Graves’ disease is characterised by diffuse toxic goitre, infiltrative ophthalmopathy and dermopathy.4
All these cardinal features may exist at one time and may precede or follow or may not occur during the lifetime. Out of these three cardinal manifestations at least two should be there to substantiate the diagnosis of Graves’ disease on clinical grounds, unless it is corroborated with estimation of TSH receptor stimulating antibodies.4
Clinically, the prevalence of thyroid associated ophthalmopathy is around 40–50%, whereas dermopathy ranges from 3–5% in association with Graves’ disease.5
Uncommonly, Hashimoto’s thyroiditis can also be associated with infiltrative ophthalmopathy in 3–5% of cases and rarely with dermopathy as well.1–4
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.
- Infiltrative ophthalmopathy and dermopathy with hyperthyroidism are the cardinal manifestations of Graves’ disease.
- Rarely, infiltrative ophthalmopathy and dermopathy may occur with hypothyroidism due to Hashimoto’s thyroiditis.