THYROID FUNCTION IN SUBACUTE THYROIDITIS

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Abstract
The status of thyroid function during the course of subacute thyroiditis has been assessed in 56 cases, 21 of which received no specific therapy to modify the natural course of the disease. In 11 very severe cases the initial extensive inflammatory necrosis presumably led to flooding of the body with thyroid hormone, thus producing symptoms of hyper-thyroidism with a high level of serum protein-bound iodine (PBI), an increased basal metabolic rate and a profound depression of thyroidal I131 uptake to virtually zero. Following the acute phase the patient passed through a euthyroid interval into a phase characterized by symptoms of hypothyroidism with a low level of serum PBI. During the later part of this phase the ability of the gland to concentrate iodine began to increase. During the recovery phase, the thyroidal I131 uptake rose to levels above normal in a rebound phenomenon, whereas the serum PBI gradually rose to levels that did not exceed the normal range. In 15 moderately severe cases, the acute phase was similar in character but usually less severe. The thyroid glands of patients in this group were not sufficiently damaged to cause a hypothyroid phase. After the serum PBI level fell to a normal range, the ability of the gland to take up radioiodine also returned to normal, without the rebound phenomenon. In the 30 milder cases, there was neither a hyperthyroid nor a hypothyroid phase, but the thyroidal uptake of I131 was usually depressed for several weeks. In all cases there appeared to be complete recovery with no permanent sequelae. Roentgen-ray or cortisone therapy modified the symptoms greatly. However, the phase of temporary hypothyroidism was not averted by therapy in very severe cases, and it is difficult to be certain (because of individual variations) whether or not the total duration of the thyroiditis was shortened.

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