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Hyperthyroidism in an elderly patient
  1. SHAILA BHATTACHARYYA,
  2. ARPANDEV BHATTACHARYYA
  1. Flat 1, Hope Hospital
  2. Stott Lane, Salford M6 8HD, UK
  3. email: Arpandev{at}aol.com

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    Editor,—We read with interest the case of hyperthyroidism in an elderly patient by Findlay and Seymour.1 We have serious reservation in agreeing with the diagnosis as suggested by the authors. The patient was clinically euthyroid; free thyroxine was marginally raised with suppressed thyroid stimulating hormone (TSH). Thyroid scan was compatible with excessive iodine exposure. The crucial feature in making a diagnosis of amiodarone induced hyperthyroidism (AIH) is a raised triiodothyronine (the authors did mention this in the discussion), as thyroxine is raised in patients who are on amiodarone and euthyroid. Therefore the triiodothyronine level is very much needed for making a diagnosis of AIH, which unfortunately has not been mentioned in the case. The question remains about the suppressed TSH. Is it surprising to have TSH suppressed in a 72 year old lady who is admitted to the hospital with a fall (and also who suffers from congestive cardiac failure)2?

    The authors did not provide us with the follow up. Was the patient treated as having AIH? Was there any improvement in the clinical status? Lastly, there was no mention of two types of AIH in the discussion. It is important to subtype a patient with AIH, as the treatment is different in the two types of AIH. Incidentally Loh has reviewed this topic in the same issue of the journal.3 In case the index patient had AIH, it would probably be type 2 where the main treatment option is corticosteroids and not antithyroid drugs.

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    The authors respond:

    I would like to thank Drs S and A Bhattacharyya for their interest and comments on the above case.

    It is quite correct to highlight the point that a suppressed TSH does not necessarily equate to a hyperthyroid state and indeed it is worth stressing that the causes of a suppressed TSH are legion. In our article we did not include the triiodothyronine which has caused my colleagues to question the diagnosis. I would, however, caution against over-reliance on triiodothyronine values in this setting. Indeed, my colleagues also mention in their letter the excellent review article by Loh on amiodarone induced thyroid disorders,1-1 which appears in the same journal. According to Loh the triiodothyronine in AIH is unreliable and may be either high or normal. For the record the value of free triiodothyronine in the case described was 12.6 pmol/l (normal range 3.0–7.0).

    The other criticism was that no information was available on the patient's progress and follow up. After discussion with the endocrinologists this patient was treated with carbimazole starting at a dose of 20 mg daily for four weeks and then reduced to a maintenance dose of 10 mg daily. Amiodarone was discontinued. The patient continues to be reviewed on a regular basis and at present is on carbimazole 10 mg daily. She remains well and her last TSH was 2.83 mU/l.

    References

    1. 1-1.
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