The Experts below are selected from a list of 237 Experts worldwide ranked by ideXlab platform
Christian Braegger - One of the best experts on this subject based on the ideXlab platform.
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Probiotics and the prevention of Necrotizing Enterocolitis.
Annals of Nutrition and Metabolism, 2010Co-Authors: Christian BraeggerAbstract:matory response of the immature intestinal immune system, resulting in rapidly evolving intestinal gangrene, perforation, sepsis, shock and death [1, 2, 4] . Probiotics have been shown to be able to modify both the intestinal microbiota as well as the intestinal immune response. On this background, several clinical trials have been carried out in order to investigate the potential role of probiotics in the prevention of Necrotizing Enterocolitis [5–13] . Most of these studies, among them many randomized controlled trials, suggest a significant benefit of probiotics in the prevention of Necrotizing Enterocolitis, confirming previous observations in experimental animal models [14, 15] . Possible mechanisms of probiotics in the prevention of Necrotizing Enterocolitis are beneficial modification of the intestinal microbiota, strengthening of the intestinal mucosal barrier and attenuating the intestinal immune response to bacteria and bacterial products. The results of the randomized controlled trials have been analyzed in several comments and reviews [16–19] . There is a general agreement that probiotic supplementation has a great potential to significantly reduce the risk of Necrotizing Enterocolitis and the overall mortality in premature infants with very low birth weight. However, there is obviously great variability of the clinical trials reported, with respect to inclusion criteria of the patients, Necrotizing Enterocolitis is one of the most serious gastrointestinal emergencies in the neonatal intensivecare unit [1] . It predominantly affects preterm infants. The onset of disease is usually between the 3rd and the 10th day of life. Necrotizing Enterocolitis presents with a wide spectrum of clinical symptoms, ranging from nonspecific gastrointestinal disturbance to a fulminant course of intestinal gangrene and perforation. Typical early signs are abdominal distension, delayed gastric emptying, diarrhea, abdominal tenderness and gastrointestinal bleeding. Characteristically, extensive hemorrhagic inflammatory necrosis of the terminal ileum and ascending colon can be found. In severe cases the entire bowel may be involved. Intramural hemorrhage, gangrene, peritonitis and edema may progress to intestinal necrosis with extensive infiltration of neutrophil leukocytes. Risk factors include prematurity, hypoxia, formula feeding, bacterial infection and intestinal ischemia [2, 3] . Mortality is high (15–30%) and related to the presence of bacteremia, disseminated intravascular coagulation, ascites and very low birth weight. Etiology and pathogenesis of Necrotizing Enterocolitis remain unknown. However, formula feeding, intestinal mucosal barrier dysfunction and dysbalance of bacterial colonization may be contributing factors, leading to an inappropriate inflam-
Victoria Niklas - One of the best experts on this subject based on the ideXlab platform.
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Lactoferrin and Necrotizing Enterocolitis.
Current Opinion in Pediatrics, 2014Co-Authors: Michael P Sherman, Mindy M. Miller, Jan Sherman, Victoria NiklasAbstract:There is an intense interest among neonatal caregivers as to whether lactoferrin given enterally may reduce the incidence of Necrotizing Enterocolitis in preterm infants. This review presents scientific and clinical evidence that lactoferrin alleviates or prevents this life-threatening disease. Preclinical studies in neonatal rats showed that lactoferrin given orally before enteral infection with pathogenic Escherichia coli reduced bacteremia and mortality. A multicentered clinical trial found that very low-birth weight preterm infants given bovine lactoferrin had a significant reduction in late-onset sepsis; there was also a trend towards a diminished incidence of Necrotizing Enterocolitis. Although multicentered trials of lactoferrin use in preterm infants are near completion, regulatory burdens required to bring lactoferrin to the bedside may limit its availability. Extremely preterm infants should receive colostrum, a natural lactoferrin concentrate, immediately after birth and, ideally, continue on breast milk throughout the hospital stay. This practice appears well tolerated, but additional experience will tell us whether this practice reduces the prevalence of Necrotizing Enterocolitis.
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Lactoferrin and Necrotizing Enterocolitis.
Current opinion in pediatrics, 2014Co-Authors: Michael P Sherman, Mindy M. Miller, Jan Sherman, Victoria NiklasAbstract:Purpose of review There is an intense interest among neonatal caregivers as to whether lactoferrin given enterally may reduce the incidence of Necrotizing Enterocolitis in preterm infants. This review presents scientific and clinical evidence that lactoferrin alleviates or prevents this life-threatening disease. Recent findings Preclinical studies in neonatal rats showed that lactoferrin given orally before enteral infection with pathogenic Escherichia coli reduced bacteremia and mortality. A multicentered clinical trial found that very low-birth weight preterm infants given bovine lactoferrin had a significant reduction in late-onset sepsis; there was also a trend towards a diminished incidence of Necrotizing Enterocolitis. Although multicentered trials of lactoferrin use in preterm infants are near completion, regulatory burdens required to bring lactoferrin to the bedside may limit its availability. Summary Extremely preterm infants should receive colostrum, a natural lactoferrin concentrate, immediately after birth and, ideally, continue on breast milk throughout the hospital stay. This practice appears well tolerated, but additional experience will tell us whether this practice reduces the prevalence of Necrotizing Enterocolitis.
Pinaki Panigrahi - One of the best experts on this subject based on the ideXlab platform.
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Necrotizing Enterocolitis
Pediatric Drugs, 2006Co-Authors: Pinaki PanigrahiAbstract:Neonatal Necrotizing Enterocolitis is the second most common cause of morbidity in premature infants and requires intensive care over an extended period. Despite advances in medical and surgical techniques, the mortality and long-term morbidity due to Necrotizing Enterocolitis remain very high. Recent advances have shifted the attention of researchers from the classic triad (ischemia, bacteria, and the introduction of a metabolic substrate into the intestine) of Necrotizing Enterocolitis, to gut maturation, feeding practices, and inflammation. The focus on inflammation includes proinflammatory cytokines such as tumor necrosis factor-α, interleukin (IL)-6, IL-18, and platelet-activating factor. Research related to the etiology of Necrotizing Enterocolitis has moved quickly from clostridial toxin to bacterial and other infectious agents. More recently, the pattern of bacterial colonization has been given emphasis rather than the particular species or strain of bacteria or their virulence. Gram-negative bacteria that form part of the normal flora are now speculated as important factors in triggering the injury process in a setting where there is a severe paucity of bacterial species and possible lack of protective Gram-positive organisms. Although the incidence of Necrotizing Enterocolitis has increased because of the survival of low birthweight infants, clinicians are more vigilant in their detection of the early gastrointestinal symptoms of Necrotizing Enterocolitis; however, radiographic demonstration of pneumatosis intestinalis remains the hallmark of Necrotizing Enterocolitis. With prompt diagnosis, a large proportion of infants with Necrotizing Enterocolitis are now able to be managed medically with intravenous fluid and nutrition, nasogastric suction, antibacterials, and close monitoring of physiologic parameters. In the advanced cases that require surgery, clinicians tend to opt for either simple peritoneal drainage (for very small and sick infants) or laparotomy and resection of the affected part. Intestinal transplantation later in life is available as a viable option for those who undergo resection of large segments of the intestine. It is becoming more evident that treatment of this devastating disease is expensive and comes with the toll of significant long-term sequelae. This has resulted in renewed interest in designing alternative strategies to prevent this serious gastrointestinal disease. Simple trophic feeding and the use of L-glutamine and arginine are novel avenues that have been examined. The use of probiotics (‘friendly’ bacterial flora) has been introduced as a promising tool for establishing healthy bacterial flora in the newborn gut to block the injury process that may ultimately lead to Necrotizing Enterocolitis.
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Necrotizing Enterocolitis: a practical guide to its prevention and management.
Paediatric drugs, 2006Co-Authors: Pinaki PanigrahiAbstract:Neonatal Necrotizing Enterocolitis is the second most common cause of morbidity in premature infants and requires intensive care over an extended period. Despite advances in medical and surgical techniques, the mortality and long-term morbidity due to Necrotizing Enterocolitis remain very high. Recent advances have shifted the attention of researchers from the classic triad (ischemia, bacteria, and the introduction of a metabolic substrate into the intestine) of Necrotizing Enterocolitis, to gut maturation, feeding practices, and inflammation. The focus on inflammation includes proinflammatory cytokines such as tumor necrosis factor-alpha, interleukin (IL)-6, IL-18, and platelet-activating factor. Research related to the etiology of Necrotizing Enterocolitis has moved quickly from clostridial toxin to bacterial and other infectious agents. More recently, the pattern of bacterial colonization has been given emphasis rather than the particular species or strain of bacteria or their virulence. Gram-negative bacteria that form part of the normal flora are now speculated as important factors in triggering the injury process in a setting where there is a severe paucity of bacterial species and possible lack of protective Gram-positive organisms. Although the incidence of Necrotizing Enterocolitis has increased because of the survival of low birthweight infants, clinicians are more vigilant in their detection of the early gastrointestinal symptoms of Necrotizing Enterocolitis; however, radiographic demonstration of pneumatosis intestinalis remains the hallmark of Necrotizing Enterocolitis. With prompt diagnosis, a large proportion of infants with Necrotizing Enterocolitis are now able to be managed medically with intravenous fluid and nutrition, nasogastric suction, antibacterials, and close monitoring of physiologic parameters. In the advanced cases that require surgery, clinicians tend to opt for either simple peritoneal drainage (for very small and sick infants) or laparotomy and resection of the affected part. Intestinal transplantation later in life is available as a viable option for those who undergo resection of large segments of the intestine. It is becoming more evident that treatment of this devastating disease is expensive and comes with the toll of significant long-term sequelae. This has resulted in renewed interest in designing alternative strategies to prevent this serious gastrointestinal disease. Simple trophic feeding and the use of L-glutamine and arginine are novel avenues that have been examined. The use of probiotics ('friendly' bacterial flora) has been introduced as a promising tool for establishing healthy bacterial flora in the newborn gut to block the injury process that may ultimately lead to Necrotizing Enterocolitis.
Thomas J. Garite - One of the best experts on this subject based on the ideXlab platform.
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Tocolysis with indomethacin increases the incidence of Necrotizing Enterocolitis in the low-birth-weight neonate
American Journal of Obstetrics and Gynecology, 1994Co-Authors: Carol Major, David F. Lewis, James A. Harding, Manuel A. Porto, Thomas J. GariteAbstract:Objective: The null hypothesis states that prolonged antenatal indomethacin exposure within 24 hours of delivery does not increase the incidence of Necrotizing Enterocolitis in the low-birth-weight neonate. Objective: The neonates of patients receiving indomethacin tocolysis admitted in preterm labor ( N = 56) were compared with the neonates of preterm labor patients who received no indomethacin tocolysis ( N = 703). These neonatal groups were then compared with regard to gestational age at delivery, birth weight, mode of delivery, antenatal magnesium and steroid exposure, incidence of respiratory distress syndrome, perinatal depression, sepsis, umbilical catheterization, and feeding rates and volumes. The overall incidence of Necrotizing Enterocolitis, mortality secondary to Necrotizing Enterocolitis, and the intervals from delivery and feeding to Necrotizing Enterocolitis diagnosis were also compared. The association between Necrotizing Enterocolitis and the duration of indomethacin exposure and the interval from exposure to delivery for both the indomethacin and control groups was determined. Results: The incidence of Necrotizing Enterocolitis in neonates who were delivered within 24 hours of maternal indomethacin therapy was 20% compared with 9% in the control group ( p = 0.005). The incidence of Necrotizing Enterocolitis in neonates with > 48 hours of antenatal indomethacin exposure was 26.4% compared with 4.1% in those with p = 0.042). The interval from first feeding to Necrotizing Enterocolitis development was significantly shorter in the indomethacin group versus the control group (2.1 ± 3.0 vs 6.8 ± 6.3 days) ( p = 0.001), as was the mean interval from delivery to development of Necrotizing Enterocolitis (10.2 ± 3.7 vs 15.2 ± 3.8 days) ( p = 0.019). Conclusions: Antenatal indomethacin exposure occurring within ≤ 24 hours of delivery and of at least 48 hours' duration is associated with a significant increase in the incidence of Necrotizing Enterocolitis in the low-birth-weight neonate.
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Tocolysis with indomethacin increases the incidence of Necrotizing Enterocolitis in the low-birth-weight neonate.
American journal of obstetrics and gynecology, 1994Co-Authors: C A Major, David F. Lewis, James A. Harding, Manuel A. Porto, Thomas J. GariteAbstract:The null hypothesis states that prolonged antenatal indomethacin exposure within 24 hours of delivery does not increase the incidence of Necrotizing Enterocolitis in the low-birth-weight neonate. The neonates of patients receiving indomethacin tocolysis admitted in preterm labor (N = 56) were compared with the neonates of preterm labor patients who received no indomethacin tocolysis (N = 703). These neonatal groups were then compared with regard to gestational age at delivery, birth weight, mode of delivery, antenatal magnesium and steroid exposure, incidence of respiratory distress syndrome, perinatal depression, sepsis, umbilical catheterization, and feeding rates and volumes. The overall incidence of Necrotizing Enterocolitis, mortality secondary to Necrotizing Enterocolitis, and the intervals from delivery and feeding to Necrotizing Enterocolitis diagnosis were also compared. The association between Necrotizing Enterocolitis and the duration of indomethacin exposure and the interval from exposure to delivery for both the indomethacin and control groups was determined. The incidence of Necrotizing Enterocolitis in neonates who were delivered within 24 hours of maternal indomethacin therapy was 20% compared with 9% in the control group (p = 0.005). The incidence of Necrotizing Enterocolitis in neonates with > 48 hours of antenatal indomethacin exposure was 26.4% compared with 4.1% in those with < 48 hours exposure (p = 0.042). The interval from first feeding to Necrotizing Enterocolitis development was significantly shorter in the indomethacin group versus the control group (2.1 +/- 3.0 vs 6.8 +/- 6.3 days) (p = 0.001), as was the mean interval from delivery to development of Necrotizing Enterocolitis (10.2 +/- 3.7 vs 15.2 +/- 3.8 days) (p = 0.019). Antenatal indomethacin exposure occurring within < or = 24 hours of delivery and of at least 48 hours' duration is associated with a significant increase in the incidence of Necrotizing Enterocolitis in the low-birth-weight neonate.
Emily S. Miller - One of the best experts on this subject based on the ideXlab platform.
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Is mode of delivery associated with the risk of Necrotizing Enterocolitis
American Journal of Obstetrics and Gynecology, 2016Co-Authors: Moeun Son, William A Grobman, Emily S. MillerAbstract:Background The pathogenesis of Necrotizing Enterocolitis remains poorly understood. Different newborn bacterial colonization due to cesarean delivery as opposed to vaginal delivery has been implicated as one potential contributing factor. Objective We sought to determine whether mode of delivery is associated with the risk of Necrotizing Enterocolitis in neonates of women who were at imminent risk of delivery Study Design This is a secondary analysis of data from a randomized controlled trial of magnesium sulfate for the prevention of cerebral palsy. The parent trial included women with pregnancies at 24 to 31 6/7 weeks of gestation who were considered at imminent risk for preterm delivery. Women with a viable singleton gestation and data available on mode of delivery and development of Necrotizing Enterocolitis were included. Neonates delivered by vaginal delivery were compared to those delivered by cesarean delivery in bivariable analyses. Multivariable analysis was used to adjust for potential confounders. Results A total of 2012 mother-neonate pairs were analyzed. Of these, 731 (36%) women delivered by cesarean delivery and 170 neonates (8.4%) developed Necrotizing Enterocolitis. In bivariable analyses, women who delivered by cesarean delivery were older (27 [interquartile range, 22-32] vs 24 [interquartile range, 20-29] years, P P = .021) compared to those who delivered vaginally. Neonates delivered by cesarean delivery were more premature (29.3 [interquartile range, 27.1-31.4] vs 30.3 [interquartile range, 27.9-31.9] weeks, P P P = .001), and had a higher frequency of proven sepsis (20.1% vs 14.7%, P = .002) compared to those who delivered vaginally. Rates of Necrotizing Enterocolitis (8.1% vs 8.7%, P = .65) and stage 2 or 3 Necrotizing Enterocolitis (4.4% vs 4.7%, P = .75) did not differ by mode of delivery. After adjusting for potential confounders, cesarean delivery continued to have no association with the frequency of Necrotizing Enterocolitis (adjusted odds ratio, 0.74; 95% confidence interval, 0.52–1.04) or stage 2 or 3 Necrotizing Enterocolitis (adjusted odds ratio, 0.73; 95% confidence interval, 0.46–1.16). This study was powered to detect a minimum relative risk of 1.5 for Necrotizing Enterocolitis associated with mode of delivery. Conclusion Mode of delivery was not significantly associated with Necrotizing Enterocolitis in neonates born to a cohort of women who were considered at imminent risk of extreme preterm delivery.
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Is mode of delivery associated with the risk of Necrotizing Enterocolitis?
American journal of obstetrics and gynecology, 2016Co-Authors: Moeun Son, William A Grobman, Emily S. MillerAbstract:The pathogenesis of Necrotizing Enterocolitis remains poorly understood. Different newborn bacterial colonization due to cesarean delivery as opposed to vaginal delivery has been implicated as one potential contributing factor. We sought to determine whether mode of delivery is associated with the risk of Necrotizing Enterocolitis in neonates of women who were at imminent risk of delivery <32 weeks' gestational age. This is a secondary analysis of data from a randomized controlled trial of magnesium sulfate for the prevention of cerebral palsy. The parent trial included women with pregnancies at 24 to 31 6/7 weeks of gestation who were considered at imminent risk for preterm delivery. Women with a viable singleton gestation and data available on mode of delivery and development of Necrotizing Enterocolitis were included. Neonates delivered by vaginal delivery were compared to those delivered by cesarean delivery in bivariable analyses. Multivariable analysis was used to adjust for potential confounders. A total of 2012 mother-neonate pairs were analyzed. Of these, 731 (36%) women delivered by cesarean delivery and 170 neonates (8.4%) developed Necrotizing Enterocolitis. In bivariable analyses, women who delivered by cesarean delivery were older (27 [interquartile range, 22-32] vs 24 [interquartile range, 20-29] years, P < .001) and had a higher frequency of chorioamnionitis (14.0% vs 10.5%, P = .021) compared to those who delivered vaginally. Neonates delivered by cesarean delivery were more premature (29.3 [interquartile range, 27.1-31.4] vs 30.3 [interquartile range, 27.9-31.9] weeks, P < .001), were smaller (1266 [interquartile range, 920-1643] vs 1465 [interquartile range, 1067-1850] g, P < .001), were more likely to be small for gestational age (4.4% vs 1.9%, P = .001), and had a higher frequency of proven sepsis (20.1% vs 14.7%, P = .002) compared to those who delivered vaginally. Rates of Necrotizing Enterocolitis (8.1% vs 8.7%, P = .65) and stage 2 or 3 Necrotizing Enterocolitis (4.4% vs 4.7%, P = .75) did not differ by mode of delivery. After adjusting for potential confounders, cesarean delivery continued to have no association with the frequency of Necrotizing Enterocolitis (adjusted odds ratio, 0.74; 95% confidence interval, 0.52-1.04) or stage 2 or 3 Necrotizing Enterocolitis (adjusted odds ratio, 0.73; 95% confidence interval, 0.46-1.16). This study was powered to detect a minimum relative risk of 1.5 for Necrotizing Enterocolitis associated with mode of delivery. Mode of delivery was not significantly associated with Necrotizing Enterocolitis in neonates born to a cohort of women who were considered at imminent risk of extreme preterm delivery. Copyright © 2016 Elsevier Inc. All rights reserved.
