Vitamin B12 status, methylmalonic acidemia, and bacterial overgrowth in short bowel syndrome.
Pediatric Gastroenterology, Hepatology, and Nutrition, University of Chicago, Chicago, IL 60637, USA.Journal of pediatric gastroenterology and nutrition (Impact Factor: 2.18). 05/2009; 48(4):495-7. DOI: 10.1097/MPG.0b013e31817f9e5b
Chapter: Bacterial Overgrowth[Show abstract] [Hide abstract]
ABSTRACT: The human gastrointestinal tract typically contains 300–500 bacterial species. Most bacterial species are acquired during the birth process and although some changes to the flora may occur during later stages of life, the composition of the intestinal microflora remains relatively constant. Small bowel bacterial overgrowth (SBBO) is defined as an excessive increase in the number of bacteria in the upper gastrointestinal tract leading to the development of symptoms. Etiologic factors in the development of SBBO include anatomic abnormalities, functional abnormalities including altered intestinal motility, and multifactorial issues such as malnutrition of the host and abnormalities of the immune system. Symptoms of SBBO include abdominal cramping, bloating, diarrhea, dyspepsia, and/or weight loss. Systemic distribution of bacterial antigen–antibody complexes may cause rashes, arthritis, and nephritis. Colitis or ileitis may also occur due to SBBO. Although diagnosis of bacterial overgrowth is classically based upon demonstration of an increase of bacterial content by aspiration and culture of upper intestinal fluids, these methods have several limitations. For this reason, a variety of non-invasive diagnostic tests have been devised for the diagnosis of SBBO. A hydrogen breath test is the most common method used. Alternative tests include the measurement of the byproducts of luminal bacteria metabolism in urine or blood and small bowel biopsies demonstrating often inflammatory changes. Treatment of SBBO commonly involves rotating broad-spectrum oral antibiotics. When significant intestinal inflammation is present, anti-inflammatory therapy with sulfasalazine or corticosteroids may be used. Regular toileting and colonic flushing with may also be used. Surgical corrections of anatomic abnormalities, such as stricture, fistula, diverticuli, are often helpful. Segments of dilated, poorly peristaltic bowel may be corrected with lengthening operations. Probiotic therapy in SBBO may be effective in reducing the use of antibiotic therapy and controlling symptoms; however, conclusive studies are needed. Nutritional support is an essential part of the management of SBBO both as a therapeutic measure and in the prevention of malnutrition.Textbook of Gastroenterology, 02/2009: pages 1284 - 1294; , ISBN: 9781444303254
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ABSTRACT: The mechanical properties of SiCf/SiC composites have been investigated, based on detailed analyses of their microstructure. SiCf/SiC composites were prepared from fiber preforms by a slurry infiltration technique, in which a mixture with SiC, Al2O3, and Y2O3 particles was impregnated into the fabric structure. SiCf/SiC composites were consolidated by liquid phase sintering process, associated with the creation of secondary phases by the addition of Al2O3 and Y2O3 particles. The reinforcing material was a plain weave Tyranno SA SiC fabric with a carbon interfacial layer. The sintered density and the pore volume fraction of SiCf/SiC composites were about 3.0Mg/m3 and about 10%, respectively. These SiCf/SiC composites had an average flexural strength of about 250MPa at room temperature. They exhibited pseudo-ductile fracture behavior, due to the carbon interfacial layer. The introduction of the carbon interfacial layer greatly improved the fracture energy of SiCf/SiC composites.Journal of Nuclear Materials 10/2011; 417(1):344-347. · 2.02 Impact Factor
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ABSTRACT: Cobalamin deficiency is relatively common, but the great majority of cases in epidemiologic surveys have subclinical cobalamin deficiency (SCCD), not classical clinical deficiency. Because SCCD has no known clinical expression, its diagnosis depends solely on biochemical biomarkers, whose optimal application becomes crucial yet remains unsettled. This review critically examines the current diagnostic concepts, tools, and interpretations. Their exploration begins with understanding that SCCD differs from clinical deficiency not just in degree of deficiency but in fundamental pathophysiology, causes, likelihood and rate of progression, and known health risks (the causation of which by SCCD awaits proof by randomized clinical trials). Conclusions from SCCD data, therefore, often may not apply to clinical deficiency and vice versa. Although many investigators view cobalamin testing as unreliable, cobalamin, like all diagnostic biomarkers, performs satisfactorily in clinical deficiency but less well in SCCD. The lack of a diagnostic gold standard limits the ability to weigh the performance characteristics of metabolic biomarkers such as methylmalonic acid (MMA) and holotranscobalamin II, whose specificities remain incompletely defined outside their relations to each other. Variable cutoff selections affect diagnostic conclusions heavily and need to be much better rationalized. The maximization of reliability and specificity of diagnosis is far more important today than the identification of ever-earlier stages of SCCD. The limitations of all current biomarkers make the combination of ≥2 test result abnormalities, such as cobalamin and MMA, the most reliable approach to diagnosing deficiency in the research setting; reliance on one test alone courts frequent misdiagnosis. Much work remains to be done.American Journal of Clinical Nutrition 07/2011; 94(1):348S-358S. · 6.50 Impact Factor
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