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Rapid Responses: Rapid Responses published:
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Ignored Science
- Eric K Pritchard (28 March 2009)
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Please go back to basic physiology
- F Davis (28 March 2009)
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Please read up to date scientific journals Dr
- D.Allen BSc Hons Allen (28 March 2009)
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Diagnosis and Treatment of Hypothyroidism
- Jim Harwood (29 March 2009)
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magnetic resonance imaging of pH using hyperpolarized : 13: C-labelled bicarbonate.
- Richard G Fiddian-Green (30 March 2009)
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When will the BTA get it's own house in order?
- E Savid (1 April 2009)
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May reality intrude?
- Charles R. Fred (1 April 2009)
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Blinkers of the NHS doctors
- Val M Stonehouse (3 April 2009)
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Lack of diagnosis & incorrect treatment
- P Lynch (4 April 2009)
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Thank you
- Bridget Harris (8 April 2009)
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Forthcoming review of joint statement by RCP et al.
- J A Cameron (15 April 2009)
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Diagnosing and treating hypothyroidism
- Philip W White (9 May 2009)
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Error in Editorial
- Azeem Majeed (16 May 2009)
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Levothyroxine only treatment
- Pamela Lynch (21 June 2009)
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Eric K Pritchard, Thinker self
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There are two problems in the general area of the diagnosis and treatment of the symptoms of hypothyroidism, language and science. The language surrounding "hypothyroidism" is not clear. The root of this is the dual meaning of "hypothyroidism." It can either mean the "clinical consquences of deficient secretion by the thyroid gland," or the "clinical consequences of inadequate levels of thyroid hormones in the body." Medical science, begun by Refetoff and Braverman, found bodily functions between the thyroid gland and the symptom producing cells. The first of these post thyroid functions is the peripheral metabolism of the relatively inactive hormone thyroxine (T4) to the active hormone triiodothyronine (T3). The second is the reception by the peripheral cells of the T3 for use by the cells' nuclei. As Dr. Ridgway noted -- the action is not T4 in the serum but T3 in the nuclei. Consequently, the two definitions of hypothyroidism are markedly different. Since the medical community does not follow its own standards of care for medical practice guidelines by stipulating the definition, confusion reigns. If the definition were stipulated, and logical consistency maintained, there would be no problem. However, the definition is not stipulated and logical consistency is not maintained. Consider the medical practice guideline for hypothyroidism by the British Thyroid Association. They use the broad definition of hypothyroidism (hormone levels in the body) but then focus on the thyroid gland only. This focus can be seen in the tests which go to the thyroid gland's input (TSH), output (fT4), and internal behavior and can be seen in the levothyroxine-only therapy, which is soley oriented to replace thyroid gland secretion deficiency. There is no logical consistency here. Just the confusion suggesting that the symptoms of hypothyroidism can be managed with levothyroxine sodium only. The supporting studies for levothyroxine-only did not use post thyroid deficient subjects, they ignored the small percentages of positive responses for T3 therapies, used insignificant doses of T3, and certainly intimated a broad interpretation of their efforts. Consequently, these studies are not broadly applicable. They are really only applicable to primary hypothyroidism. The recent statement/guideline by the Royal College of Physicians is supposed to be soley about primary hypothyroidism. However, in the concluson section, their recommendations extend beyond primary hypothyroidism and into the realm of post thyroid deficiencies -- deficient peripheral metabolism and deficient peripheral cellular hormone reception. Both of these can produce symptoms in spite of "normal" thyroid function tests -- predominately because the thyroid functions tests do not address post thyroid activity. The lack of success of the endocrinology establishment and their demand for a levothyroxine-only therapy can be seen in their 13% failure rate (Saravanan, et al.) and their proscription of the very therapies that have been proven to properly care for their failures (Baisier, et al.) Medical ethics require keeping abrest of medical science. The science of the post thryoid functions was begun in the 1960's and is now quite established -- apparently except in the minds of the endocrinolgy establishment. The American Thyroid Association claims that T3 is not needed ("Wilson's Syndrome") because the peripheral metabolism is "highly regulated." This unsubstantiated statement effectively makes the claim that a bodily function never fails in any person for all time. Medical ethics require placing the patient's well-being first and foremost. This is not done either. Rather the endocrinolgy establishment prefers to make excuses for itself with "nonspecific symptoms" or blame the patient with "functional somatoform disorders" Neither of these diagnoses can be made until all physicial etiologies have been excluded per differential diagnostic protocol. But is made anyway and contributes to the 13% error rate. If the practice of medicine were competitive, a 13% error rate would spell professional death -- as it should considering the virtual torture that the victims of post thyroid deficiencies must endure daily. Competing interests: The return to health of those suffering from post thyroid deficiencies which mimic deficient thyroid gland secretion, primary hypothyroidism |
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F Davis, Retired Pathology Laboratory Technician Rg10
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It is totally unbelievable that any doctor who genuinely cares for their patients or has any real contact with Hypothyroid patients could possibly say that Thyroxine alone is ALL thats needed. Such dogma has no basis in Human Physiology. Thyroxine is T4 ........all body tissues need T3 in order to function. If the patient for whatever reason cannot convert T4 into T3 their symptoms will not resolve on Thyroxine although their blood tests will bizarely attempt to claim otherwise . If these patients are switched to T3 a percentage of them will indeed recover. There are then a percentage who are so sensitive to chemicals that they will only recover on Armour Thyroid. There is ample documentation of Thyroxine treated patients complaining of severe muscle pains which only resolve when switched to T3 or Armour.The only reason that the UK version of Armour was stopped was due to a bad batch and the attempt to reduce the NHS drugs bill by the introduction of generics To continue to claim that "one size fits all "these days when scientists are developing drugs specifically targeted to work on different genetic types is blinkered to say the least. Clearly its high time that any Doctor treating Thyroid Patients started actually LISTENING to their patients and stopped trotting out the dogma that Thyroxine is perfect . If they actually lived with a Hypothyroid patient they would rapidly realise nothing could be furthur from the truth Competing interests: None declared |
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D.Allen BSc Hons Allen, Marine Biology Stats and Ecology YO22
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I have to respond to this. Any Dr who has read the latest science on Hypothyroidism will know that this is wrong. It is not just a case of getting a TSH result to match some marks on paper. What happened to real clinical appraisal of patients? So my blood work looks ok, my endo cannot find anything else wrong, do you give up looking because the TSH is 'within range' and the T4? What about tests for low T3 syndrome, yes it may resolve after a non thyroidal illness resolves but on the other hand it may not and it also may point to another problem. You have frightened Drs and labs into not doing any further investigations, shame on you. Also the raise in TSH requirements for diagnosis of hypothyroidism? Scandalous, haven't you read the HUNT study? Some day legal action may be started by people who have had cardiac problems due to long standing high TSH, I think you should be much more careful. Why on earth do you think so many patients are going outside the NHS? because the NHS isn't tracking down the causes of their disabilities because of the heirachy dictating the same guidelines to all Drs, and they are being failed, that is why. People who have been made well by Drs outside the NHS who test, examine and diagnose outside your advise are doing that. Thank God for them, that is all that I can say. Dawn Competing interests: None declared |
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Jim Harwood, Retired Computer Programmer 79 Central Avenue, Pinner, HA5 5BU
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Yet another "guideline" emanating from a disgruntled section of the British Thyroid Association. A few cryptic points:- This paper only addresses primary hypothyroidism. No independent thyroid patient organizations were consulted. Only 95% of the healthy population should be within a 95% reference interval (on medication or not). Armour thyroid contains a higher proportion of T3 than human serum. If this concerns you, the only logical response is to insist on a combination of Armour and thyroxine. The evidence suggests that the addition of T3 gives superior results. There is no evidence to suggest that a blood serum thyroid function test is superior to any other method of diagnosis. The patient support group "Thyroid UK" is carrying out a comparative study. There are many causes of hypothyroidism, failure of the thyroid gland is one of many possibilities. In my experience most endocrinologists have little knowledge of thyroid hormone action and are not competent to treat hypothyroidism. Competing interests: I am a patient who has been missed-diagnosed by a number of endocrinologists. |
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Richard G Fiddian-Green, FRCS, FACS None
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In addressing this subject some years ago (1) I raised the possibility of using ATP turnover as a means of improving the sensitivity and accuracy of establishing a diagnosis of hypothyroidism. I considered the diagnosis of diabetes from the same perspective (2). In so doing I raised the probability of an impairment of insulin secretion and indeed of thyroxine secretion being just two of numerous causes of "the intermittent or sustained energy deficit syndrome". If so the first step in investigation should be to determine the presence or absence of an energy deficit. In addressing metabolic screening for breast cancer (3) I introduced the possibility of using magnetic resonance imaging of pH using hyperpolarized : 13: C-labelled bicarbonate but gave an old reference. In the latest reference I intended to give (4) the limitations of current methods of NMR spectroscopy are addressed and indeed all other methods of measuring tissue pH in vivo. More importantly, from my perspective, the study would appear to have provided validation for the indirect measurement of tissue pH from the arterial bicarbonate and regional tissue PCO2 used in gastrointestinal tonometry. An exercise stress test using gastrointestinal tonometry might, therefore, provide a sensistive means of detecting of systemic energy deficit. Alternatively magnetic resonance imaging of pH of the thyroid itself, using hyperpolarized : 13: C-labelled bicarbonate, or even John McLaren-Howard’s “ATP profile test” in neutrophils (5) might be used for this purpose. 1. The pooped-out syndrome, ATP stores and hypothyroidism Richard G Fiddian-Green bmj.com, 5 Mar 2003 eletter re: Anthony D Toft and Geoffrey J Beckett Thyroid function tests and hypothyroidism BMJ 2003; 326: 295-296 2. Grounds for abandoning "diabetes" as a diagnosis? Richard G Fiddian-Green (9 March 2005) eLetter re: M K S Leow and J Wyckoff Under-recognised paradox of neuropathy from rapid glycaemic control Postgrad Med J 2005; 81: 103-107 3. Metabolic screening using thermography and magnetic resonance pH imaging. Richard G Fiddian-Green (5 March 2009) eLetter re: Peter C Gøtzsche, Ole J Hartling, Margrethe Nielsen, John Brodersen, and Karsten Juhl Jørgensen Breast screening: the facts—or maybe not BMJ 2009; 338: b86 4. Magnetic resonance imaging of pH : in vivo: using hyperpolarized : 13: C-labelled bicarbonate Ferdia A. Gallagher, Mikko I. Kettunen, Sam E. Day, De-En Hu, Jan Henrik Ardenkjær-Larsen, René in ?t Zandt, Pernille R. Jensen, Magnus Karlsson, Klaes Golman, Mathilde H. Lerche, Kevin M. Brindle. Nature 453, 940 - 943 (28 May 2008). 5. Myhill M, Booth NE, McLaren-Howard J. Chronic fatigue syndrome and mitochondrial dysfunction. Int J Clin Exp Med 2009;2:1-16. , Competing interests: Patents issued in my name |
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E Savid, Health Professional none
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The authors claim that there is no scientific evidence to support the use of T3 either when added to T4 or in the form of Armour thyroid. It's interesting then, that several recent studies by NHS endocrinologists Das et al., (2007) and Lewis et al., (2008) found that Armour thyroid treatment led to resolution of symptoms in certain groups of patients who were left unwell on thyroxine-only treatment. Given the BTA/RCP guideline authors' stated conviction that all hypothyroid symptoms resolve with sufficient levels of thyroxine-only treatment, perhaps the authors could explain how this statement can be levelled with Panicker et al.'s (2009) finding that patients with a commonly inherited variation in the D102 gene remain unwell on thyroxine- only therapy and benefit from symptom amelioration through combination T3- T4 therapy. Presumably the authors of this article have not yet had time to read the recently published rebuttal to the BTA's (2006) guidelines (Lowe, 2009) that calls into question the BTA's interpretation of studies on Armour thyroid vs. thyroxine-only therapy. It is to be welcomed that members of the BTA acknowledge that there is a high level of misdiagnosis and mistreatment of hypothyroidism in the UK. What is not pleasing however, are the attributional biases evident in this editorial. The editorial authors blame the continuing mistreatment and misdiagnosis of hypothyroidism on: the vagueness of symptoms, the rise of the internet, non-NHS doctors and the increased availability of medical information to patients. In fact the authors attribute blame to many causes, excepting of course, the BTA's own failings in the mistreatment and misdiagnosis of patients. As it happens, the internet has allowed patients in this country to compare the care and guidance they get from the NHS to that provided by healthcare systems in other countries. It is through comparison that the RCP/BTA guidelines are found wanting. We look to other countries and see professional bodies like the AACE recommending lower thresholds for diagnosis than in the UK. We are aware of foreign clinicians' higher levels of clinical autonomy and freedom to provide health-restorative medication options based on the treatment needs of the individual. British patients like myself, wonder why it is that so many people in the UK with hypothyroidism must endure crippling and life-destroying symptoms for many years before their TSH finally hits the BTA's magic number 10, all the while being told by the experts that their symptoms have 'nothing to do' with their thyroid. These same British patients also wonder why, in spite of cited scientific evidence to the contrary, the BTA continues to deny the heterogeneity of treatment needs in thyroid patients and to state that thyroxine is the only treatment that works for all hypothyroid patients. Given the difficulties in getting prompt diagnosis and individualised treatment for hypothyroidism in the UK, is it any wonder that British patients like myself with unequivocal autoimmune disease prefer to seek health-restorative care from outside the NHS rather than remain unwell for many years within the system? Does synthetic thyroid extract work for everybody? Das G, Anand S & De P Endocrine Abstracts (2007)13 P316 Improvements in quality of life in hypothyroid patients taking Armour Thyroid. Lewis D, Kumar J, Goulden P, Barnes D. Endocrine Abstracts (2008)15 P359 Common variation in the DIO2 gene predicts baseline psychological well-being and response to combination thyroxine plus triiodothyronine therapy in hypothyroid patients Panicker V, Saravanan P, Vaidya B, Evans J, Hattersley AT, Frayling TM, Dayan CM Journal of Clinical Endocrinology & Metabolism (2009) Stability, Effectiveness, and Safety of Desiccated Thyroid vs Levothyroxine: A Rebuttal to the British Thyroid Association Lowe JC Thyroid Science 4(3):C1-12, (2009) Competing interests: UK Hashimoto's patient - Took years to get a diagnosis. Made ill by NHS-prescribed Levothyroxine. Now a lot better taking Armour thyroid prescribed by a private endocrinologist. |
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Charles R. Fred, Retired New York, 11378
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May reality intrude? In 1999, my wife, age 67, had radioactive iodine thyroid reduction - followed by prescribed levothyroxine. She soon complained of depression - which she had never before experienced. Because the February, 1999 New England Journal of Medicine article connecting levothyroxine with depression had recently garnered press attention, I became aware of it and bought Armour thyroid via the internet. Without my wife’s knowledge, I switched medications. She promptly returned to her usual sunny disposition. Over the next years, her thyroid numbers were closely observed by a well qualified thyroid specialist - who was never told of the changed medication. He found no problems. In 2007, age 74, she suffered an acute ulcer bleed and was bedridden, often very near death, in a New York area teaching hospital for almost four months. She was given levothyroxine. One day she stated that she “just wanted to go home and die.” She was depressed. I informed her doctors of her thyroid history and referred them to the New England Journal article. Since their hospital formulary did not include T3, they had me bring our Armour thyroid from home. My wife promptly recovered her usual optimistic disposition, though her circumstances could scarcely have been more depressing. She has made a full recovery and continues to take Armour thyroid, now prescribed by her internist. Had she been in an NHS hospital, under the care of a well-qualified thyroid specialist, would she have been denied T3 and referred to a psychiatrist to treat dogmatically labeled non-thyroid depression? This editorial seems to say just that. One last point if I may. My wife’s depression was obvious. Since she is equipped with much the same assortment of body parts and associated physiology as others, is it not likely that many levothyroxine-treated patients suffer from less-noticeable depression? Competing interests: None declared |
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Val M Stonehouse, Community Psychiatric Nurse Community Mental Health Team,Eh28 8SQ
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I am living proof that I suffer from Hypothyroidism,but not because a blood test tells me.I have suffered for many years from various ailments.Not least of all,infertility in my early 20's.Both babies were very big,and I've had menstrual problems for years. Last year I collapsed mentally.Having worked in Acute Psychiatry for 17 years,in severe and enduring mental illness.II was diagnosed with depression,and given 2 different anti-depressants.I was utterly bone weary,had aches and pains,IBS,mind fog,at times slept for 16 hours and others couldn't sleep at all,concentration was zero,ankles swelled,put on even more weight,anxiety,panic attacks,avoided any contact with people.This and other symptoms,from a lively,fun loving professional woman. I am very aware of depressive symptoms,but this was so much more than that.My blood tests all came back "within normal limits",so my GP refused to consider I had hypothyroidism.So I searched myself,after anti- depressants lifted my mood slightly.I found TPA-UK,and learned how little the medical profession knows about this condition.Having worked in nursing for 24 years,I was astounded at the blinkered views of the medical profession. I saw a Private Dr,and within an hour of me talking about my symptoms,and taking my family history of the condition,he diagnosed me.I have now been on Armour for 5 months,I'm back to being my bubbly self.I'm only sorry that I've lost so many years,feeling so tired.I also haven't had a day off sick since starting Armour,which I buy myself. In no other condition is a "1 size fits all",as far as medication is concerned.Thyroxine is not for everyone,and it's synthetic.GP's and Primary Health needs more education,in how to diagnose and treat this condition.It is preposterous to dictate to Doctors,how to treat Hypothyroidism,without giving them the research which prove Armour is natural,and includes all 4 of the thyroid hormones which we require.There are literally 1000's of people who can disprove that thyroxine and blood tests are the only way to treat and diagnose this incapacitating illness. Val Stonehouse Competing interests: None declared |
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P Lynch, Retired CM2 6AZ
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The RCP/BTA guidelines for The Diagnosis and Management of Primary Hypothyroidism are interesting as in the 2006 BTA guidelines (1)on page 68, it states, "Routine thyroid function testing has been available for more than thirty years. Therefore, it may seem surprising that the quality of evidence to support the recommendations in these guidelines is generally poor, etc." How are the general public to have confidence in the diagnosis and treatment of hypothyroidism if these 'gold standard' tests actually aren't all they are made out to be? At the 75th Annual Meeting of the American Thyroid Association, Normal levels of TSH were quoted as 0.5-2.5, high normal as 2.5-5, mildly elevated 5-10 and clearly elevated as >10. Why do patients have to suffer for years or even decades in this country for their TSH to be elevated above 10 when they may (if they are lucky) finally receive treatment? Of course, once the diagnosis is made the main treatment offered is Thyroxine which definately does not suit us all and then once back within the reference range, medication is often kept just within the reference range even though the patient could still be suffereing severe hypothyroid symptoms. What happened to evidence based medicine? Dr A Toft (2)has stated that "In some patients, a sense of well-being is achieved only when FT4 or TT4 is raised, for example, 30pmol/l or 170nmol, and TSH low or undetectable." Dr. Toft (3)talking about the addition of T3 to a patient's medication stated that he believed that "It would appear that the treatment of hypothyroidism is about to come full circle." In 2004 Colin Dayan,(4) Endocrinologist and Consultant Senior Lecturer at the University of Bristol, stated "This house believes that thyroxine is not an adequate form of thyroid hormone replacement in everyone...",and, "Estimated that 5% are psychologically dissatisfied despite TSH levels in the reference range and that variations in 3 deoidinase anzymes, or cell membrane thyroid transporters could be factors. Finally, Prof A. P. Weetman (5) stated in 1997 in your own journal that "A high thyroid stimulating hormone concentration >2m/Ul was associated with an increased risk of future hypothyroidism", but more importantly he stated, "The simplest explanation is that thyroid disease is so common that many people predisposed to thyroid failure are included in a laboratory's reference population, which raises the question whether thyroxine replacement is adequate in patients with thyroid stimulating hormone levels >2mU/l." This all sounds very conflicting evidence to the layman. It is about time that evidence based medicine was even handed on not just on the side of the few. Isn't science meant to produce both sides of the argument? It didn't appear so in the document, 'The Diagnosis and Management of Primary Hypothyroidism'. (1) UK Guidelines for the Use of Thyroid Function Tests (July, 2006). The Association of Clinical Biochemistry, The british Thyroid Association and The British Thyroid Foundation. (2) Dr. A Toft, CBE, MD, FRCP (Consultant Physician and Endocrinologist at the Royal Infirmary, Edinburth) Toft A Understanding Thyroid Disorders. Family Doctor Publications Limited in assoc with the British Medical Association 2006) (3) AD Toft, Endocrine Clinic, Royal Infirmary, Edinburgh, UK Endocrine Abstracts 3 S40, T3/T4 combination therapy. (4) C. M. Dayan Thyroid Hormone Replacement Therapy - This house believes that thyroxine is not an adequate form of thyroid hormone replacement in everyone..." Endocrine Nurses Training Course 9-11Sept 2004 The Society for Endocrinology - Training. (5) A P Weetman, Frequencey of Hypothyroidism. BMJ 1997:314:1175 (19 April) Competing interests: None declared |
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Bridget Harris, Group Orlando 32801
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It’s reassuring to read there are medical professionals out there who care about a patient’s health above all the misleading information on the internet regarding thyroid disease; information that’s rather ubiquitous at this point. As a real thyroid patient, it’s difficult dealing with some of these issues too. Upon diagnosis, never would I have expected the kind of nonsense I’ve personally come across and dealt with when it comes to this disease. Imagine dealing with one’s own illness (including surgery), seeking out support from other patients via the internet and ending up arguing over all the charlatanisms people fall for. So far, while trying to point out the simple medical truth as I know it, I’ve been described as everything from “having evilness” to “thinking drs are gods” to “working for big pharma” to “needing to take my ‘medicine’” to “not really being a patient.” (Wish that last were true.) If you ask me, there continues to be one aspect of all this that medical professionals seem to overlook. Does anyone realize that the demographic of those seeking to get on thyroid meds when they don’t really have thyroid disease is that same demographic as those with eating disorders? Has anyone ever noticed how frequently eating, diet and weight get mentioned on most of the thyroid internet sites? To me, this seems to be where the invasion is coming from – untreated eating disorders, more specifically, bulimia. One symptom of bulimia is the desire to use thyroid medication as a compensatory measure after poor self-care behaviors. (Sort of an old-fashioned idea that’s made a comeback.) It is desiccated thyroid formulas like Armour that have the best reputation for fulfilling that. There seems to be two main reasons for this, from what I’ve read. One reason is because they include T3, which is thought to accomplish quick weight-loss. And two, is because they are natural and therefore can be justified as not really being a drug. Honestly, I could sit all day and cut-n-paste actual examples of what I’m talking about. With exaggerated language that ranges from downright silly to downright disturbing. One latest trend I notice involves the use of the term ‘no thyroid.’ That sure doesn’t mean what you’d automatically think. It now means ‘I have a thyroid gland that the dr and testing has assured me is fine but I want to be on meds so desperately that I now over -dramatize my physical state.’ I could go on, but will end by saying I hope this journal article is part of a trend toward putting the truth out there. Competing interests: None declared |
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J A Cameron, MBA Neath SA11 1RJ
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Forthcoming review of the joint statement by the RCP et al. This joint statement is of serious concern to the many thousands of hypothyroid patients who are intolerant of thyroxine (levothyroxine –T4) and/or whose blood test results do not correlate with their symptoms of hypothyroidism, to highlight just two of the issues. Therefore, all the organisations responsible have been contacted to express concerns about its content, these communications have included scientific references, which contradict assertions made within the statement. The RCP has agreed a review to consider letters and papers along with other similar communications from the many others who have written to them with concerns about the joint statement. This review is to take place very soon. The published book ‘Hypothyroidism in Childhood and Adulthood, A personal perspective and scientific standpoint,’ was also sent to all the heads of the organisations responsible for the joint statement. This book was written by C Phillips and D Roach, who are identical twin sisters and who were both diagnosed with hypothyroidism in childhood by an NHS paediatrician. Their experience provides an example of two hypothyroid patients whose clinical symptoms of hypothyroidism did not correlate with their Thyroid Stimulating Hormone (TSH) results. Thus both are exactly the type of patients whose existence, the joint statement appears to deny. Both twins are currently being treated with Armour Thyroid USP, initially provided by a private doctor and this treatment has been endorsed by two eminent NHS endocrinologists and continued via their NHS GP. This treatment is needed on an ongoing basis, as both twins are intolerant of synthetic thyroxine (Levothyroxine – T4). This book, which is illustrated with photographs, leaves no doubt that both twins are indeed hypothyroid and have been so since childhood. However, to return to the joint statement, it appears to be lacking in balance and transparency. Therefore it has been requested that when the proposed review is conducted, the Royal College of Physicians and the other organisations involved, consider the views of patients, who have been harmed or are at risk of harm as a direct result of this joint statement and to involve some such patients as part of the review. In addition, it has been requested that representatives of the patient support groups who were excluded from the deliberations the first time round are invited to participate. Furthermore, in the spirit of research and the furtherance of medical knowledge it has also been requested that doctors and researchers who have successfully treated hypothyroid patients by prescribing T3 preparations [including desiccated thyroid] and T3/T4 combination therapy are invited to attend this review to deliver their viewpoint and share their experiences and expertise with the review body. To summarise, to ensure the validity and credibility of this review, all evidence must be considered and it is essential that all the above are allowed to participate. Phillips C, Roach D. Hypothyroidism in Childhood and Adulthood A personal perspective and scientific standpoint. Nottingham University Press: 2006. Competing interests: None declared |
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Philip W White, General Practitioner Y Felinheli Surgery, LL56 4JF
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I found this a curious article as there was no mention of measuring thyroid antibodies, though current recommendations on treatment suggest if the TSH is above normal, but less than 10 one should only treat if the thyroid antibody test is positive. Another difficulty that we have been having in primary care are inconsistent standards in the levothyroxine tablets themselves, some brands disintegrating when being extracted from blister packs. We then wonder about bioavailability and compliance. Our first step now, when there are variations in response to treatment is to swap to a branded product. Often this stabilises the condition. Competing interests: None declared |
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Azeem Majeed, Professor of Primary Care Imperial College London W6 8RP
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This editorial states that one in four people in the UK have their thyroid function checked annually. Two references are given to support this statement. The first supporting reference actually states that there are approximately 10 million requests for thyroid function testing in the UK each year. [1] This equates to about one test per six people in the UK, not one per four, assuming that the tests are independent (i.e. each test is carried out on only one patient), which won't be the case. Some people will have multiple tests and hence the actual proportion of the population undergoing thyroid function testing annually will be less than one in six, and well below the authors' quoted figure of one in four. Furthermore, from reading the supporting reference, it is unclear what the provenance of the '10 million tests' statistic is or how accurate it might be. The second supporting reference does not seem to contain any statistics on thyroid function testing and so I don't know why it was cited in support. [2] If the authors can find some other evidence to support their statement, I am happy to stand corrected. References 1. http://www.british-thyroid-association.org/info-for- patients/Docs/TFT_guideline_final_version_July_2006.pdf 2. http://www.rcplondon.ac.uk/specialties/Endocrinology- Diabetes/Documents/Hypothyroidism.pdf Competing interests: None declared |
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Pamela Lynch, Retired CM2 6AZ
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I have submitted an earlier response, but would like to make another comment regarding Thyroxine as the treatment for hypothyroidism. As stated in the paper by Amit Allahabadia, secretary, British Thyroid Association, Salman Razvi, treasurer, British Thyroid Association, Prakash Abraham, assistant secretary, British Thyroid Association, Jayne Franklyn, president, British Thyroid Association, "The aim of treatment is to render the patient euthyroid; this is best achieved with levothyroxine alone." There has been a recently published paper by DH Lewis, J Kumar, P Goulden and DJ Barnes, entitled Improvments in quality of life in hypothyroid patients taking Armour Thyroid." Their conclusion was, "In appropriately selected hypothyroid patients, Armour appears to improve the quality of life in patients who have either had an inadequate clinical response to conventional T4/T3 therapy or are unable to tolerate such therapy." Maidstone and Tunbridge Wells NHS Trust, Tunbridge Wells, Kent. UK. Endocrine Abstracts (2008) 15 P359 This is a paper from doctors within the NHS and yet they are finding some patients cannot tolerate or do better on medication other than Levothyroxine, contrary to that by Amit Allahabadia, et al. In fact, one of the authors above, S Razvi was lead author of, "Quality of Life is impaired in people on Levothyroxine therapy and untreated people with sub-clinical hypothyroism." Endocrine Abstracts (2005) 9 P171. This appears to be a contradiction of views by the same author. Competing interests: None declared |
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