This Article  • Full text  • PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citing articles on ISI (1)  • Contact me when this article is cited  Related Content  • Related articles  • Similar articles in JAMA

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

To the Editor: Dr Simon and colleagues report that the hereditary pancreatitis–associated cationic trypsinogen (PRSS1) gene mutation, R122H, was present in 5 (10%) of 50 patients with idiopathic pancreatitis.¹ We have a number of concerns about this report.

First, they did not reference 3 closely related studies.^2-4 In particular, 1 study evaluated the known hereditary pancreatitis–associated PRSS1 gene mutations in a large cohort of patients with idiopathic pancreatitis.³

Second, their detection rate of 10% of the R122H mutation in patients with idiopathic pancreatitis is in sharp contrast with rates of less than 1% reported in other studies.^2-5 While a selection bias may account for this significant difference, a founder effect may also be taken into consideration. Nevertheless, most of the current data demonstrate that hereditary pancreatitis–associated PRSS1 mutations are detectable but clearly rare in idiopathic pancreatitis.

Third, the authors suggest that hereditary pancreatitis may be more common than . . . [Full Text of this Article]

RELATED ARTICLES

Idiopathic vs Hereditary Pancreatitis
Volker Keim and Niels Teich
JAMA. 2003;289(8):983-984.
EXTRACT | FULL TEXT  

Idiopathic vs Hereditary Pancreatitis
F. Ulrich Weiss, Peter Simon, Carsten Hohoff, Klaus Peter Zimmer, Wolfram Domschke, and Markus M. Lerch
JAMA. 2003;289(8):985.
EXTRACT | FULL TEXT