History
In 1811, Bernard Courtois discovered iodine was present in seaweed, and iodine intake was linked with goiter size in 1820 by Jean-Francois Coindet. Gaspard Adolphe Chatin proposed in 1852 that endemic goiter was the result of not enough iodine intake, and Eugen Baumann demonstrated iodine in thyroid tissue in 1896.The first cases of myxedema were recognized in the mid-19th century (the 1870s), but its connection to the thyroid was not discovered until the 1880s when myxedema was observed in people following the removal of the thyroid gland (thyroidectomy). The link was further confirmed in the late 19th century when people and animals who had had their thyroid removed showed improvement in symptoms with transplantation of animal thyroid tissue. The severity of myxedema, and its associated risk of mortality and complications, created interest in discovering effective treatments for hypothyroidism. Transplantation of thyroid tissue demonstrated some efficacy, but recurrences of hypothyroidism was relatively common, and sometimes required multiple repeat transplantations of thyroid tissue.In 1891, the English physician George Redmayne Murray introduced subcutaneously injected sheep thyroid extract, followed shortly after by an oral formulation. Purified thyroxine was introduced in 1914 and in the 1930s synthetic thyroxine became available, although desiccated animal thyroid extract remained widely used. Liothyronine was identified in 1952.Early attempts at titrating therapy for hypothyroidism proved difficult. After hypothyroidism was found to cause a lower basal metabolic rate, this was used as a marker to guide adjustments in therapy in the early 20th century (around 1915).
Superior limbic keratoconjunctivitis (SLK, Théodores syndrome) is a disease of the eye characterized by episodes of recurrent inflammation of the superior cornea and limbus, as well as of the superior tarsal and bulbar conjunctiva. It was first described by F. H. Théodore in 1963. Symptoms and signs
Patients present with red eye, burning, tearing, foreign body sensation and mild photophobia. Upon examination, the conjunctiva appears inflamed and thickened, especially at the limbus. Pathophysiology
The development and pathophysiology of SLK is not well understood, but appears to involve microtrauma of keratoconjunctival surfaces. This mechanical hypothesis is supported by the increased lid apposition of exophthalmic thyroid patients, who are known to have an increased incidence of superior limbic keratoconjunctivitis. Diagnosis
Treatment
First-line treatments include topical corticosteroids and artificial tears. For non-responsive cases, potential treatments include topical ciclosporin A, vitamin A, autologous serum and injections of triamcinolone. Surgical treatment options include thermocauterization of the bulbar conjunctiva and conjunctival resection, typically under rose bengal (RB) staining to visualize affected areas. Epidemiology
Superior limbic keratoconjunctivitis tends to occur more often with dry eye syndrome (keratoconjunctivitis sicca), hyperthyroidism and hyperparathyroidism. It is also a rare complication associated with rheumatoid arthritis. Rarely, it may occur as a consequence of upper eyelid blepharoplasty surgery. References


== External links ==