title: Quantitation of minimal residual disease in acute myeloid leukemia by tryptase monitoring identifies a group of patients with a high risk of relapse.
abstract: OBJECTIVE
  Recent data suggest that tryptase is produced by blast cells in a group of patients with acute myeloid leukemia (AML). In these patients, serum tryptase levels are elevated at diagnosis and decrease to normal (<15 ng/mL) or near normal values in those achieving complete hematologic remission (CR) after chemotherapy.
  
  
  METHODS
  In this study, we examined the value of tryptase as a marker of minimal residual AML. In 61 patients with de novo AML exhibiting elevated serum tryptase (>15 ng/mL) at diagnosis, tryptase levels were measured serially during and after chemotherapy by a fluoroenzyme immunoassay.
  
  
  RESULTS
  Of the 61 patients, 42 (68.9%) entered hematologic CR in response to induction chemotherapy. Twenty-nine of these 42 patients also entered biochemical remission (BR) defined by a decrease of tryptase levels to normal (<15 ng/mL). The remaining 13 patients exhibited elevated enzyme levels despite of hematologic CR. As assessed by multivariate analysis, the elevated tryptase in CR was found to be an independent prognostic variable concerning disease-free survival. Thus, AML relapses occurred in 15 of 29 patients with CR + BR (52%) and in 12 of 13 patients with CR without BR (92%), resulting in a significantly reduced probability of continuous CR for patients with CR without BR (P < 0.05). In all patients with continuous hematologic CR, tryptase levels remained constantly normal, whereas a recurrent elevation of tryptase in CR was invariably followed by a hematologic relapse.
  
  
  CONCLUSIONS
  A persistently elevated tryptase level in AML in CR is indicative of minimal residual AML and associated with a high risk of relapse.
authors.affiliation: Department of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Austria. wolfgang.r.sperr@meduniwien.ac.at
authors.forename: Wolfgang R
authors.initials: WR
authors.lastname: Sperr
authors.forename: Margit
authors.initials: M
authors.lastname: Mitterbauer
authors.forename: Gerlinde
authors.initials: G
authors.lastname: Mitterbauer
authors.forename: Michael
authors.initials: M
authors.lastname: Kundi
authors.forename: Ulrich
authors.initials: U
authors.lastname: Jäger
authors.forename: Klaus
authors.initials: K
authors.lastname: Lechner
authors.forename: Peter
authors.initials: P
authors.lastname: Valent
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D006801:Humans; D007951:Leukemia, Myeloid / Q000188:drug therapy / Q000201:enzymology / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000235:genetics; D009364:Neoplasm Recurrence, Local; D018365:Neoplasm, Residual / Q000201:enzymology / Q000235:genetics / Q000473:pathology*; D015514:Oncogene Proteins, Fusion / Q000235:genetics; D011379:Prognosis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012307:Risk Factors; D012697:Serine Endopeptidases / Q000097:blood*; D016019:Survival Analysis; D013997:Time Factors; D053802:Tryptases
chemical_list: C095514:CBFbeta-MYH11 fusion protein; D009363:Neoplasm Proteins; D015514:Oncogene Proteins, Fusion; C093476:promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; D012697:Serine Endopeptidases; D053802:Tryptases