Search

and 1 patient had 4 previous EGD's. The median time from the first EGD until the diagnostic EGD was 39 months (range: 1 month to 13 years). The same endoscopist performed the non-diagnostic and the diagnostic EGD in 10/17 patients (59%). During the prior nondiagnostic EGD, a duodenal biopsy was performed in only 41% of the patients, and ≥4 specimens (the recommended number) were submitted in 29% of the patients. On the diagnostic EGD, ≥4 specimens were submitted in 94%. CD serologies were obtained in 3/ 17 (18%) prior to the non-diagnostic EGD but were obtained in 10/17 (59%) prior to the diagnostic EGD. During the non-diagnostic EGD's, the indications were dyspepsia/abdominal pain (n=5), reflux or Barrett's esophagus (n=4), diarrhea (n=2), dysphagia (n=2), and other (n=4). During the diagnostic EGD, the indications were diarrhea (n=6), positive CD serologies (n=5), abdominal pain/dyspepsia (n=3), dysphagia (n=2), and reflux (n=1). The mean age of diagnosis of those with missed/incident CD was 53.1 years, slightly older than those diagnosed with CD on their first EGD (46.8 years, p=0.11). Both groups were predominantly female (missed/incident CD: 65% vs. 66%, p=0.94). Conclusions: Among patients with CD who had previously undergone a non-diagnostic EGD, most did not have duodenal biopsies taken on a prior EGD. Dyspepsia and reflux were the predominant symptoms among these patients, and most did not initially have CD serologies checked. Routine performance of duodenal biopsy during EGD for the indications of dyspepsia and reflux may improve the under-diagnosis rates, and shorten the time for diagnosis, of patients with CD in the United States.

Background and Aims: The association between selective complete IgA deficiency (SIgAD) and celiac disease (CD) is well recognized. However, most data come from European pediatric populations. Given that the prevalence of immunoglobulin deficiency syndromes including SIgAD varies markedly in different populations, available data may not be representative of the adult celiac population in the United States. Our objective was to determine the distribution of SIgAD in an adult U.S. celiac population compared to controls. While, SIgAD precludes use of IgA serology, the effect of partial IgA deficiency (PIgAD) on IgA tTG test performance is unknown. Thus, our secondary aim is to assess the effect of PIgAD on serologic testing for untreated CD. Methods: In adults SIgAD is defined as a serum IgA concentration of less than 7mg/dl in the presence of normal levels of other immunoglobulins. PIgAD describes a low serum IgA of less than 70 but greater than 7mg/dlis. Total IgA was measured in patients undergoing tTG testing including patients with biopsy proven CD and an equal number of tTG negative disease controls with various GI disorders. Patients were classified as having CD if duodenal pathology showed a Marsh 2 or 3 lesion and there was either positive serology or histologic response to GFD, in the absence of negative CD genetic testing (DQ2/DQ8). Controls consisted of patients on a normal diet with negative IgA-tTG or IgGDGP, and without other diagnostic criteria for CD. Results: IgA data were available for 135 CD patients and 168 disease controls. 1.5% (2 of 135) CD patients had SIgAD compared to 0.6% (1 of 168) of controls (P=0.5). A further 3.7% of CD patients and 5.9% of disease controls had PIgAD. The median age at diagnosis for IgAD CD patients was 59 yr compared to 42 yr for CD patients with a normal IgA (p= 0.05). Pre-treatment tTG serology was negative in 100% (2 of 2) SIgAD CD patients. Of note, 40% (2 of 5) of the PIgAD CD group compared to 1.7% (2 of 117) of the non IgA deficient CD group had a negative tTG at diagnosis. Interestingly, all IgAD CD patients with an IgA level >50 mg/dl had positive IgA tTG results compared to 0 of 4 with IgA levels < 50 mg/dl. Conclusions: The incidence of SIgAD was 1.5% in our CD patients which is consistent with the European literature. IgA deficient patients were older, possibly representing an association between advancing age and IgA deficiency. The high prevalence of partial IgA deficiency in non-CD gastroenterology patients (5.9%) is novel, suggesting that IgA deficiency may be a risk factor for GI symptoms, via small intestinal bacterial overgrowth or other mechanisms. This finding warrants further study. IgG-based celiac serology testing should be considered for all patients with a total serum IgA level of less than 50 mg/dl.

Background and Aims: The association between selective complete IgA deficiency (SIgAD) and celiac disease (CD) is well recognized. However, most data come from European pediatric populations. Given that the prevalence of immunoglobulin deficiency syndromes including SIgAD varies markedly in different populations, available data may not be representative of the adult celiac population in the United States. Our objective was to determine the distribution of SIgAD in an adult U.S. celiac population compared to controls. While, SIgAD precludes use of IgA serology, the effect of partial IgA deficiency (PIgAD) on IgA tTG test performance is unknown. Thus, our secondary aim is to assess the effect of PIgAD on serologic testing for untreated CD. Methods: In adults SIgAD is defined as a serum IgA concentration of less than 7mg/dl in the presence of normal levels of other immunoglobulins. PIgAD describes a low serum IgA of less than 70 but greater than 7mg/dlis. Total IgA was measured in patients undergoing tTG testing including patients with biopsy proven CD and an equal number of tTG negative disease controls with various GI disorders. Patients were classified as having CD if duodenal pathology showed a Marsh 2 or 3 lesion and there was either positive serology or histologic response to GFD, in the absence of negative CD genetic testing (DQ2/DQ8). Controls consisted of patients on a normal diet with negative IgA-tTG or IgGDGP, and without other diagnostic criteria for CD. Results: IgA data were available for 135 CD patients and 168 disease controls. 1.5% (2 of 135) CD patients had SIgAD compared to 0.6% (1 of 168) of controls (P=0.5). A further 3.7% of CD patients and 5.9% of disease controls had PIgAD. The median age at diagnosis for IgAD CD patients was 59 yr compared to 42 yr for CD patients with a normal IgA (p= 0.05). Pre-treatment tTG serology was negative in 100% (2 of 2) SIgAD CD patients. Of note, 40% (2 of 5) of the PIgAD CD group compared to 1.7% (2 of 117) of the non IgA deficient CD group had a negative tTG at diagnosis. Interestingly, all IgAD CD patients with an IgA level >50 mg/dl had positive IgA tTG results compared to 0 of 4 with IgA levels < 50 mg/dl. Conclusions: The incidence of SIgAD was 1.5% in our CD patients which is consistent with the European literature. IgA deficient patients were older, possibly representing an association between advancing age and IgA deficiency. The high prevalence of partial IgA deficiency in non-CD gastroenterology patients (5.9%) is novel, suggesting that IgA deficiency may be a risk factor for GI symptoms, via small intestinal bacterial overgrowth or other mechanisms. This finding warrants further study. IgG-based celiac serology testing should be considered for all patients with a total serum IgA level of less than 50 mg/dl.