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J Thorac Cardiovasc Surg 2004;127:1855-1856
© 2004 The American Association for Thoracic Surgery
Letter to the editor |
Department of Thoracic Surgery, Catholic University Leuven, UZ Gasthuisberg, Herestraat 49, 3000 Leuven, Belgium
To the Editor:
We thank Dr DeMeester1 for his valuable comments on our article "Extracapsular Lymph Node Involvement Is a Negative Prognostic Factor in T3 Adenocarcinoma of the Distal Esophagus and Gastroesophageal Junction."2 We fully agree with Dr DeMeester1 that the number and characteristics of lymph nodes are very important determinants of survival in esophageal cancer, and we endorse his plea for taking the number of involved nodes into account in the TNM staging system of esophageal cancer.
In his editorial,1 Dr DeMeester made some points that we would like to clarify. With regard to the survival in patients without nodal involvement versus patients with intracapsular nodal involvement, there was no significant difference in survival. This does not, however, mean that they had the same survival. Applying a Cox regression on these patients, we had a P value of .435 and a hazard ratio of 1.271 (95% confidence interval 0.696-2.322), which means that patients with intracapsular involved lymph nodes have a 27% higher risk of dying than did those with pN0 disease. This hazard ratio is not extreme relative to the hazard ratio of 3.37 in patients with lymph node involvement. There were sufficient patients at risk in each time interval: 33, 29, 24, 16, 15, and 12 for the pN0 group and 60, 53, 36, 25, 17, and 14 for the intracapsular group at 0, 1, 2, 3, 4, and 5 years, respectively.
The difference we found regarding the mean and median number of involved lymph nodes (3.68 and 3.0 for intracapsular vs 7.96 and 6.0 for extracapsular) was mainly caused by some extreme values in the extracapsular group, which could indicate that extracapsular involvement points to more advanced disease. However, we checked the interaction between lymph node status and number of involved lymph nodes by analysis of variance and ruled out significant interaction between these variables, so both can be considered as independent effects.
As to the subgroup of patients with exactly one intracapsular versus one extracapsular involved lymph node, we agree that a type II error is possible because of the small group. The reason we included this graph was merely to demonstrate the effect of intracapsular versus extracapsular involvement after having neutralized the effect of number of positive lymph nodes. Because of the small number of patients, we couldn't conclude that patients with one intracapsular lymph node have a better survival than patients with no involved lymph nodes. This graph merely shows the detrimental effect of extracapsular involvement on survival.
Again, we would like to highlight the importance of extracapsular involvement, which seems far greater than the effect of number of involved lymph nodes. As our model indicates, the effect of extracapsular involvement (237%) is much greater than the cumulative effect of, for example, 12 positive nodes (12 x 8.6% = 103.2%). For this reason we believe that in addition to the number of involved lymph nodes, lymph node status (intracapsular vs extracapsular) should be routinely incorporated in every pathology report. If our results are confirmed by other centers, then perhaps extracapsular involvement should be incorporated in the TNM staging system as well, unless indeed biologic and molecular biological markers, the Holy Grail of prognostic indicators, are able to replace the actual routine staging.
In conclusion, if you see one, ask your pathologist to look at the capsula.
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