# Acute Rhabdomyolysis as a Rare Manifestation of Hypothyroidism: A Case Report and Literature Review

**Authors:** Nada Benabdelmalek, Ali Halouache, Lhoussaine Abainou, Saadia Ait Malek, Mariam Erraoui, Imad Ghozlani

PMC · DOI: 10.7759/cureus.86675 · Cureus · 2025-06-24

## TL;DR

This paper presents a rare case of rhabdomyolysis caused by severe hypothyroidism in a 56-year-old woman with no other contributing factors.

## Contribution

The case highlights the rare but important link between profound hypothyroidism and rhabdomyolysis.

## Key findings

- The patient showed elevated CPK, LDH, and transaminases consistent with rhabdomyolysis.
- Thyroid function tests confirmed profound hypothyroidism with elevated TSH and negative thyroid antibodies.
- Treatment led to significant clinical and biological improvement.

## Abstract

Thyroid myopathy is often subtle, but massive rhabdomyolysis secondary to hypothyroidism is an exceptional phenomenon, with approximately 30 to 40 cases reported in the medical literature to date. We report a case of rhabdomyolysis secondary to profound hypothyroidism in the absence of any precipitating factor. This is a 56-year-old woman who underwent a right mastectomy six years ago for breast cancer and received adjuvant chemotherapy for two months followed by four weeks of radiotherapy. She has been on letrozole 2.5 mg daily for six years. Over the past three months, she has developed physical and psychological asthenia, constipation, muscle fatigue, and myalgia, predominantly in the proximal muscles of the four limbs. Clinical examination found signs of myxedema infiltration and signs of hypometabolism.

The laboratory assessment revealed elevated levels of total creatine phosphokinase (CPK), lactate dehydrogenase (LDH), and transaminases (aspartate aminotransferase (AST) and alanine aminotransferase (ALT)). The thyroid function test indicated profound hypothyroidism, with a significantly elevated ultrasensitive thyroid-stimulating hormone (TSHus) level. Anti-thyroperoxidase antibodies were negative, as were anti-thyroglobulin antibodies. Cervical ultrasound revealed an atrophic thyroid and loss of the musculoparenchymal gradient, suggestive of thyroiditis. Computed tomography brain was normal. The diagnosis was made based on her clinical presentation and laboratory tests. The outcome was marked, after treatment, by good clinical and biological improvement.

## Linked entities

- **Chemicals:** letrozole (PubChem CID 3902)
- **Diseases:** hypothyroidism (MONDO:0005420), rhabdomyolysis (MONDO:0005290), thyroiditis (MONDO:0004126), breast cancer (MONDO:0004989)

## Full-text entities

- **Genes:** TPO (thyroid peroxidase) [NCBI Gene 7173] {aka MSA, TDH2A, TPX}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, TG (thyroglobulin) [NCBI Gene 7038] {aka AITD3, TGN}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}
- **Diseases:** Thyroid myopathy (MESH:D013966), Rhabdomyolysis (MESH:D012206), myxedema (MESH:D009230), Hypothyroidism (MESH:D007037), constipation (MESH:D003248), muscle fatigue (MESH:D005221), myalgia (MESH:D063806), breast cancer (MESH:D001943), asthenia (MESH:D001247)
- **Chemicals:** letrozole (MESH:D000077289)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12289108/full.md

## References

25 references — full list in the complete paper: https://tomesphere.com/paper/PMC12289108/full.md

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Source: https://tomesphere.com/paper/PMC12289108