Role of juice carbohydrate malabsorption in chronic nonspecific diarrhea in children.
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Beverages↗
Biomedical subjects
J N Udall
Publications and source records attributed to J N Udall.
Treatment of infants with acute diarrhea: what's recommended and what's practiced.
In 1985, the American Academy of Pediatrics (AAP) published a policy statement on the treatment of infants with acute diarrhea complicated by mild to moderate dehydration. To determine how closely physicians in the United States follow the AAP's treatment guidelines, a questionnaire was sent to 457 pediatricians and 360 family practitioners. The questionnaire presented a hypothetical infant with acute diarrhea complicated by mild to moderate dehydration and included questions regarding the number of such patients seen yearly, length of time used to rehydrate the infant, and how formula or solids are introduced following rehydration. Complete responses were received from 53% of pediatricians and 40% of family practitioners. The number of patients with acute diarrhea seen per year did not affect physician's treatment. Pediatricians and family practitioners responded similarly to most questions. Contrary to the AAP's guidelines to rehydrate in 4 to 6 hours, 62% of responding physicians extend the rehydration period to 12 to 24 hours. Also contrary to the AAP's recommendations, 62% of pediatricians and family practitioners use a lactose-free formula. The majority of responding physicians do follow the AAP's treatment guidelines to initiate feedings with diluted formula. Significantly more pediatricians than family practitioners advance to a full-strength formula within 1 day (P = .011). Fewer than 50% of physicians polled started solids within 24 hours as suggested by the AAP. Overall, the findings suggest that very few pediatricians and family practitioners follow all aspects of the AAP's treatment guidelines for infants with acute diarrhea complicated by mild to moderate dehydration.
Acute Disease↗
Calcified thrombus in the right atrium: a rare complication of long-term parenteral nutrition in a child.
A 5-year-old boy with short-bowel syndrome who receives home parenteral nutrition developed a calcified thrombus that involved the inferior vena cava (IVC) and the right atrium. Symptoms included 3 to 4 months of intermittent fever and 2 months of vague chest pain. Blood could not be aspirated from the IVC catheter and an IVC contrast study demonstrated the calcified thrombus. The intracardiac portion of the mass was removed surgically, but the IVC mass could not be completely excised. The boy developed a pericardial effusion 6 weeks after surgery. He was treated for this and 6 months after the initial surgery the patient was asymptomatic.
Calcinosis↗
Lovastatin therapy for cholesterol ester storage disease in two sisters.
We administered lovastatin to two sisters, aged 4 and 17 years, who had cholesterol ester storage disease, an autosomal recessive disorder manifested by hypercholesterolemia and hypertriglyceridemia. The drug, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, was taken orally for 6 months. Serum lipid concentrations were determined monthly. Computed tomography of the liver was performed before and during therapy to evaluate liver fat content. The younger sister had liver biopsies before and after 6 months of lovastatin therapy to assess hepatic cholesterol stores. Both patients had marked decreases in serum levels of cholesterol, triglycerides, and low-density lipoprotein-cholesterol; high-density lipoprotein-cholesterol levels increased. Computed tomography during treatment demonstrated a significant increase in linear attenuation, suggesting a decreased liver fat content. Liver tissue obtained 6 months after lovastatin therapy was initiated had 13% less esterified cholesterol than the liver sample obtained before treatment. We conclude that lovastatin may be effective in treating children with cholesterol ester storage disease.
Adolescent↗
Gastrointestinal host defense and necrotizing enterocolitis.
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Anti-Bacterial Agents↗
Intestinal permeability to intact lactose in newborns and adults.
Small amounts of lactose have been shown to be absorbed intact across the intestine and excreted unchanged in the urine of newborns and adults. We designed a study to quantitate the intestinal uptake and urinary excretion of this disaccharide in these age groups. Similar amounts of lactose were given orally to 17 term newborns (age: 24.8 +/- 3.0 h) as a standard infant formula, and to 15 adult lactose absorbers (age: 28.1 +/- 2.6 years) and 11 adult lactose malabsorbers (age: 24.7 +/- 2.9 years) as a 20% water solution. Following lactose ingestion, breath was collected every 30 or 60 min for 3 h and analyzed for hydrogen concentration. Urine was also collected, and lactose and creatinine concentrations were determined. Peak hydrogen concentration was less than 20 ppm above baseline in newborns and adult lactose absorbers and 85 +/- 14 ppm in adult lactose malabsorbers. Urinary lactose excretion, expressed as a function of body weight (mg/ml/kg b.w.), was substantially greater in newborns (4.2 +/- 0.82) than in adult lactose absorbers (0.29 +/- 0.07; p less than 0.001) and adult lactose malabsorbers (0.55 +/- 0.04; p less than 0.01). Similarly, urinary lactose excretion expressed as a ratio of urinary lactose to urinary creatinine (mg/mg) was increased (p less than 0.001) in newborns (2.05 +/- 0.26) when compared to adult lactose absorbers (0.11 +/- 0.02) and adult lactose malabsorbers (0.20 +/- 0.02). Our data demonstrate that the intestinal uptake and urinary excretion of intact lactose is significantly increased in newborns compared to adult subjects.
Adult↗
Assessment of lactose absorption by measurement of urinary galactose.
Individuals with sufficient intestinal lactase hydrolyze ingested lactose to galactose and glucose and these monosaccharides are absorbed. Lactose is not digested completely when intestinal lactase activity is low and the disaccharide is malabsorbed. Breath hydrogen excretion after lactose ingestion is used commonly to diagnose lactose malabsorption. However, no direct tests are currently used to assess lactose absorption. We tested a new method of assessing lactose absorption in 26 healthy individuals. Each subject ingested 50 g of lactose. Participants were evaluated for lactose malabsorption using a standard 3-h breath hydrogen test. In addition, the urinary excretions of galactose, lactose, and creatinine were quantitated for 3-5 h after lactose ingestion. On the basis of breath hydrogen analysis after lactose ingestion, 12 individuals were lactose malabsorbers (defined as a rise in the breath hydrogen concentration of greater than 20 parts per million above the baseline value). The 14 subjects who did not malabsorb lactose by breath hydrogen testing (defined as a rise in the breath hydrogen concentration of less than or equal to 20 parts per million above the baseline value), had significantly more galactose in their urine 1, 2, and 3 h after lactose ingestion than lactose malabsorbers. The ratio of excreted lactose to excreted galactose was significantly decreased in lactose absorbers compared with lactose malabsorbers (p less than 0.001). Determination of the ratio of urinary galactose to urinary creatinine separated lactose absorbers from lactose malabsorbers completely (p less than 0.001). We conclude from this study that the determination of urinary galactose, urinary lactose/galactose ratio, and urinary galactose/creatinine ratio may be used to assess lactose digestion and absorption in healthy adults.
Adolescent↗
Nutritional support for pediatric patients with inflammatory bowel disease.
Pediatric patients with ulcerative colitis and Crohn's disease often suffer from malnutrition and growth failure. This is particularly true in pubertal children. Chronic insufficient nutrient intake is most often the cause of growth failure. Both parenteral nutrition and defined enteral formulas are available to rehabilitate patients with malnutrition and growth failure. Assessment of nutritional status and growth and the use of parenteral nutrition and defined enteral formulas to reverse malnutrition, growth failure, and inflammation in pediatric patients with inflammatory bowel disease are discussed.
Adolescent↗
Minimal hydrolysis of epidermal growth factor by gastric fluid of preterm infants.
Epidermal growth factor (EGF), present in high concentrations in milk, may play a role in growth of the gastrointestinal tract. Resistance to proteolytic degradation in the stomach is necessary if ingested EGF is to function within the gastrointestinal tract. Although EGF stability to low pH and proteases predicts gastric survival, the extent of digestion in the stomach remains to be defined. Consequently, we measured gastric degradation of 125I-human recombinant EGF in preterm infants with an in vitro method in which EGF was incubated at 37 degrees C with stomach fluid at pH 1.8, 3.2, and 5.8 followed by analysis of degradation products. As maximal acid proteolytic activity is present one hour after feeding in preterm infants, fluid was obtained at that time from 18 infants with a mean gestational age at birth of 30.4 (3.0) (SD) weeks and a postnatal age of 26.3 (12.7) days at sampling. Incubations for up to 60 minutes revealed minimal loss of trichloroacetic acid precipitable radioactivity, in contrast to the substantial hydrolysis of iodinated casein which occurred under the same conditions. Chromatography of reaction mixtures on Sephadex G-25 showed a single major peak of radioactivity which coeluted with EGF. Epidermal growth factor also retained greater than 75% of its ability to bind to anti-EGF affinity columns and placental membrane receptors after incubation with gastric fluid. These data support the concept of substantial gastric survival of ingested EGF in a potentially biologically active form in preterm infants.
Epidermal Growth Factor↗
Trypsin uptake and trypsin-inhibitor complexes. Differences between suckling and adult rats.
Previous studies have suggested that both newborn animals and humans absorb intact proteases from the intestine in greater amounts than do adults. Absorbed proteases are rapidly complexed in plasma by several inhibitors which inactivate free proteases. In order to confirm increased intestinal uptake in newborns, we evaluated the plasma trypsin activity in both 2-week-old and adult rats following a trypsin feed. In addition, we studied the interaction between absorbed trypsin and rat trypsin inhibitors (alpha-macroglobulin, alpha 1-inhibitor 3, and alpha 1-protease inhibitor) by determining the concentration of alpha-macroglobulin complexes both in vivo and in vitro following trypsin feeding and by evaluating the amount of trypsin activity complexed with the different inhibitors. In vivo experiments demonstrated that trypsin uptake was significantly increased in newborns compared to adult rats and that 50-70% of plasma trypsin activity was associated with alpha 1-inhibitor 3. Increased uptake was not accompanied by increased alpha-macroglobulin complexes. In vitro trypsin incubation did not lead to increased alpha-macroglobulin complexes until the other inhibitors were removed. These findings suggest that newborns have increased trypsin uptake, and the trypsin initially binds to alpha 1-inhibitor 3 before being transferred to alpha-macroglobulin for clearance. Further studies are needed in order to understand the interaction between intestinal uptake and plasma inhibition of absorbed proteases.
Aging↗
Serum antibodies to exogenous proteins: the significance?
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Antibodies↗
Flow cytometry: a new approach to the isolation and characterization of Kupffer cells.
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Animals↗
Barrier defense function of the small intestine: effect of ethanol and acute burn trauma.
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Animals↗
Elevated levels of alpha 2-macroglobulin-protease complexes in infants.
Proteases form stable complexes with alpha 2-macroglobulin (alpha 2-MG) in human plasma. We previously showed that the intestine of newborn rabbits takes up greater amounts of proteases than the intestine of weaned animals, and we suggested that the same phenomenon might occur in the human newborn. To test this possibility, alpha 2-MG complexes were sought in plasma from 3-day-old human infants and adults. In addition, the level of alpha 2-MG was measured. The concentration of alpha 2-MG complexes and of alpha 2-MG was significantly increased in the plasma of infants compared to adults. We suggest that the elevated levels of alpha 2-MG complexes in infants may reflect the enhanced uptake of proteases from the intestine. In addition, there may also be decreased clearance of complexes by the mononuclear phagocytic system in infants. The elevated levels of alpha 2-MG in the infant may reflect a response to the need for neutralizing proteases absorbed from the intestine.
Adult↗
Behavioral effects of sucrose on preschool children.
Despite speculation that sucrose consumption affects behavior, little empirical information is available. Accordingly, this study investigated the effect of sucrose consumption on the behavior of eight preschool children. Children were tested individually using a double-blind, crossover design. On separate mornings each child received 6 ounces of juice, sweetened on one morning with sucrose and on the other with an artificial sweetener. Children were observed for 90 minutes following the drinks, alternating between 15-minute sessions of work on structured tasks and 15-minute sessions of free play. Following the sucrose drink the children showed a decrement in performance in the structured testing situation, and they demonstrated more "inappropriate" behavior during free play. These differences in behavior were most pronounced approximately 45 to 60 minutes after the drinks. Thus, the study provides objective evidence in young children of a rather subtle, yet significant, time-dependent behavior effect of sucrose ingestion.
Attention↗
Liver disease in alpha 1-antitrypsin deficiency. A retrospective analysis of the influence of early breast- vs bottle-feeding.
We identified children with alpha 1-antitrypsin deficiency from the medical records of the Massachusetts General Hospital and Children's Hospital, Boston, and investigated their early feeding history. Between 1969 and 1983, forty children with the deficiency were seen at one or both hospitals. Clinical information was obtained from hospital records and from questionnaires mailed to the parents. Complete morbidity, mortality, and early feeding data were obtained for 32 of the children who were born at 38 to 42 weeks' gestation and whose weights were appropriate for gestational age. We compared the presence of severe liver disease and the death rate of those who had been exclusively breast-fed for one month with those who had been bottle-fed. Severe liver disease was present in eight (40%) of bottle-fed and one (8%) of breast-fed infants. Twenty-four of the 32 infants were still alive at the termination of the study; 12 had been breast-fed and 12 bottle-fed during their first month of life. All eight deceased infants had been bottle-fed. The mortality rate in the bottle-fed group was significantly greater than that of the breast-fed group. Our study suggests that breast-feeding may offer some protection against severe liver disease and early death in infants with alpha 1-antitrypsin deficiency.
Birth Weight↗
Development of gastrointestinal mucosal barrier. VII. In utero maturation of microvillus surface by cortisone.
When studying mucosal barrier function of developing animals, we noted that intestinal microvillus membranes (MVM) of newborn animals differ in their fluidity and binding characteristics to lectins compared with adult MVM. To further investigate these differences and determine whether maturation of the microvillus surface could be accelerated in utero, pregnant rats were given intraperitoneal cortisone beginning on the 17th day of gestation. Control and cortisone-treated animals were allowed to deliver normally, and the small intestines from newborns were used to isolate MVM. Microvillus membrane surface characteristics were evaluated by employing an 125I-labeled fucose-specific lectin, Ulex europeus (UEA). Changes in MVM proteins were monitored by disaccharidase activities and sodium dodecyl sulfate-polyacrylamide electrophoresis. MVM fluidity was accessed using a 5-doxyl stearic acid label and electron-spin-resonance spectroscopy. Results from these studies indicate that the birth weights of newborn rats exposed to cortisone in utero were significantly reduced; sucrase activity was prematurely induced and specific activities of lactase and maltase were enhanced in the intestines of the cortisone-treated newborns as contrasted with control animals. Furthermore, binding of 125I-UEA to MVM was greatly increased in treated animals. MVM fluidity decreased (P less than 0.001) compared with control animals and resembled the structural characteristics of more mature MVM. These results suggest that cortisone exposure in utero accelerate maturation of the microvillus surface of enterocytes.
Animals↗