Diagnosis and management of thyrotoxicosis

BMJ 2006; 332 doi: http://dx.doi.org/10.1136/bmj.332.7554.1369 (Published 8 June 2006)
Cite this as: BMJ 2006;332:1369

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'First , do no harm ? '

Is it not time that we abandoned this useless doctrine ?

There is not a single EFFECTIVE medical intervention that I can think of, which does not risk some harm to someone !

- Penicillin ?

- Surgery ?

- Aspirin ?

Medicines which do none harm reduce to vanishingly small concentrations of that medicine ( read Homoeopathy ).. and they, of course, are without any proven effectiveness !

We should assess the balance of harms (cautions, contraindications, risks ) against the benefits ( trialled, demonstrable, plausible ) in the individual case..

Personally, I find Radio-iodine highly efficacious in Hyperthyroidism of older people, and considerably more acceptable to Doctor and Patient than juggling Carbimazole doses with warnings, Full Blood Counts, etc. for years.. but neither my personal experience, nor my father's, should count for much - not as much as Scientific Randomised, placebo-controlled trial , surely ?

sincerely -

Competing interests: Benefit vs. Harm

Competing interests: None declared

L S Lewis, GP

Surgery, Newport, Pembrokeshire, SA42 0TJ

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The editor

I read with much interest the clinical review article 'Diagnosis and management of thyrotoxicosis'by EN Pearce in BMJ of 10 June 2006. It is an excellent article which will be of practical use in the management of cases of thyrotoxicosis by everybody. I wish to make the following comments:

Thyrotoxicosis is treated with antithyroid drugs, radioactive iodine(RAI) or by subtotal thyroidectomy. Of the three, RAI is the simplest and effective method. The absolute contraindications are pregnancy and lactation. Even in other cases it is difficult to persuade the patient to take RAI because of the following:

1. Fear of radiation. We advise them to avoid pregnant women and small children, stay off work, avoid public transport etc. after taking RAI. It is scary to think oneself of becoming radioactive! 'If it is so safe, why there are so many restrictions to save the other healthy people from coming in contact with me?'

2. Even if we suggest RAI or surgery, we start them on tablets to make them euthyroid before giving RAI or proceed with surgery. If so, then why not take the tablets for 12 to 18 months to take a 50:50 chance of going into remission!

4. Some are afraid of putting on weight after RAI. It is true if they become hypothyroid and are not given replacement dose of thyroxine.

5. RAI will result in permanent hypothyroidism in almost all patients requiring life-long thyroxine replacement.

Because of above, given the choice, the patient chooses to go on tablets first and we go along with patient's decision.

In the elderly patients, thyrotoxicosis results mainly from toxic multinodular goitre. As they may not feel unwell, it may be difficult to persuade them to take treatment. I find it useful to discuss with the patient about harms of not treating it which may result in atrial fibrillation, risk of stroke, heart failure, thyrotoxic cardiomyopathy, osteoporosis leading to fractures etc. Some will take Carbimazole long term rather than having RAI followed by life-long thyroxine. However, life -long thyroxine therapy is safer than life-long carbimazole therapy which patient understands but wouldn't want RAI.

Block-replace regime may involve fewer clinic visits. It is useful when it is difficult to get a stable carbimazole dose, partcularly to avoid fluctuation in control in presence of dysthyroid eye disease.

Yours sincerely

Dr Subrata Kumar Mallik
Locum Consultant Physician

Competing interests: None declared

Competing interests: None declared

Subrata K. Mallik, Locum Consultant Physician

St. Peter's Hospital, Guildford Road, Chertsey, Surrey KT16 0PZ

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19 June 2006

I was under the impression that treatment with iodine-131 quite often results in hypothyroidism and that it also facilitates further deterioration in thyroid eye disease.

Personally, if asked about the suitability of radioactive treatment of any illness I would be hard pressed to think of even one.

My father used to tell me horror stories about the use of "X-ray therapy" for such conditions as acne and seborrhea.

Competing interests: None declared

Competing interests: None declared

Dr. Herbert H. Nehrlich, Private Practice

Bribie Island, Australia 4507

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Graves’ disease is usually caused by production of autoantibodies against Thyrotropin receptors (TSH-R Abs). These TSH-R Abs mimic the effects of the thyroid stimulating hormone (TSH) on thyroid cells leading to autonomous production of thyroxine and triiodothyronine. In her elegant review article on Diagnosis and Management of Thyrotoxicosis, the Author Elizabeth N Pearce, has not been quite clear about the diagnostic utility of different thyroid autoantibodies. She mentions the presence of raised serum concentration of thyroperoxidase antibodies (TPO) indicating an autoimmune thyroid disease and a raised thyroid stimulating immunoglobulin (TSI) titre as indicative of Graves’ disease.

TSH-R Abs, the most specific antibodies for detection of Graves’ disease, were not mentioned in the review. TSH-R Abs do not only confer a diagnostic value, but also a prognostic one. A high titre of these antibodies reflects the “immunologic” activity of Graves’ disease. A declining titre is a good indicator of successful treatment with antithyroid drugs or radioiodine treatment. When on antithyroid drugs, a high titre of TSH-R Abs with a large goitre are two important signs of poor chance of remission. A high titre of TSH-R Abs might be associated with extrathyroidal manifestations of Graves’ disease such as Graves’ ophthalmopathy and dermopathy. A high titre during pregnancy might be a risk factor for foetal hyperthyroidism or even hypothyroidism (if the antibodies switch gear and start to block the TSH receptors of the foetal thyroid in stead of stimulating them).

TSI antibodies are a completely different set of antibodies. They do stimulate thyroid growth; they are a risk factor for goitre in Graves’ disease. I use TSI very often in Graves’ disease associated with pregnancy, but always in conjunction with TSH-R Abs. Their presence in pregnant women might be a risk factor for foetal goitre. Sometimes goitres big enough to obstruct labour.

TPO antibodies, although their titre might be high in Graves’ disease, are considered non specific for Graves’ disease, but they are usually detected in all the 3 phases of Hashimoto’s thyroiditis, including the thyrotoxic phase. We should bear in mind that not all patients with Hashimoto’s thyroiditis go through an initial thyrotoxic phase.

Competing interests: None declared

Competing interests: None declared

Shirwan A. Mirza, Clinical Assistant Professor of Medicine


37 West Garden Street, Auburn, NY 13021, USA

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Dear Sir, We offer following comments on excellent review on diagnosis and management of Thyrotoxicosis by Pearce EN [1]. The best management strategy for thyrotoxicosis is radioactive iodine [2]. It is perplexing that many physicians and endocrinologists are shy of using radioactive iodine in thyrotoxicosis. Today all patients of Graves’ disease should be treated with I-131 unless there is some absolute contraindication to its use like in pregnancy. Eighty to ninety percent of patients with Graves’ disease become euthyroid with single dose of I-131 within 8-12 weeks. There have been some controversies regarding dose of I-131 in treatment of Graves’ disease. The consensus today is that majority of the patients should be given a dose of 5 millicurie (5 mci) and only a small minority needs a second dose after 4-6 months. Based upon our experience of treating more than 1000 patients with I-131 therapy, we state that 95-98% patients of Graves’ disease become euthyroid with this treatment. The role of antithyroid drugs in management of Graves’ disease is restricted to prevention of initial worsening of thyrotoxicosis by I-131 by their use for few weeks before giving I-131, treatment of thyrotoxicosis in pregnancy by propylthiouracil, and for preparing the patients for surgery [3]. Surgery is rarely indicated in Graves’ disease. In fact we have hardly referred any patient of Graves’ disease to the surgeon in last 10 yrs or so and this has become a cause of light hearted pleading on part of surgeons for some thyroid cases. Toxic multinodular Goitre and toxic adenoma should also be treated with I-131 but response rates are lower than in Graves’ disease; surgery becoming the choice in cases not responding to I-131.

We think that the management of patient brought out in patient’s story of box 1 in the article [1] is not confirming to the current trends in management of thyrotoxicosis. Sixty five yrs old woman, suffering from Graves’ disease and who is well beyond reproductive age should have been given I-131 therapy and not subjected to misery of prolonged treatment with antithyroid drugs. This is because treatment with radioactive iodine is simple, highly effective, economical, safe and has fewer side effects as compared to antithyroid drugs.

References :

1. Pearce EN. Diagnosis and Management of Thyrotoxicosis. BMJ 2006 ; 332: 1368-1373.

2. Franklin J & Sheppard M. Radioiodine for Hyperthyroidism- Perhaps the best option. BMJ 1992; 305: 227-228.

3. Clutter WE. Endocrine diseases. In Green GB, Harris IS, Lin GA and Moylan KC (Eds) The Washington Manual of Medical Therapeutics, 31st ed. Lippincott Williams and Wilkins 2005: p 488-505.

Competing interests: None declared

Competing interests: None declared

Jainendra K Bhagat, Head dept of Nuclear Medicine

Kuldip P Anand, Ajit S Kashyap and Sukh D Duhan

Command Hospital Kolkata 700027,India

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Dear editor,

The review of diagnosis and managementof thyrotoxicosis by Elizabeth N Pearce,did not highlight the importance of psychiatric presentations in patients with thyrotoxicosis.The author mentioned anxiety disorder as a symtom of overt thyrotoxicosis, and rightly so.

The psychiatric symptom pattern in hyperthyriodism most often resembles generalised anxiety, but depression,irritability, hypomania and cognitive dysfunction are common.(refrence 1.).Presentation with irritability, emotional lability and difficulty concentrating are also common.(ref.2).

In severe cases serious manifestations include manic excitment, delusions and hallucinations, which have also been reported.(ref.3) Subclinical hypothyroidism appears to be a risk factor for depression and is a common cause of of rapid cycling in bipolar disorder.This group also often show subtle signs of cognitive dysfuntion.(ref1).

The importance of recognition of common, rare and atypical presentations, lie in the implications for management, as effective treatment can lead to rapid resolution of manifestation.


1. James L. Levenson, primary psychiatry.2006; 13(4);27-30.

2. Oxford textbook of psychiatry. Micheal Gelder et al.Fourth edition, p.489.

3.Brownlie BE,Rae AM, Walshe jw et al.Psychoses associated with thyrotoxicosis.Eur J. Endocrinol 2000: 142: 438-444.

Competing interests: None declared

Competing interests: None declared

martina .O. Esisi, senior house offiser psychiatry.

Bernard Esisi, specialist registrar in medicine,general hospital, leicester.

Leicestershire partnership nhs trurt.Brandon unit, le5, 4pw.

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To complete the excellent review of Dr Pearce on management of thyrotoxicosis, there are currently 2 clinical trials in Europe adressing the question of treatment of subclinical hyperthyroidism (NCT00213720 and NCT00151723). The protocols can be consulted on www.clinicaltrials.gov

Competing interests: None declared

Competing interests: None declared

Bernard GOICHOT, Professor of Internal Medicine

Hôpitaux Universitaires de Strasbourg, France

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