# Hypothyroidism-induced Rhabdomyolysis in a Pediatric Patient

**Authors:** Hend Abd El Baky, Danika Cziranka-Crooks, Brinda Prasanna Kumar, Meghan Jacobs, Jeremy Killion, Lucy D Mastrandrea

PMC · DOI: 10.1210/jcemcr/luae118 · 2024-07-30

## TL;DR

A 12-year-old boy with severe hypothyroidism developed rhabdomyolysis and kidney injury, showing the importance of checking thyroid function in unexplained muscle issues.

## Contribution

This case highlights a rare but critical link between severe hypothyroidism and rhabdomyolysis in a pediatric patient.

## Key findings

- The patient had severely elevated creatine kinase and creatinine due to rhabdomyolysis and acute kidney injury.
- Autoimmune hypothyroidism was confirmed with profoundly abnormal thyroid hormone levels.
- Thyroid hormone replacement and rehydration led to improvement in lab values and clinical condition.

## Abstract

Hypothyroidism is a common clinical condition with nonspecific symptoms such as fatigue, cold intolerance, and constipation. Rarely, severe primary hypothyroidism presents with rhabdomyolysis. We present a 12-year-old boy with several months of fatigue, muscle cramping, and elevated creatine kinase (CK) who was found to have severe primary hypothyroidism. Initial laboratory evaluation was significant for CK 2056 U/L (reference, 0-300 U/L; 34.34 µkat/L) and creatinine 1.39 mg/dL (reference, 0.4-1 mg/dL; 122.88 µmol/L). He was admitted for management of rhabdomyolysis with acute kidney injury. Further biochemical testing revealed profound hypothyroidism—thyrotropin 494 mIU/mL (reference, 0.40-6.00 mIU/mL) and free thyroxine (T4) less than 0.4 ng/dL (reference, 0.80-1.80 ng/dL; <5.15 pmol/L). Thyroglobulin and thyroid peroxidase autoantibodies were positive, confirming autoimmune hypothyroidism. Low-dose levothyroxine was initiated. With aggressive rehydration, creatinine and CK levels improved. The patient was discharged home with instructions to escalate thyroid hormone replacement over 8 weeks. While the etiology of CK elevation in severe hypothyroidism is poorly understood, it is hypothesized that T4 deficiency alters mitochondrial oxidative capacity and glycogenolysis precipitating muscle atrophy and breakdown with CK release. This case highlights that clinicians should consider thyroid function testing in patients with symptoms of muscle pain and unexplained elevations in CK.

## Linked entities

- **Chemicals:** creatinine (PubChem CID 588), levothyroxine (PubChem CID 5819)
- **Diseases:** hypothyroidism (MONDO:0005420), rhabdomyolysis (MONDO:0005290), acute kidney injury (MONDO:0002492)

## Full-text entities

- **Genes:** TG (thyroglobulin) [NCBI Gene 7038] {aka AITD3, TGN}, TPO (thyroid peroxidase) [NCBI Gene 7173] {aka MSA, TDH2A, TPX}
- **Diseases:** muscle pain (MESH:D063806), muscle atrophy (MESH:D009133), Rhabdomyolysis (MESH:D012206), autoimmune hypothyroidism (MESH:C562768), constipation (MESH:D003248), Hypothyroidism (MESH:D007037), fatigue (MESH:D005221), T4 deficiency (MESH:D005067), acute kidney injury (MESH:D058186), cold intolerance (MESH:D000067390), muscle cramping (MESH:D009120)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC11288370/full.md

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Source: https://tomesphere.com/paper/PMC11288370