SUN-362 A case of myopathic dysphagia caused by thyrotoxicosis

Abstract Disclosure: H. Chua: None. L. Tan: None. C. Chew: None. BackgroundMyopathic dysphagia is a less commonly seen manifestation of thyrotoxicosis. Bulbar muscle weakness may be isolated, or may be associated with preceding proximal myopathy. The pathophysiology is postulated to be via neuromuscular effects, and accumulation of glycosaminoglycans affecting swallowing function. Case report:We describe a 70 year old gentleman with newly diagnosed Graves’ disease who presented with acute dysphagia with both liquids and solids for 3 weeks, with free thyroxine (fT4) >73 pmol/L (reference range 8 to 16 pmol/L), free triiodothyronine (fT3) >40 pmol/L (reference range 3.5-6.0 pmol/L), thyroid stimulating hormone (TSH) <0.01 mIU/L (reference range 0.45-4.50 mIU/L), and TSH receptor antibody 28.6 IU/L (reference range 0.0-1.0 IU/L). This was associated with heat intolerance, palpitations, diarrhoea, proximal weakness, and loss of weight. A video fluoroscopy study confirmed moderate oropharyngeal dysphagia. The patient had recent oesophago-gastro-duodenoscopy and colonoscopy 9 months prior which did not reveal any obstructive lesions. Further evaluation was done including a magnetic resonance imaging (MRI) brain stroke protocol scan, computed tomography scan of the thorax, abdomen, pelvis (CT TAP), nasal endoscopy, and neuromuscular work up including acetylcholine receptor antibody and anti-muscle-specific kinase antibody, and myositis antibody profile - these did not reveal any other cause of dysphagia. Nerve conduction study and electromyography showed evidence of a non-irritable myopathy involving proximal muscles in both upper and lower limbs which could be due to thyrotoxic myopathy, with no evidence of post synaptic neuromuscular junction pathology. The patient’s dysphagia improved with Carbimazole doses of up to 30mg twice daily, and propranolol doses of up to 20mg thrice daily, titrated as thyrotoxicosis improved. His fT4 and fT3 level normalized within 2 months. He progressed from requiring nasogastric tube feeding, to oral feeding with regular diet and thin fluids within 7 weeks of treatment. DiscussionBased on case reports in literature, patients responded well with high doses of thionamides, and beta blockers. Our patient’s dysphagia resolved rapidly with normalization of fT4 and fT3. It is important to render the patient euthyroid as soon as possible, to minimise risks of aspiration, pneumonia and other complications. Presentation: Sunday, July 13, 2025

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Journal
Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.2372
Primary Topic
Restraint-Related Deaths
Type
article
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article

SUN-362 A case of myopathic dysphagia caused by thyrotoxicosis

Hsieh En Chua, Chee Kian Chew, Lip Hong Tan
Journal of the Endocrine Society
Restraint-Related Deaths
article

SUN-362 A case of myopathic dysphagia caused by thyrotoxicosis

Hsieh En Chua, Chee Kian Chew, Lip Hong Tan
article en

Abstract

Abstract Disclosure: H. Chua: None. L. Tan: None. C. Chew: None. BackgroundMyopathic dysphagia is a less commonly seen manifestation of thyrotoxicosis. Bulbar muscle weakness may be isolated, or may be associated with preceding proximal myopathy. The pathophysiology is postulated to be via neuromuscular effects, and accumulation of glycosaminoglycans affecting swallowing function. Case report:We describe a 70 year old gentleman with newly diagnosed Graves’ disease who presented with acute dysphagia with both liquids and solids for 3 weeks, with free thyroxine (fT4) >73 pmol/L (reference range 8 to 16 pmol/L), free triiodothyronine (fT3) >40 pmol/L (reference range 3.5-6.0 pmol/L), thyroid stimulating hormone (TSH) <0.01 mIU/L (reference range 0.45-4.50 mIU/L), and TSH receptor antibody 28.6 IU/L (reference range 0.0-1.0 IU/L). This was associated with heat intolerance, palpitations, diarrhoea, proximal weakness, and loss of weight. A video fluoroscopy study confirmed moderate oropharyngeal dysphagia. The patient had recent oesophago-gastro-duodenoscopy and colonoscopy 9 months prior which did not reveal any obstructive lesions. Further evaluation was done including a magnetic resonance imaging (MRI) brain stroke protocol scan, computed tomography scan of the thorax, abdomen, pelvis (CT TAP), nasal endoscopy, and neuromuscular work up including acetylcholine receptor antibody and anti-muscle-specific kinase antibody, and myositis antibody profile - these did not reveal any other cause of dysphagia. Nerve conduction study and electromyography showed evidence of a non-irritable myopathy involving proximal muscles in both upper and lower limbs which could be due to thyrotoxic myopathy, with no evidence of post synaptic neuromuscular junction pathology. The patient’s dysphagia improved with Carbimazole doses of up to 30mg twice daily, and propranolol doses of up to 20mg thrice daily, titrated as thyrotoxicosis improved. His fT4 and fT3 level normalized within 2 months. He progressed from requiring nasogastric tube feeding, to oral feeding with regular diet and thin fluids within 7 weeks of treatment. DiscussionBased on case reports in literature, patients responded well with high doses of thionamides, and beta blockers. Our patient’s dysphagia resolved rapidly with normalization of fT4 and fT3. It is important to render the patient euthyroid as soon as possible, to minimise risks of aspiration, pneumonia and other complications. Presentation: Sunday, July 13, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
Tan Tock Seng Hospital (SG)
Openalex Percentile: Top 55%
Restraint-Related Deaths
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