In 236 patients with fulminant viral hepatitis (FVH), type B (FBH) was most common (47.5%), followed by non-A non-B hepatitis (FNANB, 44.9%) and hepatitis type A (FAH, 7.6%). The survival rate was significantly higher in the FAH group than in the FBH and FNANB groups (61.1, 36.6 and 18.9% respectively), and was significantly higher in the FBH group than in the FNANB group. In spite of screening for hepatitis B virus (HBV), FBH was prevalent (27 of 41) in post-transfusion cases; this phenomenon is discussed in relation to a recently revealed mutation of HBV. Within a month after the onset of hepatitis symptoms all cases in the FAH, 93% in the FBH and 79% in the FNANB group, developed encephalopathy. When the duration of illness before the onset of encephalopathy was more than 10 days (a subacute form), the survival rate was significantly lower than when encephalopathy developed in less than 11 days (an acute form). This difference could be accounted for by the difference in the relative frequency of aetiological viruses in the two forms and the higher survival rate in the acute, than the subacute, form in the FNANB group.
The pathogenic ability of hepatitis B e antigen (HBeAg) to induce membranous glomerulonephritis was evaluated by the most specific method presently available. Monoclonal antibody was raised against HBeAg, and F(ab')2 fragments were obtained and labeled with fluorescence. By this reagent, 10 out of 16 patients with membranous glomerulonephritis with hepatitis B surface antigen in the serum revealed granular deposition of HBeAg along glomerular capillary walls. Among the cases with glomerular HBeAg deposits, nine had detectable HBeAg in the serum and one had antibody to HBeAg (anti-HBe). The specificity of HBeAg staining was ascertained by blocking and inhibition tests, and the fluoresceinated anti-HBe F(ab')2 reagent did not stain the glomerular immune deposits in the patients with membranous glomerulonephritis who did not carry hepatitis B virus (HBV). None of the studied patients showed deposition of hepatitis B surface or core antigens in the glomerulus. On the basis of these results, immune complexes involving HBeAg may induce membranous glomerulonephritis in persons who carry HBV.
To determine the risk of death at an early stage of fulminant viral hepatitis, we created severity indexes drawn from clinical data on the day of development of encephalopathy in 128 patients with fulminant hepatitis B and 103 with fulminant hepatitis non-A, non-B. In fulminant hepatitis B, the risk score was 2.75 x BL + 2.75 x BR + 2.7 x AG + 2.3 x WB + 1.67 x CD + 1.56 x AL - 0.098 x PR - 0.88, where BL is 1 if total bilirubin is higher than 20 mg/dl, BR is 1 if the ratio of total to direct bilirubin exceeds 2.2, AG is 1 if age is above 40 yr, WB is 1 if white blood cell count is less than 4,000 cells/mm3 or more than 18,000 cells/mm3, CD is 1 if a hazardous disease coexists and AL is 1 if ALT is less than 100 times the upper limit of normal (otherwise all are 0), and PR is prothrombin time (percentage of normal value). Using a cutoff score of 0, we found the positive predictive value, negative predictive value and predictive accuracy to be 0.90, 0.86 and 0.89, respectively. Sensitivity and specificity were 0.94 and 0.77, respectively. In fulminant non-A, non-B hepatitis, the risk score was 2.66 x BR + 2.25 x BL + 2.24 x DI + 2.05 x AL +/- 1.38 x AG + 0.00021 x WB - 6.33.(ABSTRACT TRUNCATED AT 250 WORDS)
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