Diagnosis and management of thyrotoxicosis
BMJ 2014; 349 doi: https://doi.org/10.1136/bmj.g5128 (Published 21 August 2014) Cite this as: BMJ 2014;349:g5128
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In their excellent and comprehensive review on thyrotoxicosis (1), Vaidya and Pearce do not mention an often difficult to recognise cause of thyrotoxicosis; namely thyrotoxicosis factitia due to surreptitious thyroid hormone ingestion.
Patients present with hyperthyroidism and may be mistaken for Graves’ disease, if TSH receptor positive (2), or thyroiditis because of absent uptake on a thyroid radionuclide uptake scan due to suppression of thyroid function by exogenous thyroid hormones. Suppression of thyroid function also decreases thyroglobulin secretion. Serum thyroglobulin is therefore undetectable in thyrotoxicosis factitia which differentiates it from other causes of hyperthyroidism, in which serum thyroglobulin is elevated (3). Caution, however, should be exercised in interpreting thyroglobulin results without thyroglobulin antibodies, since thyroglobulin antibodies commonly interfere in thyroglobulin immunoassays causing false positive and negative results (4) which may lead to clinical misdirection (2). In such cases, increased faecal thyroxine levels in thyrotoxicosis factitia may help differentiate it from other causes of hyperthyroidism (5).
References:
1. Vaidya B, Pearce SH. Diagnosis and management of thyrotoxicosis. BMJ 2014;349:g5128 doi: 10.1136/bmj.g5128
2. Jahagirdar VR, Strouhal P, Holder G, Gama R, Singh BM. Thyrotoxicosis factitia masquerading as recurrent Graves’ disease: Endogenous antibody immunoassay interference, a pitfall for the unwary. Ann Clin Biochem. 2008; 45: 325-7
3. Mariotti S, Martino E, Cupini C. Low serum thyroglobulin as a clue to the diagnosis of thyrotoxicosis factitia. N Engl J Med 1982; 307:410-2.
4. Clark P, Franklyn J Can we interpret serum thyroglobulin results? Ann Clin Biochem. 2012;49:313-22.
5. Bouillon R, Verresen L, Staels, F Bex M, De Vos P, De Roo M. The measurement of fecal thyroxine in the diagnosis of thyrotoxicosis factitia. Thyroid. 1993; 3:101-3.
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This is an interesting overview of the management of thyrotoxicosis. I would be interested to hear the authors' advice for acute medicine physicians when encountering patients with overt hyperthyroidism in the Acute Medical Unit. I see 2 or 3 cases per year of patients presenting with symptoms such as palpitations, tremor or new atrial fibrillation, whose blood tests reveal complete suppression of circulating TSH. In the absence of on-site endocrinologists, we often have to instigate initial treatment ourselves. When endocrine advice is sought on the phone, the variation is usually enormous and confusing. Some recommend starting carbimazole outright, some recommend starting only beta-blockers for symptom control, then referring the patient for out-patient radionuclide scanning, whereas some recommend doing nothing, merely repeating the tests in a fe weeks time (not an attractive option for the patient).
We would greatly appreciate some guidance in the management of newly diagnosed, hospitalised, symptomatic patients with thyrotoxicosis.
Yours sincerely
Ben Lovell
Competing interests: No competing interests
Diagnosis and management of thyrotoxicosis: Suspecting thyrotoxicosis factitia and acute management of thyrotoxicosis
We thank Garman and Gama for pointing out that measurement of serum thyroglobulin is a discriminant test for detecting thyrotoxicosis factitia. This state is most often due to covert ingestion of levothyroxine and in this case another giveaway feature is that the serum free T4 will be elevated out of proportion to free T3. Indeed, the free T3 may often be in the reference range, despite elevated FT4 and suppressed TSH. In typical Graves’ disease, the serum FT4 concentration is 2.5 - 3 times higher than the FT3 level (pmol/l per pmol/l). Whereas in levothyroxine-induced thyrotoxicosis factitia, the level of serum FT4 is generally 4.5 - 5 times that of the free T3. As these measurements are taken routinely in most cases of thyrotoxicosis, recognition of this pattern of test results may provide a first indication of thyrotoxicosis factitia. However, if porcine thyroid extract or tri-iodothyronine is being taken, of course, this will not be a helpful clue.
Dr. Lovell asks for guidance about management of thyrotoxicosis in the acute setting. Beta-blockers may be safely started or increased in almost all non-asthmatic patients who present acutely with thyrotoxicosis. Where there are clear contraindications to beta-blockade, diltiazem may be a useful alternative. Whether to start antithyroid drugs immediately or not is a judgement that depends on the severity of the complications and the likelihood that the diagnosis is not that of a transient thyroiditis, which will spontaneously resolve. If there is a long history of suggestive thyrotoxic symptoms prior to presentation, or some independent biochemical corroboration of the thyrotoxic state prior to presentation, then it is reasonable to start antithyroid drugs immediately. Similarly, if there are significant cardiovascular complications such as fast AF or heart failure, antithyroid drugs should not be delayed. The exception to this would be if amiodarone is implicated, in which case prednisolone might be an alternative first-line measure. If the history of thyrotoxicosis is short or non-existent, or there are no serious complications, or there is a positive indicator for thyroiditis such as thyroid pain or recent pregnancy, then it is reasonable to hold off anti-thyroid drugs pending investigation. This will include repeat serum thyroid function, thyroid autoantibodies and perhaps a radionuclide scan. Each case should be judged on its individual features and one rule can’t be applied. We would also recommend contacting the local endocrinology service for advice as soon as possible.
Competing interests: No competing interests