J. Eileen Hay, Albert J. Czaja, Jorge Rakela, Jurgen Ludwig – 1 February 1989 – To determine the nature of unexplained chronic serum aspartate aminotransferase elevations of a mild to moderate degree in asymptomatic patients, we performed systematic clinical, biochemical and histologic examinations in 47 individuals who had been screened for virus‐, alcohol‐or drug‐related disease. Serum aspartate aminotransferase levels ranged from 3‐to 8‐fold normal (mean: 156 ± 7 units per liter) for at least 6 months (mean: 30 ± 6 months).

Peter Karayiannis, Lidija M. Petrovic, Mark Fry, Duncan Moore, Mike Enticott, Michael J. McGarvey, Peter J. Scheuer, Howard C. Thomas – 1 February 1989 – Three tamarins (Saguinus labiatus), two of which had previously been infected with hepatitis A virus and parenteral non‐A, non‐B hepatitis, were inoculated intravenously with the agent of GB hepatitis. All three animals developed alanine aminotransferase abnormalities 2, weeks after inoculation. Peak alanine aminotransferase levels were recorded 4 weeks postinoculation.

Michael A. Dunn – 1 February 1989 – Cyclosporin A (CsA), administered subcutaneously as 5 daily injections of 50 mg·kg−1, reduced the numbers of Schistosoma mansoni perfused from MF1 mice at 7 weeks post‐infection. The timing of drug administration revealed that the antischistosomal effects were greater when CsA treatment coincided with or was within a few days of infection with a parasite. CsA exerted a clear prophylactic effect, which decreased with time and was virtually abolished by 4 months pre‐infection. Adult worms treated in vivo were partially susceptible to CsA.

Werner Van Steenbergen, Johan Fevery, Rita De Vos, Roger Leyten, Karel P. M. Heirwegh, Jan De Groote – 1 February 1989 – The effects of thyroidectomy and of thyroid hormone administration on the hepatic transport of endogenous bilirubin were investigated in the Wistar R/APfd rat. Hypothyroidism resulted in an enhanced hepatic bilirubin UDP‐glucuronosyltransferase activity and in a decreased p‐nitrophenol transferase activity. It caused a cholestatic condition with a 50% decrease in bile flow and bile salt excretion, and an increased proportion of conjugated bilirubin in serum.

James E. Heubi, Bruce W. Hollis, Bonny Specker, Reginald C. Tsang – 1 February 1989 – Metabolic bone disease is common in children and adults with chronic cholestasis. We evaluated baseline vitamin D (vitamin D2 and D3), 25‐OH vitamin D2 and D3, 1,25(OH)2 vitamin D, vitamin D‐binding protein, bone mineral content and dietary mineral content in six children (mean age: 12.1 years) with cholestasis since infancy. Absorption of 25‐OH vitamin D3 and vitamin D2 was evaluated by measuring serial serum concentrations after a test dose. Bone mineral content was reduced by >2 S.D.

Wolfgang E. Fleig, Gerhard Hoss – 1 February 1989 – The active principle of a cytosol extract from weanling rat liver representing a putative liver‐specific growth factor was partially purified and characterized. “Hepatic stimulator substance” was extracted from the livers of 40‐ to 60‐gm male rats by heat treatment of a homogenate in 35% (w/v) phosphate‐buffered saline and subsequent ultracentrifugation. This “heat supernatant” and fractions derived from the subsequent purification steps were tested for growth stimulatory activity in two rat hepatoma cell lines.

Kiyohiko Kurai, Shiro Iino, Kazuhiko Koike, Keiji Mitamura, Yasuo Endo, Hiroshi Oka – 1 February 1989 – The peptide which is encoded by the pre‐S(2) region of hepatitis B virus DNA, the pre‐S(2) antigen, was determined quantitatively by an enzyme immunoassay system employing monoclonal antibodies. The prevalence and titer of pre‐S(2)Ag were 91.9% (91/99) and 10,356 ± 19,053 units (mean ± S.D., arbitrary units) for hepatitis B e antigen (HBeAg)‐positive patients with acute and chronic HBV infection and 86.0% (74/86) and 952 ± 1,565 units for HBeAg‐negative subjects.

F. Trevisani, M. Bernardi, G. Gasbarrini, Udaya M. Kabadi – 1 February 1989

M. James Phillips – 1 February 1989

Robert T. Schoen – 1 February 1989 – Lyme disease, a multi‐system disorder caused by the tick‐borne spirochete, Borrelia burgdorferi, is characterized by malaise, fever, headache, arthralgia, myalgia, stiff neck, lymphadenopathy, paresthesias, and a distinctive rash, erythema chronicum migrans (ECM) in its early phase. Neurologic, cardiac, and joint abnormalities may follow within weeks to months. A patient is described in whom acute recurrent Lyme disease occurred and in which spirochetes were identified in the skin and liver histologically.