ArticlePloS one2021
Investigating myotoxicity following Australian red-bellied black snake (Pseudechis porphyriacus) envenomation.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Delayed Serum Creatine Kinase Elevation After Snakebite: Serial Changes and Clinical Correlates of Myotoxicity in a Korean Tertiary-Care Cohort.Journal of clinical medicine · 2026Article
- Delayed onset of myotoxicity following red-bellied black snake envenoming: a case report.Journal of medical case reports · 2026Article
- Doxycycline-Mediated Inhibition of Snake Venom Phospholipase and Metalloproteinase.Military medicine · 2024Article
- Dermonecrosis caused by a spitting cobra snakebite results from toxin potentiation and is prevented by the repurposed drug varespladib.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A review of 91 canine and feline red-bellied black snake (Pseudechis porphyriacus) envenomation cases and lessons for improved management.Australian veterinary journal · 2022Review
- Challenges faced when modeling clinical toxicology and toxinology events.CPT: pharmacometrics & systems pharmacology · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyotoxicity is one of the common clinical manifestations of red-bellied black snake (Pseudechis porphyriacus) envenomation characterised by elevated creatine kinase (CK) concentrations of greater than 1000 U/L. This study aimed to investigate the occurrence of myotoxicity in patients following envenomation. METHODS/PRINCIPAL
findingsPatient characteristics and serial blood samples (timed venom concentrations and CK concentrations, pre- and post- antivenom) from 114 patients (median age 41, 2-90y; 80 male) were extracted from the Australian Snakebite Project database. Patients were categorised into three groups based on peak CK concentrations [no myotoxicity (<1000 U/L), mild (1000-10,000 U/L) and severe (>10,000 U/L)]. The odds of (mild or severe) myotoxicity was lower in patients that received early antivenom (within 6 hours post-bite) compared to those that received late or no antivenom (odd ratio was 0.186; 95% confidence interval, 0.052-0.664). A population pharmacokinetic-pharmacodynamic (PKPD) model was developed to describe the relationship between the time course of venom (a mixture of toxins) and effect (elevated CK). In addition, a kinetic-pharmacodynamic (KPD) model was developed to describe the relationship between time course of a theoretical toxin and effect. Model development and parameter estimation was performed using NONMEM v7.3. No single set of parameter values from either the PKPD or KPD models were found that could accurately describe the time course of different levels of severity of myotoxicity. The predicted theoretical toxin half-life from the KPD model was 11 ± 3.9 hours compared to the half-life of venom of 5.3 ± 0.36 hours. This indicates that the putative causative toxin's concentration-time profile does not parallel that of venom.
conclusionEarly antivenom administration reduces the incidence of myotoxicity. The venom concentration profile does not appear to be the driver for myotoxicity following envenomation. Additional factors that affect the sensitivity of the patient to snake venom/toxins must be explored to understand the relationship with myotoxicity.
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