Jessica Watari1, Navinder Jassil2. 1. Internal Medicine Department, Rutgers Robert Wood Johnson Medical School New Brunswick, New Jersey. 2. Endocrine Department, Robert Wood Johnson University Hospital Somerset, Somerville, New Jersey.
Abstract
OBJECTIVE: We present a patient with long standing hypothyroidism who developed hyperthyroidism secondary to Graves disease. Recognition of this disease phenomenon is crucial to ensure prompt diagnosis and close follow-up. METHODS: The patient was evaluated with thyroid function testing and thyroid antibody testing. Further evaluation included ophthalmologic examination and radioactive iodine uptake imaging. RESULTS: A 56-year-old female with past medical history of human immunodeficiency virus, hepatitis C infection, and hypothyroidism presented for evaluation of thyroid disease. She had been off of levothyroxine for the last 8 months due to biochemical findings of thyrotoxicosis. Her family history was significant for hyperthyroidism and hypothyroidism. Laboratory tests were consistent with hypothyroidism so levothyroxine was restarted. Physical exam showed lid lag and proptosis. Ophthalmologic evaluation found bilateral 23 mm proptosis. Additional lab testing was positive for thyroid peroxidase antibody and thyroid stimulating immunoglobulin. Following levothyroxine use, the patient developed subclinical hyperthyroidism and thyroid replacement was stopped. The patient remained euthyroid for 1 year off of levothyroxine. Following 1 year, she developed mild hyperthyroidism with increased radioactive iodine uptake. She was placed on propranolol for symptomatic relief. Months later, thyroid function testing normalized. CONCLUSION: In Graves disease, hypothyroidism and conversion of hypothyroidism to hyperthyroidism are rare, yet important to recognize, clinical phenomenon. The stimulatory and inhibitory properties of thyroid-stimulating hormone receptor antibodies are speculated to play a role in individuals with alternating hypothyroidism and hyperthyroidism. These individuals can present a diagnostic and therapeutic challenge. Clinicians must maintain a high clinical suspicion for this disease entity.
OBJECTIVE: We present a patient with long standing hypothyroidism who developed hyperthyroidism secondary to Graves disease. Recognition of this disease phenomenon is crucial to ensure prompt diagnosis and close follow-up. METHODS: The patient was evaluated with thyroid function testing and thyroid antibody testing. Further evaluation included ophthalmologic examination and radioactive iodine uptake imaging. RESULTS: A 56-year-old female with past medical history of human immunodeficiency virus, hepatitis C infection, and hypothyroidism presented for evaluation of thyroid disease. She had been off of levothyroxine for the last 8 months due to biochemical findings of thyrotoxicosis. Her family history was significant for hyperthyroidism and hypothyroidism. Laboratory tests were consistent with hypothyroidism so levothyroxine was restarted. Physical exam showed lid lag and proptosis. Ophthalmologic evaluation found bilateral 23 mm proptosis. Additional lab testing was positive for thyroid peroxidase antibody and thyroid stimulating immunoglobulin. Following levothyroxine use, the patient developed subclinical hyperthyroidism and thyroid replacement was stopped. The patient remained euthyroid for 1 year off of levothyroxine. Following 1 year, she developed mild hyperthyroidism with increased radioactive iodine uptake. She was placed on propranolol for symptomatic relief. Months later, thyroid function testing normalized. CONCLUSION: In Graves disease, hypothyroidism and conversion of hypothyroidism to hyperthyroidism are rare, yet important to recognize, clinical phenomenon. The stimulatory and inhibitory properties of thyroid-stimulating hormone receptor antibodies are speculated to play a role in individuals with alternating hypothyroidism and hyperthyroidism. These individuals can present a diagnostic and therapeutic challenge. Clinicians must maintain a high clinical suspicion for this disease entity.