Serum dipeptidyl peptidase IV (DPP IV, CD26) activity in chronic hepatitisC

Background: DFP IV is a cell surface ectoenzyme widely distributed in the h uman body. It has been implicated in T-cell activation, hepatocyte-extracel lular-matrix interactions and fibroblast proliferation. Furthermore, upregu lated CD26 expression has been found on the surface of human hepatoma cells transfected with hepatitis C virus (HCV) c-DNA. We examined the serum DPP IV activity in a large number of patients with chronic HCV infection in a c ross:sectional study. We also investigated whether the activity differs fro m that in controls and depends upon the response to interferon (IFN) therap y. Methods: Serum DPP IV activity was measured by microplate-based (Multisk an-Plus-MKII, Labsystem) kinetic assay in 144 patients with chronic HCV inf ection. Seventy-four out of 144 patients (46 nonresponders, 28 responders) were formerly treated with interferon. Sixty healthy blood donors served as controls. Gly-Pro-PNA (Bachem, Torrance, USA) was used as substrate. Resul ts are expressed in nmol/ml/min (U/I). Shapiro-Wilk's test, Mann-Whitney U test and Spearman rank order correlation were used for statistical analysis . Results: Serum DPP IV activity was significantly higher (mean = 20.89 [s 9.6]) in patients with chronic HCV infection than in healthy controls (12.3 9 [2.76, P < 10(-5)]). The enzyme activities significantly differed in naiv e HCV-positive patients (22.2 [9.89, P < 10(-5)]) and nonresponders (23.28 [9.57, P < 10(-5)]) from that in the healthy controls and also from that in responders (13.69 [4.21]). Correlation was found between DPP IV activity a nd AST (r = 0.44, P < 10(-5)), ALT (r = 0.44, P < 10(-5)), GGT (r = 0.41, P < 10(-5)) levels. Conclusion: Serum DPP IV activity seems to be an indicat or of HCV induced liver injury. The activity may reflect the efficacy of in terferon therapy.