We report the presence of a patent ductus venosus in three brothers who und
erwent surgical correction. Patent ductus venosus was demonstrated by ultra
sonography. Portosystemic venous shunt ratios as evaluated by [I-123]iodoam
phetamine per rectal portal scintigraphy were 67%, 50%, and 77%, respective
ly. Histologic examination of liver biopsy specimens revealed fatty degener
ation in all cases. Portal vein pressure before and after temporarily occlu
ding the patent ductus venosus was estimated by an Anthron P-U catheter int
roduced into the portal vein via the ligament teres hepatis. Portal venous
pressure increased from 10 to 17 cm H2O, 16 to 23 cm H2O, and 14 to 27 cm H
2O, respectively. Therefore, banding of the ductus venosus with Teflon tape
was attempted to prevent portal hypertension following complete ligation.
As a result, portal venous pressures after stricture of the ductus venosus
were 12, 21, and 20 cm H-2), respectively. Bile acid and liver enzymes decr
eased and returned to normal within 14 days after surgery. Interestingly, s
erum concentrations of hepatocyte growth factor (HGF) increased significant
ly after restoration of the portal blood flow and then gradually decreased,
but remained persistently elevated for at feast two weeks in two cases mea
sured after surgical correction. One month after correction, liver function
returned to normal as assessed by serological and histological parameters
in all cases. These results suggest that it is important to determine wheth
er stricture or complete ligation is indicated for a patent ductus venosus
during surgical correction, based on the portal venous pressure after tempo
ral test occlusion of the duct. In addition, HGF may be a useful marker for
normalization of hepatic microcirculation after surgery.