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Mother to child transmission of anti- S cerevisiae mannan antibodies (ASCA) in non-IBD families
  2. B SENDID,
  4. PM DANZE,
  1. Laboratoire de Mycologie
  2. Fondamentale et Appliquée
  3. Equipe INSERM 99-15
  4. Laboratoire de Recherche sur les Maladies
  5. Inflammatoires Intestinales (CRI 4U004B)
  6. Unité fonctionnelle de génotypage HLA
  7. CH et U Lille, 59037, France
  1. J F Colombel. jfcolombel{at}
  1. J BRAUN,
  3. HY YANG,
  1. Department of Pathology and Lab Medicine
  2. UCLA and Division of Medical Genetics and
  3. IBD Research Center
  4. Cedars-Sinai Medical Center
  5. Los Angeles, CA 90095–1732, USA
  6. jbraun{at}

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    Editor,—We enjoyed the recent study by Sutton and colleagues (Gut2000;46:58–63) which confirmed our previous findings that elevated anti-S cerevisiaemannan antibodies (ASCA) are a familial trait in Crohn's disease.1 The lack of concordance in marital pairs indicated that familiality may be due to either a genetic factor or childhood environmental exposure. ASCA are present in 50–60% of patients with Crohn's disease, in 10–15% of patients with ulcerative colitis, and in 2–5% of control subjects.2-5 To gain more information on concordance for ASCA among family members, we studied ASCA distribution in non-inflammatory bowel disease (IBD) families.

    A total of 413 serum samples were collected from 94 diabetic families (table 1). One patient per family had type I diabetes. ASCA were detected by ELISA as previously described.3 Distribution of ASCA is given in fig 1 and table 1. Twenty three subjects (5.6%) were ASCA positive: six had diabetes and 14 were healthy. ASCA positive subjects were distributed within only 14 of 96 families. In seven of these families only one subject (parent) was positive for ASCA. The remaining 16 ASCA positive subjects clustered within seven families. All ASCA positive children were born of an ASCA positive mother. These results show that familiality of ASCA occurs independently of Crohn's disease and suggest vertical transmission of the marker from mother to child. Whether this is related to the observed higher risk of Crohn's disease transmission from mother to child than from father to child6 is unknown. Further work is needed to assess if the presence of ASCA may predict an increased risk of Crohn's disease in offspring.

    Table 1

    Distribution of anti-S cerevisiae mannan antibodies (ASCA) in 94 diabetic families

    Figure 1

    Pedigrees of the 14 diabetic families with at least one ASCA positive subject. +, presence of ASCA; shaded box, patient with diabetes.



    Editor,—We were interested by the letter of Poulain and colleagues on our paper Gut2000;46:58–63 and their data on familiality of this trait in non-inflammatory bowel disease (IBD) families, and evidence for mother to child transmission of anti-S cerevisiae mannan antibody (ASCA) expression. We have now re-analysed our own data set to our findings on this issue (table 1-1). We observed a strong correlation for both the mother-child and father-child pairs. This differs from Poulain and colleagues who only observed vertical transmission from mother to child. The difference may relate to distinct subject populations. Poulain evaluated a non-IBD group (diabetic families) whereas we evaluated clinically unaffected relatives from families with Crohn's disease (CD) probands. We also note that our analysis used statistical methods for quantitative data (antibody levels) which enhances statistical assessment, particularly when limited by small data sets. Poulain's analysis compares qualitative data (seropositive or seronegative), and the small number of relevant pairs may be insufficient to support their conclusion statistically. We agree with them on the need to assess the possibility that ASCA may predict increased risk for CD in unaffected individuals.

    Table 1-1

    Correlation coefficients for IgG anti-S cerevisiae mannan antibodies (ASCA) among 333 first degree relatives without evidence of Crohn's disease

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