Pediatric Celiac Disease Patients Research Articles

Unexplained Elevated Serum Pancreatic Enzymes: A Reason to Suspect Celiac Disease

The frequency of elevated serum pancreatic enzymes in patients with celiac disease (CD) is unknown. The aim of this study was to evaluate the serum levels of pancreatic enzymes in CD patients. Serum pancreatic isoamylase and lipase levels were assayed in 90 adult and 112 pediatric consecutive CD patients at diagnosis and after 12 months of gluten-free diet (GFD). Serum elastase and trypsin levels were assayed in a subgroup of adult CD patients. Pancreatic ultrasonography was also performed. Twenty-six adult (29%) and 29 pediatric (26%) CD patients exhibited elevated values of serum pancreatic amylase and/or lipase; trypsin was elevated in 69% and elastase in 19%. The frequency of elevated serum pancreatic enzymes observed was identical in the patients with "typical" and "atypical" CD symptoms and in the asymptomatic patients. Most of the elevated values were lower than 2-fold the threshold limits. Elevated pancreatic enzymes were not associated with alcohol consumption, drug use, presence of abdominal pain, or diabetes mellitus. Abdominal ultrasound scan showed no abnormal findings in the pancreatic region in any of the CD patients. After 12 months of GFD, pancreatic amylase was elevated in 3 cases and lipase in 2 cases; these patients had not strictly adhered to the GFD. We demonstrated a frequency of about 25% of elevated pancreatic enzymes values in CD patients, including subjects without gastrointestinal manifestations and apparently asymptomatic subjects. The finding of elevated serum amylase or lipase level, in the absence of signs of pancreatic disease, would appear to suggest a need to screen for celiac disease.

Immunochromatographic sticks for tissue transglutaminase and antigliadin antibody screening in celiac disease

Background & Aims: We investigated two 1-step immunochromatographic visual assays based on human recombinant tissue-transglutaminase (t-TG) as an alternative to enzyme-linked immunosorbent assays (ELISAs) for celiac disease (CD) screening. Methods: We used a tissue-transglutaminase (t-TG) stick, which detected immunoglobulin A/G (IgA/G) antibodies to t-TG, and a t-TG/antigliadin antibodies (AGA) stick, which detected IgA antibodies to both t-TG and AGA, as well as t-TG and AGA ELISAs, to determine t-TG and AGA antibodies in untreated celiac patients with subtotal villous atrophy. A total of 142 children (3 IgA-deficient sera) and 30 adults, and 140 controls (normal mucosa; 121 children and 19 adults), plus 23 sera from pediatric CD patients in remission were assayed. Results: For pediatric patients, with the t-TG stick we obtained a sensitivity of 97.1% and a specificity of 99.0%, and in adults, 83.3% and 100%, respectively. The t-TG/AGA stick displayed a sensitivity of 95.7% and a specificity of 99.0% for t-TG and a sensitivity of 89.2% and a specificity of 95.8% for AGA in children, and a sensitivity of 80% and a specificity of 100% for t-TG and a sensitivity of 83.3% and a specificity of 100% for AGA in adults. Results were comparable with the corresponding ELISAs. Conclusions: The 2 visual assays are efficient for CD screening as an alternative to ELISAs. They are simple to handle and to interpret. By the combined use of the 2 sticks, IgA-deficient patients can be identified as positive in the t-TG (IgG/A) but negative in the t-TG/AGA (IgA) stick.

Hypertransaminasemia in pediatric celiac disease patients and its prevalence as a diagnostic clue.

The aims of this study were to evaluate the following: 1) the prevalence of hypertransaminasemia (HT) in a pediatric celiac disease (CD) and its relation with clinical parameters; 2) the frequency of HT as the only manifestation of pediatric CD; and 3) the evolution of HT after a gluten free diet. A total of 114 consecutive pediatric CD patients were studied (60% with classical and 40% with atypical forms). Antiendomisyum antibodies and anti-tissue transglutaminase antibodies were determined in patients with a clinical suspicion of CD (including unexplained chronic HT), in patients at risk, and in patients with preoperative increased ALT activity for minor surgery. CD was confirmed by duodenal biopsy. At baseline, the relationship between clinical factors and aminotransferase status was univariately and multivariately assessed. After starting a gluten free diet, patients were followed up, until serological markers cleared and serum aminotransferase normalized. HT occurred in 32% of patients (37 of 114) at diagnosis. HT was the only manifestation of CD in five patients (4.3%). Patients with HT were younger (2.9 +/- 0.4 yr) than patients with normal aminotransferases (5.1 +/- 0.5 yr) (p = 0.007). A higher percentage of patients with classical CD tend to have abnormal aminotransferases (73%; 95% CI = 65-81%) than do patients with atypical CD (27%; 95% CI = 19-35%) (p = 0.068). Logistic regression analysis showed that only younger age was significantly associated with HT (p = 0.039; OR = 0.8; 95% CI = 0.71-0.99). Aminotransferases normalized with a gluten free diet in all 35 patients who were followed-up, either before (n = 18) or at the same time (n = 17) as serological markers cleared. HT is a frequent finding in pediatric CD patients and, in a substantial proportion, may be the only manifestation of CD. Thus, serological markers of CD should be introduced in the first step of the diagnostic workup of liver diseases in pediatric patients.

Hypertransaminasemia in pediatric celiac disease patients and its prevalence as a diagnostic clue

OBJECTIVES: The aims of this study were to evaluate the following: 1) the prevalence of hypertransaminasemia (HT) in a pediatric celiac disease (CD) and its relation with clinical parameters; 2) the frequency of HT as the only manifestation of pediatric CD; and 3) the evolution of HT after a gluten free diet. METHODS: A total of 114 consecutive pediatric CD patients were studied (60% with classical and 40% with atypical forms). Antiendomisyum antibodies and anti-tissue transglutaminase antibodies were determined in patients with a clinical suspicion of CD (including unexplained chronic HT), in patients at risk, and in patients with preoperative increased ALT activity for minor surgery. CD was confirmed by duodenal biopsy. At baseline, the relationship between clinical factors and aminotransferase status was univariately and multivariately assessed. After starting a gluten free diet, patients were followed up, until serological markers cleared and serum aminotransferase normalized. RESULTS: HT occurred in 32% of patients (37 of 114) at diagnosis. HT was the only manifestation of CD in five patients (4.3%). Patients with HT were younger (2.9 ± 0.4 yr) than patients with normal aminotransferases (5.1 ± 0.5 yr) ( p = 0.007). A higher percentage of patients with classical CD tend to have abnormal aminotransferases (73%; 95% CI = 65–81%) than do patients with atypical CD (27%; 95% CI = 19–35%) ( p = 0.068). Logistic regression analysis showed that only younger age was significantly associated with HT ( p = 0.039; OR = 0.8; 95% CI = 0.71–0.99). Aminotransferases normalized with a gluten free diet in all 35 patients who were followed-up, either before (n = 18) or at the same time (n = 17) as serological markers cleared. CONCLUSIONS: HT is a frequent finding in pediatric CD patients and, in a substantial proportion, may be the only manifestation of CD. Thus, serological markers of CD should be introduced in the first step of the diagnostic workup of liver diseases in pediatric patients.

A study of Italian pediatric celiac disease patients confirms that the primary HLA association is to the DQ(α1 ∗0501, β1 ∗0201) heterodimer

Celiac disease (CD) has been recently reported to be primarily associated with the DQ(α1 ∗0501, β1 ∗0201) heterodimer encoded in cis on DR3 haplotype and in trans in DR5, 7 heterozygous individuals. The high incidence of DR5, 7 heterozygotes, reflecting the high frequency of the DR5 allele in Italy, makes the analysis of the Italian CD patients critical. Polymerase chain reaction-amplified DNA from 50 CD patients and 50 controls, serologically typed for DR and DQw antigens, was hybridized with five DQA1-specific oligonucleotide probes detecting DQA1 ∗0101 + 0102 + 0103, DQA1 ∗0201, DQA1 ∗0301 + 0302, DQA1 ∗0401 + 0501 and DQA1 ∗0501 and a DQB1-sequence-specific oligonucleotide probe recognizing DQB1 ∗0201 allele. As expected by the DR-DQ disequilibria, DQA1 ∗0201 [62% in patients versus 26% in controls, relative risk (RR) = 5] and DQA1 ∗0501 (96% versus 56%, RR = 19) show positive association with the disease. Of CD patients, 92% (50% DR3 and 42% DR5,7) compared to 18% of the controls carry both DQA1 ∗0501 and DQB1 ∗0201 alleles, so that the combination confers an RR of 52, higher than both the risks of the single alleles ( DQA1 ∗0501 RR = 19, DQB1 ∗ 0201 RR = 30 ), confirming the primary role of the dimer in determining genetic predisposition to CD both in DR3 and in DR5, 7 subjects.