may not accurately identify the extent or location of a tumor. 14. Create a spreadsheet, or use a journal, to track symptoms daily. Log test results so that you can begin to see patterns. Symptoms may be as subtle as canker sores, or cracked lips or skin, a single pimple, or may be more obvious such as severe swings in mood and energy levels, insomnia, bad acne, etc. Write it all down and track it. 15. Test whenever you feel different. 16. Symptoms of a high for you may or may not match what is typically described for a high. You may experience a high differently. For example, achiness is frequently described as a low symptom, but it may occur during a high in your case. Tracking symptoms and correlating test results help to identify patterns of a high. 17. Start testing your own blood sugar to identify any possible blood sugar problems and to look for possible correlation between episodes of high blood sugar and high cortisol levels. This won't apply to everyone, and may not be useful in your case, but it was very helpful to me. A very good Walgreen's brand glucometer is only $20. 18. Get a blood pressure cuff and start checking your own bp at home. Look for patterns there as well. 19. Summarize test results for your doctor (PCP, endocrinologist, or even surgeon). Create a simple table that shows your relevant test results over time. 20. Collect photos that illustrate how your physical appearance has changed. 21. When researching surgeons, learn as much as you can about the different techniques and approaches. Some may seem similar, but there are differences that are important to understand. 22. When interviewing surgeons, the following questions may be helpful(mostly pituitary focused): a. How will you approach the tumor? b. What instruments are used? Endoscope? Microscope? Both? c. What incisions are made? d. Do you need to clear any kind of path within the nasal or sinus area for your instruments? How will you do that? e. What stitches will I have? f. Do you use a "fat plug"? g. Do you use a lumbar drain? h. Will there be any nasal packing? i. How will my head be immobilized during surgery? (Is a "halo" used?) j. Do you use Doppler to localize the carotid arteries? (not necessary in fully endoscopic procedure as I understand it) k. Describe your approach to locating any tumor seen on the MRI, and what you will do to find any other tumors that may be in, on, or around the gland. l. Under what circumstances might you find it necessary to remove either part of the pituitary gland, or all of it? m. How many of these procedures have you done? n. How long have you been performing this particular procedure? o. What are some typical complications that occur with this procedure? How do you manage those complications? p. Based on my MRI, is there anything in particular that might suggest greater risk of diabetes insipidus or other long term complications with this surgery? q. Tell me what to expect in terms of post-operative pain and how it will be managed. r. Is an ICU stay typically necessary? s. How long can I expect to stay in the hospital? t. Do you give steroids intra-operatively? u. When do you test post-op cortisol levels? What is the cortisol replacement therapy protocol? If my endocrinologist is out of state, who will be monitoring that part of my testing and prescribing cortisol replacement as necessary? v. When can I travel to return home? w. What restrictions will I have once discharged? (Lifting, noseblowing, how I sleep, driving, exercise, etc) x. How do I contact you if I should have any problems or concerns once discharged? y. How will you communicate with my endocrinologist regarding the results of my surgery? z. What is your protocol for following up with patients post-operatively? aa. What is your rate of post-operative sinus infection? bb. What is your rate of post-operative diabetes insipidus, both temporary and long-term? 23. These questions for your endocrinologist may be helpful once surgery is planned: a. How will you determine my post-op cortisol replacement needs? b. At what point will you recommend that I begin tapering my dose? What are your guidelines for each step in the weaning process? c. Based on my case and your experience with other Cushings patients, what might I experience during the recovery period? How long before I feel "better"? What restrictions will I have? d. When and how will you determine if other pituitary functions should be tested post-op? How will you test other pituitary functions post-op? e. Do you provide a prescription for emergency injectible hydrocortisone? f. Do you provide written instructions I may carry for Emergency Room staff in the event that I have an adrenal crisis? g. How long should I expect to be off work? h. How will you follow up with me post-op? i. What is the best way to reach you if I have any questions or concerns after surgery? 24. Participate on the Cushings Boards to support yourself and others through the Cushings diagnosis and treatment journey. (You'll also make some new friends.)
  16. All right, Lynn!!!!!!!!!!!!!!!!!!!!!! You and Cherri wrote excellent responses to a dangerous article. And....I'm absolutely appalled at the TV commercial, without even seeing it. How incredibly ignorant and insensitive. Do they (Toyota and ad agency) have a collective IQ of 12?
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