HOME

By Andrew J. Bauer, M.D. and Gary L. Francis, M.D., Ph.D., Reprinted, with permission, from pages 46-48 of "Thyroid Cancer in the Child and Adolescent," which is Chapter 5 of the book "Thyroid Cancer: A Guide for Patients", (Douglas Van Nostrand, M.D., Gary Bloom, and Leonard Wartofsky, M.D., editors, Keystone Press, 2004.) See http://www.thyca.org/TCGuide.htm.

In the evaluation of a thyroid nodule in a child, we often separate children into two groups: prepubertal (before the onset of puberty) and postpubertal (after puberty has begun). This separation is not absolute but does allow us to make several distincitoins. For both groups of children, however, the children look perfectly healthy except for the finding of a lump or nodule in the thyroid and/or hard, persistent swollen lymph glands in the neck. This lack of any other signs of symptoms of a potentially medical problem is routine, but this does make it more difficult to accept that a thorough evaluation is needed and that thyroid cancer may be found and will need to be treated.

In general, prepubertal children with thyroid nodules have a greater chance of having a family or genetic risk factor (a history of thyroid disease or a medical syndrome associated with thyroid disease).

Teenagers are usually sent for evaluation after an asymptomatic nodule (lump) is found in the thyroid gland during a routine exam, such as a school sports physical. Thyroid disease of all forms, to include hypothyroidism (underactive), hyperthyroidism (overactive), thyroid nodules, and thyroid cancer, are more commonly found in adolescent girls than in adolescent boys. Compared with prepubertal children, it is more common to find thyroid nodules in this age group at the onset of puberty.

This is mostly likely because nodules are more commonly associated with autoimmune disease of the thyroid, particularly Hashimoto's thyroiditis (a common cause of hypothyroidism in young adult girls). While many nodules do not turn out to be cancer, overall a greater number of nodules are medically evaluated during this time.

Lastly, it is in the late teen years that survivors of childhood radiation therapy will begin to present with thyroid disease. The thyroid gland is particularly sensitive to radiation exposure, and the younger the patient at the time of the radiation therapy, the more quickly thyroid disease may develop. After radiation exposure, thyroid disease (hypothyroidism, nodules and/or cancer) may develop as soon as five years and as late as 30 years later. Examples of patients who may have received radiation therapy include Hodgkin's lymphoma and brain tumor survivors.

Why do children develop thyroid cancer?

We do not know why children develop thyroid cancer. We know that normal cells have a time-limited life expectancy whereas cancer cells are descried as immortal-they keep on growing. One theory of cancer formation suggests that in order to become cancer, cells must be able to bypass certain key control biologic check points on growth, which then allow them to become immortal cells. Several specific abnormalities in DNA (mutations in specific genes that are associated with the development of cancer) and growth factors are believed to play a role in this process. The immune response (the system in our body that fights infections) and the fact that the child's thyroid gland is still growing even under normal conditions could also be important. As you can imagine, all of these factors are also important in the development of thyroid cancer in adults. In the final analysis, we currently do not have a unifying explanation as to what combination of the above factors makes childhood thyroid cancer behave differently than adult thyroid cancer.

Childhood cancer survivors

One subset of children at an increased risk of developing thyroid nodules and thyroid cancer are children who have been exposed to radiation. Before 1980, many children received radiation therapy for a variety of medical conditions to include ringworm of the scalp, facial acne, an enlarged thymus, and a whole host of other conditions. While these practices have been abandoned, what has been learned from this experience is that the younger the child at the time of exposure, then the greater the chance and the shorter the time for the child to develop thyroid cancer. In addition, small radiation doses appear to have a greater chance than larger doses of causing thyroid abnormalities such as cancer. This is so because larger doses usually kill all the cells whereas smaller doses cause damage to the nuclear genetic apparatus of the cell, which causes mutations through defective repair, which in turn increases the risk of developing thyroid nodules and/or cancer.

Today the children who may still receive radiation exposure to the thyroid are those who are being treated for other forms of childhood cancers such as brain tumors, leukemias, and lymphomas. Doses as small as 50 rads may cause enough damage to increase the risk of thyroid nodules and thyroid cancer, with the greatest risk occurring in patients who have received radiation doses of 200 to 2,000 cGy or rads to the head and neck prior to the age of 10 years.

In total, thyroid cancer may develop in as many as 10 percent of all tumor survivors after radiation treatments with an increasing risk related to the younger age the child was when they received radiation therapy. Most thyroid disease requires about 15 years to appear, but cases have been reported as late as 30 years after, or as short as five years later in younger children. What makes the child's thyroid gland more susceptible to radiation damage when compared to an adult's is not known.

Radiation exposure from the environment

One of our greatest concerns is the widespread increase in thyroid cancer among children exposed to environmental radiation. An extreme example of this is the Chernobyl nuclear accident in the Belarus region of Soviet Russia in April 1986. After the accident, childhood thyroid cancers began to appear around the region surrounding Chernobyl as early as five years after the accident. Because thyroid cancers usually develop slowly, the full impact of the accident may not be known for another 20 to 30 years.

In the event of a nuclear accident, there are preventive measures that can be taken against radiation damage to the thyroid gland, which include the provision of stable iodine and non-radiation-contaminated water, milk, and food. The World Health Organization recommends stable iodine in doses of 0.1 gm/day to adults, 0.05 gm/day to children over 3 years of age and 0.025 gm/day to children under 3 years of age. These doses should be given until food, water, and milk are free of contamination.

Other inherited thyroid cancer syndromes

As mentioned above, some forms of papillary thyroid cancer (PTC) are inherited (passed from one generation to the next). In these families, inheritance follows a dominant pattern of transmission (one parent may pass on the risk of cancer independent of the other parent's genes). Although uncommon, these inherited causes should be considered in any family with cancer in multiple generations. Thyroid cancer may be one feature of a group of inherited tumor syndromes that have been named after the physicians who first described them and include Gardner's syndrome, Cowden's syndrome, and the Carney complex.

Back