Isolated positive anti-gliadin immunoglobin-A antibody in children with gastrointestinal symptoms.

BACKGROUND/AIMS: The use of immunoglobulin G and A anti-gliadin antibodies for celiac disease screening has decreased due to higher specificity and sensitivity of tissue transglutaminase and endomysial antibodies. Greater values of immunoglobulin-A anti-gliadin antibody have been associated with more severe mucosal damage in proven and probable celiac disease patients. The aim of this study was to determine whether anti-gliadin antibody immunoglobulin A has any clinical importance in diagnosing celiac disease in children. Children with a chronic history of vomiting, abdominal pain, diarrhea, or constipation in the outpatient clinic were evaluated for celiac disease. MATERIALS AND METHODS: Tissue transglutaminase and anti-gliadin antibody immunoglobulin A in serum were determined by ELISA test and endomysial antibodies immunoglobulin A by indirect immunofluorescence. Most of these children with isolated positive anti-gliadin antibody immunoglobulin A were further evaluated by performing proximal gastrointestinal biopsies. RESULTS: Sixteen children had isolated positive anti-gliadin antibody immunoglobulin A (negative tissue transglutaminase and endomysial antibodies immunoglobulin A). Eight were male (mean age: 9.7 years). None had immunoglobulin A deficiency. Thirteen underwent an upper endoscopy with multiple small bowel biopsies. Two patients had villous atrophy and slightly increased intraepithelial lymphocytes (Marsh 3a), which could make the diagnosis of celiac disease likely. These two patients had high titers of anti-gliadin antibody immunoglobulin A above 70 Units. CONCLUSIONS: An isolated positive antigliadin antibody immunoglobulin A result in the absence of positive tissue transglutaminase and endomysial antibodies immunoglobulin A should raise the suspicion of the diagnosis of celiac disease. This could be a non-specific phenomenon that could be found in other gastrointestinal conditions, latent celiac disease, or gluten hypersensitivity. A longitudinal clinical follow-up is recommended in these children to confirm the diagnosis.

Evaluation of gastrointestinal pathology and treatment in children with suspected biliary dyskinesia.

AIM: Decreased gallbladder ejection fraction (GBEF) was reported in patients who had abdominal pain and gastrointestinal (GI) diseases. The study aims were to review pathology of GI tract in children with acalculous biliary-type abdominal pain and to evaluate the pain improvement after a 2-week trial of proton pump inhibitor (PPI) and laparoscopic cholecystectomy (LC). METHODS: Children below 18 years of age with a history of biliary-type abdominal pain by ROME III criteria were evaluated. All underwent an upper endoscopy and their histologic findings of the proximal GI tract were reviewed. Responses to a 2-week trial of PPI and LC were analyzed. RESULTS: Sixteen were identified with biliary-type abdominal pain with GBEF <35%. Endoscopic and histologic evidence of reflux esophagitis was observed in 11 children those of gastritis in 3 children. A GI pathology of these children is mostly acid-related and four of ten children experienced a complete response to PPIs and did not require LC. Nine children had LC; four had complete and four had partial pain improvement. CONCLUSION: A trial of PPIs may be cost-effective prior to considering LC in these patients since four of ten children experienced a complete response to PPIs without the requirement of LC, compared with four of nine children who improved completely.

Obesity and reversed growth retardation in a child with type Ia glycogen storage disease.

Type Ia Glycogen storage disease is an autosomal recessive hepatic metabolic disease due to a lack of glucose-6-phosphatase (G-6-Pase) activity presenting with growth retardation, lactic acidosis, fasting hypoglycemia with hypoinsulinemia, hyperuricemia, hepatomegaly, and hepatic adenoma with a risk of malignancy. The gene that encodes G-6-Pase was mapped to 17q21. There are some genotype-phenotype correlations. We report a case with delF327 mutation which is devoid of G-6-Pase activity; however clinical presentation in this case differs somewhat. Although correction of hypoglycemia and lactic acidosis with nocturnal intragastric feeding and uncooked starch therapy improves growth failure, mean height of the patients is often less than the target. Normal height and obesity in this case with hepatic steatosis and low hepatic glycogen storage requires clinical reevaluation since there are some overlapping phenotypes between type Ia GSD and metabolic syndrome. The phenomenon may be related to insulin resistance as a consequence of early aggressive nutrition therapy with frequent low glycemic index meals.