Project Title

A Case of Compensated Thyroid Hormone Resistance

Authors' Affiliations

Ali Bokhari, Department of Internal Medicine, East Tennessee State University, Johnson city, TN. Sathvika Gaddam, Department of Internal Medicine, East Tennessee State University, Johnson city, TN Deepika Nallala, Department of Endocrinology, East Tennessee State University, Johnson city, TN

Location

Mt Mitchell

Start Date

4-12-2019 9:00 AM

End Date

4-12-2019 2:30 PM

Poster Number

145

Faculty Sponsor’s Department

Other - please list

Endocrinology

Name of Project's Faculty Sponsor

Dr. Deepika Nallala

Type

Poster: Competitive

Classification of First Author

Medical Resident or Clinical Fellow

Project's Category

Endocrine System

Project's Category

Arts and Humanities

Abstract Text

INTRODUCTION

Impaired sensitivity to thyroid hormone is described as any process that interferes with the effectiveness of thyroid hormone and includes defects in thyroid hormone action, transport, or metabolism. Here we present a case of a 60-year-old man with resistance to thyroid hormone (RTH), the most common form of impaired sensitivity.

CASE

A 60-year-old male presented to the endocrinology clinic with complaints of fatigue, decreased concentration, and impaired memory. He denied neck swelling, neck pain, peripheral edema, or any significant changes in weight, temperature sensitivity, bowel habits, and mood. His family history was significant for difficult to control thyroid disease in his brother and son. Thyroid exam was normal. Seven years ago, he was diagnosed with hypothyroidism of undetermined etiology with an elevated Thyroid Stimulating Hormone (TSH) and started on Levothyroxine.

TSH was within normal limits in the first 3 years of therapy but TSH and free T4 remained high since then. MRI of the brain could not be done to rule out TSH secreting adenoma as he had pieces of metal in his face. In the absence of overt signs or symptoms of hyperthyroidism except atrial fibrillation, and a normal alpha subunit, IGF1, and prolactin, a TSH secreting adenoma is considered less likely.

Levothyroxine was stopped and thyroid hormone levels were rechecked in 1 month that revealed elevated TSH with normal T3 and T4, representing compensated RTH. Genetic counseling was provided to the patient but he refused genetic testing.

DISCUSSION

The incidence of RTH is approximately 1 in 50,000 live births. In approximately 85 percent of cases it is due to mutations in the gene encoding the thyroid hormone receptor beta (TR-beta), while the other 15% are yet to be determined. It is characterized by reduced responsiveness of target tissue to thyroid hormones. The hallmark of RTH is the paucity of signs and symptoms of thyroid dysfunction despite the presence of high serum T4 and T3 concentrations. Clinical features include goiters, hyperactivity, and tachycardia. It can be diagnosed after other causes of hyperthyroxinemia are ruled out and confirmed with genetic testing.

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Apr 12th, 9:00 AM Apr 12th, 2:30 PM

A Case of Compensated Thyroid Hormone Resistance

Mt Mitchell

INTRODUCTION

Impaired sensitivity to thyroid hormone is described as any process that interferes with the effectiveness of thyroid hormone and includes defects in thyroid hormone action, transport, or metabolism. Here we present a case of a 60-year-old man with resistance to thyroid hormone (RTH), the most common form of impaired sensitivity.

CASE

A 60-year-old male presented to the endocrinology clinic with complaints of fatigue, decreased concentration, and impaired memory. He denied neck swelling, neck pain, peripheral edema, or any significant changes in weight, temperature sensitivity, bowel habits, and mood. His family history was significant for difficult to control thyroid disease in his brother and son. Thyroid exam was normal. Seven years ago, he was diagnosed with hypothyroidism of undetermined etiology with an elevated Thyroid Stimulating Hormone (TSH) and started on Levothyroxine.

TSH was within normal limits in the first 3 years of therapy but TSH and free T4 remained high since then. MRI of the brain could not be done to rule out TSH secreting adenoma as he had pieces of metal in his face. In the absence of overt signs or symptoms of hyperthyroidism except atrial fibrillation, and a normal alpha subunit, IGF1, and prolactin, a TSH secreting adenoma is considered less likely.

Levothyroxine was stopped and thyroid hormone levels were rechecked in 1 month that revealed elevated TSH with normal T3 and T4, representing compensated RTH. Genetic counseling was provided to the patient but he refused genetic testing.

DISCUSSION

The incidence of RTH is approximately 1 in 50,000 live births. In approximately 85 percent of cases it is due to mutations in the gene encoding the thyroid hormone receptor beta (TR-beta), while the other 15% are yet to be determined. It is characterized by reduced responsiveness of target tissue to thyroid hormones. The hallmark of RTH is the paucity of signs and symptoms of thyroid dysfunction despite the presence of high serum T4 and T3 concentrations. Clinical features include goiters, hyperactivity, and tachycardia. It can be diagnosed after other causes of hyperthyroxinemia are ruled out and confirmed with genetic testing.