The Thyroid & Pregnancy: ATA Research Summit and Spring Symposium

The American Thyroid Association will hold its “Research Summit and Spring Symposium on the Thyroid and Pregnancy” April 16 – 17 in Washington, D.C. at the Madison Hotel, 1177 N. 15th Street, NW, Washington, DC 20005.

The two-day event features internationally prominent experts on issues such as: the changes in and the stress placed upon the thyroid gland during pregnancy, the impact of hypothyroidism and hyperthyroidism, screening during pregnancy, clinical trials and the issues regarding intervention and treatment. The Research Summit will be held April 16 and the Spring Symposium on April 17.

Pregnancy has a profound impact on the thyroid. During pregnancy, the thyroid gland produces about 50 percent more thyroid hormone as compared to when a woman is not pregnant; the glandular demand for iodine increases and, if iodine nutrition is not adequate, the thyroid increases in size and the risk for developing hypothyroidism rises.

Research Summit samples
Graham Williams, MD, PhD, FRCP, Hammersmith Hospital, London, UK, will discuss the role of thyroid hormones in fetal and post-natal bone development Thursday, April 16 from 10:00 a.m. to noon as part of a session entitled “Thyroid Hormone Action in Development.”

“Hypothyroidism delays bone formation,” says Dr. Williams. “However, thyrotoxicosis accelerates skeletal development and is an important risk factor for osteoporosis in adults.”

According to Dr. Williams, in trials with laboratory animals with mutated or deleted thyroid hormone receptors of two different types, bone growth was delayed in one case and accelerated in the other.

“The studies provide new insight regarding thyroid hormone receptor action during skeletal development and highlight a fundamental role for thyroid hormones in chondrocytes during skeletal development that ultimately establishes the structure of adult bone,” explains Dr. Williams.


“The importance of the transporter MCT8 on neural development became apparent with the identification of mutations in the MCT8 gene in humans,” explains Samuel Refetoff, MD, professor of medicine, pediatrics, genetics and molecular medicine at the University of Chicago. “Mutations of the thyroid hormone specific cell membrane transporter produce severe mental and neurological impairment in males in addition to unusual but characteristic thyroid test abnormalities.”

According to Dr. Refetoff, it is believed that the psychomotor defect is caused by the inability of thyroid hormone to reach important areas of the brain. Thus, it is not surprising that treatment with the usual doses of thyroid hormone has not been effective. Studies in mice deficient in MCT8 showed that a thyroid hormone agonist enter cells “mostly independently of MCT8.”

These issues will be discussed in Dr. Refetoff’s presentation “Role of Thyroid Hormone Membrane Transporter MCT8 in Neural Development” during the Thursday, April 16 1:00 p.m. to 2:15 p.m. session.


According to Erik. K. Alexander, MD, Division of Endocrinology, Diabetes and Hypertension at Brigham and Women’s Hospital and the Harvard Medical School, an average of a 40 percent increase in Levothyroxine is required to cope with the increasing thyroid hormone demand during early pregnancy, but large individual differences exist.

“This increase usually occurs prior to a patient’s initial obstetrical visit,” explains Dr. Alexander. “However, the demand is sustained throughout the pregnancy and returns to baseline post-partum.”

Uncertainty exists, says Dr. Alexander, over questions such as: what does thyroid sufficiency mean? how can sufficiency be maintained? how often should thyroid function be tested during pregnancy? and how should patients be counseled to modify their L-T4 dose once pregnant? These issues will be discussed in Dr. Alexander’s presentation “Maintaining Thyroid Hormone Sufficiency in Pregnancy: Thyroid Supply to Mother and Fetus” during the Thursday, April 16 2:15 – 3:30 p.m. session.

This Research Summit aims at targeting resources and setting priorities to effectively answer these unknowns, Dr. Alexander says.


Symposium samples
According to Dr. Daniel Glinoer of the Free University of Brussels, there is a vicious circle of iodine-deficiency induced thyroid changes during pregnancy by which the thyroid gland of the pregnant mother, under excessive thyroid stimulation, increases both its size and its demand for iodine to produce more thyroxin (T4).

“Goiter formation is pregnancy is the hallmark of iodine deficiency,” said Dr. Glinoer. “But, that hallmark represents only the visible tip of the ‘iceberg.’ The underlying mechanism is relative hypothyroxinemia and the resulting rise in serum Thyroid Stimulating Hormone (TSH), within or above the normal range.”
Dr. Glinoer will present “Thyroid Function and Physiology in Normal Pregnancy” Friday, April 17 at 8:40 am.


Elizabeth N. Pearce, MD, MSc associate professor of medicine at Boston University, will discuss the importance of iodine in pregnancy April 17 from 9:05 a.m. until 9:30 a.m., focusing on iodine needs, impacts and controversies.

“Iodine sufficiency in pregnant women is imperative,” explains Dr. Pearce. “Iodine deficiency has myriad potential harmful consequences for a fetus or an infant.”

The adverse effects spectrum for iodine deficiency (IDD) includes spontaneous abortion or stillbirth, increased perinatal and infant mortality, neologic cretinism, and mental deficiencies. Prenatal IDD can result in a child’s retarded mental and physical development.


Maternal hyperthyroidism can have adverse outcomes for gestational physiology and for the fetus, says Susan J. Mandel, MD, MPH of the University of Pennsylvania School of Medicine.

“Graves’ disease can complicated pregnancy and Graves’ disease diagnosed for the first time during pregnancy can have a variety of presentations,” explains Dr. Mandel, who will present her data on April 17 from 10:00 to 10:20 a.m. “Outcomes depend on the severity of the disease at the time of pregnancy.”

Dr. Mandel will discuss hyperthyroidism diagnosis in pregnancy and other therapeutic issues, including the use of TSH receptor immunoassays, the use of antithyroid drugs, and the range of adverse outcomes. One focus will be on judging how the competing inhibition of maternal antithyroid drug therapy, and the stimulation by maternal antibodies, can affect fetal thyroid.


On April 17, from 11:35 a.m. until noon, Robert C. Smallridge, MD, of the Mayo Clinic, Florida, will discuss issues in postpartum thyroid dysfunction (PPTD) including the role of autoimmunity, postpartum effect on Graves’ disease, PPTD and depression, PPTD symptoms, diagnostic approaches, and management of PPTD.

“Women with a personal or family history of thyroid disease may be at risk of developing a thyroid problem either during or after pregnancy, and should speak to their doctor about being tested for a thyroid disorder,” says Dr. Smallridge.


“What happens when mother, fetus or both are hypothyroid?” asks James E. Haddow, MD of Women and Infants Hospital and Alpert Medical School at Brown University. These questions and others will be discussed when Dr. Haddow presents study results April 17 from 1:45 p.m. to 2:10 p.m. focused on hypothyroidism and child IQ and other developmental issues.

“Published evidence shows that when the mother is hypothyroid, LT4 treatment by 10 weeks gestation preserves a child’s IQ and avoids CNS morbidity,” says Dr. Haddow. “When both mother and fetus are hypothyroid, iodine treatment up to the end of the second trimester largely protects the fetal brain from the effects of iodine deficiency. Later treatment does not improve neurologic status.”


In her presentation, Friday April 17 from 2:10 p.m. to 2:35 p.m., Dr. Rosalind S. Brown, director of clinical trials research, Endocrine Division, Children’s Hospital, Boston, will focus on fetal and neonatal “thyroidology,” describing the importance of the hormone thyroxin (T4) and T4 transfer between mother and fetus.

“Normally, unless there is a gradient between maternal and fetal circulation, there is little placental transfer of T4 between mother and fetus,” says Dr. Brown. “Babies with no thyroid gland have normal intellectual development so long as the maternal thyroid function is normal and post-natal therapy is sufficiently early and adequate.”

However, emphasized Dr. Brown, the most severe intellectual defects during child development occur when both mother and fetus are hypothyroid.
“Unlike congenital hypothyroidism, the effects of maternal hypothyroidism are not reversible with postnatal therapy,” explains Dr. Brown.


The Universal Screening Debate will be the subject of the final session April 17 from 3;45 to 4:45 p.m. as leading experts debate the pros and cons of universal thyroid screening during pregnancy.

To screen or not to screen?
* Should all pregnant women be screened for thyroid function?
* Should only ‘high risk’ pregnant patients be screened?
* Which tests should be performed and when?

Moderator Kenneth D. Burman, MD, chief of the Endocrine Section at the Washington Hospital Center and professor of Medicine at Georgetown University, Washington D.C., will be joined by Gregory A. Brent, MD (UCLA) and Daniel Glinoer, MD, PhD (Free University of Brussels) to examine the prevalence of hypothyroidism among pregnant women, the adverse effects and complications of abnormal maternal thyroid function during pregnancy, and whether all pregnant women should be screened with thyroid function test measurements.

Approximately one-third of pregnant women with thyroid disease are not identified by a strategy of testing only high-risk women. The discussion will include evaluation of case studies, the costs and benefits of thyroid function screening, and approaches to identifying pregnant women with thyroid disease.


The American Thyroid Association (ATA) is the lead organization in promoting thyroid health and understanding thyroid biology. The ATA values scientific inquiry, clinical excellence, public service, education, collaboration, and collegiality. ATA members are physicians and scientists who work to enhance the understanding of thyroid physiology and pathophysiology, improve diagnosis and treatment of thyroid diseases, and promote the education of physicians, patients, and the public about thyroid cancer. Thyroid diseases are the most common disorders of the endocrine system, affecting almost 13 million Americans.

Source: American Thyroid Association

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