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Letter

Response to Letter entitled “Cardiac toxicity following cobra envenomation”

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Page 863 | Received 17 Aug 2012, Accepted 17 Aug 2012, Published online: 12 Sep 2012

To the Editor:

While the idea of autonomic nervous system involvement is interesting, there is a lack of clear data to support such a manifestation clinically. The physiological responses to the circulating venom components are variable and complex. There is no question that Naja spp. venom can affect central nervous system (CNS) autoregulation in experimentally envenomed rats,Citation1 but if and how this occurs in humans is not well established. In the case reported earlier, the monovalent Naja kaouthia antivenom was administered and observed to reverse the bigeminy.Citation2 If the CNS was primarily responsible for the cardiac manifestation, it does not explain how the antivenom, with its generally large multi-complex aggregates, passed the blood–brain barrier and reversed the putative direct effects of venom components causing the arrhythmia. In addition, it is currently unclear how long it would take for venom components to manifest a genetically-induced clinical effect such as theoretical upregulation of transducible S-phase effectors (e.g. during DNA synthesis in cardiac cell populations) or repressor proteins on the cardiac tissue. However, we agree that unsupported speculation or unproven associations require more clinical and laboratory evidence.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

References

  • DiMattio J, Weinstein SA, Streitman J. In vivo effects of snake venoms on passive and facilitated glucose transport across blood-ocular and blood-CSF barriers of the rat. Toxicon 1985; 23:63–71.
  • Ismail AK, Weinstein SA, Auliya M, Appareo P. Ventricular bigeminy following a cobra envenomation. Clin Toxicol (Phila) 2012; 50: 518–521.

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