Age-dependency of galactose elimination capacity in healthy children and children with chronic liver disease

Figures & data

Table I. Biochemical characteristics of 30 children with liver disease.

Age interval (year)	0.25–4.9	5–9.9	10–16
No. of patients	10	7	13
Female/male	4/6	2/5	8/5
Bilirubin (μmol/l plasma)  (0–15)	17 (9–105)	23 (6–83)	13 (6–104)
Alanine aminotransferase (U/l plasma)  (5–45)	116 (40–312)	93 (66–255)	67 (21–675)
Albumin (μmol/l plasma)  (0–1 year: 455–650)  (1–7 years: 520–770)  (>7 years: 640–820)	538 (510–693)	390 (300–619)	594 (450–678)
Coagulation factors II,VII,X  (0.50–1.0)	0.69 (0.50–1.00)	0.60 (0.57–0.85)	0.72 (0.56–0.95)
Alkaline phosphatase (U/l plasma)  (6 months to 2 years: 250–1000)  (1–10 years: 145–420)  (10–15 years: 105–495)  (15–19 years: 50–260)	479 (192–1511)	830 (201–1481)	345 (130–1118)
Thrombocytes (10^9/l blood)  (1 month to 2 years: 135–620)  (>2 years: 165–435)	265 (170–359)	129 (54–303)	200 (49–356)

Results are given as median (range). In column 1, reference values are given for different age groups of healthy children in parentheses.

Figure 1. Age-dependency of GEC in children. Galactose elimination capacity (GEC) in relation to age in 10 healthy children (•; solid line) and 30 children with liver disease (Δ; broken line). The symbols indicate measured values and the lines indicate the fitted regression curves (see text).

Figure 2. Example of GEC before and after liver transplantation in a child with severe liver disease. In this boy with alpha-1-antitrypsin deficiency the age-dependent decline in GEC was markedly more pronounced than in healthy children. Following liver transplantation at the age of eight his GEC normalized and exhibited a normal age-dependent decline. The symbols connected by straight lines indicate measured values. The regression curves shown for comparison are those illustrated in Figure 1.