Subacute Hypothyroid Myopathy as an Atypical Presentation Following Radioiodine Therapy

Thesapiriya Jeyapal; Nur Aini Eddy Warman; Nur Haziqah Baharum; Aimi Fadilah Mohamad; Mohd Hazriq Awang; Fatimah Zaherah Mohamed Shah; Rohana Abdul Ghani

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Subacute Hypothyroid Myopathy as an Atypical Presentation Following Radioiodine Therapy

Author: Thesapiriya Jeyapal ¹ ; Nur Aini Eddy Warman ¹ ; Nur Haziqah Baharum ¹ ; Aimi Fadilah Mohamad ¹ ; Mohd Hazriq Awang ¹ ; Fatimah Zaherah Mohamed Shah ¹ ; Rohana Abdul Ghani ¹
Author Information

1. Department of Internal Medicine, Faculty of Medicine, Universiti Teknologi MARA
Publication Type:Journal Article
MeSH: Iodine Radioisotopes; Muscular Diseases
From: Journal of the ASEAN Federation of Endocrine Societies 2026;41(S1):105-106
CountryPhilippines
Language:English
Abstract: Introduction:Hypothyroidism is the most common outcome following radioiodine (RAI) therapy for Graves’ disease, affecting up to 80% of patients, usually within 6 months. While symptoms are often nonspecific, musculoskeletal complaints may be the predominant or sole manifestation. Hypothyroid myopathy occurs in 30–80% of patients, typically causing myalgias, cramps, fatigue, and slowly progressive, symmetric proximal weakness with delayed reflex relaxation. We report an atypical case with subacute and evolving weakness after levothyroxine initiation.
Case:A 43-year-old female with Graves’ disease underwent RAI therapy (25 mCi) and developed hypothyroidism 7 weeks later. She was started on levothyroxine 50 mcg daily. Two weeks into treatment, she presented with progressive proximal lower limb weakness (power 4/5), while distal strength and reflexes remained intact. Labs revealed elevated creatine kinase (259 U/L), hypokalemia (3.3 mmol/L), creatinine (57 µmol/L), and severe hypothyroidism (thyroid-stimulating hormone [TSH] 52.88 mIU/L, free thyroxine 4 [FT4] 7.79 pmol/L). Levothyroxine was increased to 100 mcg daily. Two weeks later, she developed proximal upper limb weakness (power 4/5), while lower limb strength had normalized. Nerve conduction studies and electromyography were unremarkable. Labs showed creatine kinase (244 U/L) and creatinine (58 µmol/L). As she remained hypothyroid (TSH 20.85 mIU/L, FT4 11.61 pmol/L), levothyroxine 100 mcg daily was continued. Her symptoms gradually improved alongside biochemical recovery (TSH 8.83 mIU/L, FT4 15.90 pmol/L) after 4 weeks, consistent with hypothyroid myopathy.
Conclusion:This case highlights an atypical subacute presentation of hypothyroid myopathy following RAI, with evolving weakness and transient worsening after starting thyroid hormone therapy. Although other serious causes should be excluded, clinicians must maintain a high index of suspicion to avoid unnecessary investigations and ensure timely optimization of thyroid hormone therapy, as clinical improvement parallels biochemical recovery.
Full text:2026080417061331522EP_A154.pdf