Despite the recent approval of lamivudine for the treatment of children with chronic hepatitis B virus (HBV) infection, there is insufficient information on the kinetics of HBV clearance and the factors that predict a favorable treatment response to lamivudine in this population. In a small retrospective study of 16 HBV-infected children treated with lamivudine, we examined changes in virus load and other factors associated with hepatitis B e antigen (HBeAg) clearance. High pretherapy alanine aminotransferase level, low serum HBV DNA load, and age at the start of treatment were independently associated with HBeAg clearance. HBeAg clearance was also associated with the achievement of specific levels of virus suppression, and failure to achieve those levels was associated with the development of lamivudine resistance. Additional studies are necessary to provide better indications and guidelines for the treatment of children with chronic HBV infection.

Although TPN is used frequently in young infants, little information is available regarding its effect on postnatal development of the gut. The effect of total parenteral nutrition (TPN) and intragastric (IG) alimentation on ontogeny of the small intestine was examined in infant rabbits starting at 10–12 days. Animals were killed at 17–19 days. Body weight, organ weight and weight of segments of proximal, mid and distal small intestine were measured. Intestinal mucosa was scraped, weighed and homogenized for estimation of protein, DNA and disaccharidases. Na⁺ transport was examined in short-circuited jejunum. Weight gain was similar in controls, sham-treated and TPN animals, but was significantly reduced in IG animals. TPN induced precocious development of sucrase and maltase activity and glucose-stimulated Na⁺ transport, despite causing a significant decrease in mucosal weight and DNA and pancreatic amylase. IG alimentation also induced precocious development of sucrase, maltase and glucose-stimulated Na⁺ transport. Thus TPN, despite producing mucosal atrophy and decreased pancreatic exocrine development, stimulates accelerated postnatal maturation of the small intestine.

The effect of oral intake and body weight on postnatal maturation of the small intestine was examined in infant rabbits with accelerated weight gain. Intestine from immature animals is characterized by large unidirectional Na fluxes, failure of Na absorption to respond to glucose but increased ability to absorb monosaccharides, and an enzyme pattern of high lactase and thymidine kinase and low sucrase. Postnatal development was monitored by measuring Na and glucose transport in short-circuited jejunum and enzyme activities in jejunal mucosa. Accelerated weight gain was achieved in the experimental group by reducing litter size to 3 animals at 24–48 hours of age. Under glucose-free conditions unidirectional Na fluxes were significantly smaller in tissue from the heavier experimental animals compared to controls. The addition of glucose had no effect on Na fluxes in control tissue but significantly increased Na absorption in the experimental group. Unidirectional and net fluxes of ¹⁴C-D-glucose were significantly smaller in the heavy experimental animals compared to controls. Isolated villus enterocytes from the experimental group had reduced lactase and thymidine kinase activities. Sucrase activity, which did not differ in isolated cells, was increased in total mucosa from the experimental group. Solute transport and the enzyme profile in jejunum from the heavier experimental suckling rabbits is characteristic of intestinal epithelium from more mature animals, indicating accelerated postnatal maturation. The findings suggest that oral nutrient intake and body weight, rather than chronologic age, act as the physiologic trigger for postnatal maturation of the small intestine.

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