THYROTROPHIN RESPONSE TO THYROTROPHIN-RELEASING HORMONE IN OPHTHALMIC GRAVES'' DISEASE: CORRELATION WITH OTHER ASPECTS OF THYROID FUNCTION, THYROID SUPPRESSIBILITY AND ACTIVITY OF EYE SIGNS

Thirty-four patients with ophthalmic Graves' disease were investigated by routine thyroid function tests, by measurement of the serum thyroid-stimulating hormone (TSH) response to thyrotrophin-releasing hormone (TRH) and by measurement of the serum triiodothyronine (T₃) levels. The patients could be divided into four groups according to their response to TRH—normal, impaired, absent and exaggerated. Those with normal responses had routine thyroid function tests and serum T₃ levels which in general did not differ from normal control values. Those with impaired and with absent responses showed routine thyroid function tests which approached the hyperthyroid range together with significant elevation of serum T₃ levels. It is suggested that they might represent examples of ‘subclinical T₃ thyrotoxicosis’. Patients with exaggerated responses had routine thyroid function tests near the lower end of the normal range and could be regarded as suffering from ‘subclinical hypothyroidism’. There was a good correlation between a normal TRH response and normal thyroid suppressibility by T₃, and between impaired and absent responses and impaired thyroid suppressibility. It is evident that the TRH test which is safer, shorter and more convenient, can replace the T₃ suppression test in routine clinical practice. The response to TRH also provided information on the activity of the eye signs, a normal response was associated with improving eye signs whereas impaired, absent or exaggerated responses were associated with static signs or actual deterioration. The TRH test is of value in the diagnosis of unilateral exophthalmos since about three-quarters of the patients in this series showed some abnormality. The wide range of TRH response and of circulating thyroid hormone levels is to be expected since the thyroid is not subject to the normal finely-balanced negative feed-back mechanism via TSH.