Myopathy due to epsilon amino-caproic acid
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Published on: July 29, 2016
Abstract:
A subacute necrotizing myopathy developed in a patient treated with epsilon amino-caproic acid (EACA) for subarachnoid hemorrhage. The muscle biopsy showed features suggesting that the muscle fiber necrosis might have been due to capillary damage. An attempt to induce EACA myopathy in the rat was made, but no abnormality developed.
Insights
Epsilon amino-caproic acid (EACA) treatment for subarachnoid hemorrhage caused a patient to develop necrotizing myopathy, potentially due to capillary damage. However, EACA-induced myopathy could not be replicated in rats.
Area of Science:
- Neurology
- Toxicology
- Pathology
Background:
- Subarachnoid hemorrhage necessitates treatment with antifibrinolytic agents like epsilon amino-caproic acid (EACA).
- Muscle damage is a potential, though rarely reported, adverse effect of EACA therapy.
Observation:
- A patient undergoing EACA treatment for subarachnoid hemorrhage presented with subacute necrotizing myopathy.
- Muscle biopsy revealed evidence of muscle fiber necrosis, with pathological features suggestive of capillary damage.
Findings:
- The observed myopathy in the patient was potentially linked to EACA administration.
- Experimental induction of EACA myopathy in rats was unsuccessful, failing to reproduce the observed muscle pathology.
Implications:
- This case highlights a potential iatrogenic cause of myopathy associated with epsilon amino-caproic acid.
- Further research is needed to elucidate the mechanism of EACA-induced myopathy and its relevance in clinical practice.
- The differential diagnosis of myopathy in patients treated with EACA should include drug-induced capillary damage.
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