Citation
M. Nakamuta et al., HIGH PLASMA-CONCENTRATION OF MYELOPEROXIDASE IN CIRRHOSIS - A POSSIBLE MARKER OF HYPERSPLENISM, Hepatology, 18(6), 1993, pp. 1377-1383
Abstract
Plasma myeloperoxidase levels in patients with cirrhosis were compared
with those in patients with chronic hepatitis and healthy controls by
means of a specific radioimmunoassay for myeloperoxidase. The mean co
ncentration of plasma myeloperoxidase in cirrhotic patients (309.1 +/-
17.2 ng/ml, n = 41) was markedly higher than that in chronic hepatiti
s patients (222.6 +/- 17.2 ng/ml, n = 21) (p < 0.01) and normal contro
ls (219.5 +/- 5.7 ng/ml, n = 50) (p < 0.01). Plasma myeloperoxidase sh
owed good negative correlations with neutrocyte count (r = -0.32, p <
0.01), thrombocyte count (r = - 0.40, p < 0.01), red blood cell count
(r = - 0.32, p < 0.01), serum albumin (r = - 0.35, p < 0.01), and chol
inesterase (r = - 0.32, p < 0.02) and positive correlations with serum
alkaline phosphatase (r = 0.49; p < 0.01) and lactate dehydrogenase (
r = 0.31, p < 0.01) in patients with cirrhosis or chronic hepatitis. A
mong lactate dehydrogenase isozymes, a good positive correlation was s
een between plasma myeloperoxidase and lactate dehydrogenase-2 (r = 0.
40, p < 0.01) and lactate dehydrogenase-1 (r = 0.03, p < 0.02). Plasma
myeloperoxidase was significantly higher in the cirrhotic and chronic
hepatitis patients with splenomegaly (34 1.1 +/- 19.4 ng/ml, n = 31)
than in those without splenomegaly (217.4 +/- 12.2 ng/ml, n = 29) (p <
0.01). We also examined the difference between plasma levels of myelo
peroxidase in the portal and peripheral blood. In the patients with no
nhepatic disease, we found a significant, portalsystemic difference (p
ortal myeloperoxidase, 221.5 +/- 19.7 ng/ml; vs. systemic myeloperoxid
ase, 179.1 +/- 10.8 ng/ml; n = 15) (p < 0.01), whereas there was no su
ch difference in the cirrhotic patients (portal myeloperoxidase, 281.5
+/- 15.2 ng/ml vs. systemic myeloperoxidase, 268.0 +/- 28.2 ng/ml; n
= 7). A significantly high concentration of plasma myeloperoxidase was
evident in the case of esophageal varices, which is a sign of portals
ystemic shunting in human beings. The results of our study imply that
the release of myeloperoxidase from destroyed neutrocytes, in addition
to its decreased hepatic clearance, are responsible for the high conc
entrations of plasma myeloperoxidase in cirrhotic patients. Therefore
measurement of plasma myeloperoxidase may be useful in assessing hyper
splenic function in liver disease.