Search

By monitoring immunobiological parameters known to be influenced by interferon (IFN), the natural killer (NK) cell activity of 10 low replication (anti-HBe) virus B-DNA (HBV-DNA) hepatitis patients receiving rIFN alpha-A, of 5 anti-HBe/delta positive hepatitis patients treated with rIFN alpha-2, and of 6 high replication (HBeAg) HBV-DNA hepatitis patients on lymphoblastoid IFN was followed-up during therapy. Overall, strong and significant (p less than 0.01) shift to increase segregated with the low replication subset; the delta positive subset was non-significantly increased (0.30 greater than p greater than 0.2); the high replication subset was depressed in a nearly significant (0.10 greater than p greater than 0.05) manner. Kinetic studies showed the activation of the first subset to follow an early steep rise and a subsequent plateau as fitted with a quadratic curve (p = 0.02); an early rise and a depression at 2 months delineated a complex cubic model (p = 0.06) in the high replication subset. The profound NK depression was clinically witnessed by a sharp rise of the aminotransferases and following drop of viremia. The study shows that i. discrete patterns of NK response as amenable to mathematical models may associate to differential patterns of virus B replication in patients responding to IFN; ii. point(s) on the NK curve may acquire clinical meaning as they coincide with a consensual or opposite shift of a clinical index.

Sixty-four heterosexual Italian carriers of HBsAg with chronic HBeAg and hepatitis B virus DNA-positive hepatitis were assigned randomly either to receive human lymphoblastoid interferon (injections of 5 million units per m2 three times per week for 6 months) or to serve as untreated controls. After 18 months of follow-up evaluation, 26 of the 33 treated patients (79%) had cleared hepatitis B virus DNA, 23 (70%) had lost HBeAg and 20 (61%) had seroconverted to anti-HBe. Fifteen of the 31 controls (48%) had cleared hepatitis B virus DNA (p = 0.01), 12 (39%) had lost HBeAg and nine (29%) had seroconverted to anti-HBe (p = 0.002). Eight treated patients but only one control had lost HBsAg and seroconverted to anti-HBs (24% vs. 3%, p = 0.01). Treated patients cleared hepatitis B virus markers after a mean interval of 4 months, compared with 8 months in the controls. All responders to interferon cleared intrahepatic HBcAg, and 50% showed histological improvement. The baseline hepatitis B virus DNA levels and the original histology were not predictive of a response to therapy; women appeared to respond better than men. Lymphoblastoid interferon provides an effective therapy in the heterosexual Italian patient with chronic hepatitis B.