0270-9139/83/0306-l013$02.

00/0
HEPATOLOGY Vol. 3, No. 6, pp. 1013-1015, 1983
Copyright 0 1983 by the American Association for the Study of Liver Diseases Printed in U.S.A.

Exudative Ascites in the Course of Acute

Type B Hepatitis
CARMEN VIOLA, LYDIAVIRETA, JAIMEBOSCH,
AND JUANRODES

Liver Unit, Hospital Clinico y Provincial, University of Barcelona, Barcelona-36, Spain

Two patients who presented with an exudative ascites in the course of typical acute type B
hepatitis are reported. In one of them, ascites was associated with an exudative pleural effusion.
In both patients, the clinical course of the hepatitis was uneventful, and ascites and pleural effusion
disappeared spontaneously. Portal hypertension and common causes of exudative ascites were
excluded. It is suggested that the development of exudative ascites in these patients represent a
hitherto unrecognized manifestation of the hepatitis itself.

Hepatitis B virus infection may produce a variety of
extrahepatic manifestations most usually involving the
skin, joints, small arteries, arterioles, and renal glomeruli
(1). The mechanism of these manifestations could be
mediated by circulating immune complexes containing
HBsAg, which can produce a localized or widespread
vasculitis, as defined by histopathological, ultrastruc-
tural, and immunofluorescent studies (1-3).
In recent years, several cases of pleural effusion asso-
ciated with acute viral hepatitis have been reported in
which the effusion was attributed to the hepatitis itself
(4-8, Cocchi, P. and Silenzi, M., J. Pediatr. 1976; 89:329-
330, Correspondence). We report here two cases of exu-
dative ascites, one of them with a concomitant pleural
effusion, appearing in the course of acute type B hepa-
titis, a hitherto unrecognized association.
CASE REPORTS
CASE1
A 48-year-old man was admitted to the hospital be-
cause of icterus and ascites. The patient had been well
until 3 weeks before admission when he developed poly-
arthralgias and an urticariform skin rash for 3 days. One
week later, he noted weakness, anorexia, and fever of
37.5"C, followed 5 days later by dark urine, clay-colored
stools, jaundice, and progressive abdominal distention.
He had no relevant past history except for pulmonary
tuberculosis at the age of 20. He was taking no drugs.
Physical examination revealed a febrile (375°C)
deeply jaundiced patient. The abdomen was distended
with obvious ascites. The liver was palpable 10 cm below
the right costal margin, and was tender. The spleen was
Received January 5, 1983; accepted May 9,1983.
Address reprint requests to: Jaime Bosch, M.D., Liver Unit, Hospital
Clinico y Provincial, Casanova, 143,Barcelona-36, Spain.
1013
not palpable, nor was lymphadenopathy noted. Cardio-
vascular, respiratory, and neurological examinations
were within normal limits. Laboratory data on admission
revealed SGOT (1,947 IU per liter), SGPT (3,000 IU per
liter), serum bilirubin (20 mg per dl), alkaline phospha-
tase (267 IU per liter), and prothrombin (68% of control
and 90% following intramuscular vitamin K). Serum
total protein was 6.8 gm per dl and albumin 3.1 gm per
dl. HBsAg was positive by radioimmunoassay. Blood
glucose, hemogram, and renal function were normal.
Paracentesis on admission revealed that the ascites had
a high protein content (refractometry). The biological
characteristics of the ascitic fluid are shown in Table 1.
Gram and Ziehl-Neelsen stains of the ascitic fluid were
negative for bacterial organisms. Cultures for bacteria
and acid-fast bacilli were negative. Cytology revealed
lymphocytes and reactive mesothelial cells without ma-
lignancies. Chest X-ray was normal, and PPD was neg-
ative.
Five days after admission, peritoneoscopy revealed a
normal peritoneum without evidence of portal hyperten-
sion and an uniformly enlarged liver with a regular,
smooth surface. Liver biopsy showed the typical histo-
logical pattern of acute viral hepatitis. Immunological
study 1 week after admission revealed immunoglobulins
in the upper normal limits: IgA, 543 mg per dl (normal
80 to 500); IgG, 1, 430 mg per dl (normal 600 to 1,500);
IgM, 168 mg per dl (normal 50 to 125); and normal
complement levels: C3, 82 mg per dl; Cq, 32 mg per dl;
CH50,560 microunits; and increased circulating immune
complexes (microconsumption test). Antinuclear,
smooth-muscle, and mitochondria1 antibodies were neg-
ative.
There was a gradual clinical improvement, with spon-
taneous resolution of the ascites within 1week of admis-
sion. Liver size decreased, and liver function tests re-
turned toward normal. The patient was discharged 20

1014 VIOLA ET AL.
TABLE FINDINGS
1. LABORATORY
Case 1 Case 2
Ascites Ascites ':s1
Total protein (gm per dl) 3.5 3.5 4.3
Sugar (mg per dl) 155 100 105
White blood cells (per mm3) 2,560 950 1,440
Polymorphonuclear leucocytes 51 48 0
(mm3)
Lymphocytes (per mm3) 2,529 902 1,440
Red blood cells (per mm3) 2,180 1,300 1,405
days after admission. On a follow-up visit 2 months later,
the patient was asymptomatic. His liver was palpable 2
cm below the right costal margin, but was not tender.
Liver tests were normal, HBsAg was negative and anti-
HBsAg positive by radioimmunoassay.
CASE2
A 21-year-old man was admitted to the hospital be-
cause of jaundice, abdominal distention, and dyspnea.
Fifteen days before admission, he developed a fever of
38"C, fatigability, anorexia, nausea, and vomiting. Two
days later, he noted dark urine, clay-colored stools, and
icterus. Ten days before admission, he developed pro-
gressive dyspnea and abdominal distention. Previous
medical history was irrelevant, and there was no drug
consumption.
On examination he was febrile (37.5"C), slightly dys-
pneic at rest, and deeply jaundiced. He had overt signs
of a large right pleural effusion, which were confirmed
radiologically. The abdomen was distended with ascites,
and hepatosplenomegaly was present 2 cm below the
right and left costal margins, respectively. Liver function
tests on admission revealed SGOT of 557 IU per liter,
SGPT of 1,114 IU per liter, and serum bilirubin of 25.2
mg per dl. HBsAg was positive by radioimmunoassay.
Serum total protein was 6.1 gm per dl and albumin 3.1
gm per dl. Prothrombin time, alkaline phosphate, he-
mogram, blood glucose, and renal function were within
normal limits. Antinuclear, smooth muscle, and mito-
chondrial antibodies were negative. PPD was negative.
Aspirations of the pleural and ascitic fluids were per-
formed on admission. Their biological characteristics are
summarized in Table 1. Gram stain, Ziehl-Nelsen stain,
and cultures for bacteria and acid-fast bacilli were neg-
ative. Cytology revealed lymphocytes and reactive me-
sothelial cells without evidence of malignancy. Perito-
neoscopy performed 6 days after admission revealed a
normal peritoneum, no signs of portal hypertension, and
a slightly enlarged, normal-appearing liver. Liver biopsy
showed a morphological pattern of acute viral hepatitis.
He improved gradually after admission and by the
tenth day ascites was no longer detectable. Liver function
tests were normal. Radiologic review of the chest showed
slow clearing which was complete 30 days after admis-
sion. Follow-up visits 2, 6, and 24 months later revealed
normal chest X-rays, liver blood tests, and HBsAg was
now negative by radioimmunoassay.
15273350, 1983, 6, Downloaded from https://aasldpubs.onlinelibrary.wiley.com/doi/10.1002/hep.1840030620 by Nat Prov Indonesia, Wiley Online Library on [26/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
HEPATOLOGY
DISCUSSION
We have described two patients with typical acute
viral hepatitis B, and the unusual presentation of an
exudative ascites (total protein above 2.5 gm per dl).
Initially, the ascites in the first patient, and the ascites
plus pleural effusion in the second were thought to rep-
resent other processes unrelated to the hepatitis. The
most likely etiology of exudative serous effusions with a
predominance of lymphocytes in Spain is tuberculosis.
This diagnosis was strongly suspected in the first case
because of his past history of tuberculosis. No evidence
of tuberculosis was found, however, to support this di-
agnosis. Ascitic and pleural fluid specimens were nega-
tive on smear and culture. No pulmonary parenchymal
lesions were evident on chest X-ray, and PPD was neg-
ative. Peritoneoscopy showed no lesions suggestive of
peritoneal tuberculosis, and the effusions resolved spon-
taneously as the hepatitis resolved. Other causes of ex-
udative ascites such as myxedema, heart failure, and
disseminated lupus were excluded by clinical and labo-
ratory data.
Another possibility to explain the presence of ascites
in our patients is that the hepatitis caused severe liver
damage which resulted in significant portal hyperten-
sion. This possibility however, seems to be highly un-
likely since peritoneoscopy disclosed no signs of portal
hypertension. Unfortunately, no direct measurements of
portal pressure were made. The fact that the ascites
appeared to be an exudate is also against this etiology.
In a retrospective survey of 45 patients admitted to our
unit for acute viral hepatitis during the past 10 years, 15
had ascites in the acute phase of the disease. In marked
contrast with the two patients who are the subject of the
present report, in these 15 patients the ascites was a
transudate (total protein C2.5 gm per dl) without an
increased number of leukocytes ( e l 0 0 per mm3),and the
hepatitis caused severe hepatic failure. Liver biopsy in
these patients when obtained showed severe necrosis and
marked distortion of the architecture of the liver which
may have induced portal hypertension.
The ascites in our patients was also characterized by
an increased number of lymphocytes (Table 1). In the
cases of pleural effusion associated with acute viral hep-
atitis that have been reported (5-8, Cocchi, P. and Sil-
enzi, M., J. Pediatr. 1976; 89:329-330, Correspondence;
Merrill, W. D. and Farris, J. R. Ann. Int. Med. 1977;
87:120, Correspondence), the effusions were also char-
acterized by having a predominance of lymphocytic leu-
kocytes with a protein concentration equal to or above 3
gm per dl, and spontaneous resolution. The similarities
of the clinical course and the characteristics of the ascitic
and pleural effusions in our patients and in those re-
ported with pleural effusion suggest that the ascites in
our patients represented a hitherto unrecognized extra-
hepatic manifestation of the hepatitis B virus infection.
The fact that one of our patients had both exudative
ascites and pleural effusion supports that view.
The pathogenesis of these exudates is not well known.
The presence of HBsAg in the pleural fluid reported in
two cases (8, Cocchi, P. and Silenzi, M., J . Pediatr. 1976;

Vol. 3, No. 6,1983 EXUDATIVE ASCITES IN ACUTE TYPE B HEPATITIS
89:329-330 Correspondence), and of skin rash, hematu-
ria, and a subnormal C3 level in another ( 5 ) , suggest that
an immunologic mechanism mediated by circulating im-
mune complexes with complement consumption may
have been responsible, as has been described in other
extrahepatic manifestations of acute hepatitis B infec-
tion (9). Immunologic study of our first case revealed
increased circulating immune complexes in the serum
with normal serum complement. The normal comple-
ment level may have been related to the fact that the
study was performed 7 days after admission when the
ascites was resolving.
Our observations suggest that the occurrence of ascites
in the course of acute viral hepatitis is not necessarily a
grave prognostic sign. Exudative ascites, unlike transu-
dative ascites, which is usually the result of severe he-
patoparenchymal necrosis, may be a self-limited, immu-
nopathic sign.
15273350, 1983, 6, Downloaded from https://aasldpubs.onlinelibrary.wiley.com/doi/10.1002/hep.1840030620 by Nat Prov Indonesia, Wiley Online Library on [26/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
1015
REFERENCES
1. Gocke DJ. Extrahepatic manifestations of viral hepatitis. Am J
Med Sci 1975; 27049.
2. Almeida JD, Waterson AP. Immune complexes in hepatitis. Lancet
1970; 2:983-986.
3. Lev0 Y. Extrahepatic manifestations of hepatitis B virus infection.
Israel J Med Sci 1979; 15276-282.
4. Isselbacher KJ, Glickman RM. Abdominal swelling and ascites. In:
Thorn GW, Adams RD, Braumwald E, et al., eds. Harrison’s
principles of internal medicine. New York: McGraw-Hill, 1977:
225.
5. Gross PA, Gerding DN. Pleural effusion associated with viral
hepatitis. Gastroenterology 1971; 60898-902.
6. Owen RL, Shapiro H. Pleural effusion, rash and anergy in icteric
hepatitis. N Engl J Med 1974; 291:963.
7. Flacks LM, Lees D. A case of hepatitis B with pleural effusion.
Aust N Z J Med 1977; 7:636-637.
8. Garau J , Hauman L. Hepatitis virica aguda y derrame pleural
exudativo. Gastroenterol Hepatol 1978; 1:180-182.
9. Alpert E, Isselbacher KJ. The pathogenesis of arthritis associated
with viral hepatitis: complement-component studies. N Engl J Med
1971; 285:185-189.