Linear growth after pediatric liver transplantation.

To determine growth patterns in a large cohort of unselected children undergoing liver transplantation, the outcomes of 294 orthotopic liver transplantations performed in 221 children at The University of Chicago between October 1984 and October 1992 were retrospectively reviewed; 66% were alive at the time of this analysis. The mean age at transplantation was 4.1 +/- 5.0 years; 44% of the children were male and 16% of the transplants were from living-related donors. The mean height z score at the time of transplantation was -1.6 +/- 1.8, and 39% of children had height z scores of < -2.0 at transplantation. When children with growth retardation at the time of transplantation (height z scores of < -2. 0) were compared with children with more normal growth, there were no significant differences in gender or re-transplantation rates, although children with growth retardation at transplantation were significantly younger than those with more appropriate growth (2.8 +/- 4.1 years vs 4.7 +/- 5.1 years, P <.05). The height z score of all children with biliary atresia at the time of transplantation was -1.9 +/- 1.7 compared with -1.2 +/- 2.0 in those children with underlying diseases other than biliary atresia. Catch-up growth was seen in 37% to 47% of children at any given time point after transplantation. Children with evidence of catch-up growth (growth velocity z score >0) 2 years after transplantation were more likely to be first-time transplant recipients, had more growth retardation at the time of transplantation, and were receiving lower doses of prednisone at 2 years after transplantation. Younger children were most likely to demonstrate catch-up growth after transplantation. In summary, a large proportion of children have growth retardation at the time of liver transplantation. This growth retardation is inversely correlated with age. Before transplantation, children with biliary atresia grow less well than children with other forms of liver disease. Up to one half of children demonstrate catch-up growth after liver transplantation. Growth after transplantation is proportional to the degree of growth retardation at transplantation and inversely correlated to age at transplantation. Children with poor growth after transplantation are more likely to be receiving higher doses of corticosteroid.

Bone mineral density assessment in children with inflammatory bowel disease.

BACKGROUND & AIMS: Children with inflammatory bowel disease (IBD) are at risk for osteoporosis because of undernutrition, delayed puberty, and prolonged corticosteroid use. The aim of this study was to compare bone mineral density (BMD) in children with IBD with that in normal children and to assess the effects of nutritional and hormonal factors and corticosteroid dosages on BMD. METHODS: One hundred sixty-two subjects (99 with IBD and 63 healthy sibling controls) were enrolled. Patients underwent anthropometric assessment, pubertal staging, bone age radiography, and BMD assessment by dual energy x-ray absorptiometry of the lumbar spine, femoral neck, and radius. Laboratory evaluations included serum calcium, phosphate, alkaline phosphatase, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, parathyroid hormone, osteocalcin, urinary N-telopeptides, albumin, insulin-like growth factor I, and testosterone or estradiol. Cumulative corticosteroid doses were calculated. RESULTS: BMD Z scores at the lumbar spine and femoral neck were lower in patients with IBD, and lower in those with Crohn's disease compared with those with ulcerative colitis. Low BMD persisted after correction for bone age in girls with Crohn's disease (lumbar spine, P = 0.004; femoral neck, P = 0.002). Cumulative corticosteroid dose was a significant predictor of reduced BMD. BMD did not correlate with measures of calcium homeostasis, except elevated serum phosphate and urine calcium levels in girls. CONCLUSIONS: Low BMD occurs in children with IBD (more in Crohn's disease than in ulcerative colitis), especially pubertal and postpubertal girls. Cumulative corticosteroid dose is a predictor of low BMD, but other factors in Crohn's disease remain undetermined.

Hepatic and cerebrospinal fluid accumulation of aluminium and bismuth in volunteers taking short course anti-ulcer therapy.

To investigate the possible absorption and deposition of bismuth or aluminium from agents used in the treatment of peptic ulcers, we have measured levels of bismuth and aluminium in the liver tissue of 15 patients undergoing elective liver biopsy and in the cerebrospinal fluid (CSF) of 15 patients undergoing elective myelography after administration of standard therapeutic doses of tripotassium dicitrato bismuthate (TBS), sucralfate or aluminium hydroxide for 1 month. Aliquots of liver or CSF were separated and levels of both aluminium and bismuth were assayed in each sample by atomic absorption spectrophotometry. The group who received TBS had significantly higher liver bismuth levels than the other two treatment groups, but there was no significant difference in CSF bismuth levels among the three groups. There was no significant difference in either liver or CSF aluminium levels among the three treatment groups. We conclude that tissue accumulation of bismuth may occur after short-course therapy with colloidal bismuth, although there is no evidence of CNS accumulation of bismuth in the present study.

Somatomedin-C levels in growth-impaired children and adolescents with chronic inflammatory bowel disease.

The relationship between caloric insufficiency and impaired growth in children with chronic inflammatory bowel disease has been increasingly recognized in recent years. The mechanism by which nutritional insufficiency leads to decreased growth in these children is unclear. Our study suggests that chronic undernutrition lowers circulating somatomedin-C, which is known to exert anabolic effects on peripheral tissues. Therapeutic intervention that increases caloric intake results in improved somatomedin-C levels and growth velocity. Monitoring somatomedin-C levels in growth-impaired children with inflammatory bowel disease provides an important marker of nutritional sufficiency and reversibility of growth retardation.