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Thyroid problems can be worrisome, but relatively few children referred for workup for an abnormal thyroid test have clinically significant disease. Choosing the right screening tests can prevent these costly encounters without compromising children whose test results warrant close follow-up and possible intervention.
DR. KAPLOWITZ is chief of endocrinology, Children's National Medical Center, and professor of pediatrics, George Washington University School of Medicine, Washington, D.C.
Referrals for evaluation of "abnormal" thyroid tests account for at least 25% of appointment requests in our department of pediatric endocrinology. The great majority of these patients do not actually have thyroid disease, need no therapy, and in many cases, no follow-up testing. They nevertheless arrive at the endocrinologist's office for three basic reasons:
This article will review some basic thyroid pathophysiology, pinpoint the indications for thyroid testing in children, and offer examples of test results that (most of the time) do not require referral to an endocrinologist.
Thyroid hormones l-thyroxine (known as T4) and triiodothyronine (known as T3) have many important functions, but those that are most critical in children are promotion of normal myelination during brain development in the first two to three years of life and normal skeletal growth. In addition, thyroid hormones regulate the rate of metabolism. Thus a severe deficiency may result in fatigue, feeling cold, low heart rate, constipation, and slow growth if the problem has been present for long enough. It is important to note that mild but biochemically detectable deficiency is often asymptomatic, and that the actual symptoms of thyroid hormone deficiency (or excess) vary greatly from child to child.
T3 is more potent as a thyroid hormone than T4, but its blood levels are lower. About 20% of T3 comes directly from thyroid synthesis and 80% from peripheral metabolism, since many tissues can convert T4 to T3 by removing an iodine atom.
Thyroid hormone production is tightly regulated by pituitary secretion of thyroid stimulating hormone (TSH), which is in turn regulated by hypothalamic thyrotropin-releasing hormone (stimulatory) and somatostatin (inhibitory). The pituitary senses the level of unbound (free) T3. When that level falls below a critical set point, TSH increases which then stimulates the thyroid gland to produce and release more thyroid hormones. When thyroid hormone levels normalize, they induce feedback inhibition of TSH release, and TSH levels return to normal. Thus a mildly increased TSH (6 to 15 µIU/mL) may be an appropriate response to a transient decrease in thyroid hormone production, and does not always signify an immediate need to start thyroid hormone replacement.
Ups and downs of thyroid function
By far the most common cause of a progressive decline in thyroid function is autoimmune or Hashimoto's thyroiditis. The hallmark of this condition is a progressive rise in TSH (usually to levels above 20 µIU/mL), accompanied by a gradual fall in circulating thyroid hormone levels. In the early stages, thyroid hormone levels may still fall within the low-normal range, but eventually, as the thyroid fails, the free T4 level will become subnormal. In most but not all cases, the rise in TSH stimulates growth of the gland itself, resulting in a goiter palpable on physical examination. Goiter may appear early in the course of disease, while symptoms are absent. Eventually, as thyroid hormone levels fall well below normal, the classic symptoms noted above will appear, although their onset is so insidious they may go unrecognized. In about 90% of cases, elevated levels of anti-thyroid antibodies, particularly thyroid peroxidase (TPO) antibodies, will be present at the time of diagnosis, thus confirming a suspicion of autoimmune thyroiditis.