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Re: Laine and Sugg—Helicobacter pylori eradication on esophagitis and GERD

TO THE EDITOR: We thank Dr. Younes et al. for an interesting discussion of the p53 immunostaining data presented in our paper (1). We agree that it is important to avoid confusion regarding data that refer to an incorporation of a potential biomarker such as p53 immunostaining into clinical practice. Therefore, we appreciate the clarification provided by Dr. Younes et al. regarding the approach to scoring of the p53 immunostaining used in their previous publication. It was our misunderstanding that even areas negative for dysplasia were considered positive when stained for p53, based not only on the statement in their paper that “biopsies that contained p53-positive high grade dysplasia or carcinoma showed positivity in adjacent nondysplastic glands,” which they mentioned in their letter, but also their finding that “p53 accumulation was detected earlier than low grade dysplasia (LGD)/indeterminate in one case” (2). As this was not the case, we acknowledge that the scoring technique was not significantly different from our approach, and apologize for unintentionally misinterpreting their data. The reason for comparing their data to ours in greater detail was an attempt to find explanations for the minor differences observed in the two otherwise fairly similar studies presented by both groups (somewhat greater progression rate of our p53-positive LGD cases compared to theirs). For this reason, the presence versus the lack of the interobserver agreement data was mentioned in the paragraph comparing Dr. Younes’ et al. results to ours. The purpose of this comparison was not to criticize their work but rather to present the immunohistochemistry data in the context of the degree of interobserver agreement on the diagnosis of LGD. We agree that a reliable separation of LGD from changes indefinite for dysplasia is difficult even by GI pathologists. However, when reviewed blindly admixed with biopsy samples showing no dysplasia, indefinite changes, or high grade dysplasia, an agreement of at least two of three GI pathologists on the diagnosis of LGD was present in the majority of the cases (88%) included in our study. The absence of the p53 expression in the LGD areas of resected esophagi observed in the study from our institution published in 1994 (3) was indeed most likely due to a different antibody as well as the use of antigen-unmasking techniques, which were used in the recent study. We hope this response will clarify the points raised in the above letter, and that the results from both of the above studies can now be viewed more clearly as concordant rather than contradictory, as we intended when we wrote this manuscript.