SAT-378 A Rare Case of Persistent Exercise-Induced Myopathy in a Patient with Treated Graves’ Disease

Abstract Disclosure: H. Diep: None. M.K. Shakir: None. G.A. Cook: None. T.D. Hoang: None. Introduction: Myopathy occurs in 30-80% patients with hypothyroidism and there have been several case studies of myopathy due to rapid correction of hyperthyroidism or Graves’ disease. We present a rare case of persistent, exercise induced myopathy after radioactive iodine therapy (RAI) in a patient with Graves’ disease. Case Report: A 25-year-old man with no family history of autoimmune thyroid disease presented with new-onset Graves’ disease treated with RAI resulting in hypothyroidism. Five months after the RAI therapy and levothyroxine replacement the patient noticed muscle spasms and cramping in his biceps, triceps, and pectoral muscles after upper body exercises that lasted for 60 seconds and were accompanied by pain and fatigue that lasted for 15-30 minutes. The patient reported his symptoms improved after stopping levothyroxine. Patient later started desiccated thyroid extract with initial improvement followed by a recurrence of myopathy symptoms. An EMG initially showed irritable myopathy, which improved on a repeat EMG a year later. Further work up with a myomarker antibody panel, muscle biopsy, and muscular dystrophy panel were unrevealing. He began taking magnesium, calcium, vitamin D, and B12 daily and prioritizing improved hydration, with no noticeable improvement. Patient was prescribed dantrolene 25mg one hour prior to exercise with mild improvement. Discussion: Thyroid hormone deficiency can result in impaired mitochondrial oxidative capacity, resulting in a selective atrophy of type II muscle fibers as they become dependent on glycolysis for energy. Oxidative damage can cause muscle cell injury and potentially rhabdomyolysis. The degree of muscle weakness does not always correlate with the severity of hormone deficiency and myopathy is also observed in hyperthyroid patients, indicating that muscle injury is likely a contributing factor to the myopathy symptoms. The cause of the patient's myopathy, whether due to Graves' disease or RAI-induced remission, is unclear. Dantrolene mildly improved the patient’s symptoms suggesting an underlying pathology with the muscle excitation-contraction coupling interaction and muscle contractility. This case outlines the variable presentation of myopathy in a patient with rapid correction of hyperthyroidism in Graves’ disease and limited treatment options. Presentation: Saturday, July 12, 2025

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Journal
Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.2295
Primary Topic
Muscle Physiology and Disorders
Type
article
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article

SAT-378 A Rare Case of Persistent Exercise-Induced Myopathy in a Patient with Treated Graves’ Disease

Glen Cook, Mohamed K.M. Shakir, Thanh D. Hoang, Hadley Diep
Journal of the Endocrine Society
Muscle Physiology and Disorders
article

SAT-378 A Rare Case of Persistent Exercise-Induced Myopathy in a Patient with Treated Graves’ Disease

Glen Cook, Mohamed K.M. Shakir, Thanh D. Hoang, Hadley Diep
article en

Abstract

Abstract Disclosure: H. Diep: None. M.K. Shakir: None. G.A. Cook: None. T.D. Hoang: None. Introduction: Myopathy occurs in 30-80% patients with hypothyroidism and there have been several case studies of myopathy due to rapid correction of hyperthyroidism or Graves’ disease. We present a rare case of persistent, exercise induced myopathy after radioactive iodine therapy (RAI) in a patient with Graves’ disease. Case Report: A 25-year-old man with no family history of autoimmune thyroid disease presented with new-onset Graves’ disease treated with RAI resulting in hypothyroidism. Five months after the RAI therapy and levothyroxine replacement the patient noticed muscle spasms and cramping in his biceps, triceps, and pectoral muscles after upper body exercises that lasted for 60 seconds and were accompanied by pain and fatigue that lasted for 15-30 minutes. The patient reported his symptoms improved after stopping levothyroxine. Patient later started desiccated thyroid extract with initial improvement followed by a recurrence of myopathy symptoms. An EMG initially showed irritable myopathy, which improved on a repeat EMG a year later. Further work up with a myomarker antibody panel, muscle biopsy, and muscular dystrophy panel were unrevealing. He began taking magnesium, calcium, vitamin D, and B12 daily and prioritizing improved hydration, with no noticeable improvement. Patient was prescribed dantrolene 25mg one hour prior to exercise with mild improvement. Discussion: Thyroid hormone deficiency can result in impaired mitochondrial oxidative capacity, resulting in a selective atrophy of type II muscle fibers as they become dependent on glycolysis for energy. Oxidative damage can cause muscle cell injury and potentially rhabdomyolysis. The degree of muscle weakness does not always correlate with the severity of hormone deficiency and myopathy is also observed in hyperthyroid patients, indicating that muscle injury is likely a contributing factor to the myopathy symptoms. The cause of the patient's myopathy, whether due to Graves' disease or RAI-induced remission, is unclear. Dantrolene mildly improved the patient’s symptoms suggesting an underlying pathology with the muscle excitation-contraction coupling interaction and muscle contractility. This case outlines the variable presentation of myopathy in a patient with rapid correction of hyperthyroidism in Graves’ disease and limited treatment options. Presentation: Saturday, July 12, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
Walter Reed National Military Medical Center (US)
Openalex Percentile: Top 73%
Muscle Physiology and Disorders
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