Normal Intestinal Absorption Research Articles

Vertebral compression fractures in pediatric patients with intestinal failure: A prospective observational case series.

BackgroundIntestinal failure associated bone disease (IFABD) poses a significant threat to bone health in pediatric patients with intestinal failure (IF) reliant on life-saving parenteral nutrition (PN). MethodsThis observational study sought to determine the prevalence of vertebral fractures (VF) detected through lateral thoracolumbar x-rays using Genant criteria in pediatric patients with IF at a single center. It was conducted as part of a larger observational database study of intestinal failure long term outcomes. ResultsFourteen out of 79 patients with IF were included in the study. The median age of our cohort was 9 years. Short bowel syndrome (SBS) was the cause of IF in nine patients (64 %), with two patients each having a pediatric onset congenital diarrhea & enteropathy (14 %) or dysmotility (14 %) as their primary IF diagnosis, and one patient (7 %) with normal intestinal length and absorption, requiring PN for growth support in the context of chronic vomiting. Three of 14 participants (21 %) had vertebral fractures confirmed on x-rays, two of whom were asymptomatic. Notably, bisphosphonate therapy was initiated in one patient with VF, highlighting the clinical impact of early detection. ConclusionDespite study limitations, including a small single center sample size, the identification of VF in 3 out of the 14 participants underscores the need for further investigation in pediatric patients with IF, especially because 2 of these 3 patients were asymptomatic. Multicenter studies in the future may explore risk factors for VF to create guidelines for radiographic screening, surveillance, and treatment in this pediatric population.

Research Progress of Intestinal Microecology in the Pathogenesis of Colorectal Adenoma and Carcinogenesis.

Colorectal adenoma is a precancerous lesion that may progress to colorectal cancer. Patients with colorectal adenoma had a 4-fold higher risk of developing colorectal malignancy than the rest of the population, with approximately 80% of colorectal cancer originating from colorectal adenoma. Therefore, preventing the occurrence and progression of colorectal adenoma is crucial in reducing the risk for colorectal cancer. The human intestinal microecology is a complex system consisting of numerous microbial communities with a sophisticated structure. Interactions among intestinal microorganisms play crucial roles in maintaining normal intestinal structure, digestion, absorption, metabolism, and other functions. The colorectal system is the largest microbial bank or fermentation system in the human body. Studies suggest that intestinal microecological imbalance, one of the most important environmental factors, may play an essential role in the occurrence and development of colorectal adenoma and colorectal cancer. Based on the complexity of studying the gut microbiota ecosystem, its specific role in the occurrence and development of colorectal adenoma is yet to be elucidated. In addition, further studies are expected to provide new insights regarding the prevention and treatment of colorectal adenoma. This article reviews the relationship and mechanism of the diversity of the gut microbiota, the relevant inflammatory response, immune regulation, and metabolic changes in the presence of colorectal adenomas.

Effects of antimicrobial peptides on growth performance and small intestinal function in broilers under chronic heat stress

Thirty-six 16-day-old broiler chicks were used to assess the effects of swine gut intestinal antimicrobial peptides (SGAMP) on growth performance and small intestinal function of broilers under chronic heat stress. The results showed that compared with the heat stress group, the SGAMP added group showed greater average daily gain and feed efficiency, less histological and ultrastructural lesions, greater height of villus and thickness of gut mucosa, greater activity of alkaline phosphatase, more intestine intraepithelial lymphocytes, higher ratio of secreting IgA, less goblet cell number, and lower ratios of proliferating cell nuclear antigen, heat shock protein 70, and glucose-6-phosphatase (P < 0.05 or P < 0.01). These results indicated that SGAMP could effectively resist the adverse effects of chronic heat stress by reducing the intestinal injury and maintaining the normal intestinal structure, absorption function, and mucosal immunity in broilers under heat stress.

Disruption of the sugar-sensing receptor T1R2 attenuates metabolic derangements associated with diet-induced obesity.

Sweet taste receptors (STRs) on the tongue mediate gustatory sweet sensing, but their expression in the gut, pancreas, and adipose tissue suggests a physiological contribution to whole body nutrient sensing and metabolism. However, little is known about the function and contribution of these sugar sensors during metabolic stress induced by overnutrition and subsequent obesity. Here, we investigated the effects of high-fat/low-carbohydrate (HF/LC) diet on glucose homeostasis and energy balance in mice with global disruption of the sweet taste receptor protein T1R2. We assessed body composition, energy balance, glucose homeostasis, and tissue-specific nutrient metabolism in T1R2 knockout (T1R2-KO) mice fed a HF/LC diet for 12 wk. HF/LC diet-fed T1R2-KO mice gained a similar amount of body mass as did WT mice, but had reduced fat mass and increased lean mass relative to WT mice. T1R2-KO mice were also hyperphagic and hyperactive. Ablation of the T1R2 sugar sensor protected mice from HF/LC diet-induced hyperinsulinemia and altered substrate utilization, including increased rates of glucose oxidation and decreased liver triglyceride (TG) accumulation, despite normal intestinal fat absorption. Finally, STRs (T1r2/T1r3) were upregulated in the adipose tissue of WT mice in response to HF/LC diet, and their expression positively correlated with fat mass and glucose intolerance. The chemosensory receptor T1R2, plays an important role in glucose homeostasis during diet-induced obesity through the regulation of yet to be identified molecular mechanisms that alter energy disposal and utilization in peripheral tissues.

New Options for Iron Supplementation in Maintenance Hemodialysis Patients

End-stage renal disease results in anemia caused by shortened erythrocyte survival, erythropoietin deficiency, hepcidin-mediated impairment of intestinal absorption and iron release, recurrent blood loss, and impaired responsiveness to erythropoiesis-stimulating agents (ESAs). Iron malabsorption renders oral iron products generally ineffective, and intravenous (IV) iron supplementation is required in most patients receiving maintenance hemodialysis (HD). IV iron is administered at doses far exceeding normal intestinal iron absorption. Moreover, by bypassing physiologic safeguards, indiscriminate use of IV iron overwhelms transferrin, imposing stress on the reticuloendothelial system that can have long-term adverse consequences. Unlike conventional oral iron preparations, ferric citrate has recently been shown to be effective in increasing serum ferritin, hemoglobin, and transferrin saturation values while significantly reducing IV iron and ESA requirements in patients treated with HD. Ferric pyrophosphate citrate is a novel iron salt delivered by dialysate; by directly reaching transferrin, its obviates the need for storing administered iron and increases transferrin saturation without increasing serum ferritin levels. Ferric pyrophosphate citrate trials have demonstrated effective iron delivery and stable hemoglobin levels with significant reductions in ESA and IV iron requirements. To date, the long-term safety of using these routes of iron administration in patients receiving HD has not been compared to IV iron and therefore awaits future investigations.

Update on intravenous iron choices

Iron deficiency is a major factor in the prevalence and severity of anemia in patients with chronic kidney disease (CKD). We review the pathophysiology impairing normal intestinal iron absorption in CKD and compare the characteristics of newer intravenous (i.v.) iron agents to the longstanding i.v. iron products in the market. The newer iron products, ferumoxytol, ferric carboxymaltose, and iron isomaltoside, more avidly bind iron, minimizing the release of labile iron during infusions, thus permitting large dose infusions. These irons also have more complex carbohydrate shells than their predecessors, which may also diminish reactions. Newer agents can be routinely administered at higher single doses, in as little as 15 min, with an acceptable safety profile. Newer i.v. iron products permit the rapid, and sometimes complete, repletion of iron-deficient patients with a single dose. However, further studies examining the long-term risks and benefits of i.v. iron repletion are needed.

Effect of quinoa (Chenopodium quinoa, W) on the intestinal mucosa of growing Wistar rats

In previous studies, we characterized the nutritional properties of quinoa from Argentinean Northwest. Moreover, quinoa seeds have a high content of saponins that give them a bitter taste and may alter the intestinal mucosa due to their detergent properties.Aimto study the effect of a variety of quinoa from Campo Tapial de Colanzuli, Iruya, Salta, without washing treatment, on the intestinal mucosa of growing rats.Materials and MethodsWistar rats (n=6/group) fed from weaning to 7 days a 10% protein diet with 1) unwashed quinoa (Q), 2) commercial washed quinoa (QR), 3) casein (C) as control group. Body weight (BW,g) and diet intake (I, g/day) were determined and ponderal growth rate (PGR, g/day/100g) was calculated. Intestines were removed and stained with Alcian Blue‐H/E. Goblets cells/100 epithelial cells (GC) were determined in 10 intestinal villi/rat. IL‐17 was characterized in lamina propria (LP) and intraepithelium (iIEL) by IFI (cells+/ 30 fields).Statistical analysisANOVA‐SNK/Kruskal‐Wallis.Results(Mean±SD) Q QR C BW 45.0±2.7a 60.0±5.4b 69.7±6.4c PGR −1.97±0.6a 1.63±0.5b 3.95±0.9c I 4.7±03 a 6.9±1.0ab 8.4±0.6b GC 24.2±6.5b 14.7±2.7a 10.9±1.2a IL‐17 LP 60.3±9.0b 41.7±4.6a 38.0±3.9a IL‐17 iIEL 9.3±4.2 a 10.5±3.7 a 9.0±1.6 a Means within rows with different superscript, differ 0.05&gt; p &lt;0.001 ConclusionGC and IL‐17 were significant increased in Q group which could indicate an inflammatory process caused by the saponins from unwashed quinoa. This could affect the normal intestinal absorption of nutrients which is reflected in BW, PGR and I, compared to QR group.Supported by UBACyT 20020100100255 y 20620100100014

Role of cysteine residues in cell surface expression of the human riboflavin transporter-2 (hRFT2) in intestinal epithelial cells.

The water-soluble vitamin B2 (riboflavin, RF) is an essential micronutrient for normal cell function and survival. Recent studies have identified a role for the human riboflavin transporter-2 (hRFT2) in normal intestinal RF absorption. However, little is known about the cell biology of this transporter and specifically about the molecular determinant(s) that dictate its cell surface expression in human intestinal epithelial cells. Here we show that the full-length hRFT2 protein fused to green fluorescent protein (GFP) (GFP-hRFT2) is expressed exclusively at the apical membrane domain of Caco-2 cells. COOH-terminal sequence was essential in dictating cell surface expression with a specific role for conserved cysteine residues (C463 and C467). Mutation of C463 and C467 ablated RF uptake, explained by retention of the constructs within the endoplasmic reticulum. Modeling analysis suggested a potential disulfide bridge between C463 and C386. Consistent with this prediction, mutating the C386 site in the context of the full-length transporter resulted in intracellular retention, whereas mutation of another conserved cysteine (C326A) was without effect on hRFT2 targeting. Intracellular trafficking of hRFT2 was also examined and appeared to involve distinct vesicular structures, the motility of vesicles critically dependent on an intact microtubule network. These results demonstrate a potential role for specific cysteine residues in the cell surface expression of the hRFT2 in human intestinal epithelial cells.

Mechanisms of Diarrhea

Diarrhea is a symptom common to a wide variety of gastrointestinal illnesses, and is an important public health challenge in underdeveloped regions of the world. Normal intestinal absorption is a complex process. Recent research offers new insights into normal physiology and pathophysiology. The role of the enteric nervous system and neurotransmitters in the pathogenesis of diarrhea in inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) is being actively investigated. In patients with IBD, ileal and sigmoid biopsies showed altered transepithelial sodium and fluid transport, specifically from decreased expression of the NHE3, NHERF-1, and NHE1 epithelial Na channel. This results in changes in normal intestinal electroneutral NaCl absorption and may be an additional factor contributing to the diarrhea in patients with IBD. Physiologic studies in humans suggest that primary bile acid malabsorption may be caused by an abnormal feedback system resulting in the increased bile salts, which may explain the watery diarrhea. Finally, the role of zinc in treatment of infectious diarrhea led to studies of its effect on intracellular human enterocyte ion secretion. Understanding such basic mechanisms may lead to better and novel therapies for treatment of diarrhea.

Intermittent dosage of imatinib mesylate in CML patients with a history of significant hematologic toxicity after standard dosing

Hematologic toxicity is reported as one of the most important problems connected with imatinib mesylate (IM) treatment in patients with chronic myelogenous leukemia (CML). Withholding the drug or application of growth factors is recommended in this situation. This study introduced a novel approach using intermittent dosage of IM in order to avoid prolonged interruptions in therapy, to allow spontaneous recovery in blood count and, simultaneously, to achieve intermittently therapeutic plasma drug levels. A retrospective analysis of intermittent therapy (iT) in 12 patients with CML is presented. All patients had intermediate-to-high prognostic scores. Two patients had history of autologous stem cell transplantation. Initial standard therapy with IM was indicated for resistance to interferon (eight subjects) and for accelerated phase in four cases (one of them cytogenetic) and lasted for 1 – 6 months. iT with 300 – 600 mg of IM 1 – 5 times a week was started after significant hematologic toxicity occurred. In three patients treated 3 – 5 times a week, hematologic recovery allowed reintroduction of full dose after 3 – 7 (mean 4.6) months. In three patients, one-to-three doses per week were sufficient to maintain the cytogenetic response for a mean of 30.6 months (range 29 – 33). Six patients tolerated more frequent dosage of 4 – 5 times a week for a mean of 17.8 months (range 3 – 28). Five patients improved their cytogenetic response during iT, while hematologic progression occurred in one patient. Development of a cytogenetic abnormality in a Ph-negative clone was observed in one patient. Overall, two complete and five major cytogenetic responses were achieved. The sensitivity of Bcr/Abl kinase to inhibition by IM was proved in seven patients tested by Crkl phosphorylation assay. Measurement of plasma IM concentrations in three subjects showed concentrations fully compatible with the dosage applied suggesting normal intestinal absorption. iT with IM is a feasible and safe strategy for short-time ‘bridging’ management of patients with significant hematologic toxicity after standard daily dosing. Long-term iT with IM does not seem to compromise the cytogenetic response in patients with sensitivity of Bcr/Abl kinase to IM and should be considered as a plausible treatment option in patients with persistent signs of myelotoxicity.

Lack of the intestinal Muc1 mucin impairs cholesterol uptake and absorption but not fatty acid uptake in Muc1-/- mice.

Before cholesterol and fatty acid molecules in the small intestinal lumen can interact with their possible transporters for uptake and absorption, they must pass through a diffusion barrier, which may modify the kinetics of nutrient assimilation. This barrier includes an unstirred water layer and a surface mucous coat, which is located at the intestinal lumen-membrane interface. In the present study, we investigated whether disruption of the mucin gene (Muc)1 may influence intestinal uptake and absorption of cholesterol and fatty acid in male Muc1(-/-) mice. The wild-type mice displayed relatively high levels of Muc1, Muc2, Muc3, and Muc4 mRNAs and relatively low levels of Muc5ac and Muc5b mRNAs in the small intestine. The absence of Muc1 mRNA and protein in the small intestines of Muc1(-/-) mice confirmed complete knockout of the Muc1 gene, but the mRNA expression for other mucin genes remained unchanged. Intestinal uptake and absorption of cholesterol but not palmitic acid were significantly reduced in Muc1(-/-) mice compared with the wild-type mice. However, knockout of the Muc1 gene did not impair either expression levels of the genes that encode intestinal sterol efflux transporters Abcg5 and Abcg8 and fatty acid transporter Fatp4 or small intestinal transit rates. We conclude that physiological levels of the epithelial mucin produced by the Muc1 gene are necessary for normal intestinal uptake and absorption of cholesterol in mice. Our study implies that because cholesterol absorption efficiency is reduced by approximately 50% in Muc1-deficient mice, there may be one or more additional pathways for cholesterol absorption.

Expression and promoter analysis of SLC19A2 in the human intestine

The molecular mechanism and regulation of the intestinal uptake process of dietary thiamine is not well understood. Previous studies have established the involvement of a carrier-mediated system for thiamine uptake in the human intestine. Recently a human thiamine transporter, SLC19A2, was cloned from a number of human tissues. Little, however, is known about expression of the SLC19A2 message along the native human gastrointestinal tract, and no analysis of its promoter in intestinal tissue is available. Therefore, the current studies were aimed at investigating the expression of SLC19A2 in the human gastrointestinal tract and at analyzing the promoter of this potential intestinal thiamine transporter. First we cloned SLC19A2 cDNA from a human intestinal cell line (Caco-2) by reverse transcriptase–polymerase chain reaction, then used this cDNA as a probe in Northern blot analysis. SLC19A2 message was found to be expressed in all gastrointestinal tissues in the following order: liver>stomach>duodenum>jejunum>colon>cecum>rectum>ileum. SLC19A2 was also expressed at the protein level in Caco-2 cells and in native human small intestine by Western blot analysis. We also cloned the 5′-regulatory region of the SLC19A2 gene and confirmed activity of its promoter following transfection into intestinal epithelial Caco-2 cells. Furthermore, we identified the minimal promoter region required for basal activity of SLC19A2 in these cells which was found to be mainly encoded in a sequence between −356 and −36, and included multiple cis-regulatory elements. Transcription initiation sites of the SLC19A2 gene in intestinal epithelial Caco-2 cells were also identified by 5′-rapid amplification of cDNA ends. These results demonstrate that SLC19A2 is expressed in various regions of the human gastrointestinal tract. In addition, the results provide the first characterization of the SLC19A2 promoter. These findings raise the possibility that SLC19A2 may play a role in the normal intestinal thiamine absorption process.

Apolipoprotein C-III deficiency accelerates triglyceride hydrolysis by lipoprotein lipase in wild-type and apoE knockout mice

Previous studies with hypertriglyceridemic APOC3 transgenic mice have suggested that apolipoprotein C-III (apoC-III) may inhibit either the apoE-mediated hepatic uptake of TG-rich lipoproteins and/or the lipoprotein lipase (LPL)-mediated hydrolysis of TG. Accordingly, apoC3 knockout (apoC3−/−) mice are hypotriglyceridemic. In the present study, we attempted to elucidate the mechanism(s) underlying these phenomena by intercrossing apoC3−/− mice with apoE−/− mice to study the effects of apoC-III deficiency against a hyperlipidemic background. Similar to apoE+/+apoC3−/− mice, apoE−/−apoC3−/− mice exhibited a marked reduction in VLDL cholesterol and TG, indicating that the mechanism(s) by which apoC-III deficiency exerts its lipid-lowering effect act independent of apoE. On both backgrounds, apoC3−/− mice showed normal intestinal lipid absorption and hepatic VLDL TG secretion. However, turnover studies showed that TG-labeled emulsion particles were cleared much more rapidly in apoC3−/− mice, whereas the clearance of VLDL apoB, as a marker for whole particle uptake by the liver, was not affected. Furthermore, it was shown that cholesteryl oleate-labeled particles were also cleared faster in apoC3−/− mice. Thus the mechanisms underlying the hypolipidemia in apoC3−/− mice involve both a more efficient hydrolysis of VLDL TG as well as an enhanced selective clearance of VLDL cholesteryl esters from plasma.In summary, our studies of apoC3−/− mice support the concept that apoC-III is an effective inhibitor of VLDL TG hydrolysis and reveal a potential regulating role for apoC-III with respect to the selective uptake of cholesteryl esters.

Choroidal calcifications in patients with Gitelman’s syndrome

Gitelman’s syndrome is a renal tubular disorder characterized by a sodium and chloride reabsorption defect in distal tubular cells that determines hypokalemia, metabolic alkalosis, hypomagnesemia, and low calcium excretion. The presence of choroidal calcifications was sought in five patients with Gitelman’s syndrome by ophthalmic examination, fluorescein angiography, indocyanine green angiography, and ocular ultrasonography. Calcifications observed in the choroid of two patients were shown by ultrasonography in both patients. Ophthalmic and fluorangiographic examinations detected this alteration in one of the two subjects. Chondrocalcinosis was found in one patient with choroidal calcifications. These findings suggest that precipitation of calcium salts can occur in the choroidal tissue of patients with Gitelman’s syndrome. Deposits appeared to be well seen by ultrasonography because of their depth in ocular tissues. Sclerochoroidal calcifications may be favored by the low calcium excretion, which is associated with normal intestinal calcium absorption in patients with Gitelman’s syndrome.

Nramp2 is mutated in the anemic Belgrade (b) rat: evidence of a role for Nramp2 in endosomal iron transport.

The Belgrade (b) rat has an autosomal recessively inherited, microcytic, hypochromic anemia associated with abnormal reticulocyte iron uptake and gastrointestinal iron absorption. The b reticulocyte defect appears to be failure of iron transport out of endosomes within the transferrin cycle. Aspects of this phenotype are similar to those reported for the microcytic anemia (mk) mutation in the mouse. Recently, mk has been attributed to a missense mutation in the gene encoding the putative iron transporter protein Nramp2. To investigate the possibility that Nramp2 was also mutated in the b rat, we established linkage of the phenotype to the centromeric portion of rat chromosome 7. This region exhibits synteny to the chromosomal location of Nramp2 in the mouse. A polymorphism within the rat Nramp2 gene cosegregated with the b phenotype. A glycine-to-arginine missense mutation (G185R) was present in the b Nramp2 gene, but not in the normal allele. Strikingly, this amino acid alteration is the same as that seen in the mk mouse. Functional studies of the protein encoded by the b allele of rat Nramp2 demonstrated that the mutation disrupted iron transport. These results confirm the hypothesis that Nramp2 is the protein defective in the Belgrade rat and raise the possibility that the phenotype shared by mk and b animals is unique to the G185R mutation. Furthermore, the phenotypic characteristics of these animals indicate that Nramp2 is essential both for normal intestinal iron absorption and for transport of iron out of the transferrin cycle endosome.

Normal intestinal dietary fat and cholesterol absorption, intestinal apolipoprotein B (ApoB) mRNA levels, and ApoB-48 synthesis in a hypobetalipoproteinemic kindred without any ApoB truncation

The purpose of this study was to characterize intestinal apolipoprotein B (apoB) metabolism in subjects with familial hypobetalipoproteinemia (FHBL), where segregation analysis supports linkage to the apoB gene but no apoB truncations are present. We investigated cholesterol and fat absorption, intestinal apoB mRNA synthesis and editing, as well as apoB-48 synthesis. Plasma triglycerides (TG) and retinyl palmitate in the chylomicron fractions were analyzed after 12 hours of fasting and then repeatedly for 14 hours after ingestion of a vitamin A—containing high-fat meal. Cholesterol absorption was assessed using a dual stable-isotope method. Mean peak times and concentrations and areas under the curve (AUCs) for fat absorption and mean percentages of cholesterol absorption were comparable in affected and nonaffected family members. Intestinal biopsies were extracted for total RNA and also incubated with 35 S-methionine for measurements of apoB synthesis. Similar quantities of apoB mRNA were found to be expressed in the intestine in affected and control subjects by RNase protection assay. ApoB mRNA editing assay showed that the majority of apoB-100 mRNA was edited to the apoB-48 form to a similar extent in both groups. Virtually no apoB-100 protein was synthesized by the intestine in any subject, and apoB-48 protein synthesis was not significantly different in the affected individuals. These data are consistent with in vivo metabolism data that show normal production rates for liver-derived apoB-100 but increased apoB-100 fractional catabolic rates in affected members of this family. Thus, the molecular defect probably does not affect transcription, translation, or secretion of apoB-containing lipoproteins, but may instead affect their clearance.

Clinical Aspects of Trace Elements: Zinc in Human Nutrition – Zinc Metabolism

Although zinc has been the most intensely studied trace element, much remains to be learned about its metabolism. Little is known about the normal mechanisms of absorption and transport across the intestinal tract. In addition, numerous unknowns surround the intricacies of bodily zinc homeostasis. Part two of this five-part review presents current views on the normal intestinal absorption, intracellular and extracellular metabolism, transport, excretion and homeostasis of zinc in the human body. The alterations in zinc metabolism that occur with age and changing physiological conditions are also discussed.

Intestinal absorption and excretion of octapeptides composed of D amino acids.

Octapeptides synthesized from D amino acids were absorbed from the intestine and excreted in urine of normal rats drinking 5% glucose/1% creatinine containing the 125I-labeled peptides at 0.1-25 mg/dl. The rats ingested fluid at the rate of about 20 ml/hr and produced urine at 15 ml/hr for several hours during the nocturnal feeding period. Sixty-one +/- 4% of the ingested creatinine and 50 +/- 3% of a lipid-insoluble D octapeptide (EASASYSA, 784 Da) were excreted intact in the urine. The steady-state molar rate of absorption-excretion of creatinine equaled or exceeded the maximum rate of carrier-mediated intestinal transport of glucose, suggesting that both the creatinine and the D octapeptide were transported paracellularly by solvent drag through absorptive cell junctions that were dilated by the glucose. More than 70% of the ingested glucose was also absorbed paracellularly. The results demonstrate that intact oligopeptides can be absorbed efficiently from the intestine when they are not hydrolyzed by membrane-bound peptidases of the brush border. The results also provide support for recent theories proposing that coupling of membrane digestion with paracellular solvent drag accounts for a major fraction of normal intestinal absorption of nutrients.

Aspergillose invasive en réanimation chirurgicale

Aspergillosis is a rare event in intensive care patients. Three cases of invasive aspergillosis due to Aspergillus fumigatus were diagnosed in a surgical critical care unit. Risk factors for aspergillosis were found in two liver transplanted patients. One of them had a primitive cutaneous aspergillosis, and the other, treatment difficulties due to the unavailability of an injectable preparation of itraconazole, a new triazole antifungal agent efficient against Aspergillus species. The third case occurred in a patient who had had surgery for gastric carcinoma with liver metastasis. The mycological examination of the air and workbench in the patients' rooms disclosed between 2 and 13 CFU · mm −3 of different Aspergillus species. Plasma itraconazole concentrations were measured in one patient only. They were below the therapeutic range, probably because of intestinal disturbances. The oral administration of itraconazole capsules through gastro-intestinal feeding tubes results in a poor availability of the drug. Such a technique of administration should therefore be undertaken with larger doses than those commonly recommended. Moreover, itraconazole plasma concentrations should be monitored. The association with amphotericin B is recommended until normal intestinal absorption has been obtained.

Microbial contamination of enteral feeding tubes occurring during nutritional treatment.

Enteral nutrition is an effective treatment for catabolic patients with normal intestinal absorption. However, tube-fed patients are at risk from superinfection. Our study is the first to evaluate in vivo the microbial contamination of solutions staying in the nasogastric tube of cancer patients receiving nutritional preparations. After daily feeding, the tube was rinsed with nonsterile tap water. Tap water staying overnight in the tube was considered as tube-rinsing solution. Microbial burden of nutritional preparations was determined on the fifth day of enteral nutrition, from opening the first container and throughout feeding. The next day, a sample of the tube-rinsing solution was cultured. All bacterial species were identified and antibiotic susceptibility pattern was assessed. Thirty-one cancer patients were included, 12 on the hospital's preparations and 19 on commercial feeding. Seven of the hospital--and none of the commercial--preparations were contaminated. Among the 48 samples collected during feeding, 16 were contaminated, including 10 hospital and 6 commercial preparations. All the 31 tube-rinsing solutions were contaminated and 102 strains cultured. Their median concentration was 10(6) colony-forming units/mL (range 10-10(10)). The strains were 48 Enterobacteriaceae, 20 group D streptococci, 9 Candida albicans, 9 Pseudomonas aeruginosa, and 16 others. Multiple antibiotic resistance was present in 12 of the 102 strains. Lower resistance was present in 33. The predominant microorganism of the tube-rinsing solution caused a bacterial colonization for three febrile patients. In conclusion, the feeding tube is an important reservoir for multiple antibiotic-resistant bacteria.