Long-term parenteral nutrition in children: liver and gallbladder disease.
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Biomedical subjects
Publications and source records attributed to C Ricour.
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The present study investigated the effects of two modalities of parenteral nutrition (continuous nutrition over the 24-hour period vs. cyclic nutrition, i.e., administered only during the night) on O2 consumption during sleep in children affected by severe gastrointestinal diseases. In both feeding modalities O2 consumption was always highest in REM sleep, intermediate in stage 2 and lowest in SWS. The trends during the night of O2 consumption (an increase from the second to the third part of the night) for different sleep stages were comparable in both feeding modalities. These results suggest that O2 consumption is not affected by the feeding modalities investigated, but is dependent on both sleep stages and time of night.
In this retrospective study the management of infants who had undergone resection of more than 50% of the small bowel as newborn infants between 1970 and 1988 was analyzed to define prognostic factors. Small bowel resections were performed for atresia (36 cases), volvulus (22 cases), gastroschisis (10 cases), necrotizing enterocolitis (11 cases), and other disorders (8 cases). Patients were classified into two groups depending on the length of residual small bowel: group 1 (n = 35) had less than 40 cm of small bowel and group 2 (n = 51) had 40 to 80 cm of residual small bowel. Patients in group 2 had significantly better survival rates than those in group 1 (92.0% vs 66.6%; p less than 0.001). The patients in group 1 who were born after 1980, when home parenteral nutrition was introduced, had better survival rates than those who were treated before 1980 (95.0% vs 65.0%; p less than 0.01). The time required for acquisition of intestinal adaptation depended on the intestinal length (average, 27.3 months for group 1 and 14 months for group 2; p less than 0.01) and on the presence or absence of the ileocecal valve. Parenteral or supportive enteral nutrition, or both, ensured normal growth in both groups. We conclude that more than 90% of infants now survive after extensive small bowel resection with parenteral nutrition and that the remaining small intestine will adapt with time. Home-based parenteral nutrition allowed children to be treated in the best psychosocial environment.
The relative effect of glucose and lipids on whole-body protein-metabolism kinetics was assessed in seven infants undergoing parenteral feeding. Protein intake was kept constant and nonprotein energy was either provided as glucose alone or as an isoenergetic glucose-lipid mixture according to a randomized crossover trial. Protein metabolism and energy-substrate utilization were assessed by a primed, constant L-[13C]leucine infusion, combined with indirect calorimetry. There was a significant difference in the pattern of energy-substrate utilization according to regime. Protein turnover (11.3 +/- 0.7 vs 9.8 +/- 0.4 g.kg-1.d-1; P less than 0.05), protein breakdown (8.4 +/- 0.6 vs 7.1 +/- 0.4 g.kg-1.d-1; P less than 0.05), and amino acid oxidation rates (2.7 +/- 0.4 vs 1.4 +/- 0.5 g.kg-1.d-1; P less than 0.05) were higher for the glucose than the glucose-lipid treatment, whereas protein-synthesis rates did not significantly differ. These results suggest that the nature of energy substrates delivered to parenterally fed infants may affect protein metabolism.
Hypercalciuria and bone disease are frequently associated with total parenteral nutrition (TPN) in children and adults. The aim of this study was to assess the influence of calcium, phosphorus, and vitamin D intakes on hypercalciuria. We observed seven children aged 4-13 years receiving home cyclic TPN for 4 consecutive years. Calcium and phosphorus intakes, constant during the 1st year, were reduced during the last 3 years to 50 and 30% of the initial intakes, and vitamin D was stopped during the 3rd and the 4th years. All children had hypercalciuria and one of them had acute painful osteopenia and nephrocalcinosis at the beginning of the study. Hypercalciuria was corrected and painful bone disease did not occur during the three following years, with TPN daily intakes of calcium, 0.35 mmol/kg, and phosphorus, 0.70 mmol/kg. Cessation of vitamin D administration during 48 months led to no further decrease in calciuria nor to the occurrence of clinical or biological signs of vitamin D deficiency. However, we hypothesize that excessive vitamin D intake may have facilitated the occurrence of the TPN-related bone disease in one patient and should be avoided. The possible role of parenteral aluminum loading is also discussed.
Thirty-eight children presenting with severe Crohn's disease (CD) were studied retrospectively over a mean period of 6 years. The severity of CD was estimated according to an activity score. This was initially 66 +/- 19 reaching 100 in 16% of cases. Initial involvement included ileon and large intestine only (n = 23), large intestine (n = 11) and ileon only (n = 4), with upper GI tract or perineal involvement in 32 and 75% of cases respectively. The treatments consisted of corticosteroids (n = 34), azathioprine (n = 11), continuous enteral feeding (CEF) (n = 25), parenteral nutrition (PN) (n = 30). Mean recurrence rates per patient and per year were 0.6 in the groups including ileon and large intestine or the large intestine only and 0.3 in the ileal group. A surgical resection was performed in 20 cases with a mean rate of reoperation of 40% at 5 years. Reoperations were necessary only in the group involving the ileon and large intestine. Mean weight catch-up in 3 months and height growth speed were 6 kg and 1.7 to 3.1 cm/year under CED and/or PN. After a 6 year follow-up the activity index was decreased by 70% with a quality of life considered to be good in 60% of cases.
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Hereditary multiple atresias involving the gastrointestinal tract from pylorus to rectum are the most unusual form of intestinal atresia; the type of inheritance was suggested to be autosomal recessive. The inheritance of the severe combined immunodeficiency syndrome can be autosomal recessive or X-linked. We report on 3 sibs with multiple-level intestinal atresias. One sib had severe combined immunodeficiency syndrome and clinical histories of the other 2 sibs strongly suggested a congenital immunodeficiency syndrome. The parents of those children were healthy and nonconsanguineous. To our knowledge, this is the first report of the association of multiple gastrointestinal atresias and immunodeficiency which appears to have an autosomal recessive pattern of transmission. Our family report suggests that, in the presence of multiple gastrointestinal atresias, attention should be given to possible associated immunological disorders.
Several experimental studies have demonstrated that activated intestinal T cells can induce villous atrophy. This observation led us to examine the possible role of activated T cells in the pathogenesis of intestinal lesions in a group of 13 children with intractable diarrhea and villous atrophy of unknown origin. Immunohistochemical study showed signs of intestinal mononuclear cell activation in seven patients. These signs included a marked increase in the number of mucosal T cells, mainly TCR alpha beta+, the appearance of lamina propria interleukin-2-receptor-bearing cells, and an increased expression of HLA-DR antigens by enterocytes. No local cause of intestinal T-cell activation was found. However, four out of seven patients had extradigestive symptoms of autoimmunity, suggesting that the intestine might also be the site of an autoimmune reaction responsible for the epithelial lesions. In these patients, presence of crypt necrosis and colic extension of the lesions suggested poor prognosis. In contrast, in six other patients, no immunohistochemical evidence of mucosal T-cell activation was obtained. In the latter cases, analysis of clinical data favored the hypothesis of a primary inborn defect of enterocyte differentiation.
The aim of this study was to determine simple predictive factors of the resting energy expenditure (REE) in children. Two groups, A (n = 14) and B (n = 23), were defined by their weight-for-height index, less than 90% and greater than 90%, respectively. Anthropometrically assessed lean body mass (LBM), 24-h urinary creatinine, and REE were measured. From multiple-regression analysis, the best-fitting equation for calculating REE (REE = 54.4 LBM (kg) + 0.095 creatinine (mmol/kg) + 4.7) was highly significant (r = 0.987, p less than 0.0001). Although the regressions of REE on weight were significantly different between the two groups, the equations using LBM or 24-h urinary creatinine did not discriminate between them. These findings suggest that an equation based on LBM or 24-h urinary creatinine excretion could be a more accurate estimate of REE than are conventional methods based on weight or height, and it may be applicable to diverse nutritional states.
Four children aged 6 months to 9 years received fully HLA-mismatched ABO identical small intestinal allografts. In order to monitor the rejection process and to study epithelial changes induced by intestinal T cells activated by an allogeneic reaction, iterative biopsies were performed through the ileal enterostomy and processed for histology and immunohistochemistry. Episodes of acute histological reaction were observed in all 4 patients between day 10 and 160. It was preceded by appearance of pericryptic CD3+CD4+ or CD8+ T cells of recipient origin, increasing numbers of which expressed CD25. Simultaneously, early epithelial changes were noted: increased HLA-DR expression by enterocytes and decreased mitotic rate as shown by decreased numbers of KI67+ cells in crypts. During acute histological rejection, massive infiltration of mucosa by CD25+CD3+ T-cells and activated macrophages (KIM6+CD25+), was associated with crypt necrosis and then, destruction of surface epithelium. Successful treatment of graft rejection episodes with antilymphocytic serum (2), anti-CD3 monoclonal antibody (2), anti-CD25 monoclonal antibody (1) resulted in a rapid decrease of CD3+ cells, a more progressive decrease of CD25+ and KIM6+ macrophages, reappearance of KI67+ cells in crypts followed after a variable delay by recovery of villous architecture. Chronic histological rejection was observed in 1 patient after 7 months. It was characterized by total villous atrophy, fibrosis, endarteritis, infiltration of lamina propria and epithelium by CD3+CD8+ cells, a small number of which CD25+, strong HLA-DR expression by crypt and surface epithelium, increased numbers of KI67 enterocytes. Altogether these data suggested that activated T cells can induce two types of villous atrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
The aim of a combined liver/intestinal transplantation experimental model in rats is the study of the liver-induced tolerance of a solid, vascularized and highly immunogenic organ. Animals. Inbred Lewis rats were divided in two syngenic groups: 1. small intestine grafting (n = 10); 2. combined liver/intestinal grafting (n = 10). Intestinal grafting was performed 15 days after liver transplantation. Results. 10/10 animals were alive after 60 days in the first group and 7/10 in the second. Intestinal graft viability was good and 3 intestinal biopsies were done without any complication in each animal. All samples were histologically normal. Our study using syngenic animals prove that combined liver/intestinal transplantation is technically possible and reliable.
Digestive and/or nutritional manifestations of Henoch-Schoenlein purpura (HSP) in childhood may be so severe as to require nutritional assistance. The study of 19 cases with this form of the disease allows to suggest a therapeutic protocol. When enteral nutrition cannot be used from the onset, parenteral nutrition is required. Associated steroid therapy may prove helpful for the regression of the digestive signs. The observed slowness of the weight catch-up, in spite of high protein-energy intakes, emphasizes the severity of catabolism in these severe forms of HSP.
Ten infants on continuous total parenteral nutrition (TPN) were infused with NaH13CO3 for 6 h in order to assess the amount of 13C recovered as breath 13CO2. Protein intake was 2.8 +/- 0.3 g/kg/d and non-protein energy intake 107 +/- 4 kcal/kg/d (447 +/- 18 kJ/kg/d), provided either as glucose alone or as an isoenergetic glucose-lipid mixture. In the five infants receiving glucose as the sole non-protein energy source, total CO2 production (559 +/- 50 mumol/kg/min), natural 13C abundance of breath CO2 (-11.8 +/- 0.6 delta % versus PDB) and basal 13CO2 production (6.1 +/- 0.6 mumol/kg/min) were higher than in the five infants infused the glucose-lipid mixture (465 +/- 30 mumol/kg/min, P less than 0.02; -16.1 +/- 0.5 delta %, P less than 0.01 and 5.0 +/- 0.3 mumol/kg min, P less than 0.02, respectively). There was a good agreement, in the glucose-infused infants, between the net glucose oxidation rate measured by indirect calorimetry (25.6 +/- 2 g/kg/d) and the glucose oxidation rate estimated from the 13C natural abundances of breath CO2 and infused substrates (23.5 +/- 3 g/kg/d). Steady state 13C enrichment of breath CO2 was reached in all infants after 120 min infusion and ranged from 11.0 to 21.5 delta % over baseline. Steady state 13C enrichment was negatively related to total CO2 production (r = -0.72; P less than 0.02). In contrast, steady state 13CO2 production in excess of baseline was only correlated to bicarbonate infusion rate (r = 0.95; P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
The gastrointestinal tract is particularly sensitive to stress, especially in children. The specificity of the gastric, intestinal and colonic microcirculation explains the high risk of ischemia during septic and hemorrhagic shock. The consequences of digestive ischemia vary from mucosal ulceration to transmural necrosis. Tissue hypoxia, the production of superoxide radicals and luminal factors explain these lesions. Some drugs are proposed which may limit the extent of these ischemic lesions; however to prevent them the author advises, on anticipating stress and complete hemodynamic monitoring of infants at risk.