Richard H. Goodman, Andrew Leiter, Malcolm J. Low, Marc R. Montminy, Toshihiko Tsukada, J. Stephen Fink, Gail Mandel – 1 January 1987

Boris H. Ruebner, Mary Patricia Pauly, Neville Pimstone, Richard E. Ward, John M. Vierling, Robert H. Fennell, Antonio Monarca, Roberto Natangelo, Valeria Azzolini, B. A. Runyon, Y. Peled, J. Rattan, T. Gilat, Z. Fireman – 1 January 1987

S. W. Hosking, A. G. Johnson – 1 January 1987

1 January 1987

Yun‐Fan Liaw, Dar‐In Tai, Chia‐Ming Chu, Chia C. Pao, Tong‐Jong Chen – 1 January 1987 – The incidence, clinicopathological features and etiology of acute exacerbation occurring in patients with chronic type B hepatitis were assessed prospectively among 385 patients who had HBeAg and 279 who had anti‐HBe in serum. During an average follow‐up of 23.5 months, acute exacerbations occurred in 197 HBeAg‐positive patients and in 56 anti‐HBe positive patients, with a calculated annual incidence of 28.6 and 10.3%, respectively (p < 0.001).

Atsushi Kanno, Hitoshi Ohori, Keizaburoh Matsuda, Haruo Nakayama, Yutaka Miyazaki, Motoyasu Ishii, Hiroshi Suzuki, Masao Ohtsuki, Yoshio Goto – 1 January 1987 – In order to establish the virological significance of HBeAg subtypes (HBeAg/1 and HBeAg/2) during hepatitis B virus infection, HBsAg, HBeAg and hepatitis B virus DNA in serum and HBeAg in liver were determined quantitatively in relation to the detection of HBeAg subtypes in agar gel diffusion.

Jan Van Hattum, Geziena M. Th. Schreuder, Solko W. Schalm – 1 January 1987 – The course after hepatitis B virus infection seems to be determined by the host's immune response, which in turn may be regulated by the major histocompatibility complex. In order to find a possible relationship between the course of disease and the phenotype frequency of HLA determinants, we studied 396 Dutch subjects of northern European local race. Six groups of individuals with various courses after hepatitis B virus infection were compared to healthy controls.

Paul D. Berk, Barry J. Potter, Wolfgang Stremmel – 1 January 1987

James E. Heubi, John C. Partin, Jacqueline S. Partin, William K. Schubert – 1 January 1987

Laurence M. Blendis, Michael J. Sole, Peter Campbell, Alan G. Lossing, Paul D. Greig, Bryce R. Taylor, Bernard Langer – 1 January 1987 – The elevated catecholamine levels in cirrhotic patients with ascites have been proposed to be due to sympathetic overactivity secondary either to reduced intravascular volume or to an underlying cardiovascular abnormality such as reduced pressor responsiveness. Furthermore, these elevated catecholamine levels have been proposed to be involved in the pathogenesis of salt and water retention.