The mechanism of fibrogenesis in the pancreas is not well known. We analyze
d the role of prolylhydroxylase and collagenase activities in the developme
nt of fibrosis in chronic alcoholic pancreatitis (CAP). Nineteen patients w
ith CAP and 11 controls (organ donors) with normal pancreatic histology wer
e included in the study. Pancreatic tissue was obtained from all subjects t
o measure (a) area of fibrosis (histomorphometric method); (b) prolylhydrox
ylase activity (PHase), which reflects the intracellular synthesis of colla
gen (Hutton's method); and (c) collagenase activity, which reflects the deg
radation of collagen (collagenase assay system, H-3). The percentage of the
fibrosis area in relation to the total area of pancreatic tissue was signi
ficantly higher in CAP than in the control group (70.6 +/- 20.2% vs. 4.6 +/
- 1.8%; p < 0.001). Mean pancreatic PHase activity was also significantly h
igher in CAP than in the control group (775 +/- 258 cpm/mg protein/h vs. 40
5 +/- 151 cpm/mg protein/h; p < 0.001), The collagenase activity was signif
icantly lower in CAP than in the control group (8.7 +/- 3.5 cpm/cpm added/m
g protein vs. 18.0 +/- 3.9 cpm/cpm added/mg protein; p < 0.001). A signific
ant correlation was observed between percentage fibrosis evaluated histomor
phometrically and PHase activity in all patients (r = 0.72; p < 0.001), and
between PHase and collagenase activities in controls (r = 0.70; p = 0.024)
, but not in CAP. Pancreatic tissue in CAP has an increased fibrogenic acti
vity and an impaired collagen-degradation capacity. These findings might ex
plain the excessive development of fibrosis in CAP.