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OBJECTIVES: Anti-Saccharomyces cerevisiae antibodies (ASCAs) are present in 50-60% of patients with Crohn's disease (CD) and in 20-25% of their healthy relatives (HRs). The yeast, Candida albicans, has been shown to generate ASCAs, but the presence of C. albicans in the digestive tract of CD patients and their HRs has never been investigated. Therefore, we studied C. albicans carriage in familial CD and its correlation with ASCAs. METHODS: Study groups consisted of 41 CD families composed of 129 patients and 113 HRs, and 14 control families composed of 76 individuals. Mouth swabs and stool specimens were collected for isolation, identification, and quantification of yeasts. Serum samples were collected for detection of ASCAs and anti-C. albicans mannan antibodies (ACMAs). RESULTS: C. albicans was isolated significantly more frequently from stool samples from CD patients (44%) and their HRs (38%) than from controls (22%) (P < 0.05). The prevalence of ACMAs was similar between CD patients, their HRs, and controls (22, 19, and 21%, respectively, P = 0.845), whereas the prevalence of ASCAs was significantly increased in CD families (72 and 34% in CD and HRs, respectively, in contrast to 4% in controls, P < 0.0001). AMCA levels correlated with C. albicans colonization in all populations. ASCA levels correlated with C. albicans colonization in HRs but not in CD patients. CONCLUSIONS: CD patients and their first-degree HRs are more frequently and more heavily colonized by C. albicans than are controls. ASCAs correlate with C. albicans colonization in HRs but not in CD. In HRs, ASCAs could result from an altered immune response to C. albicans. In CD, a subsequent alteration in sensing C. albicans colonization could occur with disease onset.
Keywords
INFLAMMATORY-BOWEL-DISEASE, ANTI-SACCHAROMYCES-CEREVISIAE, ANTINEUTROPHIL CYTOPLASMIC AUTOANTIBODIES, MANNAN ANTIBODIES ASCA, ULCERATIVE-COLITIS, BINDING LECTIN, MOLECULAR CHARACTERIZATION, INTESTINAL PERMEABILITY, ANTIBIOTIC-THERAPY, CONTROLLED TRIAL

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Chicago
Standaert-Vitse, Annie, Boualem Sendid, Marie Joossens, Nadine Francois, Peggy Vandewalle-El Khoury, Julien Branche, Herbert Van Kruiningen, et al. 2009. “Candida Albicans Colonization and ASCA in Familial Crohn’s Disease.” American Journal of Gastroenterology 104 (7): 1745–1753.
APA
Standaert-Vitse, A., Sendid, B., Joossens, M., Francois, N., Vandewalle-El Khoury, P., Branche, J., Van Kruiningen, H., et al. (2009). Candida albicans colonization and ASCA in familial Crohn’s disease. AMERICAN JOURNAL OF GASTROENTEROLOGY, 104(7), 1745–1753.
Vancouver
1.
Standaert-Vitse A, Sendid B, Joossens M, Francois N, Vandewalle-El Khoury P, Branche J, et al. Candida albicans colonization and ASCA in familial Crohn’s disease. AMERICAN JOURNAL OF GASTROENTEROLOGY. 2009;104(7):1745–53.
MLA
Standaert-Vitse, Annie et al. “Candida Albicans Colonization and ASCA in Familial Crohn’s Disease.” AMERICAN JOURNAL OF GASTROENTEROLOGY 104.7 (2009): 1745–1753. Print.
@article{8540949,
  abstract     = {OBJECTIVES: Anti-Saccharomyces cerevisiae antibodies (ASCAs) are present in 50-60\% of patients with Crohn's disease (CD) and in 20-25\% of their healthy relatives (HRs). The yeast, Candida albicans, has been shown to generate ASCAs, but the presence of C. albicans in the digestive tract of CD patients and their HRs has never been investigated. Therefore, we studied C. albicans carriage in familial CD and its correlation with ASCAs. 
METHODS: Study groups consisted of 41 CD families composed of 129 patients and 113 HRs, and 14 control families composed of 76 individuals. Mouth swabs and stool specimens were collected for isolation, identification, and quantification of yeasts. Serum samples were collected for detection of ASCAs and anti-C. albicans mannan antibodies (ACMAs). 
RESULTS: C. albicans was isolated significantly more frequently from stool samples from CD patients (44\%) and their HRs (38\%) than from controls (22\%) (P {\textlangle} 0.05). The prevalence of ACMAs was similar between CD patients, their HRs, and controls (22, 19, and 21\%, respectively, P = 0.845), whereas the prevalence of ASCAs was significantly increased in CD families (72 and 34\% in CD and HRs, respectively, in contrast to 4\% in controls, P {\textlangle} 0.0001). AMCA levels correlated with C. albicans colonization in all populations. ASCA levels correlated with C. albicans colonization in HRs but not in CD patients. 
CONCLUSIONS: CD patients and their first-degree HRs are more frequently and more heavily colonized by C. albicans than are controls. ASCAs correlate with C. albicans colonization in HRs but not in CD. In HRs, ASCAs could result from an altered immune response to C. albicans. In CD, a subsequent alteration in sensing C. albicans colonization could occur with disease onset.},
  author       = {Standaert-Vitse, Annie and Sendid, Boualem and Joossens, Marie and Francois, Nadine and Vandewalle-El Khoury, Peggy and Branche, Julien and Van Kruiningen, Herbert and Jouault, Thierry and Rutgeerts, Paul and Gower-Rousseau, Corinne and Libersa, Christian and Neut, Christel and Broly, Franck and Chamaillard, Mathias and Vermeire, Severine and Poulain, Daniel and Colombel, Jean-Frederic},
  issn         = {0002-9270},
  journal      = {AMERICAN JOURNAL OF GASTROENTEROLOGY},
  language     = {eng},
  number       = {7},
  pages        = {1745--1753},
  title        = {Candida albicans colonization and ASCA in familial Crohn's disease},
  url          = {http://dx.doi.org/10.1038/ajg.2009.225},
  volume       = {104},
  year         = {2009},
}

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