Hocaoglu C. Clozapine-induced rabbit syndrome: a case report


Comment to: Significant endothelin release in patients treated with
foam sclerotherapy by Frullini A, Barsotti MC, Santoni T, Duranti E, Burchielli S, Di Stefano R. Dermatol Surg 2012;38:741–7.

Francesco Ferrara

Napoli Monaldi Hospital Cardiovascular Surgery, Italy



E-mail: frferr@tiscali.it

  



	Abstract

      A greater incidence of cough, transient visual and neurological disturbances have been reported with foam rather than with liquid sclerosant. These complications have often been associated with migraine and patent foramen ovale (PFO), a common condition affecting approximately 25% of the whole adult population.
Foam bubbles may pass through a PFO to the left heart chambers, with consequent paradoxical systemic embolization.
Visual and neurological disturbances have often been reported also with liquid sclerosants which conflicts with the bubble theory. In a recent study, the same Authors1 demonstrated that POL foam is capable of significantly elevating endothelin 1 (ET-1) in an animal model. It is feasible that the release of ET-1 is a source of neurological and visual disturbances after sclerotherapy.
In the first part of this study, the Authors tested ET-1 release in 11 rats treated with STS 1% (Fibro-vein).
Five were treated with liquid STS and 6 with STS foam. A significant difference was found between ET level at 1 min and at 5 min with foam STS (P



Comment by Francesco Ferrara

Recent studies have shown that the visual and neurological disturbances that can be observed after liquid or foam sclerotherapy are due to the release of two different chemical mediators: histamine and endothelin 1. The increase in both the mediators has the same source: damage to the edothelium membrane. These two theories can live side by side. But a preventive therapy with vasoprotectors cannot be proposed as this treatment contrasts with the action of the sclerosing agents. However, a preventive antihistaminic therapy can be used selectively only versus the mediator of the neurological disturbance.  



Reply by the author (Frullini)  

I thank Francesco Ferrara for her comments but have to disagree. Pharmacological antagonism can be exerted in very different ways and this includes endothelin synthesis inhibition, competitive links with receptors or binding with circulating endothelin. None of these is related to vasoprotection. Only inhibition of ET-1 release from vacuoles could be considered a protective action but I still think that such an approach could be helpful. In fact, when injecting a sclerosant, by definition its action cannot be limited to the target vessel. It could be interesting to develop the concept of how to protect the veins that we do not want to sclerose.





References

1. Frullini A, Felice F, Burchielli S, Di Stefano R. High production of endothelin after foam sclerotherapy: a new pathogenetic hypothesis for neurological and visual disturbances after sclerotherapy. Phlebology 2011;26:203-8.[CrossRef][PubMed]

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