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In response to the letter of Harlozinska-Szmyrka and Strutynska-Karpinska (Gut 2004;53:469–70) commenting on our study,1 we agree with the remarks made in relation to the difficulties in discriminating between chronic pancreatitis and adenocarcinoma using currently employed diagnostic imaging and tumour marker analysis. Our study was aimed at determining the risk of cancer development in patients with proven chronic pancreatitis,1 examining age and sex standardised incidence ratios calculated from the number of observed cases of pancreatic cancer in our cohort of 373 patients with predominantly alcohol related chronic pancreatitis to the number of cases expected in the National Cancer Registry. Our study design did not take into consideration diagnostic dilemmas and focused purely on cancer risk in our cohort of patients using defined stringent criteria. Indeed, we previously underlined the interest of biological markers in this situation (for example, CA19-9 and circulating K-ras)2,3; however these markers have problems with both sensitivity and specificity.
We acknowledge that given the difficulties in diagnosing cancer in this situation, the establishment of new tumour markers such as tissue polypeptide specific antigen (TPS)4 with proven good sensitivity and specificity should provide for progress in the future. Is has to be stressed however that TPS, a marker of proliferation activity, is not specific to pancreatic cancer, and other digestive and non-digestive cancers as well as benign chronic disorders may have high levels of this marker.5–7 Thus validated data concerning tumour markers, either alone or in combination, in distinguishing pancreatic cancer from chronic pancreatitis should prove important in diagnostic situations.
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