摘要:

For centuries, fermentation of milk products using specific bacteria or cultures has been a way to preserve dairy foods. In 1908, Metchnikoff suggested that ingested lactobacilli could displace toxin-producing microorganisms in the gastrointestinal (GI) tract and thus promote health and prolong life (1). In the latter half of this century, evidence mounted in support of the concept that the preservation of gut microflora in animals is necessary to prevent infections. It was recognized that germ-free animals are more susceptible to infection than animals colonized with microflora (2) and that giving fecal suspensions orally to animals could prevent infection (3). Fecal enemas were successfully administered to humans to controlC. difficileinfection (4); conversely, it was recognized that antibiotics can alter intestinal flora and induce diarrhea. All this information led to the concept that a healthy or balanced microflora is necessary for maintaining the health of the host; one way to maintain balanced microflora is to ingest exogenous bacteria in order to incorporate them into the gut milieu. Many published observations have claimed a variety of health benefits from several microbial agents. Among the benefits attributed to the consumption of these organisms are improvement of lactose absorption and tolerance, control of intestinal infections, anticarcinogenic properties, anticholesterolemic effects, and improvement of GI motility (5,6). These attributions became part of the nutritional folklore that has conferred upon yogurt and other cultured milk products the status of “health foods.‘’

ISSN:0277-2116    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

“We need to look again, without preconceived ideas, at the conditions of children in regions where the weaning diet is particularly low in protein”

ISSN:0277-2116    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Summary:With the improved therapy for acute diarrhea, persistent diarrhea (> 14 days) is emerging as a major problem in developing countries. However, the etiologies and pathogenesis of persistent diarrhea remain poorly understood. We conducted a prospective case-control study in children <3 years old presenting to the hospital with persistent diarrhea in Fortaleza, Brazil. Over the study period (August 1988 to March 1991), 56 children seen with persistent diarrhea, 52 children seen with acute diarrhea, and 42 controls attending the same hospital/clinic for illnesses other than diarrhea were enrolled. A potential pathogen was found in 91% of children with persistent diarrhea and 90% of those with acute diarrhea versus 45% of controls (bothp‘s < 0.01). Thirty-four percent of persistent (19/56) and 38% of acute (20/52) diarrhea cases versus 2% (1/42) of controls (bothp’s < 0.01) had multiple pathogens. EnteroaggregativeEscherichia coli(EAggEC) were found in 68% (38/56) of children with persistent diarrhea versus 31% (13/42) of controls (p< 0.01) and in 46% (24/52) of those with acute diarrhea. Furthermore, when the EAggEC were subdivided into aggregative adherence (AA) gene probe positive (18/56; 32%) and negative (20/56; 36%), both subgroups were still significantly different from controls [6/42 (14%) and 7/42 (17%), respectively; bothp‘s < 0.05]. EAggEC were the sole pathogen in 17 of 56 (30%) of patients with persistent diarrhea [vs. 11/94 (11.7%) in those with acute diarrhea and controls;p< 0.01], and AA gene probe-positive EAggEC were the sole pathogen in 20% of children with persistent diarrhea, whereas only 6% of those with acute diarrhea and 7% of controls had AA probe-positiveE. coli(persistent diarrhea vs. acute diarrhea and controls;p< 0.03) Cryptosporidia were found in 25% (14/56) of children with persistent diarrhea (vs. 5% of controls;p< 0.02). Of 32 children with persistent diarrhea who had quantitative small bowel cultures, 13 (41%) had ≥ 104/ml EAggEC (2 had AA probe-positive EAggEC) in the upper small bowel. Of 10 EAggEC isolated from the small bowel of seven patients with persistent diarrhea, 6 significantly colonized and caused diarrhea in the rabbit-reversible ileal tie model. Both AA gene probe-positive and AA gene probe-negative EAggEC andCryptosporidiumare important potential pathogens in young children with persistent diarrhea and warrant further study to improve our understanding of their pathogenesis and control.

ISSN:0277-2116    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Summary:The American Academy of Pediatrics recommends oral rehydration and early refeeding for management of infants with diarrhea and mild to moderate dehydration. However, intravenous rehydration is still widely used for treatment of infants hospitalized for dehydration. The administration of oral rehydration solution via continuous infusion through a nasogastric tube facilitates its delivery in hospitalized children. The purpose of this study is to compare intravenous and nasogastric rehydration in children hospitalized for mild to moderate dehydration. Infants who failed attempts at oral rehydration and were hospitalized for dehydration due to acute diarrheal illness were randomized to receive intravenous or nasogastric rehydration. Following rehydration, infants received soy formula and a maintenance oral electrolyte solution to replace ongoing stool losses, as directed by the attending physician. Patients were discharged from the hospital once oral feeding was tolerated, and the vomiting and diarrhea resolved. Twenty-four patients, from 2 to 19 months of age, were enrolled in the study. Rehydration was successful in 11 of 12 patients in the nasogastric rehydration group and in all 12 patients who received intravenous rehydration. The degree of dehydration, severity of vomiting and diarrhea, and duration of rehydration were similar in both groups. The duration and cost of hospitalization were less for patients receiving nasogastric rehydration compared to those who were rehydrated intravenously. Rehydration by infusion of oral rehydration solution via a nasogastric tube is a safe and effective treatment for infants with mild to moderate dehydration. Rehydration with infusion of oral rehydration solution through a nasogastric tube should be considered for in-patient management of infants with diarrhea.

ISSN:0277-2116    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Summary:The perianal complications of Crohn's disease (CD) seen in children and adolescents include skin tags, anal fissures, fistulae, and abscesses. White these lesions are often chronic and variably responsive to medical therapy, only rarely are they severely destructive. In this report, we characterize the frequency, severity, and clinical course of a highly destructive form of perianal disease (HDPD) that we have noted in a number of children and adolescents with Crohn's disease. A database containing records from 350 children with inflammatory bowel disease was reviewed to identify all children with CD treated between 1970 and 1993. For each, the occurrence or absence of significant perianal pathology, including fistula, abscess, and HDPD, was determined. Pertinent clinical details were recorded for all patients. In addition, the clinical characteristics of those children with HDPD were compiled, and the courses of those with HDPD characterized. A search of the database identified 230 children and adolescents with CD followed for a total of 1,518 patient years. Sixty-seven of these patients (29% of the CD population) had significant perianal pathology. This included 6 with HDPD, 8 with complicated fistuale [rectourethroperineal (1), rectovaginal (1), rectolabial (2), and multiple communicating perineal (4)], and 53 with simple perianal fistulae or abscesses. All six with HDPD had deeply destructive perineal ulcerations, marked undermining of the perineal and perirectal tissues, and copious exudate, and often there was a deeply cleaved or fileted perineum on separating the buttocks. Two children with HDPD had fecal incontinence. Apart from race (five of six with HDPD were black), there were no significant demographic characteristics that differentiated the children with HDPD from those with perianal fistulae and abscesses. No patient with HDPD had had anal intercourse, lymphogranuloma venereum, condylomata accuminata, or sarcoidosis. None had been sexually abused. In five of six patients with HDPD, perianal disease was the initial and primary manifestation of CD. Three patients failed aggressive medical management [intravenous (iv)/oral (po)/intrarectal corticosteroids + metronidazole (MTZ) (2); iv/po cyclosporine + MTZ + 6-mercaptopurine (1)] and surgery was performed [diverting colostomy (2) with eventual reanastomosis (1), total proctocolectomy (1)]. The HDPD healed completely in two of the three operated patients but remains active, although much improved, 15 months after colostomy in the third. Two patients improved with iv steroids + MTZ and were left with shallow fissures and skin tags or persistent, shallow perianal ulcerations. The remaining child had unchanged HDPD after 2 years of inconsistent MTZ therapy. HDPD is an unusual but important perianal complication of CD for which black children may be at increased risk. The perianal disease is a cause of significant morbidity, is highly resistant to medical therapy, and in some cases only slowly improves following diversion of the fecal stream. Why HDPD occurs is unknown, but the extent of destruction and the resistance to medical therapy make HDPD a difficult problem with a poor prognosis.

ISSN:0277-2116    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Summary:Nonsteroidal antiinflammatory drugs (NSAIDs) are widely used and may cause small intestinal inflammation and damage. Reactive oxygen metabolites are involved in various gastrointestinal inflammatory processes, but there is little information about their role in small intestinal mucosal damage induced by NSAIDs. We studied the effect of the oxygen radical scavengers superoxide dismutase (SOD), catalase (CAT), and allopurinol (ALLO) on indomethacin (INDO)-induced intestinal ulceration in the rat. Ulceration was produced by s.c. injection of 30 mg/kg of INDO 30 min after refeeding 24 h-fasted rats. Total ulcer area was measured 24 h after INDO administration. Study groups each consisted of eight animals which received either i.p. CAT, SOD, or both together, at a dosage of 5,000 U/kg each. All drugs were divided into five doses, given once an hour over a 4-h period, starting at the time of INDO injection. Another group received 100 mg/kg ALLO in two doses. Total ulcer area was reduced by SOD from 228 ± 12 (sq mm, mean ± SEM) to 153 ± 12 (p< 0.001), by CAT to 179 ± 13 (p< 0.01), and by both together to 95 ± 5 (p< 0.0001). ALLO administration reduced the total ulcer area to 176 ± 7 (p< 0.003). The protective effect of oxyradical scavengers supports the hypothesis that oxygen radicals are involved in the pathogenesis of INDO-induced small intestinal ulceration in the rat.

ISSN:0277-2116    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Summary:Partial resection of the small intestine results in compensatory proliferation and adaptation in the remaining small intestinal mucosa. The molecular mechanisms governing the proliferative response are not known, nor has the timing of events associated with proliferation been adequately defined, particularly during the period just after resection. We designed experiments to characterize early (within 24 h) proliferative events associated with proximal intestinal resection and sought to determine the cell type that first responds to proliferative stimuli. Twenty-one day old male Sprague-Dawley rats underwent a 70% proximal intestinal resection or transection (control). Poly(A) RNA was isolated from the distal (ileal) remnants. Northern blots showed a marked induction of the immediate early genes zif-268, nup-475, andc-myc1–3 h following resection, but not following transection. Immunohistochemical analysis ofc-mycexpression in ileal crypt epithelial cells showed a biphasic induction that was most marked 6 h after resection and less prominent 24 h after resection. Immunostaining with 5-bromodeoxyuridine (5-BrdU) was restricted to ileal crypt nuclei and was maximal 24 h after resection. All these events were observed in the absence of nutrient intake. Taken together, these data show that a potent nutrient-independent stimulus for intestinal epithelial cell proliferation occurs within minutes of partial small intestinal resection and that the first targets of this stimulus are crypt epithelial cells in the residual intestine.

ISSN:0277-2116    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Summary:This study was designed to determine whether dietary lipids influence the development of intestinal cell glycosylation, in relationship to diet-induced changes in phospholipid fatty acid composition. The ability of two different lectins, wheat germ agglutinin (WGA) andMaackia amurensisagglutinin (MAA), to combine specifically with particular carbohydrate residues was used to investigate the surface characteristics of epithelial cells of rats fed different dietary lipids from birth to 6 weeks of age. Diets contained 5% (weight) peanut oil (PO), rich in n-6 fatty acids; salmon oil (SO), rich in n-3 fatty acids; hydrogenated palm oil (HPO), deficient in both n-6 and n-3 fatty acids or a PO and rapeseed oil (RO) mixture (PRO), the control diet. Pieces of jejunal and ileal villi were excised from postweanling rats and prepared for lectin histochemical study. Concurrently, epithelial cells were removed from jejunal and ileal segments for determining their phospholipid fatty acid compositions. Polyunsaturated fatty acid (PUFA) deficiency was evidenced in the HPO group by the appearance of eicosatrienoic acid (20:3n-9) in both jejunal and ileal phospholipids, which paralleled the decrease in arachidonic acid content. Accretion of 18: ln-9 and 20:3n-9 in cell phospholipids of group HPO was not sufficient to match the unsaturation level in rats fed nonhydrogenated vegetable oils (PRO, PO) or fish oil (SO). The lectin histochemical study showed that WGA strongly labelled the brush border membrane microvilli whereas binding of MAA was specific to goblet cells and mucus. Regardless of the type of diet, WGA binding was weaker in the ileum than in the jejunum. In comparison to all other groups, WGA-labelling of villi was less intense in the jejunum and disappeared almost completely in the ileum of HPO-fed rats. Although SO- and PO-fed rats had, respectively, very low and high ratios of n-6 to n-3 in their intestinal phospholipids, binding of WGA in both groups was not markedly different from that in the control (PRO). MAA-labelling was very intense in jejunal and ileal villi of n-3-fed (SO) rats, whereas it was strongly attenuated in the n-3− and n-6 deficient (HPO) group. These results suggest that intestinal glycosyltransferase activities involved in cell differentiation were altered relative to the overall unsaturation index of dietary fatty acids. Alterations of epithelial glycosylation mainly resulted from a drop in total n-6 and n-3 fatty acids, although it may be speculated that there is a specific effect of n-3 fatty acids.

ISSN:0277-2116    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Summary:We assessed the growth, tolerance, and acceptability as well as fecal flora composition and stool pH of 20 healthy full-term infants fed with a fermented whey-adapted infant formula containing viable bifidobacteria (106/g of powder) during the first 2 months of life. This fermented infant formula, first biologically acidified byStreptococcus thermophilusandLactobacillus helveticus, was compared to a whey-adapted, nonacidified, low-phosphate infant formula in a double-blind, randomized controlled study. The results were compared to a control group (n = 14) of fully breast-fed infants. The fermented whey-adapted formula containing viable bifidobacteria induced a prevalence of colonization with bifidobacteria at 1 month of age similar to that of breast-fed infants (12/20 versus 8/14) but significantly higher than in the group fed the standard infant formula (4/20). The mean bacterial count of bifidobacteria was similar in all colonized infants; however, fecal pH was significantly lower in the breast-fed infants than in the nonacidified bottle-fed infants. This kind of infant formula was well tolerated and promoted a normal growth during the first 2 months.

ISSN:0277-2116    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Summary:Very low-birth weight (VLBW) infants fed high-calcium and high-phosphorus (10.74 and 6.93 mmol/MJ; 180 and 90 mg/100 kcal, respectively) infant formulas were randomized to one of three levels of vitamin D intake to approximate 200, 400, and 800 IU/day. Sixty-two infants completed the study (24 to 29 days), with actual mean daily vitamin D intakes of 161, 361, and 766 IU, respectively. Outcomes were not different by group: gains in body weight, length and head circumference, serum calcium, magnesium, phosphorus, alkaline phosphatase, osteocalcin, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and urine calcium:creatinine and magnesium:creatinine ratios. There were no radiographic fractures and/or rickets. A subset of 19 infants was followed between 173 and 380 days to determine descriptively if there was any delayed effect of earlier manipulation of vitamin D intake. They were fed standard infant formulas with a vitamin D content of 400 to 420 IU/L. No significant differences were present among the three groups, and data were combined. Serum 25-hydroxyvitamin D increased (p< 0.05), osteocalcin decreased (p< 0.05), and 1,25-dihydroxyvitamin D decreased (p= 0.06) at follow-up. Thus, for VLBW infants fed high-calcium and high-phosphorus milk, an average daily vitamin D intake as low as 160 IU maintains normal and stable vitamin D status and normal physical growth, biochemical and hormonal indexes of bone mineral metabolism, and skeletal radiographs versus randomized infants receiving about 400 or 800 IU of vitamin D per day. On follow-up, vitamin D status remained normal for ≥ 6 months while infants received <400 IU of vitamin D per day.

ISSN:0277-2116    

出版商:OVID    

年代:1995

数据来源: OVID