The patient was evaluated outside earlier and diagnosed as having thyroprivic hypothyroidism: serum total T3 (tri-iodothyronine) 1.45 nmol/l (normal range (NR) 1.2–3.0); total T4 (thyroxine) 47.62 nmol/ (NR 61.8–163.4); and thyroid stimulating hormone (TSH) 43.47 mU/l (NR 0.27 – 4.2). He was started on L-thyroxine 50 μg replacement and he felt some symptomatic improvement, but his proptosis and skin lesions persisted. He was referred to our institute for further management.

On examination, his height was 176 cm, weight 69 kg, pulse rate 80 beat/min, and blood pressure 130/80 mm Hg. He had diffuse firm grade I goitre and pandigital clubbing. He also had periorbital puffiness and bilateral severe proptosis (28 mm both eyes) with clinical activity score of 2/7 (fig 1A). His visual acuity was 6/6 in the right eye and 6/9 in the left eye. The skin over both the lower limbs was hyperpigmented and showed pronounced induration (fig 2A). His deep tendon reflexes were delayed.

With the availability of better techniques, the TSH receptor stimulating as well as blocking immunoglobulins have been demonstrated in autoimmune thyroid disorders,^6,7 and the clinical state depends upon the predominance of either of these. TSH receptors are distributed not only on thyroid follicular cells but also on orbital and dermal fibroblasts, therefore these thyroid stimulating immunoglobulins act on these extra-thyroidal receptors, and produce the manifestations—namely, infiltrative ophthalmopathy and dermopathy.⁶ In patients with Graves’ disease the above said three cardinal manifestations can easily be explained by the presence of TSH receptor stimulating antibodies. But all these manifestations are usually not present together, possibly because TSH receptor density may be variable at different sites or TSH receptor blocking antibodies might be interfering with its actions at those sites.

Hashimoto’s thyroiditis as corroborated by high TPO antibody titre in our patient suggests that ongoing autoimmune destruction was responsible for his hypothyroid state. Autoimmune thyroprivic hypothyroidism is usually not associated with thyroid associated ophthalmopathy or dermopathy, despite increased concentrations of TSH which may act on TSH receptors present on ocular or dermal fibroblasts similar to thyroid stimulating immunoglobulins (TSI). The probable reasons are that autoimmunity in Hashimoto’s thyroiditis is confined to thyroid gland only and/or thyroid stimulating immunoglobulins possibly act on some other orbital or dermal antigens other than TSH receptors. A limitation of our case study is the lack of measurement of TSH receptor antibodies, and therefore these remain as postulations.

Therefore, these two infiltrative complications occurring in the above case can possibly be explained by the complex interplay between TSH receptor stimulating and blocking immunoglobulins.