Digestive Diseases and Sciences, Vol. 29, No. 5 (May 1984), p. 479 LETTER TO THE EDITOR SERUM TRYPSINOGEN To The Editor: The Steinberg letter raises a relevant point as to the potential use of serum trypsinogen assay in differentiating pancreatic from nonpancreatic causes of steatorrhea in patients with signs and symptoms of malabsorption/maldigestion. Indeed, a formal study of the above problem is lacking at the moment, but preliminary results are available from the limited amount of data so far published (1-3). From these reports and from our experience, it appears that all patients with nonpancreatic steator- rhea have normal levels of trypsinogen with a specificity rate of 100%. However, the sensitivity of the assay varied from 100% (1, 3) to 36% (2). We have already reported in cases of pancreatic stea- torrhea the finding of normal trypsinogen values in the sera of 4 of 24 chronic pancreatitis patients (4) and in 18 of 33 cystic fibrosis children (5). Our suggestion was that while low serum trypsinogen levels were limited to pancreatic steatorrhea, the reverse did not hold true since normal values were detected in patients with abnormal fecal fat loss secondary to pancreatic insufficiency. The underlying assumption of these findings is the hypothesis that serum trypsinogen levels do reflect the functioning mass of pancreatic acinar cells. The claim seems to be strongly supported by data reporting a clear relation between the amount of trypsinogen into the blood and duodenal output of pancreatic trypsin secretion (6, 7). Our explana- tion for why patients with pancreatic steatorrhea present normal values of serum trypsinogen is that other factors, ie, rebound of pancreatic enzymes into the circulation, apart from reduction of func- tioning acinar cell mass may influence the amount of serum trypsinogen (4, 6). An interesting observation has been made by Adrian et al (1): they have reported that of 17 patients with chronic pancreatitis without overt exocrine dysfunction three had low trypsinogen concentrations in their sera; all three subjects de- veloped clinical evidence of steatorrhea in the 18 months since the study. The authors indicate that the finding of a low serum trypsin concentration might predate the onset of steatorrhea in these patients. The data should be pursued in a larger series of such patients to establish this point in clinical practice. We have found that serial serum trypsinogen measurement is a useful way to assess the progressive involvement of the pancreas in children with cystic fibrosis (5). ANGELO ANDRIULLI, MD GUYA MASOERO, MD Ospedale Mauriziano Torino, Italy REFERENCES 1. Adrian TE, Besterman HS, Mallinson CN, Pera A, Redshaw MR, Wood TP, Bloom SR: Plasma trypsin in chronic pancre- atitis and pancreatic adenocarcinoma. Clin Chim Acta 97:205-212, 1979 2. RuddeU WSJ, Mitchell CJ, Hamilton J, Leek JP, Kelleher J: Clinical value of serum immunoreactive trypsin concentra- tion. Br Med J 283:1429-1432, 1981 3. Jacobson D, Curington C, Toskes P, Connery K: Sensitivity and specificity of decreased serum trypsin-like immunoreac- tivity as a test of pancreatic exocrine insufficiency. Clin Res 30:284A, 1982 4. Andriulli A, Masoero G, Felder M, Vantini I, Petrillo M, Cavallini G, Bianchi Porro G, Dobrilla G, Verme G: Circulat- ing trypsin-like immunoreactivity in chronic pancreatitis. Dig Dis Sci 26:532-537, 1981 5. Masoero G, Andriulli A, Santini B, Benitti V, Ansaldi N, Verme G: Serum trypin-like immunoreactivity in cystic fibro- sis: An aid in assessing the progressive involvement of the pancreas. Am J Dis Child 1983 (in press) 6. AndriulliA, Masoero G, Benitti V, Amato A, Piantino P, Gaia E: Relation between serum cathodic trypsinogen levels and exocrine pancreatic function. J Clin Gastroenterol (submit- ted) 7. Koop H, Lankisch PG, St6ckmann F, Arnold R: Trypsin radioimmunoassay in the diagnosis of chronic pancreatitis, Digestion 20:151-156, 1980 Digestive Diseases and Sciences, Vol. 29, No. 5 (may 1984) 479 0163-2116/84/0500-0479503.50/0 9 1984 PlenumPublishing Corporation