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PE1463: SUBMISSION FROM DR GORDON SKINNER

*20 February 2013

FOR THE ATTENTION OF MR DAVID STEWART, CONVENER, SCOTTISH PARLIAMENT, REFERENCE: PE01463

Dear Mr Stewart,

It was most gratifying to learn that a petition on the subject of hypothyroidism was received by the Scottish Parliament and followed by a constructive discussion towards proper debate on this serious shortfall in the care of patients with hypothyroidism.

I have been striving to engage argument with the relevant authorities and my medical colleagues particularly Endocrinologists for some 20 years in my capacity as Director of the Louise Lorne Clinic in Moseley, Birmingham, UK which is dedicated to the diagnosis and management of hypothyroidism. I am not embarrassed to assert that many patients deemed to be healthy and well on account of thyroid chemistry have been returned to optimal health by appropriate thyroid medication. It is regrettable that the earnest solicitations of these patients that they did not feel well were roundly ignored with (often) significant detriment to marriage, family life and social interactions, their present and future employment and indeed many patients became virtual recluses with a pitifully low quality of life.

I have been in correspondence for a number of years with The Department of Health (UK) and Royal College of Physicians and have enclosed relevant correspondence with a Document of Record which is intended to be a reference point for the profession and laity. This document has already been lodged with the Department of Health, Regulatory Authorities for example the General Medical Council and the Care Quality Commission, The Royal Colleges, Endocrinological Societies, Thyroid Health Groups for example Thyroid UK, Thyroid Patient Advocacy, The British Thyroid Foundation and the World Thyroid Register. It would be very much appreciated if I might lodge this Document with the appropriate office of the Scottish Parliament.

On a lighter note, I have enclosed a book on the subject which I penned as palatable for lay readers. Unfortunately I am advised that the preponderance of `Scottishisms’ has reduced its UK-wide palatability although some of my colleagues have advised that at least it helps them get off to sleep at night.

1 urge that you give your reasonable consideration to the contents of this note and enclosures contained therein.

Yours sincerely,

Gordon R B Skinner MD, DSc, FRCOG, FRCPath
Enclosures:

    • Letter from Mr Chris Harris D of H 23.11.2012

 

    • Letter from Dr Skinner to Mr Harris 28.11.2012

 

    • Letter from Mr Charles Dobson D of H to Dr Skinner 09.01.2013

 

    • Letter from Dr Skinner in response to Mr Charles Dobson 18.01.2013

 

    • Document of Record concerning UK Guidelines for thyroid function test October 2005

 

    • Letter to Dr G H Beastall from Dr Skinner 22.12.2005

 

    • Letter to Professor Gill. Royal College of Physicians. 05.02.2009

ENCLOSURE (1 ) Letter from Mr Chris Harris D of H. 23.11.2012

Dear Ms Wright,

Thank you for your letter of 7 November 2012 to the Chief Medical Officer containing patient testimonials in support of Dr G R B Skinner in relation to his General Medical Council (GMC) hearing. I have been asked to reply on the CMO’s behalf.

The GMC is a statutory body, independent of Government but accountable as an organisation to Parliament, via the Privy Council. Neither ministers nor officials have any role or powers in relation to individual cases. I also note that the testimonies have already been sent to the Fitness to Practise department at the GMC.

I hope this reply is helpful.

Yours sincerely
Chris Harris

Professional Standards Division Department of Health

ENCLOSURE (2) Letter from Dr Skinner to Mr Harris 28.11.2012

Dear Mr Halrris,

Thank you for your courteous and polite response to my note to Chris Harris.

Mr Harris has kindly made response but you yourself raise some other issues on which I would like to make a few comments although I understand that you are probably bogged down by thousands of similar approaches by the profession and the laity.

I do think that the Department of Health has a remit to take this matter seriously as thousands of patients are presently in ill health in the UK following what is one of the major faux pas of the last three decades particularly as the pivotal reliance on thyroid chemistry has no evidential basis and was never validated in proper clinical trial.

The concerns to which you refer are indeed genuine and arise from patients because they are receiving a sub-standard level of care and a somewhat tangential point I rather assume that by private individuals you are referring to medical practitioners in private practice. Having worked for many years in the NHS, the University sector and private practice, I wondered if that is a somewhat unworthy assertion and takes little account of the present regulatory controls, the CHQ and the appraisal systems.

The crux of this matter is that the only real voice to support this non-validated medical strategy is the BTA and ACB who then cajoled or asked or whatever the Royal College of Physicians to endorse their guidelines which they did endorse and indeed endorsed in spades and reconfirmed the findings of the ACB and BTA; it would be tedious and inappropriate to go into this in detail at this point but one of the most extraordinary contentions to emerge from these guidelines is that the diagnosis of hypothyroidism requires a TSH level of over 10 which is not only disconsonant with medical practice in the field but is astonishingly wayward on the statistical basis giving the mean TSH levels in the population and the standard error of this estimation; this erroneous purport is presently condemning thousands of patients to poor quality health.

I fully understand that these bodies are not being asked by the Department to withdraw their guidance and fortunately there are many other organisations both professional and lay who are pursuing sensible debate on the issue. Your perfectly sensible suggestion that we approach these organisations directly has been the focus of attention for some ten or more years and I regret that it has not even possible to engage in sensible debate on the issue and thus the position of the Department of Health and indeed the organisations to which you refer leaves nowhere to go. I do sincerely believe that this is one of the most shameful episodes in modern medicine where it would appear that nobody cares at all about these patients.

Kind regards,

Gordon RB Skinner MD, DSc, FRCPath, FRCOG

ENCLOSURE (3) Letter from Mr Charles Dobson D of H to Dr Skinner 09.01.2013

9 January 2013

Dear Dr Skinner

My colleague Chris Harris from the Professional Standards Division has passed on to me your letter of 28 November about the care of patients with suspected hypothyroidism. I am very sorry you have not had an earlier reply.

We are of course well aware of the controversy over the diagnosis of hypothyroidism and in particular over the use of blood serum tests as an indicator for treatment. Our view is that the current RCP guidelines, originally issued in 2008 and reissued with minor revision in 2011, were derived by an appropriate methodology from the available evidence. We also understand that these guidelines are supported by all the main professional organisations and also by two leading patient organisations, the British Thyroid Association and the patient support group of the British Thyroid Foundation. In these circumstances we have no reason to query conclusions that appear to represent the consensus view of the great majority of professional opinion in this country.

If any clinician believes that these guidelines are not supported by the evidence base, their proper course would be to seek publication of their views in a professional journal. Alternatively, they would be free to propose a NICE clinical guideline or (on the narrow issue of the use of a specific diagnostic test) a NICE technology appraisal, using the proposal form available on NICE’s website.

I am sorry if this is a disappointing reply.

Yours sincerely

Charles Dobson
Deputy Director
NHS Medical Directorate

ENCLOSURE (4) Letter from Dr Skinner in response to Mr Charles Dobson 18.01.2013

18 January 2013

Dear Dr Dobson,

Thank you for your note on the question of the diagnosis of hypothyroidism. I would like to make a few points and respectfully reque rt that you commit these comments to record.

The problem in any medical controversy is that while there is no evidence for the original assertion on the pivotality of thyroid chemistry, it then seems to require that a contrary view must disprove the original assertion which was never proved in the first place.

It is really only NICE who are empowered to make Guidelines and it is surely relevant that NICE have refused to issue Guidelines and in consort vNith the Department of Health have emphasised the importance of pivotality of’ clinical judgement. I hope you will understand I am not being unduly confrontational but many citizens both professional and lay might query your appellation `main professional organisations’ and will see far otherwise than purporting that the British Thyroid Association and the British Thyroid Foundation are `leading patient organisations’. They may feel uncomfortable tt,at these parties should be given extra weighting than some of the other excellent organisations for example Thyroid UK or Thyroid Patient Advocacy who are diligently striving to encourage open debate on this serious shortfall in patient care which is condemning many many patients in the United Kingdom and worldwide to continuing ill-health.

We have established a World Thyroid Register with active membership in the UK, USA, Europe and Scandinavia, inter alia. We ar<~ endeavouring on a world-wide basis to encourage open debate; we organised a World Thyroid Forum last yew which obtained a consensus that there is crucial need to prosecute a formal multi-centre clinical trial on the pivotality or otherwise of thyroid chemistry as an exclusive criterion of hypothyroidism.

I submit that the consensus view of the lay and professional opinion in the t K and the considerable body of peer reviewed literature unequivocally indicates that thvroid chemistry will not safely exclude this diagnosis. Opinion is changing towards amore critical evaluation of thyroid chemistry as a pivotal criterion; our concern is the number of patients who will have suffered by the time this re-evaluation rea-ises into modification of clinical practice.

Thank you again for your courteous response to my note; I ask if you would incorporate this response with my Document of Record which has already been submitted to the Department of Health.

Yours sincerely

Gordon RB Skinner MD, DSc, fRCPath, FRCOG

Enclosure (5) Document of Record concerning UK Guidelines for thyroid function test October 2005

In October 2005 the Association for Clinical Biochemistry, British Thyroid Association, and British Thyroid Foundation kindly prepared the document named as above and invited comment and input through the medium of e-mail with assurance that due consideration would be given to any such advice.

Some eight weeks have elapsed and it is unclear how such input has been integrated or its authorship or indeed when will be the next consultation paper. These are not criticisms but we feel that there is need to enshrine a Document of Record as a future point of reference for both the profession and patients. The latter in particular may find themselves in a difficult position if the Department of Health and the medical profession adopt or even advocate these Guidelines. This is important; there is little doubt that as time goes by

Guidelines soon become Rules and the profession will believe and not without justification in the present environment that report of non adherence to Guidelines to the General Medical Council can result in adverse outcome or civil litigation. We require clear directives from the General Medical Council and Defence Societies that sensible decision-making outside Guidelines does not engender disciplinary action for the Practitioner.

A second concern is that once Guidelines have transmuted into Rules, the precise authorship of these Guidelines and, importantly, any caveats or arguments against precepts contained within the Guidelines slip into obscurity; it is then assumed that Guidelines represented a majority view of the wise and any deviation from that view bespeaks a certain charlatanry or marginality in the medical practice of that colleague.

This document focuses specifically on hypothyroidism. This Working Group believes that too many patients have suffered at the hands of a non-evidence-based mantra which (ironically) has been paraded as evidence based where there is no evidence for example to support the core precept of Guidelines that thyroid chemistry is an independent and reliable marker of illness or health. This is purposefully stated in the simplest terms to avoid any possible confusion on this fundamental misconception which will result in continuing ill health for many patients and will continue so to do if these Guidelines are enshrined in stone for the future diagnosis and management of hypothyroidism.

We respectfully submit that we do not accept the following precepts contained in the Guidelines.

1. EXCLUSION OF HYPOTHYROIDISM ON THE BASIS OF THYROID CHEMISTRY

There is no evidence that free thyroxine or thyroid stimulating hormone levels within 95% reference intervals exclude a diagnosis of hypothyroidism. If there is contrary evidence to this view then it should be presented and further time allowed for analysis and discussion of such evidence; if there is no such evidence, then this must be unequivocally stated towards redirection of medical practice vis-a-vis management of hypothyroidism.

2. THERAPEUTIC BENEFIT IN RELATION TO DIAGNOSIS BY CLINICAL OR THYROID HORMONE LEVELS.

There is no evidence on a crucial therapeutic issue namely that the outcome of thyroid replacement is better or worse if the diagnostic criterion has been based on clinical features of thyroid chemistry. Pending formal clinical trial, we argue that patients will fare better if diagnosis is based on clinical features.

3.INTERPRETATION OF THYROID HORMONE LEVELS AND REFERENCE INTERVALS.

There is little discussion in the Guidelines concerning possible technical and pharmacological shortfalls in a non critical interpretation of free thyroxine, thyroid stimulating hormone and 95% reference intervals as pivotal criteria in the diagnosis of hypothyroidism; various arguments on these issues have been presented in the following references (1, 2, 3, 4).

4. THYROID HORMONE REPLACEMENT AS MONITORED BY THYROID HORMONE LEVELS.

Levels of thyroid replacement or choice of thyroid preparation should be monitored by clinical considerations rather than thyroid chemistry which is virtually an axiomatic proposition. In the present environment, chronic hypothyroid ill health is too often accepted from an unfounded anxiety over perceived pathogenicity of raised FT4 and/or low TSH levels outwith 95% reference intervals; we have provided evidence in publication that clinical outcome is not related to thyroid chemistry but more closely to thyroid dosage level which was based on clinical evaluation of the patient (!)

5. RELATIVE THERAPEUTIC EFFICACY OF AVAILABLE THYROID PREPARATIONS

There is no evidence teaching advantage of thyroxine versus triiodothyronine versus Armour Thyroid excepting observation of practitioners who have used all three preparations over a number of years. It is thus unreasonable that there is repetitive suggestion from a number of colleagues in the field that Armour Thyroid must prove its mettle when it was actually first at the post by a long way. We ask for a measure of equability in the evaluation of medicinal products; there is urgent need for a comparative evaluation.

6. LONG TERM HEALTH DETRIMENT FROM ABNORMAL THYROID HORMONE LEVELS

Long term adverse outcome from abnormal thyroid chemistry has been exaggerated from non cognisance of the clinical status of patients in long-term studies of this issue. It is realised of course that patients with long term evidence of thyrotoxicity may well develop pathological sequelae but there is no secure evidence that suppressed TSH in clinically euthyroid patients carries such detriment. If there is such evidence, it should be stated but, if not, we feel the document should make unequivocal statement to the contrary. It is considered highly improbable that continuance of hypothyroidism with its manifest pathological sequelae including the oft-ignored long term complications of increased cholesterol level and atheromic deposition is a safe alternataive to clinical euthyroidism and optimal health.

CONCLUSION

We submit that the diagnosis of hypothroidism and evaluation of replacement dosage levels should not be pivotally dependent on thyroid chemistry but on clinical evaluation of the patient with sensible cognisance of thyroid hormone levels as an adjunct if required in patients where there might be dubiety or uncertainty on the evidentiality of clinical features. There is no evidence from clinical trial to support the relative therapeutic benefit of either of the three available thyroid preparations in single or combinative use. There is urgent need to subject unresolved issues as highlighted above in 1 6 to the scrutiny of formal clinical trial.

REFERENCES

    1. Clinical response to thyroxine sodium in clinically hypothyroid but biochemically euthyroid patients. G.R.B. Skinner MD DSc FRCpath FRCOG., D. Holmes., A. Ahmed PhD., J.A. Davies., BSc and Benitez MSc. Journal of Nutritional & Environmental Medicine (2000) 10, 115 124

 

    1. Thyroxine should be tried in clinically hypothyroid but biochemically euthyroid patients. G R B Skinner, R Thomas, M Taylor, M Sellarajah,S Bolt, S Krett, A Wright. Letter to the Editor. BMJ. 14th June 1997.

 

    1. Diagnosis and Management of Hypothyroidism. Gordon R B Skinner. Louise Lorne Publication. Birmingham, UK. 2003.

 

    1. Communication to Dr G H Beastall in response to proposed UK Guidelines 22.12.2005 (Enclosed)

ENCLOSURE (6) Letter to Dr G H Beastall, Secretarty, Guidelines Development Group from Dr Skinner – 22.12.2005

Dear

      Dr Beastall,

 

      I thank you for allowing comment on your consultation document.


I. General Comments

      One of the difficulties with Guidelines in modern day medicine is that they cannot be divorced from political and regulatory influences. I hope you will thus forgive a few comments on your hard work.

 

      There is no doubt that in the present environment Guidelines tend to transmute into rules and caveats or reasonable argument against any aspect of such Guidelines becomes lost in time. In the unusual environment of modern day clinical practice, there is little doubt that to waver from Guidelines once they have become enshrined in publication becomes dangerous territory for a practitioner; indeed colleagues involved in regulation of medical practice tend to rely more and more on Guidelines compounded by the difficulty that expert witnesses will often be lauded for quoting Guidelines rather than invoking their own (sometime) extensive experience in a subject which will not be considered evidence based medicine albeit culled over forty years of hard won toil. It is thus crucial that the medical profession acknowledge and state in the public domain that Guidelines are there to assist practitioners but are not sticks to beat them if they fall out of line.

 

      Guidelines usually proclaim the value of evidence based medicine wherein clinical evidence, for example if the patient says he/she is not feeling well is somehow less weighty than evidence based on laboratory findings albeit that this philosophy is selectively applied and there is little laboratory evidence for the extensive display of Prozac, Seroxat etc. Endocrinology and particularly hypothyroidism have elevated laboratory based medicine to a level which frequently gainsays unequivocal clinical evidence and the clinical features are then bizarrely ascribed to depression, a peri-menopausal state (which used to be considered physiological) or overeating or a somatiform illness albeit the patient has classical features of hypothyroidism. This situation is compounded by the political legal regulatory pressures wherein a practitioner who disclaims the diagnosis of hypothyroidism if the thyroid chemistry is normal usually within 95% reference range will receive no disapprobium from peers or regulatory bodies while practitioners who diagnose and treat patients with due cognisance of clinical evidence in the face of normal thyroid chemistry are in treacherous territory and is usually considered the province of marginal practitioners (often private) who have not quite got their heads round the concept of evidence based medicine albeit the patient returns to optimal health following thyroid replacement.

 

      In summary there is a significant pressure on practitioners to use laboratory chemistry as a keep-safe to not make a diagnosis in the face of overwhelming evidence of the condition.

 

      It is pivotal that there is no confusion on this issue. Few practitioners will not agree that if a patient has high TSH level or a low FT4 level that that patient is likely to be unwell and suffering from the clinical features of hypothyroidism. The mischief lies in assumption of the reciprocal and I am unaware of any evidence which teaches that if you have clinical features of hypothyroidism with reasonably normal thyroid chemistry that the patient does not suffer from hypothyroidism and will not benefit from thyroid replacement. Two studies have tried to examine this issue.

 

      Dr McLarens group examined this matter in a left handed way although this was not the primary purpose of this study (1). The study identified patients who were deemed to have hypothyroid features but normal thyroid chemistry which in itself somewhat supports the notion. However treatment in these patients did not reveal significant improvement. It is the easiest thing in this world to criticise a colleague or a colleagues work but there were certain aspects of this trial which might explain the poor response to treatment and these points are engrossed in an enclosed note (3) where I have tried to argue these issues and encourage investigation of this whole question of the diagnosis of hypothyroidism.

 

      In our own centre we conducted a temporal analysis of the results of treatment in patients who were diagnosed largely with depression or chronic fatigue type syndromes and who had normal thyroid chemistry but clinical features of hypothyroidism and it did seem that these patients improved significantly (2). This was not a placebo controlled trial but the importance of the two studies rests in the original observation and selection of patients where it did seem that there were patients who had clinical features of hypothyroidism with normal thyroid chemistry and certainly in one of these studies there was improvement in the clinical status of most of the patients following thyroid replacement. It is crucial to institute formal clinical trial but to date we have been unable to obtain funding for this purpose.

 

      The only other evidence (which one hesitates to include in these strange times) is clinical observation over many years and in my own practice I have seen many patients in this situation who returned to optimal health following thyroid replacement. While appreciating that statements of this nature will not only be discounted by (particularly) younger colleagues and considered to be yet another example of the kind of thing that colleagues who do not understand evidence based medicine are inclined to say I feel I am a (relatively) sane citizen (and indeed lectured in statistics in the University of Birmingham in an earlier life) and am not embarrassed to make such a statement and request that it be entered into the portfolio of information of this matter.

 

      I earnestly urge that this document makes an unequivocal statement that there is no evidence to suggest that normal thyroid chemistry excludes a diagnosis of hypothyroidism; this simple statement written in bold (I trust) may save literally thousand of patients during the next two decades from the unqualified misery of untreated hypothyroidism.

II. Thyroid hormone levels

      Reliance on thyroid chemistry is a backward rather than a forward step and I have previously presented a number of arguments in support of this view (1,2,3 and 4). Two additional general points may be germaine.

 

      1. Critically the tests measure the presence of thyroid hormones by immunological methods and it is well recognised that antigenicity and indeed immunogenicity will survive deactivation for example, formalin or phenol treated vaccines and the immunological epitope can and often does survive in a chemical moiety but there is no hormonal or enzymatic activity left in the molecule; this is well recognised in cellular biology. There is indeed clinical evidence of this in that I have come across a few patients where by mischance they had staggeringly high levels of thyroid hormones for example FT4 reading above 100.0 yet the patient seemed not in the slightest thyrotoxic and indeed one of the patients was still clearly hypothyroid; it is also true that many patients feel best when their FT4 readings are over 30.0 and have no clinical evidence of thyrotoxicity and until there are measures of the biological activity of these hormones, it is surely errant to equate biological activity with immunological presence; a graveyard has a high density of people but little activity.

 

      Reference intervals which depend on the size and nature of the population selection often mislead. The distributions are skewed and a 95% reference interval indicates that 5% of the global population lie out-with this range which is cheerily ignored when a patient has their level of medication slashed if their FT4 (for example) is a decimal point above the upper limit of a 95% reference interval; moreover if a patient is just within 95% interval they are deemed for some obscure reason to be in good health thyroidwise but if as obtains with 5% of the globe some five hundred million people are just above the upper limit of the reference interval few practitioners would seek to proclaim that they are hyperthyroid! it should be emphasised that the statistical concept of a reference interval is a different issue from a health cut-off point or some kind of regulatory meter in a machine where there is a safety zone and cut-off zone and where to stray out of the zone is dangerous or instantly indicative of good or bad health. I hope you will not feel I am over labouring this point but there is little doubt that this mode of thinking is operative for many practitioners when assessing the diagnosis of hypothyroidism and the notion that the patients personal computer which is their brain can incorporate, integrate, and distil a multitude of information is lost in a legally driven misinterpretation of statistical scatter.


III. Miscellaneous comments on text

3.1.1 Para 1

      . Patients who have no symptoms are surely not suffering from hypothyroidism; I wonder if this would not be defined as sub-clinical hypothyroidism if there is coincident abnormal thyroid chemistry.


Paragraph 2

      . The first sentence is self obvious as everyone will agree that, for example, fatigue has a large number of diagnostic aetiologies. I really do not agree with the second sentence; I think most colleagues would agree that goitre with an enlarged tongue would point in the direction of hypothyroidism and over the years I have found that patients with side vision hallucinations or hallucination of objects on the floor relating to mucopolysaccharide opacities in the eyes tend to be associated with hypothyroidism. Most patients can be diagnosed by clinical features and this was once the only system of diagnosing hypothyroidism; I am unaware that results were worse prior to institution of thyroid chemistry but I have no evidence that this is the case. The last sentence of Paragraph 2 again suffers from the assumption of reciprocal; are you really contending that a patient with a TSH of 9.9 should be considered to not have hypothyroidism? I think an unequivocal statement in this matter would be important.


Paragraph 3

      . Is there a mix up between sub-clinical which means no symptoms and mild hypothyroidism which would mean symptoms of hypothyroidism in small measure? I have seen many patients who have normal FT4 readings and are in fact very ill and I do think this statement will confuse colleagues for years to come.


Paragraph 4

      . I do strongly disagree with this paragraph in that it is at odds with clinical experience of many practitioners over many years.

 

      The first two bullet points I think are not true and the second bullet point again suffers from the danger of assumption of the truth of the reciprocal which would leave many patients untreated.


3.1.2

      I feel I am being tedious but titrating dosage by laboratory tests may have become the mainstay with certain practitioners but this should not be construed an optimal approach. It was shown, for example, some decades ago that smaller doses of thyroid replacement would reduce TSH level but many patients do not feel well until the TSH approaches zero. You are surely not advancing that a TSH level just below the upper limit of the reference interval indicates satisfactory replacement as in quoted references 18 and 19; the average for healthy patients lies around 1, a TSH of four times the average would be (usually) within a 95% reference interval and surely not the objective of treatment.

 

      I do earnestly urge that this concept is removed from Guidelines and the mainstay of treatment should be when the patient has returned to feeling well with no residual hypothyroid features; this principle will ensure that the present catastrophic situation where patients continue to be unwell on account of TSH level will not continue for future decades.


Paragraph 2

      . (Page 27) I did wonder if this was unnecessarily complicated in that preventing over-replacement is an axiomatic schedule. However if patients are replaced in small increments then this will not occur and if clinical features of over treatment develop then the dose can simply be reduced again. It would simplify matters if all patients short of hypothyroid emergencies are started at 25 ?g thyroxine for one week and then proceeding in 25 ?g integers at sensible intervals. Cardiac complications have been seriously over emphasised and I think it would be useful in the Guidelines to mention that the main threat to cardiac status is continuing hypothyroidism with low physical activity , hypercholesterolaemia and deposition of atheroma; the latter has been significantly under noted in recent years but featured highly in the earlier literature on the subject.


Paragraph 3

      . Again the assumed reciprocal; one asks the development group how secure they feel is the information that patients do not feel better if the TSH is below 2.0. In my own experience and indeed in our published work we found a rather poor relationship between TSH levels and clinical well being.


Paragraph 5

      . The most crucial aspect is how the patient feels and not levels of these hormones. I would seriously contend that there are thousand of patients who are maintained in a state of sub-health because it is deemed that either TSH or FT4 are at satisfactory level and indeed some in measure the next paragraph (Paragraph 6) does address issue of the perfidy of using these levels as exclusive criteria.


Paragraph 6

      . I cannot agree with bullet points 1 and 2 particularly 2; surely a primary target of replacement is to restore clinical wellbeing.


3.1.3

      . I agree with the FT4 reading in patients taking tri-iodothyronine. I have come across a few patients who were taking T3 only and had a FT4 of zero which rather confused certain laboratories.

 

      Again we are back to the reciprocal point and to my knowledge there is no evidence advocating that thyroxine alone is preferable to the combined therapy and dare I say it I have often noted patients to be considerably better using the combined therapy but it is possible that the patient is merely having a higher level of replacement. On balance I think that certain patients do benefit from combined therapy.


3.1.4

      . Again I do not agree with the objective of therapy which should be return of well being and it happens in many patients who are still unwell and in fact do not become well until the TSH is well below the lower end of the reference interval.


SUMMARY POINTS ON GUIDELINES

      .

 

      The following are major points with which I am in disagreement

vis–vis

      the Guidelines. I would preface these points by indicating that I appreciate only too well how much hard work and consultation has gone into preparation of these Guidelines although I do wonder if perhaps rather more consultation with patients or even thyroid self-help groups who might have perhaps influenced some of the major conclusions. I do formally thank Dr Beastall and his colleagues for carrying out what is often a somewhat thankless task ; it is only too easy these days to put ones head below rather than above the parapet.


Summary comments

      .


1

      . The predication that criteria for diagnosis and dose level of thyroid replacement should be based on thyroid chemistry is doomed to failure; I have observed this over many years of practice.


2

      . Thyroid hormones levels in particular thyroxine and thyroid stimulating hormone within 95% reference interval does not equate with health or euthyroidism; there is no evidence to support this contention but a measure of evidence from two studies (1, 2) and from clinical experience over many years that this is not the case. I believe that this must be clearly stated in the Guidelines to avoid condemnation of many patients to continuing hypothyroidism based on this misassumption.


3

      . Laboratory tests for thyroid hormone levels do not measure biological activity and the adoption of reference ranges as action parameters is a significant problem in the diagnosis and treatment of hypothyroidism. This results in a serious short-fall in care with inadequate replacement based on the notion that TSH levels should be returned to somewhere within the reference interval. TSH values have a left-sided skewed distribution and a value of say 2.5 is well above the average TSH level which runs around 1.0 in most laboratories; thus the contention that a patient is satisfactorily treated if they have a TSH which has declined to a level of (approximately) twice the healthy average is clearly in error. This mischief is compounded by anxiety over suppressed TSH. I believe that any perceived long term detriment from suppressed TSH levels in a healthy patient is infinitesimal compared to the unequivocal detriment of inadequate replacement and continuing ill health.

 

      Advice on FT4 higher levels seems overly cautious. While some patient are returned to optimal health with an FT4 reading towards the upper end of the 95% reference interval; I would have thought that a number of

 

      Endocrinologists would agree that in a patient with no clinical evidence of thyrotoxicity there is a little to be feared from a patient with FT4 readings even approaching 35.0; it is difficult to believe that clinical euthyroidism is accompanied by unsuspected detriment from a raised FT4 reading. Account must be taken of previous caveats concerning thyroid hormone estimation and pharmacological considerations where intracellular uptake rate or deactivation or neutralisation of thyroid hormones highlight the ill advisability of equating thyrotoxicity with a high level of a hormone which may not be de-iodinated effectively or may be inactivated or may not be uptaken by the cells in vivo; it has always been a mystery to me that my colleagues purport thyrotoxicity solely based on a hormone level in patients who are manifestly not thyrotoxic.

 

      In summary the major point of disagreement with these Guidelines rests on my earnest belief that exclusion of hypothyroidism through the criterion of normal thyroid chemistry will frequently miss the diagnosis and titration of dose levels through thyroid chemistry will result in patients being chronically under treated with serious health risk. There is an overwhelming need for a properly controlled clinical trial to assess the results of thyroid replacement in patients who are clinically hypothyroid with normal thyroid chemistry and a prospective or even retrospective investigation of any detriment to health in a patient who is clinically euthyroid but whose thyroid chemistry falls outwith 95% reference intervals. Both of these studies are ethical and should be undertaken with expedition.

 

      Yours sincerely,

 

      Gordon RB Skinner MD DSc FRCPath FRCOG

REFERENCES

      1. Thyroxine treatment in patients with symptoms of hypothyroidism but thyroid function tests within the reference range: randomised placebo controlled crossover trial. Pollock M. A., Sturrock A., Marshall. K., Davidson K.M., Kelly C.J.G., McMahon A. D., McLaren. E.H., BMJ 2001; 323; 891- 895 (20th Oct).

        Clinical Response to Thyroxine Sodium in Clinically Hypothyroid but Biochemically Euthyroid Patients. G.R.B. Skinner MD DSc FRCpath FRCOG., D. Holmes., A. Ahmed PhD., J.A. Davies., BSc and Benitez MSc. Journal of Nutritional & Environmental Medicine (2000) 10, 115 1

Letter to Sir Patrick Cormack, F.S.A; MP. 02.12.2005.

Diagnosis and Management of Hypothyroidism. G R B Skinner. Louise Lorne Publication. Birmingham, UK. 2003.

ENCLOSURE (7) Letter to Professor Gill. Royal College of Physicians from Dr Gordon Skinner 05.02.2009

            Dear Professor Gill,
            I note your recent documentation and press release entitled RCP: Thyroxine is the only treatment for primary hypothyroidism; I respectfully submit the following comments on the contents thereof.

 

            I have no formal training in terms of College further education in this specific field and I trust you will indulge my solicitation. In mitigation I have published on the subject of hypothyroidism and have seen many patients during the last fifteen years and I think provided reasonable service to these patients. In a sense, the absence of formal training issue has motivated my note; I am concerned that the contents of the RCP document will be incorporated into future formal training of medical practitioners with (I believe) detrimental consequence to the diagnosis and management of hypothyroidism.

 

            I should like to provide evidence in two sections.


1. General comments.

            i) There should surely be an acknowledgement of alternative views on these issues; there is a significant body of contrary opinion. Admittedly this is not from what might be viewed traditionally as the Establishment but the Establishment do not have a monopoly over truth and unilateral somewhat cavalier pronouncements do or perhaps should engender a measure of incertitude in those who are in receipt of this kind of communication; I respectfully refer to my document which has been lodged in a number of appropriate Institutions including the Royal College of Physicians and Royal College of General Practitioners. I have enclosed a copy which I hope provides a reasonable balanced counter-argument to some of the views expressed in the RCP document (Enclosure A).

 

            ii) Secondly, it would be insensitive person indeed who would not detect a measure of adversiality to (presumably) private practice perhaps not in the words but within the spirit vaguely implying poor practice outside the NHS. The College represents both public and private sectors and if this is a College view, they should stand up and enter public debate if the College believe that private medical practitioners are serving their patients to a poorer level than in the public sector. I would remind the College that Mr Bevan introduced the NHS with a clear mandate to work with the private sector.

 

            (iii) Thirdly, the document presents material in journalese mode where, for example, overwhelming evidence on the value of thyroxine alone is purported albeit there is no evidence at all, the proportion of thyroid hormone in Armour Thyroid is receiving disapprobium while contemporaneously advocating T4 alone which has infinite proportion of T4 over T3; this is hardly good enough in a formal document from the Royal Colleges.

 

            (iv) Finally there is to the easy observer at least an anonymity in this documentation which is unacceptable in a matter of such critical importance for the future health of the nation.


2 Specific contentions.

i)) Armour Thyroid/T3 should not be used

            I am unaware of any clinical trials comparing the efficacy of T4, T3 and/or Armour Thyroid. There is in fact theoretical advatages in Armour Thyroid and in my experience it has a role and value in certain patients particularly patients (for obvious reasons) who have had thyroidectomy. May I beg preemption of the tired old mantra that this last contention is anecdotal, the overwhelming evidence that T4 is preferable is not anecdotal, it does not exist at all.


(ii) Diagnosis of hypothyroidism should be made by validated by blood tests

            Hypothyroidism was not defined by thyroid chemistry but by clinical criteria. It is astonishing intellectual servility to assume that a Gaussian interval particularly when TSH values are manifestly not distributed according to Gaussian distribution but have a distinct left sided skewed distribution will precisely define the frequency of hypothyroidism but even more astonishing and never validated an inviolate criterion for excluding diagnosis if TSH or FT4 values lie within 95% interval. This will only obtain if the condition was defined ab initio by biochemical criteria for example hypercholesteraemia or other conditions thus defined. I have seen thousands of patients over many years with unequivocal clinical evidence of hypothyroidism and thyroid chemistry within 95% reference intervals who were returned to optimal health by thyroid replacement and have yet to see a significant irreversible adverse effect of this practice.

 

            I contend that this non-validated and unproven position is presently resulting in a poor quality existence for many patients in not only the national but international arena.


(iii) Laboratory tests must be validated

            One naturally applauds this view albeit presented in a somewhat unwelcoming facon de parler. There is a certain imbalance in that the present blood tests of thyroid chemistry have not been validated in terms of their relation to disease frequency and treatment outcome and one would imagine that the author (anonymous) of the document would welcome a less invasive investigation for example saliva or urine; I do feel that an academic institution has a duty to inspire proper investigative research rather than dampen with faint anticipatory condemnation which is rather the spirit of the document.

 

            I sincerely urge reconsideration by the College of this document. It will cause untold damage to the future diagnosis and management with unnecessary and unproven restriction of the therapeutic armamentarium. The views advanced are not even consonant with Endocrinological practice which I have indicated from my small pilot survey (Enclosure B). This Document from the College will I fear be considered one of the great howlers within the next ten years and I beg your reconsideration with further discussion in an open forum taking proper and wider representation on these issues.

 

            I so advise.

 

            Yours sincerely,

 

          Gordon RB Skinner MD DSc FRCOG FRCPath

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