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The thyroid blood test, TSH, is the most sensitive test for detecting primary hypothyroidism in non-pregnant adults.
TRUE: The thyroid stimulating hormone (TSH) has the most sensitivity for detecting primary hypothyroidism in ambulatory patients. This sentence is is very concise and is loaded with specific terms. All medical tests, whether a blood test or as simple as a physician asking a patient a question about symptoms, have an associated sensitivity or specificity. A test with high sensitivity are defined as tests that are very good at ruling out a disease. Medical tests with high specificity are very good at ruling in a disease. The TSH test has a high sensitivity and when used with the Free T4 has a high specificity. Primary hypothyroidism the most common type of thyroid function abnormality where the thyroid gland itself is producing insufficient thyroid hormones T4 and T3. This type of hypothyroidism does not include low thyroid function due to brain disorders of the pituitary or hypothalamus. Ambulatory patients are those that are otherwise healthy, not suffering from an acute medical condition. The texas endocrinologists Dr. Jogi and Dr. Elhaj can fully explain the use of blood tests in the management of thyroid disease.
The TSH blood test can be misleading.
TRUE: The TSH testing is accurate only when 6 major assumptions are met. 1) Steady state conditions 2) Normal TSH-to-target organ hormone relationship 3) Tissue responsiveness proportionality to hormone concentration 4) The TSH assay measures active hormone 5) The assay can reliably distinguish low from normal values 6) The reference ranges are appropriate. Your Houston Thyroid and Endocrine endocrinologist should ensure that interpretation of the thyroid blood testing is done in light of these assumptions. For further detail on each of these assumptoms please click here.
The primary way to diagnose hypothyroidism in patient with pituitary or hypothalamic brain disease is how the patient feels and using the Free T4 levels.
TRUE: The TSH reference "normal" intervals are based on the 95% confidence limits of the log-transformed values of at least 120 rigorously screened normal euthyroid volunteers who have no detectable thyroid autoantibodies (TPO antibodies or Thyroglobulin antibodies), no personal of family history of thyroid dysfunction, no visible goiter, and who are not taking any medications other than estrogen. (1) Patients with pituitary diseases and/or hypothalamic disease (central hypothyroidism or TSH secreting pituitary tumors) may have paradoxically normal, high, or low TSH values because the current blood testing for TSH does not distinguish between the normal and biologically altered TSH isoforms that may be present in those diseases. (2) Fortunately these pituitary and hypothalamic diseases are very rare and usually obvious to an endocrinologist. Thus, if pituitary disease is suspected, an endocrinologist should be involved and the patient's symptoms along with the Free T4 levels become more important in management of the thyroid disease. The TSH is considered to be the most important thyroid test for assessing the early development of either primary hypothyroidism or primary hyperthyroidism. This is because the log/linear TSH to Free T4 relationship dictates that an altered TSH will be the first abnormality to appear - as soon as the pituitary registers that FT4 has changed from its genetically-determined setpoint for that particular individual (3)
The TRH stimulation test is a historically useful test for diagnosing pituitary disease.
TRUE: The TRH test is a historically useful test and is no longer a useful in the 21st century. To understand this testing the physiology of thyroid disease should be understood first. The TSH assay "quality" is defined by its clinical sensitivity, ie// the ability to differentiate between hyperthyroid and normal thyroid levels. The "first generation" TSH assays were used between 1965 and 1985 and were based on radio immunoassay (RAI) methodology that had limited functional sensitivity (~ 1.0 mIU/L), thus they were only useful to help identify hypothyroidism, but not helpful to decide if a patient had truely normal thyroid levels. (4) In 1970, the hypothalamic hormone,Thyrotropin Releasing Hormone (TRH) (Thyroliberin) was created and used to stimulate serum TSH upwards into the measurable range in all patients with normal thyroid levels, but not patients with hyperthyroidism or hypopituitarism. This was useful because a low TSH can indicate pituitary disease in rare patients. (5) The use of TRH testing fell into decline after the more sensitive immunometric assay (IMA) methodology (also called "sandwich" or "noncompetitive" methodology) became available in the mid-1980s. It is also difficult to obtain TRH itself. By 1990, IMA non-isotopic methods had replaced most TSH RIA methods and as a result of inherently greater assay sensitivity and specificity resulted in narrowing the TSH reference range by reducing glycoprotein hormone cross-reactivity and improving precision The development of high-sensitivity TSH assays has almost eliminated the need for TRH testing in clinical practice because TRH testing does not provide much of a diagnostic advantage over an accurate basal measurement of TSH. The one situitation in which this testing might be useful is to distinguish among the extremely rare cases of thyroid hormone resistance versus pituitary dependent hyperthyroidism caused by TSH-secreting tumors. But, there are multiple other methods to diagnose these conditions. (6,7)
Based on a patient's symptom scores and physical examination only, a physician can diagnose thyroid disease accurately.
FALSE: Large objective studies have shown that in over 3000 unselected patients who were assessed by both clinical and laboratory criteria, a thyroid disorder was not suspected by primary care physicians in more than 90% of those who tested positive for a thyroid problem, even when clinical features were apparent in retropect. (8,9) Even thyroid specialists can be mislead by clinical information alone. In one study, once specialists had the laboratory information avaialble, the specialists had to revise their diagnosis in up to 33% of patents evaluated for a clinically suspected thyroid disorder. (10) In general, clinical assessment identifies about 40% of patients with overt hypothyroidism since classical signs were only present in the most severely affected. Importantly, both overt hyperthyroidism and overt hypothyroidism can have detrimental clinical consequences before the usual clinical features become obvious. As patients age, the typical classical symptoms of hyperthyroidism become much less obvious with advancing age. (11)
Taking excessive thyroid hormone replacement has dangerous side effects
TRUE: Long term treatment with thyroxine medication when properly monitored, is generally very safe with no significant increase in morbidity or mortality (12). Thyroxine (T4) treatment reduces the TSH. When the TSH is lowered too much there is an association with detrimental effects on the heart and the bones. A TSH value of less than or equal to 0.1 mU/l has been identified as a risk factor for the development of atrial fibrillation (13). Atrial fibrillation is an abnormal heart rhythm which can cause strokes. Long term thyroxine therapy to TSH-suppressive doses may cause the heart to become enlarged (14) and increases the risk of ischemic heart disease in patients under the age of 65 years (15). TSH-suppressive doses of levothyroxine have been associated with bone loss in some but not all studies. A meta-analysis (compilation of many scientific studies) concluded that bone mineral density was reduced in hypothyroid patients with a suppressed TSH due to excessive levothyroxine therapy in postmenopausal women (16). This suggests an increase risk for fracture but this is not conclusive since no or a minimal excess of bone fractures has been observed in patients on levothyroxine even if TSH is suppressed (17, 18). Cardiovascular disease, dysrhythmias, and fractures were increased in patients with a high TSH (>4.0 mU/l) and especially in patients with a suppressed TSH (< or = 0.03 mU/l) when compared to patients with a TSH in the laboratory reference range. (19) These risks occur in patients taking any form of thyroid hormone: desiccated, "bio-identical", compounded, or synthetic thyroid hormone replacement.
High levels of iodine intake will help thyroid function
FALSE: Iodine deficiency can adversely affect thyroid function and conversely iodine excess can adversely affect thyroid function. The effect of iodine on the thyroid gland is complex with a “U shaped” relationship between iodine intake and risk of thyroid disease. Paradoxically, low and high iodine intake are associated with an increased risk of thyroid function problems (hyperthyroidism, hypothyroidism, or thyroiditis). (23, 24, 25) Healthy adults can tolerate up to 600-1100 μg iodine/day without any side effects (20, 21). These levels are variable based on pregnancy status and age of patient. An exception to these levels of intake is in populations which has been exposed to iodine deficiency for a prolonged period in the past: these patients can develop hyperthyroidism when exposed 600 - 1100 μg iodine/day. The optimal level of iodine intake to prevent any thyroid disease may be a relatively narrow range around the recommended daily intake of 150 μg (22). For 2011, the recommended daily allowance (RDA) for iodine by the Institute of Medicine (IOM) Food and nutrition board is 90mg/day for children, 150mg/day for adults, and 220 mg/day for pregnant women. The World Health Organization defines adult iodine nutrition with urine testing as excessive iodine intake which is >300 ug/L, adequate as 100-199 ug/L, mild iodine deficiency as 50-99 ug/L, and moderate iodine deficiency as 20-49 ug/L, and severe iodine deficiency as <20 ug/L.
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