Hypothyroidism to Graves' disease and late appearance of pretibial myxoedema from The Lancet

[holyshedballs]

The Lancet

CLINICAL PICTURE| VOLUME 394, ISSUE 10206, P1364, OCTOBER 12, 2019

Eveline Bruinstroop, Irina Cairo, Paul Drillenburg, P Sytze van Dam

Published:October 12, 2019DOI:doi.org/10.1016/S0140-6736(...

thelancet.com/journals/lanc...

A 57-year-old man attended our clinic complaining of orbital pain, anxiety, and a tremor. On examination, he had oedema and retraction of his eyelids and an obvious tremor. 6 months earlier, he had been diagnosed with autoimmune hypothyroidism after he began to gain weight and complained of feeling tired: his thyroid-stimulating hormone (TSH) concentration was raised at 83 mIU/L (normal range 0·3–4·6), free thyroxine (T4) concentration was 5·9 pmol/L (normal range 10–23), and the antithyroid peroxidase antibody concentration was markedly elevated at 1488 IU/mL (normal level <101). The thyroid gland was recorded as being minimally enlarged. At that stage the patient had been started on levothyroxine.

When we saw him, his TSH concentration was 0·02 mIU/L and his free T4 concentration was 35 pmol/L, and we concluded that he was hyperthyroid because of treatment with excessive levothyroxine; we reduced the dose and arranged to see him 1 month later. At that time, his serum TSH concentration remained suppressed (0·01 mIU/L) and the concentration of TSH receptor antibodies (TRAb) was high at more than 20 IU/mL (normal level <1). We made a diagnosis of Graves' disease and treated the patient with block and replace therapy—giving him thiamazole 30 mg daily followed by levothyroxine 75 μg daily. We also made an urgent referral to an ophthalmologist: the patient had progressive retraction of both eyelids and a scleral show of 1 mm, and was diagnosed as having Graves' opthalmopathy.

1 year after starting the block and replace treatment, the patient visited a dermatologist, complaining of large, red-orange plaques on both shins. They were not painful or itchy (figure). On examination, he had sharply demarcated, waxy, peau d'orange texture, firm, non-pitting plaques. He was euthyroid and continued with the block and replace therapy. Histological examination of a skin biopsy specimen showed mucopolysaccharide deposition localised to the reticular dermis and attenuation of collagen fibres such that they were frayed, fragmented, and widely separated, confirming a diagnosis of pretibial myxoedema. Our patient was treated with topical corticosteroids and compression stockings. After 6 months, the skin was less firm, but there was no significant improvement in his condition; we advised him to only continue with the compression stockings. A blood test taken after a trial of stopping block and replace therapy showed a serum TSH concentration of 0·01 mIU/L, free T4 concentration greater than 100 pmol/L, and TRAb concentration greater than 20 IU/L (see appendix for complete blood results). An ultrasound—2 years after the initial diagnosis of Graves' disease—showed diffuse enlargement of the thyroid.

Conversion of Graves' disease to hypothyroidism is not uncommon. However, the reverse is rare: in our patient, autoimmune hypothyrodisim switched to hyperthyroidism, caused by TSH receptor stimulating antibodies. Pretibial myxoedema or Graves' dermopathy is an infrequent, but classic, sign of Graves' disease that should be recognised as an extrathyroidal manifestation. It can develop years after the hyperthyroidism and as a result may present to a dermatologist rather than an endocrinologist. Although pretibial myxoedema is a relatively benign condition, it is often resistant to treatment and can cause a great deal of distress—as in our patient—for cosmetic reasons.

Contributors

All authors were involved in the clinical care of the patient and writing of the manuscript. We would like to acknowledge Kees Brinkman (OLVG, Netherlands), Eric Fliers (Amsterdam UMC, Netherlands), and Paul M Yen (Duke-NUS Medical School, Singapore) for their suggestions. Written consent for publication was obtained from the patient.

[hilary77]

I was diagnosed hyperthyroid 2008 after treatment my thyroid went back to normal then in 2010 I became hypothyroid started on Levothyroxine my weight started ballooning from 8st 2lbs to 10st 7lbs then in 2013 whilst still taking levothyroxine my eye became swollen & I had an aversion to light my weight had dropped to 7st 1lb I had tremors & felt really ill, saw my doctor & he sent me to an endocrinologist who diagnosed hyperthyroidism with Graves & TED told to stop levothyroxine, put me on block & replace but they couldn’t control my thyroid the endocrinologist said it was very rare & he hadn’t seen it before, he said that my thyroid could swing from hyper to hypo to hyper so recommended a total thyroidectomy but they needed to control my thyroid they were going admit me to hospital to put me on a drip I can’t remember what for but whilst awaiting admission my thyroid decided to play along, I had the operation & have been fine since my weight has stayed pretty much the same I also take Liothyronine as well as Levothyroxine. only one eye was affected with TED but the last 8 months my eye has started to pop again ache & have a slight aversion to light again, can this be right seeing i don’t have a thyroid gland?