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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nenatal necrotizing enterocolitis (NEC) is a disease mainly affects premature infants. It is well known that prematurity, enteral formula feeding, and bacterial colonization are three major risk factors for NEC. Acetic acid, propionic acid and butyric acid are short chain fatty acids (SCFAs), which are produced mainly in the colon by bacterial fermentation of undigested carbohydrates. Although luminal production of modest quantities of SCFAs is essential for normal colonic mucosal function, excessive production/accumulation of SCFAs may arise in premature infants due to increased luminal carbohydrates malabsorption and poor gastrointestinal motility, and may have deleterious effects on mucosal integrity. Therefore, it is proposed that too much luminal short chain fatty acids cause neonatal NEC.
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PMID:Too much short chain fatty acids cause neonatal necrotizing enterocolitis. 1496 41

Glucagon Like Peptide 2 (GLP-2) has been proposed as an important regulatory hormone in nutrient absorption. The present study was conducted in human infants with intestinal dysfunction undergoing surgery, correlating postprandial GLP-2 levels with intestinal length, nutrient absorption, and patient outcome. We hypothesized that GLP-2 levels would be inversely related to nutrient absorption; we further hypothesized that post prandial GLP-2 levels would be predictive of the ability to wean patients from total parenteral nutrition (TPN), and tolerance of enteral feeding. Infants prospectively identified with nutrient malabsorption following intestinal surgery were monitored and after initiation of feeds GLP-2 levels were measured in the fed state. Intestinal length was recorded intraoperatively and nutrient absorption was quantified using both a balance study, and carbohydrate probe method. 12 infants had GLP-2 levels successfully measured; two patients had repeated studies. Average gestational age was 32.7 +/- 3.4 wk, age at testing was 1.7 +/- 1.4 mo and average weight was 3.5 +/- 1.1 kg. Causes of intestinal loss were necrotizing enterocolitis, atresia and volvulus. Five patients had severe short bowel syndrome (<50% of normal small intestinal length), 3 died. GLP-2 levels were best correlated with residual small intestinal length (r2 = 0.75). Correlations with total intestinal length including colon were less significant; residual colon appeared to not contribute to measurable GLP-2 production. GLP-2 levels were well correlated with tolerance of enteral feeds. Contradicting the initial hypothesis, GLP-2 levels were directly correlated with nutrient absorptive capacity (correlation with fat absorption: r2 = 0.72, carbohydrate = 0.50 and protein = 0.54 respectively). There were no apparent changes in GLP-2 levels with gestational or postnatal age. As a corollary to the correlation with bowel length, a postprandial level of 15 pmol/L appeared to be discriminatory; infants with postprandial GLP-2 levels of > 15 pmol/L were able to be weaned from total parenteral nutrition, while 3 of 4 infants who had GLP-2 levels less than 15 could not be weaned by one year. These results show that in infants with intestinal dysfunction, GLP-2 levels are correlated with residual small bowel length and nutrient absorption, and may be predictive of outcome. In contrast to adults with intact colon and SBS, infants with SBS and intact colon do not appear able to produce GLP-2 in response to feeding stimulation. Further studies are suggested to examine the ontogeny of the GLP-2 axis and the possible therapeutic role of GLP-2 supplementation.
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PMID:GLP-2 levels in infants with intestinal dysfunction. 1520 2

The short bowel syndrome is the result of a congenital or acquired loss of a large part of the small intestine. The most frequent causes of surgical resection of the intestine in infants are arterial or venous thrombosis, intestinal volvulus, necrotizing enterocolitis, and Crohn's disease. Symptoms include nutrient and electrolyte malabsorption, steatorrhea and diarrhea, which can result in failure to thrive. The consequences of extensive small bowel resections consist of nutritional deficiencies, gastric acid hypersecretion, nephrolithiasis, cholelithiasis and lactic acidosis. Of these, D-lactic acidosis is an infrequent but important complication because of the symptoms that it can produce. D-lactic acid in the human organism is generated by intestinal bacteria, D-lactate ingestion, or endogenous production in the methyl glycoxylase pathway. Neurological symptoms such as somnolence, ataxia or altered behavior in a patient with short bowel syndrome should make us think of D-lactic acidosis caused by bacterial overgrowth. We present the case of an 11-year-old boy with short bowel syndrome secondary to multiple resections during the postnatal period who was admitted to hospital for episodes of confusion and altered behavior. The diagnosis was lactic acidosis. Outcome was favorable due to prompt instauration of treatment.
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PMID:[D-lactic acidosis in an 11-year-old patient with short bowel syndrome]. 1660 77

Short bowel syndrome (SBS) refers to the malabsorption of nutrients, water, and essential vitamins as a result of disease or surgical removal of parts of the small intestine. The most common reasons for removing part of the small intestine are due to surgical intervention for the treatment of either Crohn's disease or necrotizing enterocolitis. Intestinal adaptation following resection may take weeks to months to be achieved, thus nutritional support requires a variety of therapeutic measures, which include parenteral nutrition. Improper nutrition management can leave the SBS patient malnourished and/or dehydrated, which can be life threatening. The development of therapeutic strategies that reduce both the complications and medical costs associated with SBS/long-term parenteral nutrition while enhancing the intestinal adaptive response would be valuable. Currently, therapeutic options available for the treatment of SBS are limited. There are many potential stimulators of intestinal adaptation including peptide hormones, growth factors, and neuronally-derived components. Glucagon-like peptide-2 (GLP-2) is one potential treatment for gastrointestinal disorders associated with insufficient mucosal function. A significant body of evidence demonstrates that GLP-2 is a trophic hormone that plays an important role in controlling intestinal adaptation. Recent data from clinical trials demonstrate that GLP-2 is safe, well-tolerated, and promotes intestinal growth in SBS patients. However, the mechanism of action and the localization of the glucagon-like peptide-2 receptor (GLP-2R) remains an enigma. This review summarizes the role of a number of mucosal-derived factors that might be involved with intestinal adaptation processes; however, this discussion primarily examines the physiology, mechanism of action, and utility of GLP-2 in the regulation of intestinal mucosal growth.
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PMID:Gut hormones, and short bowel syndrome: the enigmatic role of glucagon-like peptide-2 in the regulation of intestinal adaptation. 1683 Mar 59

This article presents a case study of a newborn with gastroschisis, followed by a retrospective analysis of gastroschisis cases admitted in a single tertiary neonatal intensive care unit over a 5-year period in terms of maternal age, prenatal diagnosis, type of repair, length of stay, and complications. Gastroschisis is an abdominal wall defect resulting from ischemia to blood vessels that supply the abdominal wall during the first trimester of pregnancy. The injury results in an opening in the abdominal wall that allows the abdominal contents, most often intestines and stomach, to develop outside the abdominal cavity. The incidence of gastroschisis is rising, primarily in young mothers aged 20 years or younger. Environmental factors including medication use and nutrition are proposed mechanisms for this association. Surgical management includes techniques for primary repair in which the intestinal contents are immediately closed inside the abdomen, or staged repair if the abdominal cavity is not able to accommodate the volume of intestine. Exposure of the fetal intestine to amniotic fluid can cause inflammation and damage, and significant gastrointestinal problems occur during the neonatal period after closure of the defect. Complications include prolonged ileus, sepsis, associated intestinal atresias, malabsorption, wound infection, and necrotizing enterocolitis.
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PMID:Gastroschisis: incidence, complications, and clinical management in the neonatal intensive care unit. 1730 69

Children with ileostomy can develop short bowel syndrome (SBS), characterized by malabsorption of nutrients and consequent malnutrition. Continuous extracorporeal stool transport (CEST) consists of collecting and transporting the intestinal effluent drained from the proximal stoma to the portion of the distal intestine. Thus, intestinal flux can be maintained, while digestion and absorption approximate real physiology until defecation. We describe the case of a preterm newborn who suffered from necrotizing enterocolitis and who underwent resection of the small intestine and implantation of four stomas. CEST was applied, allowing early reduction of total enteral nutrition and its subsequent withdrawal. This in turn allowed the reduction of those complications associated to the continous use of this therapy (risk of infection and hepatobiliary alterations) and permited keeping the distal intestine in optimal conditions until reconstructive surgery could be performed. Our experience demonstrates that CEST is a safe and relatively simple technique with good results that allows restoration of intestinal homeostasis in neonates with SBS.
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PMID:[Continuous extracorporeal stool transport (CEST) in a preterm infant with proximal ileostomy: report of a case]. 1803 42

Necrotizing enterocolitis (NEC) causes morbidity and mortality among preterm infants and is associated with nutrient malabsorption. Therefore, a preterm pig model that spontaneously develops NEC was used to investigate the relationship between severity of NEC lesions and galactose absorption in vivo and carrier-mediated glucose absorption by intact mid small intestine. Preterm pigs collected by caesarian section at 92% of gestation received parenteral nutrition with and without minimal enteral nutrition for 48 h before conversion to enteral nutrition with colostrum or an enteral formula. Pigs were killed when symptoms of NEC were observed or after 36-40 h of enteral nutrition. NEC lesions decreased in vivo absorption of galactose and mannitol by more than 50% and abolished carrier-mediated glucose uptake by tissues with lesions. Moreover, when NEC lesions were restricted to the colon, small intestinal tissues that seemed clinically healthy had decreased in vitro glucose absorption due to reduced uptake via the sodium-dependent glucose transporter with little or no involvement of the apical facilitative glucose carrier. The present findings reveal a direct relationship between the severity of NEC lesions and the magnitude of sugar malabsorption that is detectable before clinical symptoms are evident.
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PMID:Aldohexose malabsorption in preterm pigs is directly related to the severity of necrotizing enterocolitis. 1835 43

Short bowel syndrome (SBS) is a malabsorptive state occuring as a result of surgical resection or congenital disease of a significant portion of the small intestine . The amount of resection or remaining bowel generally dictates the degree of malabsorption and consequentely the need for specialized enteral nutrition or parenteral nutrition (PN). Intestinal failure in the context of SBS is defined as a dependence on PN to maintain minimal energy and fluid requirement for growth in children. Common causes of SBS in infants and children include necrotizing enterocolitis, midgut volvulus, intestinal atresia, and gastroschisis. Early identification of patients at risk for long-term PN dependency is the first step toward avoiding severe complications. Close monitoring of nutritional status, steady and early introduction of enteral nutrition, and aggressive prevention, diagnosis, and treatment of infections such as central venous catheter sepsis and bacterial overgrowth can significantly improve the prognosis. Intestinal transplantation is an emerging treatment that may be considered when intestinal failure is irreversible and children are experiencing serious complications related to TPN administration.
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PMID:Overview of pediatric short bowel syndrome. 1866 16

Wernicke's encephalopathy (WE) is a metabolic disturbance resulting from severe thiamine deficiency classically described in malnourished alcoholics. Untreated, it can result in stupor, coma, and death. WE has previously been reported as a complication of pregnancy in women with hyperemesis gravidarum. We report a case of WE complicating pregnancy in a woman with chronic malabsorption secondary to premature birth and subsequent necrotizing enterocolitis (NEC). Our patient progressed through classic stages of WE before lapsing into a coma. She made a complete recovery after aggressive intravenous thiamine and nutritional support. This is the first report of WE in pregnancy secondary to NEC-related chronic malabsorption. We report this case to bring attention to a potential pregnancy complication affecting women with malabsorptive conditions.
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PMID:Wernicke's encephalopathy complicating pregnancy in a woman with neonatal necrotizing enterocolitis and resultant chronic malabsorption. 1928 94

Short bowel syndrome (SBS) is the most common cause of intestinal failure in children. It is defined as the inability to maintain adequate nutrition enterally as a result of a major loss of the small intestine. SBS is a life-threatening entity associated with potential significant morbidity and mortality. The etiology in the pediatric age group includes necrotizing enterocolitis (32%), atresia (20%), volvulus (18%), gastroschisis (17%), and aganglionosis (6%). It is characterized by substrate malabsorption, electrolyte imbalance, intestinal bacterial overgrowth, steatorrhea, and weight loss. Current medical management includes parenteral nutrition, progressive feeds as tolerated, various medications, and surgical manipulations. However, frequently this management is not successful in achieving the goal of attaining normal growth and development without parenteral nutrition. It has been known for decades that there is a normal physiologic response of the residual intestine to massive bowel resection referred to as intestinal adaptation. The mechanisms that control this process are unknown. Unfortunately, intestinal adaptation and the current management are not always successful. As a result of new knowledge regarding the pathophysiology of SBS over the past two decades, several novel strategies have been developed in experimental animal models as well as limited clinical trials in infants and children. They can be divided into several categories that potentially influence intestinal (1) absorption, (2) secretion, (3) motility, and (4) adaptation. More recently, newer modalities have been studied including small intestine transplantation, and the use of specific intestinal growth factors. Ultimately, tissue and organ engineering will become the treatment for infants and children with SBS.
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PMID:Novel therapies for the management of short bowel syndrome in children. 2398 26


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