Sick Euthyroid Syndrome – Unraveling the Mystery of the Sick Euthyroid Syndrome
The sick euthyroid syndrome can be described as abnormal findings on thyroid function tests in a patient with no known thyroid condition or nonthyroidal illness (NTI). After recovering from the illness, the abnormalities are reversible. However, most of these patients are admitted into the Intensive Care Unit so it is of utmost important that the syndrome be differentiated from a real thyroid disorder.
There are many forms of the syndrome but one such form is most common. In this form, there are low or lower than normal levels of total thyroxine and triiodothyronine. In cases of true hypothyroidism, the low levels of thyroid hormones would send a feedback signal to the pituitary gland to increase secretion of thyrotropin or thyroid-stimulating hormone (TSH) but not so in this condition. In this form of the syndrome, TSH levels remain within the normal range.
Pathophysiology
One such explanation for the abnormal findings in the syndrome involve the distinction between type 1 deiodinase and type 2 deiodinase enzymes. Type 1 deiodinase is usually found in the periphery while type 2 deiodinase is found mainly in the pituitary gland. In this particular condition, it is the activity of type 1 deiodinase which is decreased, resulting in less conversion of thyroxine to triiodothyronine.
Despite all this, the type 2 deiodinase is not as affected as the type 1 deiodinase and the pituitary gland continues to sense normal levels of triiodothyronine. Because of this, the pituitary gland will inhibit the secretion of TSH due to what it perceives as normal concentrations of triiodothyronine. However, other factors should be considered and this theory does not account for the low levels of thyroxine as well.
Another explanation suggests that the serum thyroid hormone abnormalities may be due to inhibition of hormone-binding proteins, which consequently prevents test from reflecting normal free hormone levels. This binding inhibitor can be found in both serum and tissues and could inhibit binding to nuclear triiodothyronine receptors or prevent uptake of the thyroid hormones by the cells of the body. However, some studies have failed to exhibit such a binding inhibitor.
Cytokines, too, have been thought to play a role in this particular syndrome. These cytokines in particular are interleukin-1 and interleukin-6, tumor necrosis factor-alpha, and interferon-beta. They were thought to exert an effect on the hypothalamus, pituitary gland, and other tissues, inhibiting the production of thyroid-releasing hormone, thyroid-stimulating hormone, triiodothyronine, thyroid-binding globulins, and thyroglobulin. They were also thought to decrease the activity of type 1 deiodinase and the binding capacity of triiodothyronine nuclear receptors.
Treatment
Although patients with the sick euthyroid syndrome may exhibit signs of hypothyroidism such as hypothermia and a sluggish sensorium, they are not hypothyroid and should not receive thyroid hormone replacement as treatment. Treatment of such patients with thyroid hormone may, in fact, yield either no improvement or a worse outcome.
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