280 PRESI ~0 PRES2 P~ITIGEFIS ~ONG HBsAp CARRIERS: RELATION WITH VIRAL REPLI~TION ~D REACTIVATION IN #fTI-HBe PATIENTS. _H2,lbarra, l,Hora, J,Bartolml~, F.La Banda, JC,Porres, C.Hero~dez-Guio, V.Cirreno. Department of Gastroenterology, FundaciGn Jim~nez D;az. Madrid. GRAIN,

The pre-S region of the HBU genome codes the expression of two antigens different from the HBs~g: preSl (P39/GP42) and preS2 (GP33/GP36). The aim of the study was to analyze the presence of those antigens in the serum of HBV chronic carriers, in relation with the viral replication level.

Thirty-two HO~g positive patients histologically diagnosed were included, and as control group 30 healthy subjects with normal l iver function tests and negative to all HBV markers, In addition 16 anti-HBe positive patients followed during 21.6~13,5 months a who sutfered a viral reactivation (increase of OPT and reappearance of HG'V-[/~el), were also included.

PreS[ and preS2 antigens were detected by R]A using polystyrene beads coated with anti-preSl or anti-preS2 (Dr. W. Gerlich, GGttingen) and zzaI-anti-HDs as tracer.

All the controls were negative for preS] and preS2. Presence of both viral antigens was detected in 24 (7~/,,) out of the 32 patients included. The other 8 patients who resulted negative were anti-HBe positive, asymptomatic carriers.

We found a good relation between preSI, preS2 and H~ replication, since the level of these antigens was significantly higher in HBeAg, HBV-OIt~ positive patients than in the rest (p(O.05) (Table).

preSl (S/N) preS2 (S,'N)

GROUP 1 (HBeAg +/HB'J-Oh~ ÷) 151.1 ~ 84.1 ° 62.9 ± 34.8" ] GROUP II (HBeAg ÷/HBV-OI~ -) 127.2 ~ 79.6 ~ 39.9 ± 26.2 b

I GROUP 111 (Anti-HBe +/ abnormal OPT) 66.6 ± 54.4 26.7 ± 19.9 °: p(O.OO5 GROUP IV (Anti-HBe +/ normal OPT) 0.8 ± 0.4 1,3 ± 0.4 b: p(O.05

~ong anti-HBe + patients suffering a reactivation a significant increase of preSl and preS2 leve]swas observed concurring with GPT exacerbation and HGV-DIt~ poslt lvl ty. After reactivation, the level of preS antigens returned to the basal values.

]n conclusion the detection of preSl and preS2 antigens in serum, is more frequent in those patientswhlt high viral replication. Furthermore. among anti-HOe carriers with a viral reactivation, synthesis of preS antigens takes place again.

281 THE EFFECT OF VASOPRESSIN ON INDOCYANINE GREEN ELIMINATION IN

PATIENTS WITH CIRRHOSIS

S. ISLAM, F. BALLET, Y. CHRETIEN, R. POUPON. S e r v i c e d ' h ~ p a t o l o g i e ,

HGpital Saint-Antoine 75571 Paris Cedex 12 - France -

Vasopressin (Vp) has both hemodynamic and metabolic effects on the liver. We have previously shown that intravenous administration of Vp to cirrhotics reduces the intrinsic hepatic clearance (Vmax/km) of Indocyanine green (ICG). This may be either due to reduction of Vmax by a direct metabolic effect of Vp on the exposed hepato- cytes or to the increase of apparent km by decreasing the fraction o£ hepatic blood flow wich perfuses the functional areas of the liver. In order to elucidate the mechanism for the reduction of clearance Vmax/km of ICG by Vp we studied in 10 cirrhotic patients its effect on first order hepatic clearance and Vmax, a flow independent parameter. Under Vp clearance of ICG was reduced from 4.07 ~ O.67 to 3-09- 0.53 ml/min/kg body weight (P< O.02), Vmax was not modified significantly

+ + .

(42.23- 2/70 vs 40.67- 2.71 pg/mxn/kg body weight), calculated Kmwas zncreased ÷ + /

from 9-59- 0.96 to 12.03- 1.17 pg/ml and the clearance Vmax/km was reduced from + + . .

4.95- O.72 to 3.82- O.59 ml/mzn/kg body wezght (P< 0.02). These data suggest that the reduction of the clearance Vmax/km of ICG by Vp is not due to a direct metabolic effect on the hepatocytes but probably results from a decrease of the functional hepatic blood flow.

S146