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: 2.87). 05/2009; 48(4):495-7. DOI: 10.1097/MPG.0b013e31817f9e5b
Source: PubMed
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    ABSTRACT: Functional diarrhea (FD) or non-specific chronic diarrhea (NSCD) is considered as the most frequent cause of chronic diarrhea without failure to thrive in toddlers. According to the Rome III classification, this clinical entity is defined as a daily painless, recurrent passage of three or more, large, unformed stools during a period of at least 4 weeks, with an absence of alarm signs such as failure to thrive if caloric intake is adequate, abdominal pain, or blood in the stool and emesis. The clinical history is the key point to identify patients with FD. Minimal blood and stool tests may help to differentiate between the causes of diarrhea such as infection, celiac disease, and inflammatory conditions. The pathophysiology of FD is not well understood. Starch, fructose, and sorbitol malabsorption have been implicated as important nutritional substances in the development of FD. In the same hand, parental factors are important in the perpetuation of functional diarrhea and induction of complications such as malnutrition. Functional diarrhea in childhood is a self-limiting disease and therefore no treatment is necessary. The recognition that dietary factors play a key role in the majority of these children has focused awareness upon the dietary intervention of this FGID. Key WordsFunctional diarrhea-Toddler’s diarrhea-Unspecific diarrhea-Chronic diarrhea
    10/2010: pages 341-356;
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    ABSTRACT: Endocrine neoplasms of the gut are a rare cause of chronic diarrhea and account for <1% of patients who present with chronic diarrhea. However, diarrhea associated with endocrine neoplasms can cause significant morbidity and mortality, and clinicians should recognize the diarrheal syndromes associated with endocrine neoplasms. This chapter discusses pathophysiology, diagnostic tests, and treatment options for diarrhea associated with endocrine neoplasms. Key WordsChronic diarrhea-Secretory diarrhea-Neuroendocrine tumors
    10/2010: pages 265-279;
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    ABSTRACT: Celiac disease (CD) is an autoimmune disorder occurring in genetically susceptible individuals, triggered by gluten and related prolamins, and plant storage proteins found in wheat, barley, and rye. It affects primarily the small intestine, where it progressively leads to flattening of the small intestinal mucosa and subsequent nutrient malabsorption. Its pathogenesis involves interactions among genetic, environmental, and immunological factors. Well-identified haplotypes in the HLA class II region (DQ2, DQ8) confer a large part of the genetic susceptibility to CD. Four possible presentations of CD are recognized: (1) typical, characterized mostly by gastrointestinal signs and symptoms; (2) atypical or extra-intestinal, where gastrointestinal signs/symptoms are minimal or absent and a number of extra-intestinal manifestations are present; (3) silent, where the small intestinal mucosa is damaged and CD autoimmunity can be detected by serology, but there are minimal or no symptoms; and finally (4) latent: these individuals, who possess genetic compatibility with CD and may also show positive autoimmune serology, have a normal mucosa morphology and may or may not be symptomatic. The diagnosis of celiac disease still rests on the demonstration of changes in the histology of the small intestinal mucosa. Currently, serological screening tests (serum levels of IgA–anti-tissue transglutaminase are generally acknowledged as the first choice) are utilized primarily to identify those individuals in need of a diagnostic endoscopic biopsy. Serology, including the newer anti-deamidated gliadin peptides, is also employed in monitoring the response to a gluten-free diet, which constitutes the only available treatment. Newer forms of treatment which will probably be available include enzymes degrading gluten to be ingested with meals; the use of substrates regulating intestinal permeability so as to prevent gluten entry across the epithelium; the development of genetically modified grains; and finally the development of different forms of immunotherapy. Key WordsCeliac-Malabsorption-Chronic diarrhea-Autoimmunity-Diabetes-Down syndrome-Short stature-Gluten-Gliadin-Tissue transglutaminase-Anti-endomysium antibodies-Deamidated gliadin peptides-Marsh-Villous atrophy-Intraepithelial lymphocytes-Refractory sprue-EATL-Enamel hypoplasia
    10/2010: pages 209-224;