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Transient Creatine Kinase Elevation Followed by Hypocomplementemia in a Case of Rotavirus Myositis
Yuka Rokugo1, Satoru Kumaki1, Ryoichi Onuma1
1Department of Pediatrics, Sendai Medical Center, 2-8-8 Miyagino, Miyagino-ku, Sendai, Miyagi 983-8520, Japan.
Insights
This study investigates rotavirus myositis in an infant, finding that complement activation results from skeletal muscle damage, not the cause. This rare complication offers new insights into viral-induced myopathy.
Area of Science:
- Pediatrics
- Virology
- Immunology
Background:
- Rotavirus infection can lead to rare complications like myositis.
- Previous reports suggested complement activation as a cause of rotavirus myositis.
- Complement levels were not measured at onset in prior cases.
Purpose of the Study:
- To investigate the role of complement in a case of infant rotavirus myositis.
- To clarify the temporal relationship between complement activation and skeletal muscle damage.
Main Methods:
- Case report of an infant with rotavirus myositis.
- Monitoring of serum creatine kinase (CK) and complement levels.
- Analysis of temporal changes in CK and complement levels.
Main Results:
- The infant presented with rotavirus myositis.
- Complement levels remained normal during peak serum creatine kinase (CK) levels.
- Complement levels decreased as CK levels normalized.
Conclusions:
- Complement activation in this case was a consequence, not the cause, of skeletal muscle damage.
- This finding contrasts with previous hypotheses on rotavirus myositis pathogenesis.
- The study provides new evidence on the mechanisms of viral myositis.
Abstract:
We report an infant case of rotavirus myositis, a rare complication of rotavirus infection. Complement levels of the patient were normal when serum creatine kinase (CK) level was at its peak and then decreased when the CK level became normalized. In a previous case report of rotavirus myositis, transient decrease of serum albumin, immunoglobulin, and complement levels was reported. The authors speculated that intravascular complement activation was caused by rotavirus and resulted in the pathogenesis of myositis, although complement levels at onset were not measured by the authors. In this report, however, we demonstrate that the complement activation of our patient is a result of, rather than the cause of, skeletal muscle damage.
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