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cat lady

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  1. I posted about Henry VIII a while back. There were a bunch of articles on him about a year ago or so. And I vote for Sally Struthers. Poor woman has been picked on for years.
  2. How Should a Nonfunctioning Pituitary Macroadenoma be Monitored After Debulking Surgery? Yona Greenman; Naftali Stern Published: 09/10/2009 Summary and Introduction Summary Transsphenoidal surgery is the treatment of choice for nonfunctioning pituitary macroadenomas but is seldom curative. Tumour progression rates are high in patients with postoperative remnants. Therefore, long-term monitoring is necessary to detect tumour growth, which may be asymptomatic or manifest with visual field defects and/or pituitary dysfunction. In view of the generally slow-growing nature of these tumours, yearly magnetic resonance imaging, neuro-ophalmologic and pituitary function evaluation are appropriate during the first 3-5 years after surgery. If there is no evidence for tumour progression during this period, testing intervals may be extended thereafter. Introduction Most clinically nonfunctioning pituitary adenomas (NFPA) are of gonadotroph cell origin, but rarely manifest with clinical signs or symptoms related to gonadotropin excess. Headaches, visual field compromise and decrease in visual acuity, as well as hypopituitarism are the most common presenting features of NFPA, and are all induced by pressure of the tumour on surrounding structures. Therefore, tissue decompression is the main therapeutic goal in NFPA, being effectively achieved in most cases through transsphenoidal excision of the tumour. Nevertheless, these usually large and invasive tumours often cannot be completely resected. NFPA patients need long-term surveillance, although the best means and frequency of follow-up have not been clearly established. The monitoring strategy used in our institution and presented herein has evolved based on published observational studies on the natural history of NFPA, and clinical experience. The Problem of Lack of Secretory Markers In clinically functioning pituitary adenomas, circulating hormone levels are accurate tumour markers. Hence, the presence of elevated serum hormone concentration may indicate incomplete surgical resection or tumour recurrence even in face of an apparently normal imaging study. This important tool is lacking for the follow-up of most NFPA, as elevated gonadotropins are detected only in a minority of patients on basal conditions, and the TRH-induced increase in β-subunits is not a sufficiently reliable marker for the presence of residual tumour.[1] Consequently, detection of recurrence or residual tumour growth relies directly on imaging studies, or is indirectly based on appearance of new defects or deterioration of previously impaired visual and pituitary function. Early Postoperative Assessment Visual Fields Resolution of headaches and amelioration of visual field defects occur shortly after surgery in the majority of patients. The recovery of visual fields is progressive, with an early fast phase of improvement during the first week after surgery, an early slow phase (4-6 months postoperatively) by the end of which most of the eventual recovery takes place and a late phase (up to 3-5 years) in which mild further improvement may still occur.[2] Overall, normalization of visual function occurs in 35-39% and improvement in 50-60% of patients.[2,3] Worsening of vision is reported in 0?5-2?4% of patients, and as with other surgical complications, its prevalence depends on the experience of the neurosurgeon and the volume of operations performed in a particular centre.[4] Based on these data, a neuroophthalmological assessment should be performed 1 week and again after 3-6 months following surgery. The visual status obtained in these evaluations will be the baseline for subsequent comparisons. Pituitary Function In most[5] but not all[6] series, normalization of one or more hypothalamo-pituitary-axis function has been reported after surgery, whereas worsening of pituitary function is less common. The degree of improvement is variable, occurring in 15-50% of patients.[5] This variability probably reflects the actual degree and duration of the preoperative impairment, surgical expertise, the use of different endocrine tests and criteria for the diagnosis of hypopituitarism as well as the surgical route of operation. Pituitary function normalized in 19?6%, improved in 30?1%, remained unchanged in 48?9% and worsened in 1?4% of patients following surgery by the transsphenoidal route; whereas after transcranial surgery, none of the patients had normalization, only 11?3% had improvement and 15% had deterioration of pituitary function, as reported by Nomikos et al.[7] Transient diabetes insipidus (DI) complicates up to 15% of surgeries, but permanent DI is less frequent, occurring in 0?9%[8] to 2% of patients. Transient hyponatremia secondary to ADH excess may occur in the context of a triphasic pattern of DI or as an isolated event, peaking at postoperative day 7.[9] During the immediate postoperative period (7-10 days), emphasis should focus on evaluation and correction of corticotroph and posterior pituitary deficits. The recovery of the hypothalamo-pituitary adrenal-axis occurs very early in the postoperative period, as ACTH levels increase within hours after surgery in patients who recover adrenal function,[10] and an insulin tolerance test (ITT) performed within 8 days after surgery was 100% sensitive and specific in predicting long-term normalcy of the axis.[11] In practice, morning serum cortisol levels are measured 3-7 days after surgery depending on the schedule of perioperative glucocorticoid coverage, and indicate the need for continuing steroid replacement until definitive testing is performed. Thus, morning cortisol levels less than 100 nmol/l or over 450 nmol/l are consistent with ACTH deficiency and sufficiency, respectively, and intermediate levels require further testing.[12] ACTH stimulation tests, while easier and safer than ITT, are not a reliable enough means to detect new onset of postoperative secondary hypoadrenalism in the first 4-6 weeks, as adrenal cortical mass and response may be still preserved during this time interval, but the low-dose 1 μg ACTH test is a powerful and sensitive tool thereafter.[13] The time frame for recovery of other hypothalamo-pituitary-axes has not been longitudinally studied and the best timing for testing has not been established. Although this is traditionally performed 4-6 weeks after surgery,[9] the long-term predictive value of tests conducted at this time is not known. It is reasonable to re-assess the function of axes found to be impaired at the first postoperative evaluation 3, 6 and 12 months thereafter, both to assess the current status of pituitary function and need for hormone replacement, and to establish the baseline for subsequent follow-up. Imaging Early postoperative magnetic resonance images (MRI) are difficult to interpret owing to intrasellar fluid and blood collection, the presence of implanted sealing materials and incomplete descent of residual suprasellar tumour remnants. Therefore, the completeness of tumour resection and assessment of remnant size are better achieved by MRI performed at least 3-4 months after surgery.[14] In some cases, even at this point, the distinction between adenomatous tissue and postoperative changes and fibrosis may be difficult. In this context, 11C-methionine PET, which detects protein synthesis in viable tissue, could be helpful, but its place in the management of pituitary tumours needs further validation.[15] The initial postoperative MRI will be the baseline against which subsequent imaging will be compared with for the detection of recurrence or tumour progression. Long-term Monitoring The long-term follow-up strategy is based on the slow-growing nature of NFPA and on the reported rates of recurrence or tumour remnant progression. The calculated tumour volume doubling time (TVDT) is variable and ranges from 0?8 to 27?2 years.[16] Patients with TVDT under 5 years were younger (50 ? 15 years) than those with TVDT over 5 years (69 ? 7 years).[17] The true recurrence/progression rate of NFPA is difficult to assess because of selection bias (more aggressive tumours being referred to radiotherapy)[18] and variable surveillance methods. Most series are retrospective in nature and lack a pre-established protocol for imaging intervals. Tumour growth may be detected earlier, at an asymptomatic stage, through serial MRI imaging, or later, when patients present with mass-related symptoms. Despite these caveats, patients in whom complete tumour resection has been achieved have, in general, a low risk for recurrence, whereas those with residual tumours have high long-term progression rates (13% and 41%, respectively).[5] Longer follow-up duration is associated with increased detection of recurrence/progression.[6] The mean time for detection of tumour progression varies between 2?2 and 7?5 years ( Table 1 ), ranging from 6 months to 20 years. Some clinical aspects, such as young age[3] and extent of suprasellar extension in the residual tumour,[19] have been associated with a higher risk of tumour enlargement. This may indicate the need for more careful surveillance for these patients. Nevertheless, in general, our ability to predict tumoural biological behaviour is poor. Morphological features in the pathologic specimen, such as cytological atypia, and presence of mitoses do not reliably reflect tumour aggressiveness. Similarly, markers of cell proliferation, such as Ki-67, PCNA and p53, do not consistently correlate with tumour invasiveness or recurrence.[20,21] Therefore, we perform MRI yearly for the first 3-5 years after surgery in all patients, for the detection of more rapidly growing tumours. The detection of an increase in tumour mass not leading to prompt re-operation will require a repeat imaging study at an earlier time. In the absence of such progression, however, imaging intervals may be then spaced to every 2 years and later on to every 3 years, as at this point we are dealing with stable or very slow growing tumours. Technical aspects of MRI interpretation and tumour size evaluation should be established a priori and standardized to allow for accurate comparisons over time. Another aspect to be emphasized is the need to compare the most current imaging study not only with the previous, but also with earlier studies, as this is the only way to reliably detect small size changes over time. Visual field testing should be performed generally every 12 months, especially when the tumour margins are in relative proximity to the optic chiasm, or in between imaging studies in other instances. More frequent visual assessment is needed for tumours quite adjacent to the optic chiasm, as appearance of new or deterioration of existing visual field defects is reported in nearly half of the patients in whom tumour growth occurs during conservative follow-up.[22] Pituitary function should also be assessed on a yearly basis, as it may become compromised with tumour growth. Table 1. Postoperative Recurrence of NFPA Not Treated With Radiation, According to Degree of Surgical Resection, in Series in Which Time to Recurrence Was Specified Series Ref. N No residual tumour in postoperative MRI Residual tumour Recurrence Mean time to detection (year) 5 year RFS (%) Growth Mean time to detection (year) 5 year PFS (%) 10 year PFS (%) Soto-Ares et al. (2002) 27 51 0/17 (0) 13/34 (38?2) 2?2 ? 1?4 60?9 Greenman et al. (2003) 19 108 6/30 (20) 5 ? 2 84 41/78 (52?5) 2?2 ? 1?1 30 Dekkers et al. (2006) 6 97 0/27 (0) 9/70 (12?8)* 6?3 92 74 Ferrante et al. (2006) 28 150? 14/73 (19?2) 7?5 ? 2?6 45/77 (58?4) 5?3 ? 4 Van den Bergh et al. (2007) 29 28 16/28 (57) 2?5 49 22 Total 434 20/147 (13?6) 124/287(43) Values in parentheses are percentages. RFS = recurrence-free survival; PFS = progression-free survival. *Including six patients who received radiation therapy and had no evidence of tumour growth. ?After exclusion from the initial cohort of patients who received radiation therapy or were reoperated. Does Treatment Choice Affect Monitoring? Patients in whom tumour has been completely excised usually undergo expectant follow-up as recurrence rates are low, as detailed earlier. In contrast, the optimal management of patients in whom residual tumour is detected on postoperative MRI is controversial, and may include observation alone,[6] the use of dopamine agonists (DA)[23] or radiation therapy.[24] Discussion on the merits or indications for the different therapeutic approaches is beyond the scope of this document. Nevertheless, the choice of treatment may influence some aspects of long-term monitoring. For example, particular attention should be given to pituitary function evaluation of irradiated patients in view of the high incidence of radiation-related hypopituitarism that is insidious and may take up to 20 years to develop.[24] Patients on DA therapy may need periodic echocardiograms in view of the increased incidence of valvular heart disease reported in cabergoline treated patients with Parkinson's disease,[25] although the lower doses used for treatment of pituitary disease have not generally been associated with clinically significant alterations in most studies.[26] Radiation and DA treatment reduce tumour progression rates to 8-20%[5] and 21%, respectively,[23] but because the anatomical response of an individual tumour to therapy cannot be anticipated, the imaging strategy should be similar to that of untreated patients. [ CLOSE WINDOW ] References 1. Greenman, Y., Tordjman, K., S?mjen, D. et al. (1998) The use of β-subunits of gonadotrophin hormones in the follow-up of clinically non-functioning pituitary tumours. Clinical Endocrinology, 49, 185-190. 2. Gnanalingham, K.K., Bhattacharjee, S., Pennington, R. et al. (2005) The time course of visual field recovery following transsphenoidal surgery for pituitary adenomas: predictive factors for a good outcome. Journal of Neurology, Neurosurgery and Psychiatry, 76, 415-419. 3. Losa, M., Mortini, P., Barzaghi, R. et al. (2008) Early results of surgery in patients with nonfunctioning pituitary adenomas and analysis of the risk of tumor recurrence. Journal of Neurosurgery, 108, 525-532. 4. Ciric, I., Ragin, A., Baumgartner, C. et al. (1997) Complications of transsphenoidal surgery: results of a national survey, review of the literature and personal experience. Neurosurgery, 40, 225-236. 5. Molitch, M.E. (2008) Nonfunctioning pituitary tumors and pituitary incidentalomas. Endocrinology and Metabolism Clinics of North America, 37, 151-171. 6. Dekkers, O.M., Pereira, A.M., Roelfsema, J.H.C. et al. (2006) Observation alone after transsphenoidal surgery for nonfunctioning pituitary macroadenoma. Journal of Clinical Endocrinology and Metabolism, 91, 1796-1801. 7. Nomikos, P., Ladar, C., Fahlbusch, R. et al. (2004) Impact of primary surgery on pituitary function in patients with non-functioning pituitary adenomas - a study on 721 patients. Acta Neurochirurgica, 146, 27-35. 8. Nemergut, E.C., Zuo, Z., Jane, J.A. et al. (2005) Predictors of diabetes insipidus after transsphenoidal surgery: a review of 881 patients. Journal of Neurosurgery, 103, 448-454. 9. Ausiello, J.C., Bruce, J.N. & Freda, P.U. (2008) Postoperative assessment of the patient after transsphenoidal pituitary surgery. Pituitary, 11, 391-401. 10. Arafah, B.M., Kailani, S.H., Nekl, K.E. et al. (1994) Immediate recovery of pituitary function after transsphenoidal resection of pituitary macroadenomas. Journal of Clinical Endocrinology and Metabolism, 79, 348-354. 11. A., R.J., Shewbridge, R.K. & Shepherd, M.D. (1997) Which patients benefit from provocative adrenal testing after transsphenoidal pituitary surgery? Clinical Endocrinology, 46, 21-27. 12. Inder, W.J. & Hunt, P.J. (2002) Glucocorticoid replacement in pituitary surgery: guidelines for perioperative assessment and management. Journal of Clinical Endocrinology and Metabolism, 87, 2745-2750. 13. Kazlauskaite, R., Evans, A.T., Villabona, C.V. et al. (2008) Corticotropin tests for hypothalamic-pituitary-adrenal insufficiency: a metaanalysis. Journal of Clinical Endocrinology and Metabolism, 93, 4245-4253. 14. Kremmer, P., Forsting, M., Ranaei, G. et al. (2002) Magnetic resonance imaging after transsphenoidal surgery of clinically nonfunctional pituitary macroadenomas and its impact on detecting residual adenoma. Acta Neurochirurgica (Wien), 144, 433-443. 15. Tang, B.N.T., Levivier, M., Heureux, M. et al. (2006) 11C-methionine PET for the diagnosis and management of recurrent pituitary adenomas. European Journal of Nuclear Medicine and Molecular Imaging, 33, 169-178. 16. Honegger, J., Zimmermann, S., Psaras, T. et al. (2008) Growth modeling of non-functioning pituitary adenomas in patients referred for surgery. European Journal of Endocrinology, 158, 287-294. 17. Tanaka, Y., Hongo, K., Tada, T. et al. (2003) Growth pattern and rate in residual nonfunctioning pituitary adenomas: correlations among tumor volume doubling time, patient age, and MIB-1 index. Journal of Neurosurgery, 98, 359-365. 18. Turner, H.E., Stratton, I.M., Byrne, J.V. et al. (1999) Audit of selected patients with nonfunctioning pituitary adenomas treated without irradiation - a follow-up study. Clinical Endocrinology, 51, 281-284. 19. Greenman, Y., Ouaknine, G., Veshchev, I. et al. (2003) Postoperative surveillance of clinically nonfunctioning pituitary macroadenomas: markers of tumour quiescence and regrowth. Clinical Endocrinology, 58, 763-769. 20. Gejman, R., Swearingen, B. & Hedley-Whyte, E.T. (2008) Role of Ki-67 proliferation index and p53 expression in predicting progression of pituitary adenomas. Human Pathology, 39, 758-766. 21. Dubois, S., Guyetant, S., Penei, P. et al. (2007) Relevance of Ki-67 and prognostic factors for recurrence/progression of gonadotropic adenomas after first surgery. European Journal of Endocrinology, 157, 141-147. 22. Karavitaki, N., Collison, K., Halliday, J. et al. (2007) What is the natural history of nonoperated nonfunctioning pituitary adenomas? Clinical Endocrinology, 67, 938-943. 23. Greenman, Y., Tordjman, K., Osher, E. et al. (2005) Postoperative treatment of clinically nonfunctioning pituitary adenomas with dopamine agonists decreases tumour remnant growth. Clinical Endocrinology, 63, 39-394. 24. Gittoes, N.J.L. (2003) Radiotherapy for non-functioning pituitary tumors- when and under what circumstances? Pituitary, 6, 103-108. 25. Zanettini, R., Antonini, A., Gatto, G. et al. (2007) Valvular heart disease and the use of dopamine agonists for Parkinson's disease. New England Journal of Medicine, 356, 39-46. 26. Molitch, M.E. (2008) The cabergoline-resistant prolactinoma patients: new challenges. Journal of Clinical Endocrinology and Metabolism, 93, 4643-4645. 27. Soto-Ares, G., Cortet-Rudelli, C., Assaker, R. et al. (2002) MRI protocol technique in the optimal therapeutic strategy of non-functioning pituitary adenomas. European Journal of Endocrinology, 146, 179-186. 28. Ferrante, E., Ferraroni, M., Castrignano, T. et al. (2006) Non-functioning pituitary adenoma database: a useful resource to improve the clinical management of pituitary tumors. European Journal of Endocrinology, 155, 823-829. 29. van den Bergh, A.C.M., van den Bergh, G., Schoorl, M.A. et al. (2007) Immediate postoperative radiotherapy in residual nonfunctioning pituitary adenoma: beneficial effect on local control without additional negative impact on pituitary function and life expectancy. International Journal of Radiation Oncology, 67, 863-869. [CLOSE WINDOW] Authors and Disclosures Yona Greenman and Naftali Stern, Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center and the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel Correspondence to Yona Greenman, Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv-Sourasky Medical Center, 6 Weizmann Street, Tel Aviv 64239, Israel. Tel: +972 36973899; Fax: +972 36973053; E-Mail: greenman@tasmc.heatlh.gov.il Clin Endocrinol. 2009;70(6):829-832. ? 2009 Blackwell Publishing
  3. VIDEO LINK Woman With Hormone Condition Stands 6-Feet, 6-Inches; Weighs 476 Pounds A woman suffering from a rare hormonal disorder stands 6-feet, 6-inches, weighs 476 pounds and is still growing, the Daily Mail reports. Tanya Angus is believed to be one of the tallest and heaviest women on the planet and doctors say her condition cannot be stopped by medication. Angus, who appeared on NBC's Today show in June, lives in Nevada and suffers from a condition known as acromegaly, also referred to as gigantism. At 20-years-old, Angus stood 5-foot, 11-inches and weighed just 115 pounds, but her height and her weight soon started to spiral out of control. Her doctor diagnosed her with gigantism and she was sent to a specialist, the Daily Mail reported. RELATED: Doctor Discovers Man's Brain Tumor Through 'Spongy' Handshake An MRI scan showed she had a tumor the size of a grapefruit in her brain which had wrapped itself around her inner carotid artery, causing an overproduction of growth hormones. In 2003, she underwent surgery to remove most of the tumor, although small parts of it were too difficult to separate from her brain. She was then given a cocktail of drugs to try to control the huge amounts of growth hormones still in her body. Her growth hormones totaled 3,000. An average person has about 250. Despite the drugs, her growth hormone level has never fallen below 900. At 6ft6ins and 34stone, meet one of the largest and heaviest women on the planet - and she's still growing Standing at 6ft 6ins and weighing 34 stone, this woman has been dubbed a modern-day giant - and, alarmingly, she is still growing. Tanya Angus, who suffers from a rare growth condition, is already one of the tallest and heaviest women on the planet. Now doctors say she is the only woman in the world whose growth cannot be halted by medication. Suffering from a rare disease known as Acromeglia, a condition often referred to as 'gigantism', (which means her body is producing too much growth hormone), Tanya rocketed from a slender 5ft 8ins at the age of 18 to a massive 6ft 6ins and 34 stone. 'I'm staying hopeful,' says 30-year-old Tanya, from Nevada, USA. 'Without hope you don't have anything. I hope they can stop me growing one day so I can try to live as normally as possible.' Tanya's troubles began in her late teens when she noticed that her feet, face and figure were continuing to grow at an alarming rate. 'I started to feel unhappy with my appearance. I started spending a fortune on make-up, trying to make myself look better. I couldn't understand why my face didn't look as attractive any more,' she said. Tanya also began suffering severe migraines and felt run down and depressed, as if she was suffering from constant flu. But though she kept going to see her GP, he believed the 20-year-old was just an attention-seeker hoping to be given anti-depressant drugs, and refused to help. Even more shockingly Tanya's figure started to alter. Her once-womanly body became larger overall, and straight up and down - like a man's. 'Someone at work actually asked me if I used to be a man,' she said. 'My voice had also changed and become deeper. I was devastated and started to feel very shy and insecure.' Things finally came to a head when her own boyfriend also asked her about her new shape, and got his mum to ask her whether she'd had a sex change. 'I was heartbroken and I decided I didn't want any more to do with him,' she said. 'I phoned my mum and said I wanted to come back to Nevada. 'As soon as my sister saw me at the airport, she knew I'd changed, and she called my mum and told her we needed to see a doctor.' The family GP immediately recognised the signs of gigantism and referred Tanya to a specialist. At that stage she was 6ft 1ins tall, and a size 14 to 16, with a size 10 feet. An MRI scan eventually showed a tumour the size of a grapefruit in her brain which had wrapped itself around her inner carotid artery, causing an overproduction of growth hormone. It was so big, doctors at first said there was nothing to be done. But Tanya's mum Karen, EMT-1 medical professional and firefighter, searched the Internet and medical publications until she finally found a doctor who said he could operate. In 2003, she Tanya finally underwent surgery to remove most of the tumour, although small parts of it were too difficult to separate from her brain. She was then given a cocktail of drugs to try to control the huge amounts of growth hormones still in her body. Tanya had a count of 3,000 of the hormones, compared to an average person's of just 250. Doctors were anxious to bring the level down to less than 1,000, but they were barely able to do that. Her height had crept up to 6ft 3ins, and she was now a size 20. Unable to walk properly, she had to live with her mother and stepfather. She barely went out and was subjected to stares and make rude comments in the street. 'It was horrible,' she said. 'My whole life had to change, and I couldn't do anything for myself any more. 'The hardest thing is that people kept thinking I was man, and calling me sir, which really annoys me. I try to dress in feminine clothes and wear make-up to look nice, but it's really hard when you're my size.' Two years later in 2005, the hormone levels again began to soar, and Tanya's mum sought out a second specialist who discovered the tumour had grown again and was now the size of an orange. She underwent further surgery, and fat from her stomach had to be used to pad out areas of brain tissue from where the tumour had been removed. Tanya was put on another set of medication to reduce the growth hormone, but her levels have never sunk to below 900 and are now over 1,000. She is now one of the world's tallest women, and also one of the heaviest. Then two years ago, Tanya also suffered a stroke, caused by the pressure her massive body was putting on her heart. She had to learn how to walk and talk again, and now suffers hearing difficulties. She recovered and went to live with her sister, but still struggles to get around, and now uses a wheelchair. 'Doctors just say there is nothing we can do for her,' said Karen. 'You don't know how many doctors we have called to try and help us. We've spent all our savings, over $200,000 (?122,300) trying to help her. 'One doctor even told me that my daughter had only two months to live. That was eight months ago, but I refused to believe it. 'I won't stop until we can find something to halt the growth.' Now Tanya has a new doctor, who she's been seeing for three months, and he is hopeful of finally finding a drug combination to slow down her growth. 'I'm doing this story because I want people to understand why I'm this way,' she says. 'It's not my fault I ended up like this. 'People even in my home town are still so hurtful, and I'd like people to be educated so they can treat me as a real person at last.' She?s 6-foot-6, 480 pounds ... and still growingTanya Angus, 30, has rare disorder that causes uncontrolled growth
  4. King size! Henry VIII's armour reveals he had a 52in girth - for which he paid a terrible price He was an immense figure in the history of England. Just how immense, however, has finally been revealed after a study of his body armour exposed Henry VIII's extraordinary vital statistics. It found that by the end of his reign the 6ft 1in Tudor king had a whopping 52in waist and 53in chest - enough to make him severely obese by modern standards. The study by the Royal Armouries coincides with a forthcoming exhibition of his supersized battle dress at the Tower of London to mark the 500th anniversary of him taking the throne. Here, Philippa Gregory reveals the heavy price he paid for being a very tubby Tudor. He was a lithe and handsome lothario who went on to acquire a truly legendary waistline. Until now, however, we haven't quite appreciated just how much larger than life Henry VIII really became. But as we approach the 500th anniversary of his coronation, new research by the Royal Armouries in Leeds reveals the full scale of his gargantuan girth. Analysing his suits of armour, many of which will be brought together in a new exhibition at the Tower of London in April, the researchers discovered that by the final years of his life, the 6ft 1in Tudor boasted a whopping 52in waist. In other words, the one-time royal pin-up was now barely taller than he was round. New research has shown that by the age of 45, Henry VII's weight had started to balloon as he suffered increasingly from chronic constipation and his body succumbed to hideous sores and repeated infections Of course, years earlier, life had started rather well for young Hal. The twentysomething Henry VIII was tall, muscle-bound and supremely fit - a talented athlete and a courageous jouster at the grand tournaments of the age. His armour from that period reveals some impressive dimensions: a 32in waist and a 39in chest. According to the Venetian Ambassador, he was 'the handsomest potentate I ever set eyes on, with an extremely fine calf to his leg . . . and a round face so very beautiful that it would become a pretty woman'. But not even Henry, who believed himself directly favoured by God, could stay young for ever. Indeed, physically and mentally, the final 15 years of his life saw the most astonishing deterioration. The golden Prince Hal became old, very likely mad - and monstrously fat. By his late 40s, he measured 48 inches around the middle and soon expanded to the colossal measurements of his twilight years. Peter Armstrong, the director of the Royal Armouries, describes him simply as 'an absolute monster'. Not that you would have known that from his portrayal by Jonathan Rhys Meyers in the recent hit TV series The Tudors. The final episode reached the mid-1530s, which meant that Henry was in his mid-40s and courting his future third wife, Jane Seymour, while still married to his second, the doomed Anne Boleyn. Expanding waistline: A suit of armour worn by the king in his early 20s But Rhys Meyers looked as slim and fresh-faced as he had at the start of the first series. In the 16th century, the life expectancy of the average man was 45. As for Henry, the new research confirms, by this age his weight had started to balloon as he suffered increasingly from chronic constipation and his body succumbed to hideous sores and repeated infections. Mentally, he was also beginning to show the first signs of madness. However, he probably did not have syphilis, as is often alleged. Nor is there any record of him being prescribed mercury, the highly toxic metal that was used to treat the disease. But he may have had Cushing's syndrome (a rare hormonal disorder) which could account for the obesity and the mental instability. And there were a host of other problems, too. I would think it likely that Henry was also experiencing bouts of impotence during his marriage to Anne Boleyn; certainly, she is said to have complained of such a problem to her brother. And while he successfully sired a son - the future Edward VI - with Jane, he never managed intercourse with wife number four, Anne of Cleves. Not surprisingly, his next marriage - to the young and sexually active Catherine Howard - was said to have rejuvenated and exhausted him. But she was executed by him for no good reason other than malice in little over a year. By this time, the King weighed more than 20st, was enduring regular and very painful enemas and had a foul-smelling open wound on his leg that the royal physicians - based on the then accepted medical knowledge - refused to let heal, believing that illness must be allowed to flow out of the body. Whenever it threatened to close up, the wound would be cut open, the flesh pulled apart and tied open with string and the abscess filled with gold pellets to keep the sore running. The constant pain must have been unimaginable and certainly goes some way to explaining the legendary royal rages that characterised Henry's later years. Armed with modern medical knowledge, historians now believe this wound, which marked the onset of Henry's long decline into chronic ill health, was the result of a varicose ulcer he developed on his left thigh in his mid-30s, probably brought on by his habit of wearing tight garters on his famously handsome legs. Alternatively, it could have been caused by a condition called chronic osteitis, a bone infection that certainly fits reports of constant ulcers opening up. In 1536, Henry also suffered a particularly nasty fall from a horse while participating in one of the tournaments he so enjoyed. He was unconscious for about two hours - a period long and worrying enough for Anne Boleyn later to blame for the miscarriage she suffered soon afterwards. Some medical historians now believe his head injury was severe enough to cause permanent brain damage. Certainly, from that time, Henry's furious temper and unpredictability got even worse. He would issue orders in the morning and then countermand them in the afternoon - then plunge into an ever darker rage on discovering his instructions had already been carried out. My own research makes me believe that some sort of brain damage also goes a long way to explaining his persecution of Anne Boleyn - accusing her of adultery (not with just one man but five), witchcraft, treason and even incest, and then insisting on her execution when almost everyone, Anne included, expected her to be granted a royal pardon. Typically, at the hour of the execution of the woman he had so adored, the King was dancing with Jane Seymour. Just a few years later, in 1540, the onset of madness could also explain the savage humiliation and botched execution (carried out by a nervous teenager with a blunt axe) of Thomas Cromwell, once the King's closest adviser. Within months, Henry bitterly regretted the execution - an irrational about face that was becoming all too common. By this time, Henry was becoming a tyrant. In writing my historical novels, I apply very strict rules of accuracy to facts when they are known. But when it comes to Henry VIII, there's just no need to invent or significantly change events to improve the story. We are faced with this extraordinarily charismatic king who married six times, who broke with the Roman Catholic Church and then went mad, all before his death at the age of 55. Indeed, it is the question of human mortality that makes history so interesting. The true story of Henry VIII is a parable of the corruption of power and the frailty of the body. He got old, he became disgusting and dangerous and he grew enormously fat. But in many ways, England's most enigmatic king remains all the more interesting for his viler features. Philippa Gregory is author of The Other Boleyn Girl (HarperCollins).
  5. Interesting article. Oddly enough, the endocrinologist that told me all my diagnostic labs were invalid and that I should get gastric bypass since medical science would never figure me out specifically told me to get a Roux-en-Y bypass because it would short circuit the brain/stomach loop of ghrelin and simple banding would not (Despite the fact that I and my husband both told him I hardly eat at all). Needless to say I tossed the GI surgeon's card he gave me and didn't follow up with him. Still, it is an interesting article. Gastric Artery Embolization Stops Weight Gain in Animal Study NEW YORK (Reuters Health) Sept 17 - In a porcine model, catheter-directed chemical embolization of the gastric artery suppressed release of ghrelin, an appetite-inducing hormone, and prevented weight gain. Researchers are hopeful that this treatment could offer a less invasive alternative to bariatric surgery. "With gastric artery chemical embolization, called GACE, there's no major surgery," lead author Dr. Aravind Arepally, from Johns University School of Medicine in Baltimore, said in a statement. "In our study in pigs, this procedure produced an effect similar to bariatric surgery by suppressing ghrelin levels and subsequently lowering appetite." In the study, reported in the September 16th online issue of Radiology, five pigs were treated with the artery-ablating compound sodium morrhuate and five were treated with saline. The assigned treatment was delivered via catheter to the gastric arteries under x-ray guidance. In the active treatment group, ghrelin levels at weeks 1, 2, 3, and 4 were significantly reduced relative to baseline values. By contrast, levels in the control group were increased at all points relative to baseline values. At 4 weeks, continued weight gain was still observed in the control group, whereas in the active treatment group weight had stabilized. "With the minimally invasive nature of the GACE procedure, further refinements could provide the ability to deliver a variety of novel agents directly to the gastric fundus that would provide sustained suppression of ghrelin," the authors conclude. Radiology 2008.
  6. Australia. I saw that too. Why is it that all these doctors aren't jumping on some kind of international doctor forum when they get stumped with something like this. We see right away about 10 things that could be wrong. MOMO, acromegaly, Cushings,...not to mention they have these BIG MEDICAL BOOKS they all had to read in order to get their degrees. Crack one open and spend a weekend reading and taking some notes and set a game plan to figure it out. I know I would as a physician.
  7. Interesting. Mine was 15 in January and 10 in April. I just haven't had the energy to deal with that issue too since I had the bad reaction to the supplements. I should though.
  8. World's Tallest Woman Dies at Age 53 The world’s tallest woman, Sandy Allen, died early this morning at a nursing home in Shelbyville, Ind., at the age of 53. No cause of death has been released, but a family friend told the Indianapolis Star that Allen had been sick for several months. Allen, who was 7-foot-7, is listed by the Guinness Book of World Records as the tallest living woman, and has appeared in the publication since the mid-1970s. She came into the world weighing an average 6.5 pounds – but her abnormal growth began soon after her birth in June 1955. By the age of 10, Allen stood at 6 feet 3 inches tall and by the age of 16 she towered over 7 feet tall. Her height was due to a tumor in her pituitary gland that caused it to release growth hormones uncontrollably, according to the world record book. At the age of 22, she underwent surgery to correct the condition. When a tumor produces too much of one or more hormones, several conditions can occur including gigantism, the National Institutes of health reported on its Web site. In her first letter to the Guinness Book of World Records in 1974, Allen wrote, “I would like to get to know someone that is approximately my height. It is needless to say my social life is practically nil and perhaps the publicity from your book may brighten my life.” Following the letter, there was an offer from film director Federico Fellini to take a role in his film "Casanova" in 1975, and then her first date with a 7 foot Illinois man. In the last years of her life, Allen suffered from poor circulation and weak leg muscles which resulted in her being dependent on a wheelchair.
  9. Measurement of urinary free cortisol by tandem mass spectrometry and comparison with results obtained by gas chromatography-mass spectrometry and two commercial immunoassays Lisa Wood1, David H Ducroq2, Helen L Fraser2, Scott Gillingwater3, Carol Evans1, Alan J Pickett1, Derek W Rees1, Rhys John1 and Atilla Turkes1 1 Department of Medical Biochemistry and Immunology, University Hospital of Wales, Heath Park, Cardiff CF14 4XW, UK; 2 WEQAS, Reference Laboratory, The Quadrant Centre, Cardiff Business Park, Llanishen, Cardiff CF14 5WF, UK; 3 Waters Corporation, MS Technologies Centre, Atlas Park, Simonsway, Manchester M22 5PP, UK Corresponding author: Dr A Turkes. Email: atilla.turkes@cardiffandvale.wales.nhs.uk Background: Determination of urinary free cortisol (UFC) is an important adjunct for the assessment of adrenal function. In this study, we have analysed cortisol concentrations in urine samples by gas chromatography-mass spectrometry (GC-MS), liquid chromatography-tandem mass spectrometry (LC-MS/MS) and two immunoassays. The results were compared with GC-MS. The interference of cortisol ring-A metabolites in immunoassays was also assessed. Methods: The GC-MS technique involved solvent extraction, LH-20 clean-up and derivatization. Only solid-phase extraction procedure was used for LC-MS/MS. The samples were analysed in positive electro-spray ionization mode, monitoring the transitions for cortisol and deuterated-cortisol at m/z 363.3 > 121.2 and m/z 365.3 > 122.2, respectively. Immunoassays were performed according to the manufacturer's instructions. Results: When compared with GC-MS results both immunoassays (Coat-A-Count; approximately 1.9-fold, Centaur; approximately 1.6-fold) overestimated UFC concentrations. Cortisol ring-A dihydro- and tetrahydrometabolites contribute significantly to this overestimation. There was no interference by these metabolites in either GC-MS or LC-MS/MS methods. The sensitivity of the LC-MS/MS procedure was 2 nmol/L and the intra- and inter-assay variations were <5% in each quality-control sample. The comparison of the UFC results achieved by assaying the study samples with GC-MS and LC-MS/MS indicated that the agreement between the two methods was excellent (LC-MS/MS = 1.0036GC-MS ? 0.0841; r2 = 0.9937). Conclusions: The interference of cortisol ring-A metabolites in immunoassays contribute to overestimation of UFC concentrations. The LC-MS/MS procedure had the sensitivity, specificity, linearity, precision and accuracy for the determination of UFC concentrations. The method is suitable for routine use provided that method-dependant reference values are established.
  10. Happy to pay in advance for one when/if you get a pool of us that want a batch? Sorry you got stuck with some too.
  11. I tried to get one of the magnets. I wasn't fast enough I guess. If you get another batch of those, I'd bet interested!
  12. I think the biggest disservice doctors do is assume that each disease/condition is acting in a vacuum or that because you have one condition you can't possibly have another. It's like assuming you're brakes can't be bad on your car because you need new headlights. Or as I'm learning...that if one thing goes wrong in your emissions system there's a huge and expensive cascade effect through the entire system and fixing one problem can unmask another problem. I don't know the Medicare answer but I'd think since it's Federal there'd be some crossover? Anyone else with more knowledge that can chime in?
  13. Phaeochromocytoma combined with subclinical Cushing's syndrome and pituitary microadenoma GF Yaylali, F Akin, M Bastemir, YT Yaylali, and A Ozden Clin Invest Med, January 1, 2008; 31(3): E176-81 Pamukkale University, School of Medicine, Department of Endocrinology and Metabolic Diseases, Denizli, Turkey. guzinf@gmail.com OBJECTIVES: Phaeochromocytoma (PHEO) occasionally associates with pathological lesions of the adrenal cortex. The coexistence of PHEO and pre-clinical Cushing's syndrome (PCS) of the same adrenal gland has rarely been reported. We report a case of PHEO and PCS originating from the same adrenal gland and discuss the peculiar diagnostic aspects of this entity. CLINICAL PRESENTATION: A 64 yr old man was hospitalized to evaluate the right adrenal mass which was discovered incidentally by ultrasonography. He had a history of type 2 diabetes mellitus and hyperlipidemia. Blood pressure measurements were all normal during his hospital stay. Laboratory examination showed: urinary catecholamines were markedly increased. HbA1C of 14.3 %, midnight cortisol of 11(microg/dL), cortisol was not suppressed after the overnight 1 mg oral dexamethasone suppression test (DST): 3.42(microg/dL), 24 hr free cortisol in the urine : 213 microg/day (10-100), cortisol levels were suppressed more than 50% with 8 mg of dexamethasone. CT scan of the adrenal glands showed a 6 cm well encapsulated right adrenal mass together with a clearly normal left adrenal gland. MRI investigation of the sella turcica revealed a pituitary microadenoma on the right side of the adenohypophysis He was treated with alpha and subsequent beta blockers after the diagnosis of PHEO and PCS was made. Right adrenalectomy was performed. The pathology showed typical PHEO with adrenocortical hyperplasia. VMA, metanefrin and free cortisol levels were normalized one month after surgery. CONCLUSION: The present report is a rare case of PHEO combined with PCS in the same adrenal gland. Publication Type: * Journal article PMID: 18544281
  14. I tried to find the complete article but wasn't able to access it. This is the abstract...(and based on what I read in the abstract I'm still looking for the punchline. Did I miss the big story in it?) Lower Growth Hormone and Higher Cortisol are Associated with Greater Visceral Adiposity, Intramyocellular Lipids and Insulin Resistance in Overweight Girls Madhusmita Misra1*, Miriam Bredella2, Patrika Tsai3, Nara Mendes3, Karen K. Miller3, and Anne Klibanski3 1 Pediatric Endocrine Unit, MassGeneral Hospital for Children and Harvard Medical School, Boston, Massachusetts, United States 2 Radiology, Massachusetts General Hospital, Boston, Massachusetts, United States 3 Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, United States * To whom correspondence should be addressed. E-mail: mmisra@partners.org. Background: Although overweight adolescents have markedly altered body composition, insulin sensitivity and lipids, hormonal associations with these parameters have not been well characterized. Growth hormone (GH) deficiency and hypercortisolemia predispose to abdominal adiposity and insulin resistance, and GH secretion is decreased in obese adults. Objective: We hypothesized that low peak GH on the GHRH-arginine stimulation test, and high cortisol in overweight adolescents would be associated with higher regional fat, insulin resistance and lipids. Design/Methods: We examined the following in 15 overweight girls and 15 bone-age-matched controls 12-18 years: (i) body composition using DXA and MR [visceral and subcutaneous adipose tissue (VAT and SAT) at L 4-5, and soleus-intramyocellular lipid (IMCL) (1H-MRS)], (ii) peak GH on the GHRH-arginine stimulation test, (iii) mean overnight GH and cortisol, (iv) 24-hour urine free cortisol (UFC), (v) fasting lipids, and (vi) an OGTT. Stepwise regression was the major tool employed to determine relationships between measured parameters. Results: Log peak GH on the GHRH-arginine test was lower (p=0.03) and log UFC higher (p=0.02) in overweight girls. Log mean cortisol (overnight sampling) was associated positively with SAT, and with BMI-SDS accounted for 92% of its variability, whereas log peak GH and BMI-SDS accounted for 88% of VAT variability, and log peak GH for 34% of the IMCL variability. Log mean cortisol was independently associated with log HOMA-IR, LDL and HDL and explained 49- 59% of the variability. Conclusions: Lower peak GH and higher UFC in overweight girls are associated with visceral adiposity, insulin resistance and lipids.
  15. Thanks! Yeah...I'm so tired of the if/then and multiple choice answers. I'd be okay with an essay answer at this point. It doesn't have to be A, B, C, or D...it could be all of the above or none of the above...or not even be in the book!
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