418 CLINICAL SIGNIFICANCE OF DELTA ANTIBODY IN HBsAg+ CHRONIC LIVER DISEASE

E. Vallebona, A. Solinas, G. Faa$ R. Carruxi, G. Sanna, F. Pitzus and

L. Demelia Istituto di Clinica Medica and *Istituto di Anatomia Patologica,

University of Cagliari , Italy

HDV infection has been proved to play an important role in the progression of HBsAg+ CLD.

For this purpose we followed 60 HBsAE+ CLD pts durin E 27 months (ZI8 SD). Twenty-one (35%)

were AntiHD+ (mean age 35 3rcs) and 39 (mean age 43 yrs) AntiHD-. Histological features and

HBeAg/Ab status at presentation are shown below:

No. HBeAb+ HBeAg+ CPH CLH CAH IC AC

AntiHD+ 21 16 2 2 1 15 0 3

AntiHD- 39 30 7 I0 2 19 4 4

After follow-up period, histological pattern and HBeAg/Ab status underwent the following

changes:

No. HBeAb+ HBeA~+ CPH CLH CAH IC AC

AntiHD+ 16 15 i 2 0 12 0 2

AntiHD- 40 35 3 5 I 6 4 2

A clinical and histological remission was observed in four HDAb+ pts and an inprovement in

one (AC-~IC) (24%) with a simultaneous seroconversion from HDAb+ to HDAb-. Nineteen HDAb-pts

(61%) remitted completely. Three HDAb- pts died: one of massive variceal bleedin E and two of

liver failure. Signs of mai'ked activity persisted in 12/15 (80~) HDAb+ CAH pts compared to

6/19 (32%) of HDAb-CAH group. No progression to cirrhosis was observed in either group proba

bly because of short follow-up period. Anyway, we believe that HDV infection may represent a poor prognostic sign in the outcome of CLD.

419 PROGNOSTIC FACTORS FCR ~E COURSE A~'i'Ju.,{. ESCE~=F_AL VARICEAL ~7,~ING: NEW FACTS A~D ~ 1 ' ~ .

H.R. van Buuren, A. ~ , S.J.A.J. Rikken, J. Boot, S.W. Scha/m. Depart- m~%t of Internal Medicine II, University Hospital Dijkzigt, Dr. Mole~terplein 40, 3015 ~ Rmtterdan, The Netherlands.

To find prognostic factors amenable to therapeutic intervention a retrospective study was u~n~vtaken of all patients admitted for esophageal variceal bleeding to our hospital from 1984 till 1986. The follow-up ("time zero") started directly after admission, was at least 6 mc~ths and averaged 22 months. The standard treatment was endoscopic sclezotherapy, initially wBekly till Qbliteration, later 3-6 monthly. Of the 88 patients studied 44% had alcoholic cirrhosis, 49% nc~-alcoholic liver disease and 7% a pre-hepatic cause of portal hypertension. According to Child-Pugh, 28% of patients were in class A, 44% in B and 28% in C. Early (one month) mortality w~s correlated with the Child class (8% for ~ A, 20% for B and 40% for C) and with the severity of the bleeding. Variceal rEbleeding occurred in 46% of the patients. ~he survival after z~bleeding was identical to that after the index bleeding. Late mortality was identical for alcoholic and nun-alcoholic liver disease (beyond one month) but correlated with disease activity. Patients with inactive liver disease (repeatedly normal SGOr during follow-up) all survived, although 40% had a variceal rebleeding and 54% were Child class B or C patients. In contrast 58% of patients with mild activity (SGUf<2 x upper normal limit) and cnly 30% of patients with moderate or severe activity (SGOI~2 x) survi~sd 35 munths (p<0.005). We conclude that early mortality depends on the severity of the bleeding and the remaining functicr~l capacity of the liver (Child class). Despite intensive sclerotherapy varioeal rebleeding occurs in nearly 50% of patients with a prognosis at rebleeding similar to that at the index bleeding. Late mortality is not determined by the etiology but by the persistence of active liver ~isease. After variceal bleeding all efforts should be made to inactivate the liver disease.

$215