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Ann Thorac Surg 2006;81:1947-1948
© 2006 The Society of Thoracic Surgeons
Hôpital Européen Georges Pompidou, 20-40 rue Leblanc, Paris, Cedex 15 75908 France
(Email: marc.riquet{at}hop.egn.ap-hop-paris.fr).
We thank Shimizu and colleagues [1] for their comments on our article on skip mediastinal lymph node (LN) metastases (N1-)N2 [2], and we are pleased to see that we both take the same interest in visceral pleural invasion (VPI).
Our observation that VPI was correlated with an important N2 involvement prompted us to support Brewer's hypothesis [3] that the dissemination of tumor cells (TC) throughout the pleural cavity and reabsorbed by parietal subpleural lymphatics was possibly accounting for the lymphatic TC dissemination, with the hypothesis reinforced as Shimizu remembered by an anatomical study. We were also disappointed not to find more (N1-)N2 associated with VPI, which could have added evidence to confirm this mode of spread and be another explanation for (N1-)N2 origin. Nevertheless we discussed this hypothesis as a theoretical explanation with supporting anatomical evidence. Shimizu and colleagues' [4] results also question this hypothesis, but do not conclusively discount it either.
Concerning (N1-)N2 origin, we mentioned Yoshino and colleague's [5] suggestion that the "biological" behavior of TC could be another explanation. Now, this suggestion, which was purely hypothetical at that time, has more support since Shimizu and colleagues' [4] study; tumors with VPI are more likely to be of moderate or poor differentiation, high scar grade, nuclear atypic grade, mitotic index, and serum carcinoembryonic antigen level. These biological criteria indicate a more aggressive nature, which we also consider as an explanation for worsening prognosis. Shimizu and colleagues' tumors with VPI are also associated with more lymphatic, vascular and intrapulmonary, and mediastinal LN invasion. These are histologic criteria of an invasive nature, as VPI itself. The biological aggressiveness of the tumor may explain this locoregional invasiveness, but we cannot agree with Shimizu and colleagues' suggestion that the VPI TC pathway is through hilar and mediastinal LN, because (N1+)N2 are more frequent in the VPI group. The (N1+)N2 involvement reflects more the local invasiveness of aggressive TC than a preferential pathway.
This does not rule out other explanations for (N1-)N2, such as direct lymphatic drainage to distant mediastinal LN, and it does not explain the TC outcome once desquamated within the pleura, with their presence being confirmed by pleural lavage. These TC do not appear to seed over the diaphragm nor invade the juxta-diaphragmatic LN. Do they join the thoracic duct after reabsorption by lymphatics located in the posterior diaphragmatic recess? Such lymphatics are also demonstrated by an anatomical study [6] and could contribute to the highest frequency of systemic metastases we also observed in VPI patients.
Many studies are still needed to explain (N1-)N2 and VPI. Be that as it may, the main conclusion and primary point of our article was that (N1-)N2 has a better prognosis. The VPI that appears due to a more aggressive TC type and that is less frequent in the (N1-)N2 group also supports this conclusion.
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