Rapid Responses to:
|
|
Rapid Responses: Rapid Responses published:
-
![[Read Rapid Response]](/icons/misc/sectionDOWN.gif)
Iodine Deficiency and Thyroid Function Tests
- Eleanor Allen (19 October 2001)
-
Its Thyroxine thats the problem
- Pat Davis (19 October 2001)
-
What does this study mean?
- June Hyslop (20 October 2001)
-
Its the Thyroxine Stupid!
- W John Diamond (21 October 2001)
-
Reverse T3 and thyroxin binding globulin were not measured.
- Andrea Corsonello (22 October 2001)
-
Trial of Armour is required
- Carol Foster (23 October 2001)
-
Reference ranges
- Simon Waters (23 October 2001)
-
Flaws in the Study
- Lois Sommerfield (29 October 2001)
-
A VTS critical appraisal.
- M Duncan (7 November 2001)
-
More Elegant Research Needed
- Jim Harwood (12 November 2001)
-
Surprise!
- A Mark Clarfield (30 November 2001)
-
Other Paths to Consider
- Eric K Pritchard (20 September 2008)
|
|
|||
|
Eleanor Allen, Health Writer Ottawa
Send response to journal:
|
Dear Editor, Re: Thyroxine treatment in patients with symptoms of hypothyroidism but thyroid function tests within the reference range Iodine deficiency might explain the persistence of the anecdotal belief in a connection between thryoxine treatment and the relief of hypothyroid symptoms despite thyroid function tests within the reference range. While serum thyroid hormone and thyroid stimulating hormone levels change with iodine deficiency, in adults they nonetheless stay within the reference range, except in cases of severe deficiency(1). Of course, for neonates with iodine deficiency, thyroid stiumlating hormone is above the reference range. Hetzel and Delange note that in adults this compensation for deficiency comes about because triiodothyronine is being converted from thyroxine that is taken "from peripheral tissues containing type II 5'deiodinase like the brain." In studies of rats, the results (sensitivity to cold, reduced growth hormone) have suggested hypothyroidism in some tissues, despite normal serum triodothyronine concentrations (2). A 1985 German study found that 100 mg thyroxine and 500 mg iodide were equally effective at reducing goitre size, the only difference being that the thyroxine led to increases within the normal range in serum thyroxine and free thryoxine levels within one month, while the iodide treatment led to the same changes only after three months. They found no change in triiodothyronine levels(3). Perhaps in the open studies there are some people with undetected mild or moderate iodine deficiency who are finding real benefit from thyroxine treatments. Iodine supplements might have done the trick just as well. Yours truly, Eleanor Allen
References: 1 Dr. John Dunn, MD, Executive Director of International Council for the Control of Iodine Deficiency Disorders. Interview. 26 February 2001. 2 Delange F, Hetzel B. The Iodine Deficiency Disorders. In: Hennemann G, DeGroot L, editors. The Thyroid and Its Diseases. Massachusetts: Endocrine Education, Inc.; August 2001; Sect. Endemic Goiter, Pathophysiology. Last revision 18 July 2001. Available from: URL: http://www.thyroidmanager.org/Chapter20/20- frame.htm 3 Olbricht T, Hoff HG, Benker G, Wagner R, Reinwein D. [Sonographic volumetry of the thryoid gland in the control of thryroxine and iodide treatment of non-toxic goiter] Sonographische Volumetrie der Schilddruse zur Verlaugskontrolle bei der throxin- un Jodidbehandlung der blanden Struma. Dtsch Med Wochenschr 1985 May 31;110(22):863-6. |
|||
|
|
|||
|
Pat Davis, Thyroid Group Helper
Send response to journal:
|
Not once in this article is it recognised that thousands of correctly diagnosed Hypothyroid patients throughout the world feel very little benefit from any amount of Thyroxine .......yet when they explain this situation to their GPs or Endocrinologists they are ridiculed and their situation is ignored in the totally rigid belief that both Thyroid Blood tests and Thyroxine are perfect . The FDA are not happy about the quality of Synthyroid ( thyroxine )which is a grandfathered drug which has never been tested but just assumed to work and have forced drug manufacturers to submit it to proper testing . Researchers in Spain have proved that its whats happening at a cellular level that needs evaluation but currently there are no available tests to prove how a patients cells use or respond to Thyroid Hormone , or indeed tests to prove whether the patient is actually able to convert Thyroxine T4 into the T3 their cells need Reverse T3 testing is not done so false assumptions are made and thousands of patients who are genetically resistant to Thyroid hormone and thereby exhibit Hypothyroid symptoms go ignored and untreated www.drlowe.com is the work of years of research which is backed by other innovative doctors across the USA and Canada like Dr Domininesse, Dr David Derry etc who have proved time after time that these patients only respond to either T3 Cytomel or Armour dessicated thyroid .........both of which are denied to UK patients Thyroid patients in the UK are treated like idiots who dont know just how rotten they feel or just what a poor quality of life they have all because of one influential persons rigid doctrine that Blood tests and Thyroxine are perfect As the long suffering wife of a Hashimotos Hypothyroid Man who despite 10 yrs of optimum doses of Thyroxine and so called perfect blood tests is very far from well or able to enjoy life and being on the end of a helpline I sure know the subject and the suffering better than the majority of doctors |
|||
|
|
|||
|
June Hyslop
Send response to journal:
|
What does this study mean for patients with hypothyroid symptoms who are within 'normal' reference ranges on thyroid functions tests? I do not think the picture presented in this research is at all clear. The sample is, as the authors acknowledge, very small and the findings do seem at odds with other published research in this area. The study may therefore ultimately be viewed as of limited value. Some information which I would consider useful is not discussed. For example did the either of the patient groups exhibit any ill effects from taking the thyroxine as opposed to the placebo and if not why not? Did the researchers consider that the dose of thyroxine may have been too small to make a difference and what investigations did they make to ascertain what would be the optimal dosage? It would have been interesting to have had a further group take Armour Thyroid and/or T3 and conduct the same tests and measurements as there is evidence that this improves cognitive function and general wellbeing for people for whom thyroxine does not work. I would also point out that, in my experience, thyroxine may help alleviate hypothyroid symptoms for a short period of time and then some kind of resistance (like insulin resistence) kicks in and symptoms return. It is not known whether this has been accounted for in the study. I note that the authors state that the T3 conversion/uptake issue warrants further investigation - this could explain the results - and I very much hope that the research group will go on to further study of this area as this is very necessary. The authors note that one patient 'normalised' a TSH of 5.8mU/l on placebo to 4.5mU/l but they do not hypothesise on what mechanisms may be at work here. It seems to me that this would also warrant further investigation. For information I would point out that there is a view that a TSH of over 2.5mU/l is suspicious and indicative of possible longer term problems and that 4.5mU/l cannot therefore be viewed as 'normal'. In summary this research appears to raise more questions than it answers and a more extensive study in terms of both participant numbers and treatment options appears warranted. Finally, I feel I should declare my interest - I am a patient who is clinically hypothyroid but whose thyroid function tests are within the 'normal reference range'. I do not know what is normal for me however as my thyroid function was never tested when I was well. I have had tremendous difficlty getting what I consider to be appropriate treatment for my condition on the NHS. I am however currently functioning very well on a combination of Armour Thyroid and T3, NHS homeopathy and a wheat free diet. June Hyslop |
|||
|
|
|||
|
W John Diamond, Medical Director, Integrated Medicines, LLC
Send response to journal:
|
Dear Sirs: Excuse the somewhat insulting title, but its hard to believe that rational, well trained doctors are so endocrinologically blind as to still be using thyroxine only in their hypothyroid patients. Almost all of these patients have problems with T4 to T3 conversion, and many others have refractory T3 binding sites. Clinical experience overwhelmingly demonstrates immediate response to either Armour Thyroid or Thyrolar (mixed T4/T3)in the majority of these patients. STOP treating the Lab values and start treating the patient! Sincerely, W. John Diamond,MD. |
|||
|
|
|||
|
Andrea Corsonello, Via D. Frugiuele, 39. I-87100 Cosenza. Italy Italian National Research Centres on Aging (INRCA). I-87100 Cosenza. Italy
Send response to journal:
|
This is an interesting paper, which raises some questions. Above all, the sample is too small, as the Authors acknowledge. Furthermore, it is not clear what means that "all participants were required to have no current medical disorder". The fact that patients are not acutely ill does not rule out the possibility that a chronic disease may interfere with thyroid hormones metabolism, as it happens in the euthyroid sick syndrome (ESS). Additionally, the reverse T3 is not measured in this study. So it is likely that patients genetically resistant to thyroxine treatment and those with a ESS due to a inhibition of the tissue 5'-deiodase activity remain not identified. The Authors acknowledge that an impairment in the peripheral conversion of thyroxine to triiodothyronine may have affected their results. However, although it is known that thyroxine-resistant patients may respond to Armour thyroid and/or T3, this treatment has not been considered in this study. In our experience, elderly patients frequently present with symptoms of hypothyroidism and normal routine thyroid function tests. Reverse T3 measurement may be useful to identify subjects which are more likely to be not-responders to thyroxine treatment. Why thyroxine binding globulin (TBG) was not measured in this study? A reduction in circulating TBG can allow proportionally more thyroid hormone to be free. In this case, thyroxine treatment may be more disadvantageous than advantageous, leading to a tissue hyperthyroid state (which will not be reflected by anything we can measure) with a consequent impairment in tissue function. The limited possibility to study the thyroid status at the cellular/tissue level remains an unresolved problem: what we need is a specific cellular/tissue marker for hypothyroidism. In conclusion, this study should be considered as preliminary. Further investigations with a better biochemical description of the health and thyroid status of enrolled patients, and with other treatment options may be helpful to delineate the rationale for a correct pharmacological management of patients with hypothyroid symtpoms and normal thyroid function tests. Yours Sincerely Andrea Corsonello, MD
Francesco Corica, MD
|
|||
|
|
|||
|
Carol Foster, Policy Officer Dept Work & Pensions
Send response to journal:
|
As a policy officer with a masters degree in research I know that any study of such a small number of people cannot be used to make generalisations applicable for the population as a whole. A more statistically valid sample is required, and for completeness the study should look at varying doses of thyroxine, and alternative treatments such as Armour, and Homeopathy. I also am a hypothyroid sufferer, having to obtain treatment privately because my condition is not recognised by the NHS. I had below- normal levels of FT4 for many years, but this was discounted because of a 'normal'TSH. I had wide-ranging symptoms, all consistent with hypothyroidism, but was told I had depression. I became increasingly more ill and was finally diagnosed with ME. Luckily I found Dr Skinner,and am now on Armour therapy. Over three months I have noticed some improvement - I am now back at work - but I am still by no means better. So perhaps any future study needs to look at people for longer than three months, particularly where the individual has had hypothyroid symptoms for many years. The study suggests that patients did well because of a placebo effect. I can only say this is not the case with me.If all I had wanted was a placebo, why didn't the anti depressants work? I think they actually made my symptoms much worse. But despite a long list of side effects, some of them very serious, anti depressants are handed out so easily. Thyroid medication, provided it is used in conjunction with regular blood tests to ensure over-medication does not occur, is harmless. And for many people it can be a life-saver, literally. I would like to know why GPs insist that Armour cannot be prescribed on the NHS, when it can? Why do GPs insist on perpetuating the myth that Armour is unsafe? The FDA in America think it is safe, and I dont think American's have a different biological make-up to us? Can I please appeal to all doctors reading this, can you approach this with a little more of an open mind, and listen to your patients? Have a look at the stuff on the internet and find out what is going on across the world. It is no good telling patients their blood tests show they are Ok when they are feeling very ill indeed. There are so many people now, in the UK, Europe, US and elsewhere, all saying the same - we think we are hypothyroid but we are not getting the treatment we need. Please will someone now start to take this more seriously! |
|||
|
|
|||
|
Simon Waters
Send response to journal:
|
Just to emphasise June's comments on in reference range thyroid results. The BMJ has previously covered the issue of TSH results in the upper part of the reference range being indicative of hypothyroidism, or the likelihood of developing hypothyroidism. The mean and std of scores for the patient group implies some (more than the control group) of these patients were in this category, which may have affected the results. I am curious as to whether the data shows a stronger signal with this group excluded. Any attempt to put more scientific rigour into this area has to be good. I concur with Dr Diamond that further research on the clinical use of T3 supplements also seems appropriate, a this is a topic that has generated more heat than light in the past. |
|||
|
|
|||
|
Lois Sommerfield, thyroid support group volunteer
Send response to journal:
|
While I applaud research in the area of hypothyroidism and "normal" thyroid hormone levels, this study has too many flaws for it to be conclusive.
First, what did the participants have in common? The starting thyroid test levels were not included; we were only told that they were "within the reference range." Based on personal experience and on observation of many other people with hypothyroidism, I can say that the reference ranges are too wide, but it is important to know where within the ranges the numbers were. Assuming that the pituitary and the hypothalamus are functioning properly (which we can't assume), a TSH level of 1.2, for example, is far different from a TSH of 4.2, and it makes all the difference to many thyroid patients whether their T4 and T3 levels are in the upper or lower part of the ranges. Putting aside the TSH, why weren't those with low T4 and T3 levels separated from those with high (but still in range) T4 and T3 levels? Participants with close-to-ideal and far-from-ideal test results were presumably lumped together. In addition, the patients all had at least three out of six symptoms, but not necessarily the same ones. While not all symptoms of hypothyroidism present themselves in most hypothyroid people, the differences of symptoms in the study group meant that the group was not homogenous. Was any screening done to rule out other causes of the symptoms, such as (depending on which of the symptoms each participant had) Cushing's, PCOS, chronic infections, etc.? Second, why was no improvement in cognitive function and psychological well-being considered significant when T3 is necessary to improve these, and only T4 was used in the study? Eighty percent of T3 comes from conversion of T4, and for participants who had T4-to-T3 conversion problems (suggested by "the lack of significant increase in free triiodothyronine in patients taking thyroxine"), no amount of T4 alone was going to achieve the desired results. Third, looking at just T4, starting and finishing with a dosage of 100 mcg is doomed to be ineffective for many hypothyroid patients. It is too high a starting dosage for many people, and this can make some truly hypothyroid people (and perhaps others) feel worse at the beginning of treatment. Moreover, once the thyroid gland gets the message that it doesn't need to work as hard, it often reduces its output of thyroid hormone. As a result, if a patient adjusts to 100 mcg of T4 and still needs more but doesn’t receive it, that patient may start to feel more hypothyroid again. This could explain why many of the participants couldn't tell the difference between the T4 and the placebo. Six weeks is the usual time to test because it takes that long for the full effects of T4 to be reached. Yet it takes more than six weeks for most hypothyroid patients to become stabilized on thyroid medication. A study based only on the "before" levels and the levels after one six-week period does not show the full response of patients who are receiving proper treatment for hypothyroidism. If the objective of this study is to be realized, I suggest the following: -- that only patients with similar hypothyroid symptoms and free T4 and T3 results in the lowest third of the range be included; -- that other possible causes of the symptoms be ruled out first; -- that T4 be introduced at a more typical, lower, starting dosage and then raised gradually; -- that the study continue for longer than six weeks before the washout period; -- and that those who show little or no improvement in cognitive function and mental well-being then be given a trial of T3 in addition to T4. Also, whatever the results, the patients should taper off the T4 (or the placebo) gradually after each part of the study rather than quitting it cold turkey, to avoid causing more health problems. |
|||
|
|
|||
|
M Duncan, GP Registrar Sheffield
Send response to journal:
|
As practice for the MRCGP exam our VTS group decided to critically appraise your paper. Here is what we observed. To begin with some of us were unclear about what the actual research question aimed to answer."to determine whether thyroxine treatment in patients with symptoms of hypothyroidism but normal TFT's is effective". Effective at what? Effective in what way? Certainly not at getting rid of the original symptoms as they were not measured. Looking at the study design, we thought it was an appropriate design to address the research question, (despite the question being dubious), and being a randomised controlled double blind placebo controlled trial, we thought the results might be likely to alter practice.It is an original study from two case studies which the authors themselves reported. The major downfall, and the authors are acutely aware of this, is the very small size of the study. This in effect means that the power of the study may not have been sufficient to eliminate a possible biological effect of thyroxine. Moving on to the methodology. The symptomatic subjects recruited for the trial were hospital subjects, GP referrals, hospital clinician referrals or by self selection through an article in the local rag.Some of these methods bring about selection bias, what kind of person self selects themselves for a trial like this, local rag excludes minority groups etc. There is no mention of what that article said. More interestingly the control group were personal contacts of the investigators. What does that mean? Were they all doctors, medical student (both groups hardly representative of your average Joe Public), drinking partners??!!!!! Inclusion criteria for the trial were that patients were required to have three out of a possible eight symptoms for six months and "normal" TFT's. Exclusion criteria were that no patient should have a history of any current medical problem or history of thyroid disease. Matching, the authors admit, was a problem presumably due to the tiny numbers but if you log on to the BMJ website and get to the article , then click on the box thet tells you where to go for the table A and B, you can see that the match wasn't too bad. No mention though of the fact that 6 out of the 23 symptomatic patients had previous psychiatric contact. The intervention was pretty straightforward, thyroxine or placebo both made to look the same. Why though was the first 20 patients given capsules and thereafter tablets. Was this another effect of lack of funds? We were slightly dubious about the method used for randomisation, done by "toss of a coin in batches of four" The gold standard is of course by computer. Moving on to bias again, we have talked about selection bias but there is also measurement or information bias. The authors are clear to point out the ways in which blood samples are analysed to avoid variations and which lab/equipment used etc. Physical measurements were done on standard, well recognised equipment and cognitive function and psychomotor skills were assessed using recognised scales. There was no mention of whether the questionnaires were done by post or face to face as this can sometimes introduce bias however since the authors mention that two patients failed to complete a page of one questionnaire we presume some of them were not done face to face. Interestingly, the authors make up for this lack of infomation by taking the mean scores of their remaining two visits to replace the missing values. We wondered if there may be any confounding factors in the study.Confounders are things which the study overlooks that may have produced the result that they attained. The fact that the symptoms are so wide-ranging and non-specific may account for other chronic unrecognised disease but this isn't really a confounder. Likewise the large proportion of psychiatric history in the patient group may also produce confusion but you may expect to get more of a placebo effect in this group. We thought that the follow up period of 12 weeks for each treatment phase was probably enough though we had some disagreement as to how quickly patients respond to treatment. The overall thought was that very hypothyroid patients cognitive function responds pretty quickly but how does this equate to the type of patients we are looking at here. May they need much longer? None of us knew enough about thyroxine to know if six weeks was a long enough wash out period or not. There were 22 patients and 19 controls completing the study. Three withdrew at an early stage. There was no mention of intention to treat. Looking at the main outcome measures, there were biochemical measures, basic clinical measures, cognitive functioning scores and psychological functioning scores. If there were measuremnts of the original symptoms that was not made clear. It is difficult to gauge if these were approporiate indicators to answer the research question, they seem appropriate. They are all pretty soft indicators though which makes them difficult to quantify and validate, however it is difficult to think of what else you could use. We therefore didn't think there were any surrogate endpoints in the study. The results in the study were presented in several tables. Tables 1 and 2 were fairly clear but table 3 was presented in a confusing manner. Table 4 was fairly self explanatory. The effect of treatment on each variable was studied using analysis of varience models in relation to patient, period and treatment. They tried to use parametric tests firsts but the results were not normally distributed so they went on to use non-parametric tests. The p-values and confidence intervals are given in the tables and as we would expect from the small power of the study many of the CI overlap zero confidence. There was local ethical approval granted for the study and funding was from a scientific development scholarship from the Association of Biochemists. The authors declare that there are no competing interests. For us in our general practice VTS group we thought this paper might have influenced us, however the size of the study is far to small to glean any real conclusions. On the other hand, we spent an enjoyable afternoon critiquing it and the way may now be paved for a much bigger study. We look forward to that and try to ignore the cynics among us who believe that thyroxine is so cheap that there are no incentives from the drug companies to market it as a pick-me-up!! Drs M.Duncan,R Kennedy,A.Hobbs,D.Puxley,R.Clarke,M.Tomson,C.Kerry and C.Mills.(3rd year VTS,Sheffield) |
|||
|
|
|||
|
Jim Harwood, Computer Programmer! 79 Central Avenue, PINNER, HA5 5BU.
Send response to journal:
|
This paper raises a number of issues:- Selection for the trial was the first twenty five patients who exhibited at least three of six symptoms over a period of six months. For research purposes, a more rigorous selection using a clinical scoring system(1) might give more significant results. Patients who completed the trial all had recent thyroid function tests within the reference range and all but one responded normally to a TRH stimulation test. It is therefore, unlikely that these patients had a failing thyroid or pituitary ("subclinical hypothyroidism"). Hypothyroidism, if present, would be due to other causes, such as impaired T4 -> T3 conversion, or end organ resistance to thyroid hormones. These patients would require higher doses of thyroxine and / or triiodiothyronine. Supplying 100 mmg thyroxine will have little effect, the hypothalmic pituitary thyroid axis will compensate. (There were no significant changes in blood pressure, pulse or weight and neither patients or controls were able to identify thyroxine or placebo.) Skinner et al.(2) in an open trial reported improvement in clinical features using incremental thyroxine doses, stabilizing in the range 50 - 300 mmg. A TRH stimulation test was not used to exclude primary hypothyroidism, it is possible that some of the patients had mild primary hypothyroidism and responded to the lower doses of thyroxine.(3) Clearly many of the patients required high dosage thyroxine. The study outcome was assessed on the basis of cognitive and psychological tests. Bunevicius et al.(4,5) showed that neuropsychological function responds to triiodothyronine plus thyroxine rather than thyroxine alone. They hypothesize a specific effect of triiodothyronine normally secreted by the thyroid gland. The patients in this study did not show a significant increase in triiodothyronine levels, nor did they receive exogenous triiodothyronine. The triiodothyronine produced by peripheral conversion of the thyroxine 100 mmg administered may cause a reduction in that produced by the thyroid gland. TSH increases exponentially in response to lowered thyroid hormones, but is usually reported linearly. The results of this study are repeated below along with the log natural values for TSH:- Thyroxine Placebo Difference TSH ln TSH ln ln Patients 0.66 -0.42 1.77 0.57 0.99 Controls 0.32 -1.14 1.55 0.44 1.58 This indicates the TSH response to thyroxine in the patients (0.99) was less than the controls TSH response (1.58). It is regrettable that TSH is not reported in logarithmic values. This trial has demonstrated an impaired peripheral conversion of thyroxine to triiodothyronine in the patient group and possibly a reduced response of TSH to exogenous thyroxine. Further, more sophisticated research, with an incremental trial of thyroxine, thyroxine plus triiodothyronine and natural thyroid extract is needed. The consequences of undiagnosed / untreated hypothyroidism are loss of quality of life, unnecessary health care expenditure, morbidity and mortality. 1. Zulewski H, Muller B, ExerP, Miserez AR, Staub JJ. 1997 Estimation of tissue hypothyroidism by a new clinical score: evaluation of patients with various grades of hypothyroidism and controls. J Clin Endocrinol Metab Mar;82(3):771-6. 2. GRB Skinner, D Holmes, A Ahmad, A Davies, J Benitez. 2000 Clinical response to thyroxine sodium in clinically hypothyroid but biochemically euthyroid patients. Journal of Nutritional & Environmental Medicine 10:115-124. 3. Jean-Jaques Staub et. al. 1992. Spectrum of subclinical and overt hypothyroidism: Effect on thyrotropin, prolactin, and thyroid reserve, and metabolic impact on peripheral target tissues. The Am J of Med 92:631-641. 4. Bunevicius R, Kazanavicius G, Zalinkevicius R, Prange AJ Jr. 1999. Effect of thyroxine as compared with thyroxine plus triiodothyronine in patients with hypothyroidism. N Engl J Med 340(6):424-9. 5. Bunevicius R, Prange AJ Jr. 2000. Mental improvement after replacement therapy with thyroxine plus triiodothyronine: relationship to cause of hypothyroidism. Int J Nueropsychopharmacology 3:167-174. |
|||
|
|
|||
|
A Mark Clarfield, Head of Geriatrics and Professor Soroka Hospital and Ben Gurion University, PO Box 151, Beersheva, 84101, Israel
Send response to journal:
|
Dear Dr. Smith, We were surprised by the decision of the BMJ to publish the paper by Pollock et al (BMJ 2001;323:891-5) concerning the treatment of patients with symptoms of hypothyroidism but with normal thyroid function tests. In our opinion, there are two problems with this study. First, it suffered from a lack of statistical power due to the small sample size . As such this clinical trial was doomed from the start either to offer negative findings or to be inconclusive, unless by some miracle the effect size turned out to be enormous. Despite the authors’ apparent a priori knowledge of this fatal flaw, they went ahead with the study.(Approval by the local Helsinki[IRB] Committee in no way excuses this decision.) A more serious critique relates to the decision to expose patients who were essentially normal (except for minor symptoms that could have been due to any number of causes) to pharmacological doses of thyroxine . Clinical trials require sufficient equipoise, as well as a patho- physiological rationale in order to justify the time, trouble, expense and possible side-effects to which patients are exposed. Reports “in a local newspaper” do not seem to us to offer sufficient reason to perform such an experiment on human subjects . We shudder to think of other trials which could be motivated by reports in the popular press. As well, given the fact that thyroxine can cause serious adverse side effects , especially in the elderly and those suffering from coronary artery disease, we were perplexed to find no mention either of the patients’ age or of the presence of co-morbidity. We are surprised that this trial took place, but not with its results. Yours sincerely, Prof. A. Mark Clarfield, MD, FRCPC
Dr. Ora Paltiel, MD, FRCPC
|
|||
|
|
|||
|
Eric K Pritchard, Thinker Self, 290 Pritchard Lane, Berkeley Springs, WV 25411
Send response to journal:
|
There numerous other paths to consider when the thyroid gland assays are normal and symptoms persist. The first path recognizes the medical science, circa 1970, and tests for the deficiency in triiodothyronine. As suggested earlier, there is the rT3 test, which, according to Brady, finds post thyroid deficiencies in either conversion to or reception of triiodothyronine (T3). This would suggest a triiodothyronine replacement. Although these replacements have been disparaged, they are approved and indicated by the US Food and Drug Administration. The other paths recognize that hormone effects are more like shotgun blasts than rifle shots. Per Thierry Hertoghe's book, most hormones effect most everything to some degree. Thus, fatigue can be created by a deficiency in any of several hormones... However, and unfortunately, the hypothyroidism niche would rather declare the patient is dreaming up her misery than to recognize these potentials. Consequently, there is the overabundant and improper use of "functional somatoform disorders" and "nonspecific symptoms." These simply produced continued suffering from a chronic deficiency. It would be quite beneficial if the hypothryoidism niche would lose its innocence of medical ethics, make the patient the first concern, keep up with medical science, etc. Competing interests: None declared |
|||