Amiodarone-induced hyperthyroidism

HOSP # WARD Endocrine clinic
CONSULTANT   Jody Rusch / Khalid Aligail DOB/AGE 21 y female

Abnormal Result

TSH: < 0.01 mIU/L (0.27 – 4.2)

Free-T4: 80.9 pmol/L (12 -22)

Free-T3: 10.8 pmol/L (3.1 – 6.8)

Presenting Complaint

Started to have frequent supra-ventricular arythmias – hence placed on amiodarone by the cardiologists

History

Mitral valve repair in 2018.

Started Warfarin, then later stopped.

Upon routine visit for follow-up 1 w before, the cardiologist requested TFT’s.

Examination

  • Denies chest pain, shortness of breath and has no symptoms of dyspnoea
  • No lower limb oedema
  • No sweating
  • No abdominal complaints
  • Patient is comfortable, no distress
  • CVS unremarkable
  • Muffled systolic murmur, JVP normal, No lower limb oedema.
  • Fine tremor, pulse rate 84
  • No eye signs
  • Gland diffusely enlarged, and no focal nodules detected
  • Bruit was clearly audible

Laboratory Investigations

TSH receptor antibodies = 3.3 U/L (<1.8)

Other Investigations

Radio-active Iodine thyroid uptake scan showed no uptake in the thyroid gland – not indicative of Graves Thyrotoxicosis.

Final Diagnosis

Summary: 21 y female, 1 y after mitral valve replacement placed on amiodarone now presented with a diffusely enlarged thyroid gland with a bruit clearly audible and no signs or symptoms of hyperthyroidism, but with biochemical evidence of significant hyperthyroidism

DDx: No symptoms pointing towards overt thyroid problems before initiating, thus this is likely Amiodarone – induced thyrotoxicosis

2 types are known, differentiated by either a diffusely enlarged thyroid which is more likely type 2 than type 1 .

Take Home Message

Rx differs between type 1 and type 2:

High iodine uptake is usually type 1 : usual Rx of Hyperthyroidism is given, thus Lugol’s iodine, else if non-responsive: radio-active Iodine or surgery.

If not much uptake on the uptake scan: Type 2 : points towards destruction of the gland : Rx = steroids

Which is more common?

In a local study of ~250 patients in 10y period it was found the longer it is left, the higher the chance of thyrotoxicosis. “Type 2 is likely more common”- prof Ross.

How does lithium thyroid disease work?

Lithium increases the enterothyroidal iodine recirculation : characteristically causing a : goiter with hypo or hyperthyroidism (thyroiditis).

Lithium inhibits proteases which liberates T3 and T4, hence inhibiting Iodine recirculation.

Interestingly, despite having a free T4 of ~80pmol/L, the patient had no symptoms whatsoever.

Also, of note, amiodarone more often causes hyperthyroidism than hypothyroidism.