Diagnostic efficacy of the ELISA test for the detection of deamidated anti-gliadin peptide antibodies in the diagnosis and monitoring of celiac disease.

BACKGROUND AND AIM: We evaluated the diagnostic performance of an ELISA test for anti-gliadin IgA and IgG antibodies, which uses synthetic deamidated gliadin peptides (anti-gliadin antibodies, AGAs) as coating; the results were compared with a test that uses extracted gliadin (AGAe). METHODS: The study was conducted on the sera of 144 patients suffering from celiac disease (CD), including 20 patients with IgA deficiency and 9 who were following a gluten-free diet (GFD), and 129 controls. RESULTS: In the 115 CD patients (without IgA deficiency), the sensitivity of AGAe IgA and IgG was 32.2 and 60.9%, whereas that of AGAs IgA and IgG was 59.1 and 72.2%. The specificity for AGAe IgA and IgG, and AGAs IgA and IgG was 93.8 and 89.9%, and 96.9% and 99.2%, respectively. Of the 20 patients with CD and IgA deficiency, 7 tested positive for AGAe IgG and 14 for AGAs IgG. The test using deamidated gliadin peptides performed better in terms of sensitivity and specificity than the AGA tests with extracted antigen. CONCLUSIONS: The very high specificity of the AGAs IgG test (99.2%) also suggests that patients who test positive with this assay require a thorough followup, even if the anti-tissue transglutaminase antibodies (anti-tTG) and anti-endomysial autoantibodies (EMA) assays are negative.

Hospital discharge diagnoses in patients with positive blood cultures in an Italian academic hospital.

OBJECTIVE: To assess the sensitivity of hospital discharge diagnoses for identifying sepsis in patients with blood culture confirmation. METHODS: A cross-sectional study was conducted at the Italian 1000-bed University Hospital of Udine. The administrative databases of the Hospital were used as the source of information. Laboratory data were linked with hospital discharge data. We estimated the proportion of hospitalizations with at least 2 positive blood culture tests in which at least one discharge diagnosis indicated bloodstream infection. RESULTS: From 2011 to 2017, 3571 hospitalizations (1.2%) had positive blood culture tests. Of them, only 49.5% had at least one ICD-9-CM discharge diagnosis code of sepsis, with lower proportions in surgical than in medical wards. CONCLUSIONS: The sensitivity of ICD-9-CM discharge codes for sepsis is low as compared with the blood culture gold standard. Using discharge codes for epidemiological estimates of sepsis, health planning and risk management may yield biased results. Audits and ICD coding training are needed.

B-lymphocyte stimulator and a proliferation-inducing ligand serum levels in IgA-deficient patients with and without celiac disease.

IgA deficiency (IgAD) is the most common form of immunodeficiency and frequently associates with autoimmunity, especially with celiac disease (CD). The mechanisms underlying IgAD and the development of autoimmunity are still relatively unknown. Elevated B-lymphocyte stimulator (BLyS) and APRIL (a proliferation-inducing ligand) serum levels characterize several autoimmune diseases. We herein investigated BLyS and APRIL serum levels in IgAD patients with and without CD and compared these patients to CD patients with normal IgA and control patients (HBDs). Compared to HBDs, IgAD patients demonstrated a significant increase of BLyS (P < 0.0001) and APRIL (P = 0.003) levels, and no differences were seen between patients with or without CD. While BLyS appeared similarly overexpressed in IgAD and CD patients, APRIL was significantly increased only in IgAD patients. Because APRIL promotes IgA production, its overexpression may represent a physiological mechanism of compensation. BLyS upregulation may be involved in the increased risk of autoimmune disease development characterizing people carrying IgAD.

Elevated B cell-activating factor of the tumour necrosis factor family in coeliac disease.

OBJECTIVE: The B cell-activating factor of the tumour necrosis factor (TNF) family (BAFF) was recently described as a critical survival factor for B cells, and its expression is increased in several autoimmune diseases. Abnormal production of BAFF disturbs immune tolerance allowing the survival of autoreactive B cells and participates in the progression of B-cell lymphomas. Coeliac disease (CD) is a common autoimmune disorder induced by gluten intake in genetically predisposed individuals, associated with autoantibody production and with an increased risk of lymphoma at follow-up. The purpose of this study was to investigate the possible implications of BAFF in CD. MATERIAL AND METHODS: Seventy-three patients with small-bowel biopsies and laboratory-proven diagnosis of CD were included in the study. All serum samples were analysed before the start of a gluten-free diet (GFD). In 12 cases, one or more samples were analysed during follow-up of the GFD. Seventy-seven blood donors were taken as controls. Serum BAFF levels and anti-transglutaminase (a-tTG) antibodies were assessed by ELISA and endomysial antibodies by indirect immunofluorescence. RESULTS: Serum BAFF levels appeared to be significantly more elevated in CD patients than in controls (p<0.0001) and, compared with other autoimmune diseases where BAFF is increased, a much larger percentage (80.8%) of CD patients presented BAFF levels above the normal range. In addition, serum BAFF levels were found to correlate with a-tTG antibody levels (p =0.0007) and there was a significant reduction of BAFF after introduction of a GFD. CONCLUSIONS: BAFF may represent a possible pathogenic factor in CD. Its implications for the diagnosis, prognosis and treatment of CD should also be assessed.