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Rapid Responses: Rapid Responses published:
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Biophysical-Semeiotic Bed-Side Assessment of Thyroid Function, even in preclinical Phase.
- Sergio Stagnaro (7 February 2003)
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Here We Go Again !
- Jim Harwood (8 February 2003)
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thyroid function tests in special situations.
- dr.manan vasenwala md,mrcp (10 February 2003)
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Coexistence of Addison's Disease, Ulcerative Colitis and Sub-clinical Hypothyroidism
- Daniel Cuevas-Ramos, Daniel Cuevas-Ramos, Carlos Gutierrez-Cirlos, Jorge Hernández-Calleros, (10 February 2003)
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Continuing Debate is the Essence of Good Science
- Madge Hirsch (14 February 2003)
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Is delayed presentation partly due to mode of onset?
- Ahmed Waise (21 February 2003)
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Response to editorial on thyroid function tests and hypothyroidism
- Barry J Durrant-Peatfield (27 February 2003)
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Reducing TSH levels further would be harmful.
- Mike Crilly (3 March 2003)
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The pooped-out syndrome, ATP stores and hypothyroidism
- Richard G Fiddian-Green (5 March 2003)
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AUTOIMMUNE HYPOTHYROIDISM AND RESPIRATORY DISEASE
- Surinder S Birring, Ronak B Patel and Ian D Pavord. (20 March 2003)
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Streptococci induce Rheumatism and Thyroiditis
- Friedrich Flachsbart (21 March 2003)
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Biochemists already know how Bacteria induce Thyroid Dysfunction
- Trevor G Marshall, PhD (23 March 2003)
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Patient co-operation begins with clarity
- Simon M. Clarke (29 April 2003)
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Open questions to the authors
- Simon R Cains (5 June 2003)
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High dosage thyroid replacement should be considered in 'refractory' hypothyroidism
- Gordon R B Skinner (8 January 2004)
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Severe Hypothyroid symptoms with normal TSH
- Maureen hallett (31 August 2008)
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Sergio Stagnaro, Specialist in Blood, Gastrointestinal, and Metabolic Diseases. Researcher in Biophysical Semeiotics. Via Ersmo Piaggio 23/8 16037 Riva Trigoso (Genoa) Italy
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Sirs, I find A.D.Toft and G.H. Beckett’s paper really interesting, since it uderlines, fortunately, the paramaount importance of physical semeiotics, even in present Medicine, ruled by high technology, as I am suggesting since five decades (1). In a 45-year-long clinical experience I have been observing patients presenting aspecific symptoms of thyroid failure and showing normal serum concentrations of both thyroxine (T4) and thyroid stimulating hormone (TSH). These patients, however, were suffering for hypothyroidism, when examined by means of Biophysical Semeiotics (2) (See:HONCode site 233736, http://digilander.libero.it/semeioticabiofisica). In fact, they promptly recovered under hormone replacement treatment, as a lot of other people with preclinical hypothyroidism, but showing clear biophysical-semeiotic signs of such as endocrine disorder. As a matter of fact, this original method, reliable at the bed-side in recognizing endocrine disorders, even sub-clinical, is based upon microcirculatory modifications present under different pathological conditions of both neuronal centres secreting releasing hormones and hypohysis as well as all other endocrine glands, comprising endocrine pancreas, under pathological conditions. According to Tischendorf’s well-known concept, microcirculatory modifications parallell parenchymal alteration, both functional and structural. 1) Toft A.D., Beckett G.H. Thyroid function tests and hypothyroidism Measurement of serum TSH alone may not always reflect thyroid status. BMJ 2003;326:295-296 ( 8 February ) 2) Stagnaro-Neri M., Stagnaro S., Semeiotica Biofisica: valutazione clinica del picco precoce della secrezione insulinica di base e dopo stimolazione tiroidea, surrenalica, con glucagone endogeno e dopo attivazione del sistema renina-angiotesina circolante e tessutale – Acta Med. Medit. 13, 99,1997. Competing interests: None declared |
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Jim Harwood, Information Systems 79 Central Avenue, Pinner, HA5 5BU
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Yet again it is proposed that hypothyroidism with a normal TSH level rarely - if ever - exists. The testimony of a large number of patients fails to impress, or stimulate a spirit of inquiry. Let my own story be an example. I had the usual hypothyroid symptoms, including extreme tiredness with a inability to concentrate and failing memory. Puffy eyes and dry skin were symptoms with good specificity for hypothyroidism. TSH: 1.0 (0.4-5.5), T4: 13.3 (9.0-20.0), fT3: 4.9 (3.5 – 6.5), Total Cholesterol: 7.0, Creatinine 120. The body said hypothyroid, interpretation of the biochemistry said euthyroid. I now take Thyroxine with a small amount of Tertroxin and am fully recovered. My thyroid biochemistry is outside the reference range, my cholesterol 3.9 and creatinine 90. I now have to apply pressure when using a nail clipper. I have no hyperthyroid symptoms. We live in an age when the Hypothalamic-Pituitary-Thyroid axis is king. So impressed by the sensitivity of the pituitary and its ability to indicate subclinical hypothyroidism we forget that the supply of thyroid hormones is only half the story. We forget about the many organisms that do not have a pituitary, but nonetheless utilize thyroid hormones. Utilization is as important as supply. Patient experience indicates it is rash to assume that the pituitary and end organs respond equally to thyroid hormones in all cases. The suggestion that patients feel “below par”, or have “psychosocial reasons”, is a disservice to the patients and to the author. There is a need for effective research; this so far amounts to one small trial led by a GP, endocrinologists have failed to accept the challenge. Until there is better knowledge, treat the patient not the numbers. Competing interests: None declared |
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dr.manan vasenwala md,mrcp, consultant-cardiologist (non-invasive) k.k.heart center, aligarh.202002,INDIA
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i have come across many patients, some with overt cardiac disease being inappropriately treated with thyroxine. many of this patients have underlying neurosis, and thyroxine can further increase anxiety. also increasing symptoms of anxiety may be attributed to an under dosage or under-replacement and lead to further increase in dosage setting up a vicious cycle. as treatment is life long it is better to confirm diagnosis irrespective of cost rather than pursuing an incorrect treatment. once a label is put on patient as hypothyroid, few will dispute it and the treatment is likely to be continued despite a change in treating physician. i therefore feel that a correct diagnosis based on laboratory tests should be adhered to. in a majority of cases diagnosis is simple based on t3,t4 and tsh, the latter being the best screening test.subclinical state of hypothyroidism is usually associated with rise of tsh which compensates for hypothyroidism. there is no hurry for treatment in this case, as it is soon followed by overt disease.this developing state can be confirmed by tpo antibodies.if a tsh value is suspect, a free t4 estimation usually will rule out non-thyroidal causes of abnormal tsh. one other area of concern is maternal hypothyroidism. pregnancy induces a wide variety of changes in thyroid binding proteins. one needs to do free t3, free t4 and tsh for diagnosis. the old conventional tests are too cumbersome. also maternal hypothyroidism can have devastating effect on fetal brain maturity, thus treatment is a matter of urgency in this case. another intriguing situation is posed by use of a cardiac drug amiodarone. this drug, antiarrythmic class 111 was initially confined to Europe. now its use is worldwide.it produces a range of effects on thyroid, some transient and some permanent. the patient can remain euthyroid, he may become hypothyroid or more devastatingly he may become hyperthyroid.because of high iodine load which gets deposited in fat depots, its half -life is a year. stopping the drug thus will not help.any patient on this drug should have regular monitoring of tsh.and t3 . t4 may actually be raised due to iodine load, thus not helpful.in hyperthyroidism, a low tsh and high t4 is found, but confounded by fact this is seen also in early phase of amiodarone treatment. thus one should rely on t3 which is unaffected. a raised t3 would indicate thyrotoxicosis, while a low free t3 indicates hypothyroidism. a tpo antibodies- positivity indicate hypothyroidism. treatment of thyrotoxicosis is problematic and may involve subtotal-thyroidectomy. finally, algorithm are found in textbooks for evaluating thyroid status in patients on amiodarone. Competing interests: None declared |
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Daniel Cuevas-Ramos, Resident of Internal Medicine Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán". Department of Internal Medic, Daniel Cuevas-Ramos, Carlos Gutierrez-Cirlos, Jorge Hernández-Calleros,
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Coexistence of Addison's Disease, Ulcerative Colitis and Sub-clinical Hypothyroidism Editor - We have read with special interest the excellent editorial by Toft and Beckett in which they mention the largely unwritten story of the asymptomatic and unexpected finding of mildly raised serum thyroid stimulating hormone (TSH).1 In accord with that comment, we would like to let you know a singular clinical experience. During the last year, a 20 year old woman was hospitalized with abdominal pain, weakness and diarrhea containing small amounts of blood and mucus. Since 1999, she presented to another hospital with physical debility, skin hyperpigmentation, vomiting and weight loss. Addison's disease, of unspecified origin, was then diagnosed. From then up to now, she has been on prednisone 7.5 milligrams (mg) and fludrocortisone 0.1 mg, both doses every 24 hours. We suspected that the etiology of this disease could be of autoimmune nature and, in fact, antiadrenal antibodies were present (>1:8 titers). Furthermore, the clinical examination practiced to her by us, revealed diffuse abdominal pain and, in rectal exploration, the fecal occult blood test was positive. She does not have extra- intestinal symptoms, but we also realize that she was too thin and presented a doubtful protrusion of both eyes. Colonoscopic examination showed diffuse erythema and granular appearance, with loss of the usual fine vascular pattern in the colon mucosa. In the rectum also was appreciated little ulcerations irregularly distributed on the mucosa. Multiple biopsies were obtained and showed loss of the normal architecture with irregular distribution of glands and moderate infiltration of neutrophils and plasma cells. The picture was consistent with moderate chronic ulcerative colitis. Stool culture did not reveal any pathogens. Against our original suspect, thyroid function tests results showed mildly raised serum TSH values (3.8 micro-Units/milliliter; the normal range in our Institute's laboratory is from 0.3 to 3.5 µU/mL), with normal serum concentrations of both thyroxine (T4) (97.3 nano-molls/Liter) and triiodothyronine (T3) (1.72 n-mol/L), laboratory findings, as it is known, compatible with the presumptive diagnosis of sub-clinical hypothyroidism.2 Antithyroid antibodies were not detected and not treatment was given. At the beginning, the patient was treated with intravenous hydrocortisone to prevent acute adrenal failure. Once the diagnosis of ulcerative colitis was established, she was also treated with mesalamine 400 mg tablets to be taken three times a day. Her symptoms improved dramatically and a week later she can leave hospitalization. In our Institute, in 16 years (1986-2002), it is the first case with the coexistence of these two entities: Addison's disease and ulcerative colitis. In their paper, Govindarajan and Galpin cited that as early as 1966, Wright and Trulove thought that ulcerative colitis was either autoimmune in origin or had external antigens in their etiology; likewise, they noted that autoimmune disorders of a broad spectrum had detectable auto- antibodies and were present in 15% of patients with ulcerative colitis.2 Janerot described the association between ulcerative colitis and thyrotoxicosis,3 a similar association was found by Clubb et al4 and also by Modebe.5 Snook et al, in their extensive survey of 858 patients with ulcerative colitis, did not come across with a single patient with Addison's disease, but they also reported the coexistence of other autoimmune diseases and ulcerative colitis.6 Approximately one-half (56%) of patients with autoimmune adrenal insufficiency have one or more other autoimmune endocrine disorders but, on the other hand, patients with the more common autoimmune endocrine disorders, such as type 1 diabetes mellitus or chronic autoimmune thyroiditis, rarely develop adrenal insufficiency.7 Therefore, the clinical and laboratory facts that we are reporting, maintain the question if the etiology of the ulcerative colitis is also autoimmune, and if both entities studied by us, in this young woman, share some etiological factors. Findings also relevant with Toft and Beckett's comments about "patients with autoimmune thyroid disease who continue to complain of non-specific symptoms".1 Daniel Cuevas-Ramos, MD, resident of Internal Medicine. Carlos Gutierrez-Cirlos, MD, consultant of Internal Medicine. Jorge Hernández-Calleros, MD, resident of Internal Medicine. Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán". Department of Internal Medicine. Calle Vasco de Quiroga # 15. Deleg. Tlalpan, CP 14000, México, D. F. México. References 1. Toft AD, Beckett, GJ. Thyroid function tests and hypothyroidism. BMJ 2003;326:295-296. 2.Govindarajan R, Galpin OP. Coexistence of Addison's Disease, Ulcerative Colitis, Hypothyroidism and Pernicious Anemia. J Clin Gastroenterol. 1992; 15(1): 82-83 3. Janerot G, Azad Khan AK, Trulove SC. The thyroid in Crohn's disease and ulcerative colitis. Acta Med Scand 1975; 197:83-87 4. Clubb, JS. Block PJ, Wallace DC. An association of thyroid disease, ulcerative colitis and diabetes mellitus- a report of three cases in young women. Aust Ann Med 1970; 19:159-163 5. Modebe, O. Autoimmune thyroid disease with ulcerative colitis. Postgrad Med J 1986;62:475-6 6. Snook JA, DeSilva HJ, Jewell DP. The association of autoimmune disorders with inflammatory bowel disease. Q J Med. 1989; 269: 835-840. 7. Zelissen PM, Bast EJ, Croughs RJ. Associated autoimmunity in Addison's disease. J Autoimmun 1995; 8: 121. Competing interests: None declared Editorial comment
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Madge Hirsch, none none
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The opening sentence of Toft’s editorial “Thyroid Function Tests and Hypothyroidism”, “It is extraordinary that more than 100 years since the first description of the treatment of hypothyroidism and the current availability of refined diagnostic tests, debate is continuing about its diagnosis and management”, exemplifies his blinkered attitude which seems to be that we know all there is to know about the diagnosis and management of this condition so that further research and debate are unnecessary. It is this reluctance to listen to different ideas coupled with rigid adherence to the view that a diagnosis of primary hypothyroidism cannot be made if the patient’s TSH is within the normal range which has condemned many patients to miserable lives. Some medical professionals take the view that the THS measurement tells us what is happening only as regards the pituitary-thyroid axis and does not correlate well with what is going on in the patient’s body tissues. Perhaps Toft would label them too as “misguided”. It is worth remembering that Galileo, Pasteur, Darwin and others too numerous to name started as minorities of one and were doubtless regarded as “misguided” and “vociferous”. Is it not in the nature of things that any pioneer, no matter how important and well directed, will be abused in this way? The study by Meier et al. reviewed by Toft shows that “TSH is a poor measure for estimating the clinical and metabolic severity of primary overt thyroid failure”. Rather than saying that it is extraordinary that debate about the diagnosis of this condition continues would it not be more appropriate to encourage research into whether Meier’s conclusions were also applicable to sub-clinical hypothyroidism (mild thyroid failure)? Instead, Toft has used Meier’s study as a hook on which to hang an attack on “misguided medical practitioners” who differ from the current orthodoxy and prescribe thyroid hormones to patients with “normal” TSH. He attacks the belief (supported by the hypothesis that a doctor cannot know whether a given concentration of free T4 or TSH within wide reference ranges is normal for a particular patient) that hypothyroidism may co- exist with normal serum concentrations of both thyroxine and TSH, calling it the view of a “vociferous minority” of patients. Perhaps he is not aware of the study by Andersen et al. indicating that each individual’s thyroid function is unique and that “a test result within laboratory reference limits is not necessarily normal for an individual.”. (1) They also concluded that their data indicated “that the distinction between sub-clinical and overt thyroid disease is somewhat arbitrary”. Toft states “patients with non-specific symptoms of hypothyroidism and unequivocally normal T4 and TSH concentrations do not benefit from treatment with thyroxine” and gives as reference the study by Pollock et al. “Thyroxine treatment in patients with symptoms of hypothyroidism within the reference range – randomized double blind placebo controlled cross over trial” BMJ 2001; 323:891-895. One has only to read the many rapid responses to this study in the BMJ to see that it was seriously flawed and showed only that thyroxine administered for 12 weeks in the particular dosage used was no better than placebo. Subjects were not introduced to the thyroxine gradually as is usual in clinical practice but were given 100 mgs straight off. They were not given the opportunity to progress to a higher dose or to a T4/T3 combination. A long term sufferer of tissue hypometabolism is unlikely to see much noticeable improvement after only 12 weeks given that half that time is necessary for the thyroxine to reach a constant level in the blood. Toft does concede that there is “the difficulty of interpreting a serum concentration of TSH in isolation”. Unfortunately, this difficulty is ignored in clinical practice up and down the U.K. Many NHS hospital labs will not perform free T4 tests in cases where TSH is within range even if the GP has asked for it and this is due not just to penny-pinching but also to near religious devotion to TSH as the definitive thyroid function test. As a result, many patients who may be suffering from hypothyroidism have no option but to seek treatment from “misguided medical practitioners” or to continue to suffer their symptoms and, even worse, to run the risk of future cardiac complication from untreated hypometabolism (2). Furthermore the NHS wastes money on treating such patients’ individual symptoms such as high cholesterol, depression and fibromialgia with expensive drugs which are known to have undesirable side effects when thyroid hormone treatment is cheap. Instead of trying to close down debate it might be more appropriate to note the growing unease (partly generated by the recent large population studies done in the USA and Norway (3 & 4)) about the TSH ranges in current use. Thyroid Disease Manager reports in News Feb 2003 “there are recent suggestions that we have to redefine the normal serum TSH. Spencer et al. (5) suggest a range between 0.4 and 2.0 mIU/l as values < 2.0 mIU/l may represent early hypothyroidism. Others advise an optimal “normal TSH range of 0.4 to 1.5 mIU/l for patients substituted with T4 only”. Spencer et al. point out that “in the future it is likely that the upper limit of the serum TSH euthyroid reference range will be reduced to 2.5 mIU/l because <95% of rigorously screened normal euthyroid volunteers have serum TSH values between 0.4 and 2.5 mIU/l (5). Given this controversy over the ranges it is hard to see how it is “misguided” to treat with thyroid hormone patients whose TSH falls into the range 2-6 mIU/l, particularly if they have positive scores for clinical and metabolic markers of hypothyroidism as used by Meier et al. to evaluate thyroid hormone action at tissue level. Toft concludes by saying “Although the potential improvement in the well being of patients with hypothyroidism while taking a combination of T3 and T4 is of great interest, the greatest advantage will be the security of a normal TSH while taking physiological replacement removing the anxiety about whether a little too much thyroxine alone is harmful.”. Unsupported assumptions about where “the greatest advantage” lies are unhelpful when what is needed is more research so we can better understand the effect of a T4/T3 combination treatment. If that research were to show that the combination medication helped patients to recover from their debilitating symptoms without undesirable side effects surely that would be a greater advantage. What is clear is that this is not happening for all patients who use T4 alone, particularly with the doses given to patients who are being monitored by TSH alone as is current practice (6). Toft’s interpretation of where the greatest advantage might lie flows from the current disregard of what is happening at the tissue level in favour of TSH measurement. These “adequate” doses of T4 which keep the TSH within the reference range have a very modest effect on lowering cholesterol while doses which suppress TSH have a much greater effect(7). One has only to visit internet forums for thyroid patients to see how current treatment with “replacement” doses of T4 only leaves thousands of patients dissatisfied. Fortunately, patients can now communicate with others all over the world and learn that they are not the only ones who, when consulting their GP or endocrinologist with continuing symptoms of tissue hypometabolism are told “Your TSH is in the normal range. These symptoms are nothing to do with your thyroid. You can’t have an increase in dose as your TSH tells us your present dose is fine. There is no need for T3 as the body converts T4 into T3. Perhaps you should consider an antidepressant.”. They can also communicate with patients who have been fortunate enough to consult “misguided medical practitioners” who diagnose and treat hypothyroidism as it was treated successfully for many decades before the advent of the TSH test – by taking a detailed clinical history and examining the patient carefully and then instituting a trial of thyroid hormone – starting off cautiously and gradually increasing the dose while monitoring the patient’s response. They can communicate with patients who have spent 20 or more miserable years on Levothyroxine alone with little amelioration of their symptoms and then made complete recoveries when switched to Armour Thyroid or had synthetic T3 added to their T4. I would say that it is far from extraordinary that debate on the diagnosis and management of hypothyroidism is continuing 100 years after the first description of the disease. Since the advent of insistence on biochemical verification of hypothyroidism and the inadequate practice of testing for TSH and T4 serum concentrations only (how many people in the cash-strapped NHS actually ever get a Free T3/ Thyroid antibodies/ TRH stimulation test?) the under-diagnosis and under-treatment of hypothyroidism has become a real problem and has led to widespread patient dissatisfaction. Thanks to the internet those patients need no longer suffer in isolation, and those with a scientific background can research this disease for themselves and discover that the views upheld by clinicians such as Toft are not universally accepted and that, whether he likes it or not, the research and debate which are the essence of good science continue. Yours faithfully Madge Hirsch References. (1) Narrow Individual Variations in Serum T4 and T3 in Normal Subjects: A Clue to the Understanding of Subclinical Thyroid Disease. Stig Andersen et al. Journal of Clinical Endocrinology and Metabolism Vol 81 No3 1068 -1072 (2) Sub-clinical Hypothyroidism is an Independent Risk Factor for Atherosclerosis and Myocardial Infarction in Elderly Women: The Rotterdam Study. Hak A E et al. Ann Intern Med 2000: 132: 270-270. (3) Serum TSH, T4 and Thyroid Antibodies in the United States Population (1988 to 1994): National Health and Nutritional Examination Survey (NHANES III) Joseph G. Hollowell et al. Journal of Clinical Endocrinology and Metabolism Vol 87 No.2 489-499. (4) Prevalence of Thyroid Disease, Thyroid Disfunction and Thyroid Perioxidase Antibodies in a Large, Unselected Population. The Health Study of Nord-Trǿndelag. Bjǿro et al. European Journal of Endocrinology 200 143 639-647. (5) National Academy of Clinical Biochemistry “Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease’’ Spencer et al. The American Thyroid Association Newsletter (on-line www.thyroid.org) (6) Psychological Well Being in Patients on “Adequate” Doses of L- thyroxine: Results of a large controlled community based study. Saravanan P. et al. Clinical Endocrinology Vol 57 Issue 5 Nov.2002. Thyroxine Replacement Therapy and Circulating Lipid Concentrations. Franklyn J.A. et al. Clinical Endocrinology (Oxf) 1993 May: 38(5) 453-9. Competing interests: None declared |
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Ahmed Waise, Consultant Chemical Pathologist York Hospital, York YO31 8HE, UK
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Dear Editor, The article and leader emphasise that, even in severe primary hypothyroidism, there may be poor correlation between TSH level and tissue markers of thyroid hormone action1,2. The discrepancy between markers of thyroid under activity may indeed extend to the clinical presentation, where by patients may not testify to have significant symptoms of hypothyroidism. This is despite the findings of physical signs and tissue markers indicating hypothyroidism as well as having severe biochemical hypothyroidism, i.e. TSH> 20 mU/l and very low thyroxine levels. Equally some patients are found to have severe hypothyroidism when they are being assessed for non specific symptoms. This lack of correlation may, as least in part, be related to the insidious onset of autoimmune hypothyroidism. This sharply contrast with the development of transient or permanent hypothyroidism, which may happen within the first few months after radioactive iodine therapy. Under these circumstances symptoms tend to be ‘acute’ with pronounced tiredness, exhaustion and weight gain and with patients reporting these features sooner. As the authors also indicate, titration the dose of thyroxine to bring down TSH level to ‘ within the normal range ’ may be inadequate, particularly in patients who continue to experience symptoms. There is probably a strong case for having a different range for TSH in patients on thyroxine replacement. A range of 0.5 to 1.5 mU/l has been recommended3. The study showing that a TSH above 2 mU/l is associated with an increased probability of future hypothyroidism tends to lend support to such recommendation4. Finally we have, in this journal, previously also highlighted clinical histories and progress of six patients with pituitary disorders and in whom the diagnosis would have been delayed or missed altogether, if TSH only had been used as first line thyroid testing5 1. Meier C, Trittibach P, Guglielmetti M, Staub J-J, Müller B. Serum thyroid stimulating hormone in assessment of severity of tissue hypothyroidism in patients with overt primary thyroid failure: cross sectional survey. BMJ 2003; 326: 311-312 2. Toft A.D., Beckett G.H. Thyroid function tests and hypothyroidism Measurement of serum TSH alone may not always reflect thyroid status. BMJ 2003;326:295-296 3. L M Demers, C A Spencer. Laboratory support for the diagnosis and monitoring of thyroid disease (accessed 20.2.2003) http://www.nacb.org/lmpg/thyroid_lmpg_pub.stm 4. Vanderpump MPJ, Tunbridge WMG, French JM, Appleton D, Bates D, Clark F, et al. The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham survey. Clin Endocrinol 1995;43:55-68 5. Waise A, Belchetz PE. Unsuspected central hypothyroidism. BMJ 2000; 321: 1275-1277 Competing interests: None declared |
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Barry J Durrant-Peatfield, Retired Physician DA13 0NY
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Dear Sir The editorial in the BMJ 2003, 8th February, by Toft and Beckett is disappointing in a number of regards. The opening paragraph encapsulates the generalised and arrogant approach taken by Dr Toft together with so many of his colleagues. His suggestion that patients with symptoms of hypothyroidism, but normal blood tests, are a “vociferous minority” who have psychosocial problems, is entirely misleading and quite insulting to a great many patients. If he could be persuaded to take the trouble to undertake a full clinical appraisal, including the invaluable basal temperature test, suggested by Barnes as long ago as 1945 in the Lancet, he would doubtless be able to make a diagnosis of hypothyroidism on clinical grounds, and learn for himself the pitfalls of an uncritical reliance on blood tests. His second paragraph, concerning “misguided medical practitioners” who in their alleged unwisdom actually try to solve their patients’ problems by using T3 as well as T4, or natural desiccated thyroid, is again gratuitously insulting. These practitioners do not attempt to hit some desired T4 or TSH level, but actually titrate the dosage to their patients’ needs. A process called listening to the patient. Reliance on the “sensitivity” of the TSH, expressly disregarding the clinical response, is misplaced; the test approach must have a sensitivity of at least 0.02 mu/l, which is difficult to reliably achieve and thus affords a frequently seen cause for error. He raises again the spectre of iatrogenic hyperthyroidism as a cause of osteoporosis and atrial fibrillation. Although a theoretical possibility, there is no evidence for this and I have never seen it in many thousands of patients. It is particularly unlikely when patients have been taught the value of self-monitoring. Dr Toft refers to Pollock et al, who purported to demonstrate, in a much criticised paper, that thyroxine helped a little in patients with incontrovertible hypothyroidism but didn’t at all if they hadn’t. As with the authors, Dr Toft confuses symptoms with a full clinical appraisal providing a consequent diagnosis, which it is perfectly proper for an experienced physician to make despite a normal TSH and T4. Neither this paper nor Dr Toft’s comments have furthered understanding in any way. Again, he refers to “the exquisite” sensitivity of the TSH which leads him and his colleagues astray. He is right to point out that pituitary or hypothalamic weakness, very much more common than he believes, will provide a false low TSH; he would do well to remember that a hypometabolic pituitary/hypothalamic axis is a commonly met cause of unreliable TSH estimations. However his observation that a replacement providing a higher than normal T4 and suppressed TSH allows for greater patient well-being is to be welcomed. Further is to be welcomed his consideration concerning the addition of T3 to T4, if somewhat rather late in the day. Perhaps he might in due course be persuaded that the use of T2 as well, as with desiccated thyroid, confers additional advantage. Yours faithfully Dr Barry Durrant-Peatfield M.B., B.S., L.R.C.P, M.R.C.S. Competing interests: None declared |
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Mike Crilly, Senior Lecturer in Clinical Epidemiology & Public Health Medicine Aberdeen University Medical School, AB25 2ZD
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DEAR EDITOR - In their recent editorial on thyroid function tests and hypothyroidism, Toft and Beckett discuss the target TSH (thyroid stimulating hormone) concentration for patients receiving thyroxine replacement therapy for primary hypothyroidism.[1] They suggest that patients with continuing non-specific symptoms (despite a TSH within the laboratory reference range) are ‘under-replaced’. They conclude that simply satisfying the recommendations of the American Thyroid Association and restoring TSH concentrations to normal is inadequate. They state that “some patients only achieve a sense of well-being if their TSH is low or undetectable” and that “most patients feel well only with a low normal TSH concentration”.[1] Primary care physicians in the UK provide sole continuing clinical care for majority of patients (82%) with primary hypothyroidism.[2] Before considering changing their clinical practice, physicians should know that almost no empirical evidence exists to support the assertion that hypothyroid patients feel better with a TSH concentration that is ‘low normal’, undetectable or suppressed.[1] By comparison, two systematic reviews with meta-analysis have found that reducing TSH levels with thyroxine therapy increases the risk of osteoporosis - particularly in post-menopausal women.[3,4] An issue of considerable clinical importance as women over the age of 50 years comprise 84% of patients prescribed thyroxine replacement therapy in primary care.[2] TSH suppression also increases the risk of atrial fibrillation.[5] Existing levels of TSH suppression in the community already pose a threat to women’s health. Many hypothyroid patients are currently over- replaced with thyroxine in the UK. The proportion of patients with suppressed levels of TSH is over 20% [2,6] in primary care, whilst undetectable TSH levels (on ultra-sensitive assay) are 12%.[2] A change in routine clinical practice which further reduces women’s TSH on thyroxine replacement therapy is likely to increase both osteoporosis and atrial fibrillation - without any good evidence that these women will feel any better. Dr Mike Crilly
Conflicts of interest: None References [1] Toft AD, Beckett GH. Thyroid function tests and hypothyroidism Measurement of serum TSH alone may not always reflect thyroid status. BMJ 2003;326:295-296 (8 February) [2] Crilly,M. Thyroid adherence study. Impact of an educational booklet on thyroxine adherence inpatients with primary hypothyroidism: a randomised controlled clinical trial in primary care. [MD Thesis: submitted University of Manchester UK, 2002] [3] Faber J, Galloe AM. Changes in bone mass during prolonged subclinical hyperthyroidism due to L-thyroxine treatment: a meta-analysis. Eur J Endocrinol 1994;130(4):350-6. [4] Uzzan B, Campos J, Cucherat M, Nony P, Boissel JP, Perret GY. Effects on bone mass of long term treatment with thyroid hormones: a meta- analysis. J Clin Endocrinol Metab 1996;81(12):4278-89. [5] Sawin CT, Geller A, Wolf PA, Belanger AJ, Baker E, Bacharach P, et al. Low serum thyrotropin concentrations as a risk factor for atrial fibrillation in older persons. N Engl J Med 1994;331(19):1249-52. [6] De Whalley P. Do abnormal thyroid stimulating hormone level values result in treatment changes? A study of patients on thyroxine in one general practice. Br J Gen Pract 1995;45(391):93-5 Competing interests: None declared |
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Richard G Fiddian-Green, None None
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William Silen, formerly Johnson and Johnson Professor of Surgery at Harvard and Chief of the Surgical Services at the Beth Israel in Boston, used to speak of the pooped-out syndrome that developed in patients after major surgery. Depression is a common feature in these patients. He ascribed the syndrome to hypothyroidism. It is now appreciated that many patients develop haemodynamically compensated shock, or an inadequacy of mitochondrial oxidative phosphorylation, during or immediately after major surgery. Organ dysfunctions and failures tend to occur almost exclusively in these patients. If persistent this might lead to a depletion in adenine nucleotide stores and hence in the capacity to replenish ATP stores after the demand for energy release by ATP hydrolysis. ATP depletion is a serious biochemical abnormality for I may take as long as 300 days to replenish (1). It may take much longer and might not even be possible if a significant degree of impairment of mitochondrial oxidative phosphorylation persists. Any impairment of ATP resynthesis is likely to compromise the replenishment of endocrine pools and the electrohemical gradients needed to release them in a timely and appropriate manner (2). Thyroid hormones open the permeability transition pores on mitochondrial membranes and thereby decrease the magnitude of the protonmotive force driving ATP resynthesis. Oxidative phosphorylation is thus uncoupled and the generation of heat increased. An increase in metabolic rate is required to accommodate these changes. This effect appears to be beneficial for in hypothyroidism it is deficient. If increased to to excessive degrees, however, opening the permeability transition pores may induce apoptosis and even cellular necrosis (3,4). ATP turnover would seem to be a far more sensitive measure of the adequacy of ATP resynthesis than measures of ATP, ADP, adenine nucleotide energy charge, or phosphorylation potential (1). I suspect the same applies to the assessment of thyroid function, hormonal turnover rates being likely to be far more sensitive than the conventional measurements. But what of the ATP pools upon which thyroid hormonal function would appear to depend? Should ATP turnover rates be included in the assessment of thyroid function (5)? 1. Ingwall JS. ATP synthesis in the normal and failing heart. In: Heart failure, Poole-Wilson PA, Colucci WS, Massie BM, Eds, Churchill Livingston, New York, 1997 2.Treating dementia with light and near infrared waves Richard G Fiddian-Green bmj.com/cgi/eletters/325/7376/1312#29607, 12 Feb 2003 3. Madness, hyperhomocysteinemia, metabolic rate and body temperature Richard G Fiddian-Green bmj.com/cgi/eletters/325/7378/1433#28469, 6 Jan 2003 4. Coronary revascularisation: treatment or prevention? Richard G Fiddian- Green bmj.com/cgi/eletters/326/7381/134#29010, 22 Jan 2003 5. Thyroid function tests and hypothyroidism Anthony D Toft and Geoffrey J Beckett BMJ 2003; 326: 295-296 Competing interests: None declared |
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Surinder S Birring, Specialist Registrar in Respiratory Medicine Institute for Lung Health, Department of Respiratory Medicine, Glenfield Hospital, Leicester, LE39QP, Ronak B Patel and Ian D Pavord.
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Editor- Toft and Beckett finish their review of thyroid function tests in hypothyroidism with the intriguing statement that residual symptoms in treated patients might relate to the underlying chronic inflammatory disorder rather than subtle abnormalities of thyroid hormone status.(1) This struck a cord with us since we have noted a striking excess of cases of treated hypothyroidism amongst a population of idiopathic chronic cough(2) and in non-smokers with fixed airflow obstruction(3) and have shown that idiopathic chronic cough is associated with a bronchoalveolar lavage lymphocytosis.(2) We have suggested that this may be due to homing of activated lymphocytes from the primary site of autoimmune inflammation to embryologically related structures such as the airways.(2-4) The mechanism of airway inflammation and damage in autoimmune thyroid disease may be analogous to that thought to be responsible for airway complications of inflammatory bowel disease. The concept that inflammatory bowel disease and autoimmune thyroid disease are associated with airway disease and that the pathogenesis is similar and not related to thyroid hormone status is supported by a recent study showing a 2-3 fold excess of cough, sputum production and breathlessness, and a remarkably similar profile of respiratory symptoms, amongst a cohort of patients with inflammatory bowel disease and another with treated autoimmune thyroid disease.4 Further evidence for a link between thyroid disease and respiratory disease independent of thyroid hormone status has been reported in a study showed a 2-3 fold increase in death from respiratory disease in a large cohort of patients with normal thyroxine but suppressed thyrotropin.(5) These findings would be consistent with the view of thyroid disease as a generalised, rather than organ-specific autoimmune disease. It is tempting to speculate that other non-specific symptoms as well as recognised complications of hypothyroidism such as ischaemic heart disease are related to similar inflammatory mechanisms. References 1. Toft AD,.Beckett GJ. Thyroid function tests and hypothyroidism. BMJ 2003;326:295-6. 2. Birring S.S., Brightling, C. E., Symon, F. A., Barlow, S., Wardlaw, A. J., and Pavord ID. Lymphocytic bronchoalveolitis in idiopathic chronic cough. Thorax 57, iii1. 2002. 3. Birring SS, Brightling CE, Bradding P, Entwisle JJ, Vara DD, Grigg J et al. Clinical, radiologic, and induced sputum features of chronic obstructive pulmonary disease in nonsmokers: a descriptive study. Am.J.Respir.Crit Care Med. 2002;166:1078-83. 4. Birring S.S., Morgan A.J., Prudon B, McKeever T.M., Lewis S.A., Falconer Smith J.F., Robinson R.J., Britton J.R., and Pavord ID. Respiratory symptoms in patients with treated hypothyroidism and inflammatory bowel disease. Thorax in press. 2003. 5. Parle JV, Maisonneuve P, Sheppard MC, Boyle P, Franklyn JA. Prediction of all-cause and cardiovascular mortality in elderly people from one low serum thyrotropin result: a 10-year cohort study. Lancet 2001;358:861-5. Competing interests: None declared |
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Friedrich Flachsbart, General medicine 37085 Göttingen
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Dear Sir, the connections between acute respiratory infections, acute rheumatic fever and hyperthyreoidism were first described by v. Basedow, 28. March 1840. The connections between acute respiratory infections, acute rheumatic fever and diabetes mellitus were first described by Ebstein, 1876. And Veil again focussed these lines of evidence to the central point: Induction by streptococcal infection. We only have to look into the old books to find the new things. W. H. Veil: Der Rheumatismus und die streptomykotische Symbiose. Enke, Stuttgart, 1939. All the best to You Yours Competing interests: None declared |
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Trevor G Marshall, PhD, Research Director Sarcinfo, Thousand Oaks California, 91360-1122
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Biochemists have known for some time that the Thyroid and Parathyroid are both profoundly affected by the secosteroid hormone 1,25-dihydroxyvitamin-D (1,25-D) [1]. There is an excellent drawing illustrating the systemic effects of this steroid available online from University of California, Riverside, Dept of Biochemistry (click here to view it). Unfortunately, clinical medicine has been slow to use this knowledge, and this secosteroid is rarely measured, even today. I have some 1,25-D data which demonstrates that between 20% and 50% of euthyroid patients are suffering from undiagnosed inflammation, most probably as the result of an undiagnosed immune condition. This data would indicate that a significant percentage of the population could be at risk. The 1,25-D secosteroid is formed in large quantities in inflamed tissue. It is a component of the immune system's Th1 inflammatory response. Angiotensin II is also involved. We have recently proposed a working description of the Th1 endocrine biochemistry [2]
The Th1 inflammatory cycle is mounted in response to infection. It has been shown, in-vitro, that gram-negative bacteria release lipopolysaccharides and lipopeptides [3]. Most folks' immune systems seem to neutralize the infective agent and recover, but a proportion of the population does not manage to immediately kill all the bacteria, and those which remain continue to secrete lipopolysaccharide and lipopetides. Consequently, the body's immune reaction is sustained for long periods, sometimes for life. A small proportion of these continuing immune reactions are severe enough to cause the most chronic immune disease, Sarcoidosis [4]. We have found that measuring the elevated production of 1,25-D steroid gives a reliable indication of the degree of immune dysfunction. We have achieved excellent results using antibiotics to induce remission in chronic sarcoidosis, but, at this point, have been unable to get our results through peer-review. Give it time... maybe another decade or two... Half a century ago, Thomas McPherson Brown reported positive results with antibiotics in Rheumatoid Arthritis [5], but, despite significant popular acclaim [6] his discovery has still not been acknowleged by the mainstream clinical community. 'Therapeutic probe' with some older antibiotics is now reliably curing 'autoimmune' disease, and this has given reasonable confirmation that the so-called 'autoimmune' diseases are actually due to Cell Wall Deficient bacteria [7,8]. These are species of resistant bacteria (including strep species) which have developed resistance to the antibiotics whose mode of attack on the organism is destruction of the cell walls (such as the penicillins). I would therefore caution against using the "auto"-immune word, as the immune system is clearly reacting to a simulus, not to itself. Unfortunately I suspect it may take a very long time for this pathogenesis to be recognized, and fully adopted into clinical practice. It is becoming clear that recognition of the (relatively simple) biochemistry whereby bacteria affect the thyroid and parathyroid via Th1 and 1,25-D will take equally as long to transition from the realm of Molecular Biochemistry into clinical practice. Guy Scadding first noted the links between this secosteroid's metabolism and Immune Disease in the BMJ back in 1950 [9]. I agree with Dr. Flachsbart, "we only have to look into the old books to find the new things". Unfortunately, most of these old books were burned during the 'wonder-drug' and 'Evidence Based Medicine' revolutions... 1. Norman AW, Adams D, Collins ED, Okamura WH, Fletterick RJ: Three-dimensional model of the ligand binding domain of the nuclear receptor
for 1alpha,25-dihydroxy-vitamin D. J Cell Biochem 1999 Sep 1;
74(3):323-33 [PubMed Abstract]
2. Marshall TG, Marshall FE: New Treatments Emerge as Sarcoidosis Yields Up its Secrets. Clinmed 2003 Jan 27;2003010001. clinmed.netprints.org/cgi/content/full/2003010001 (accessed 27 Jan 2003) [Full Text] 3. Mühlradt PF, Kiess M, Meyer H,Süssmuth R, Jung G. Structure and Specific Activity of Macrophage-Stimulating Lipopeptides from Mycoplasma hyorhinis. Infect Immun 1998 Oct; 6(10): 804-10 [Full Text] 4. Marshall TG, Marshall FE: Brown, et al, ACCESS Study finds Bacterial Pathogens in Sarcoidosis Patients. [Electronic Letter] Chest 2003: Feb 12. Available from URL http://www.chestjournal.org/cgi/eletters/123/2/413#96 5. Brown TMcP, Wichelhausen RH, Robinson LB, Merchant WR: The in-vivo action of aureomycin on pleuropneumonia-like organisms associated with various rheumatic diseases. J Lab Clin Med 1949; 34: 1304-1410 6. The Road Back Foundation: Rheumatic Treatment and Research. Available from URL http://www.roadback.org 7. Cantwell AR Jr: Variably acid-fast bacteria in a case of systemic sarcoidosis and hypodermitis sclerodermiformis. Dermatologica 1981; 163(3):239-48 [PubMed Abstract] 8. Almenoff PL, Johnson A, Lesser M, Mattman LH: Growth of acid fast L forms from the blood of patients with sarcoidosis. Thorax 1996 May; 51(5):530-3 [PubMed Abstract] 9. Scadding JG: Sarcoidosis, with special reference to lung
changes. BR
Med J 1950; 1: 745-753 Competing interests: None declared |
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Simon M. Clarke, Hypothyroid Patient Cornwall, PL14 4EQ
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Whilst beginning with a strong backlash against the 'rogue medical professionals' and almost certainly the self-diagnosing internet browsing patients, the article makes a strong case for TSH testing as a basis of diagnosis. However... Medical professionals must have guidelines in which to work, and base their decisions upon. Patients, such as myself, understand this. Problems quickly arise when a patient feels unwell, yet often has just a few minutes of their GPs time in which to voice their concerns. A check of the most recent blood works on their computer screen, and the GP assures/dismisses (depending on which side of the desk you sit) based upon the numbers being within the regarded range. The internet savy or just plain unconvinced patient search the internet and finds.... widely differing suggested ranges! Several UK sources suggest a TSH reference range of 0.4 - 4.5 whilst my GP insists it should be 0.3 - 5.5 This may not seem a huge difference, but it's highly significant to me as I'm currently 4.6, feeling unwell but my GP will not increase my T4 dosage. (my current T4 being 13.6 in a stated range of 10 - 23) Now it appears that the USA have amended their range to peak at 3.0 ! With UK GP's working to differing ranges, and most unable or unwilling to consider supplementing T4 with T3 for patients who are still feeling unwell, patients comments and 'gut feelings' MUST take a higher significance than mere numbers. Medical professionals need to look beyond the figures to the quality of life of their patient. It is us, after all, that have to live with our widely differing blood results long after our three-minute consultation with you has ended. Competing interests: None declared |
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Simon R Cains, Senior geophysicist Not medical
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Dear Sirs, I have no training or clinical experience of endocrinology, so I will not attempt to present any evidence which would contradict your views. ( Although my wife developed a hoarse voice with all the other symptoms, the ENT hospital department have suggested hypothyroidism, but of course they cannot prescribe thyroxine.) However as the husband of one of the people you condemm as having "psycho- social problems" I feel at least I am entitled to ask some very basic questions. 1) The reference level for TSH for "healthy patients" is 0.5 to 5.0. Can you explain why certain patients function normally at 0.5 and others at 5.0 ? If you could accurately predict a healthy patient's TSH from some other factors, this would remove any doubt about an individual patient's reference level. If you have no idea, doesn't this suggest some lack of certainty concerning TSH and the other hormones ? 2) Without knowing a reference level, would you agree there will be cases where 2 patients both present to an endocronologist with TSH levels, say 5x their normal level; one patient is diagnosed and treated, the other patient is told their problems are all due to over-eating, clinical depression, and the many other symptoms are due to an unfortunate coincidence or just unexplained. The reason for this of course is patient A had a reference level of 0.5, the other had nearer to 5. Patient A despite their 5x increase is still in the "normal" range, patient B is above the range. Would you agree this is a thyroid lottery, those lucky enough to be born with a higher level are more likely to be treated ? If the exact range from 0.5 to 5 is as irrelevant as you say, why are patients with 5.1 diagnosed hypothyroid, while 4.9 are hypochondriac ? 3) Reducing the method to its basics:- All healthy patients have a TSH level of 0.5 to 5.0. Therefore all patients with a TSH of 0.5 to 5.0 are healthy. Does it not occur to you there may be a slight flaw in this logic ? In most fields of science, we would also test the contrary, i.e. do all unhealthy patients have a TSH range outside 0.5 to 5.0 ? If this test had been done in 1973, when the hormone test was first introduced, we know the answer would have been no, many patients present with numerous specific clinical symptoms (not just overweight and tired) but have TSH in the normal range. How different the diagnosis of hypothyroidism might been, if this had been done before taking the TSH range as gospel and throwing out all the symptoms. 4) Do you or indeed any endocrinologists have any psychiatric training ? What are your qualifications to diagnose all these patients with depression ? If you could take the time to read all the patients' accounts published, you would find that all patients sent to psychiatrists from endocrinology are diagnosed as mentally normal, the only thing making them depressed is all the symptoms that the doctor cannot explain. Your absolute certain diagnosis of every symptom, from hoarse voice, dry skin and deafness to severe fluid retention as due to "psycho-social problems" is a very confident diagnosis outside your field, something you deplore in those outside the endocrine speciality. 5) Would you at least agree that some patients are in-appropriately treated, after the thyroid cause has been eliminated ? For instance Diana Holmes was treated for 6 severe conditions such as Myasthenia Gravis, coeliac disease, etc, treated with massive doses of steroids, antibiotics, Mestinon, etc (Tears Behind Closed Doors, Normandi Publishing 2002). None of these had any effect, and she was only cured and back to full health after being treatd with thyroxine. Of course your diagnosis would be that all her disabilities were due to some psychological reason and the thyroxine had the "magic" placebo effect that can explain everything (but why didn't the previous 6 treatments have this effect ?). Therefore none of the previous treatments were appropriate. So why are you so opposed to patients trying a short-term test of a low dose of thyroxine, to try to cure these symptoms that leave doctors baffled ? ( A simple medical waiver form would remove any risk of patient litigation if anything went wrong). The alternatives can be also be drastic. The antidepressents that you and collegues hand out like sweets are also not without side effects. 6) If you have seen the patient-oriented websites, you will know that many patients are having to dose themselves with thyroxine with no medical supervision, since they cannot find a GP who will consider the symptoms. Would you not agree that GPs should at least be allowed to monitor and advise patients even though they are not prescribing the hormone ? I would be very interested to hear your replies. You state it is only a vociferous minority who claim that throxine has cured them ( so obviously they must be wrong). Of course the rest, the majority of patients diagnosed as normal by the GP and endocrinologist simply accept the diagnosis, because they are never told that some medical staff do have doubts. Of this minority who do decide to and have the resources to research deeper, a much smaller minority actually manage to find a GP who will try out thyroxine on them. So it is even more surprising that so many hundreds of people have mananged to find a way through this process and found a cure. I have a nagging suspicion that the medical profession have seized on these hormone levels as an OBJECTIVE method to decide the course of treatment, without having to make any clinical judgement which they fear might result in litigation. But gentlemen I must point out that litigation can work both ways. If one day a high court judge finally decides that hundreds, thousands of patients have suffered crippling illness and disability due to medical neglect, the litigation will be severe indeed against those who so "vociferously" blocked any patient choice. So once again, are you still totally opposed to seriously disabled patients being give a small test of thyroxine if all else has failed ? Your banning policy may not quite be as risk-free as you think. Competing interests: None declared |
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Gordon R B Skinner, Private Practitioner 22 Alcester Road, Moseley, Birmingham B13 8BE
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High dosage thyroid replacement should be considered in 'refractory' hypothyroidism Dear Sir, There has been correspondence in the British Medical Journal (8th February 2003) discussing tangentially risk assessment in patients receiving high dosage thyroid replacement. As my practice is mainly concerned with problems of thyroid function, I seek advice from colleagues on the advisability of long term high dosage thyroid replacement in patients with refractory hypothyroidism. Hypothyroid patients who do not respond to thyroid treatment comprise two groups namely patients who show no improvement but become clinically thyrotoxic and patients who show no improvement nor adverse effect. The latter creates a frustrating and difficult situation for both patient and doctor which is often compounded by FT4 or FT3 levels above the upper limit of the 95% reference interval and TSH levels approaching zero. During the last decade I have treated at least fifty patients who had irresolvable or refractory hypothyroidism with sodium thyroxine at dosages over 350µg per day or natural Armour Thyroid extract at over 4 Grains per day or a combination of the two medications at equivalent dosage. These patients have been returned to optimal or near optimal health with no evidence of adverse effect. The critical question concerns possible long term adverse effects. A priori, it is unlikely that restoration of a patient to health where she is up and about and living a full life will be detrimental or associated with long term pathological sequelae. Perceived complications are unproven. Cardiac irregularity is a well recognised feature of hypothyroidism and usually disappears on thyroid replacement and (in my experience) asymptomatic thyroxine induced irregularity is rare but is easily detected by physical examination and is reversible within 1-2 days. Evidence of osteoporosis is insecure and may have arisen from the purported association of osteoporosis with chronic hyperthyroidism where there may also be accompanying hyperparathyroidism with bone demineralisation but this is speculation. The author has never encountered significant adverse effects in patients restored to euthyroidism by high dosage thyroid replacement. There is a second more philosophic consideration; many patients unequivocally state that they would rather run the gauntlet of putative and unproven pathological sequelae than continue a wretched hypothyroid existence. This raises an ethical question on the degree of self determination or self selection of medical care which is desirable, acceptable or indeed is a patient¹s right in a society based on consensual rather than dictatorial principles. However it remains an unpalatable fact that many patients are receiving inadequate and ineffective thyroid replacement from unfounded fears that return of a patient to euthyroidism will be accompanied by crumbling bones or undiagnosable cardiac pathology. It is suggested that the efficacy and safety of higher dosage thyroid replacement be subjected to the scrutiny of formal clinical trial. Yours sincerely,
Competing interests: None declared |
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Maureen hallett, RN (retired ) due to ill health 32766
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I read with interest your article which at first seemed to state that TSH is the "gold standard " in the first line of diagnosing Hypothyroidism and your early statements about patients insisting they have hypothyrodism when the TSH is los even though they have symptoms is egged on by some clinicians.Well what I found odd was your article then gave proof at the end that people can and do have normal TSH and Hypothyroid disease and should be checked for it with symptoms...I don;t get the point of your article... I myself had a rapid weight gain after a lifetime of being a very thin person even after four children..I was an ER nurse at the time and was also getting weaker and weaker,,I also had asthma and fibromyalgia and undiagnosed Rheumatoid arthritis..By the time I left my primary doctor to find another I had gained 80 lbs!!! One particular time I remember was when I had come home from a camping trip with my husband where we had been hiking 20 miles every day this is while I was around the 40lb overweight stage and I had gained 7 lbs,,,the doctor was not concerned,.,,As a nurse I realized that it was impossible to hike like this and gain weight without a serious metabolic disorder...but since my TSH was normal..still nothing was done.. Worse still I have a mother with Hashimotos and a sister with Graves ...this did not phase them.. I was still working and going to other docs for my other troubles so having little time to search for new docs but when my GYN saw me for my routine visit he ordered a T4 and T3 resin uptake and these were abnormal but really not that awful but sent me to an endocrinologist...I had brittle hair,nails that bent in half and peeled,my legs had three plus pitting edema by this point ,my heels of my feet were so dry a thick layer of skin fell right of of both heels...I was now so tired I could no longer drive,,,,My eyes were puffy and I had a sed rate of 54 my cholesterol was and is high at 250 I am now on Synthroid and very slowly getting better Competing interests: None declared |
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