Effect of Altered Thyroid Function on Critically Ill Patients

Abstract

The thyroid gland is one of the largest endocrine glands of the body. The gland has two primary functions, secretion of thyroid hormones, which maintain the level of metabolism in the tissues that is optimal for their normal function. And secretion of calcitonin, a hormone that regulates circulating levels of calcium. The thyroid gland is prone to a number of diseases that can alter its function and structure. These diseases frequently have wide-ranging systemic effects because thyroid hormones regulate the metabolism of almost every cell in the body. The main diseases are Hypothyroidism, Hyperthyroidism, Subclinical thyroid disease Thyroiditis Non-Thyroidal Illness and Thyroid neoplasms. Thyroid function tests are used to evaluate thyroid status, and the laboratory tests are used to confirm the clinical diagnosis of thyroid disease and to monitor patient with thyroid disease who have been treated. It is widely recognized that certain drugs can alter thyroid hormone measurements and can cause confusing laboratory test results in subjects without thyroid disease. The non-thyroidal illness syndrome, also known as the low T3 syndrome or euthyroid sick syndrome, describes a condition characterized by abnormal thyroid function tests encountered in patients with acute or chronic systemic illnesses. The laboratory parameters of this syndrome include low serum levels of tri iodothyronine T3 and high levels of reverse T3, with normal or low levels of thyroxine T4 and normal or low levels of thyroid-stimulating hormone (TSH). This condition may affect 60 to 70% of critically ill patients. During acute illness, surgery, or other types of severe physical stress, there is a very rapid decline in the circulating amount of T3, whereas plasma concentrations of rT3 rise acutely. Most often plasma TSH concentrations are in the normal range in patients admitted to the ICU. However, by analyzing TSH time series, it has become clear that in this acute phase of illness, the normal nocturnal TSH surge is absent. The magnitude of the decrease in circulating T3 during the first 24 hours after the onset of acute illness reflects the severity of illness and correlates with mortality. It is very difficult to normalize plasma thyroid hormone concentrations by using T4 and/or T3 in the context of critical illness. As the cause of the problem in the prolonged phase of critical illness is not the thyroidal capacity to produce or release thyroid hormone, nor the peripheral metabolism or uptake, but instead lies in a suppressed hypothalamic expression of releasing factors, such as TRH but also GH-releasing hormones, may be such peptides are a better and a more rational alternative.