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Disaccharidase Deficiencies in Children With Chronic Abdominal Pain
Khalil El-Chammas1, Sara E Williams1, Adrian Miranda1
11 Department of Pediatrics, Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Insights
Many children with chronic abdominal pain (CAP) have disaccharidase deficiencies, particularly lactase deficiency. Clinical features like bowel habits or pain location do not predict these common digestive issues.
Area of Science:
- Pediatric Gastroenterology
- Digestive Health
- Malabsorption Syndromes
Background:
- Carbohydrate intolerance is a potential cause of chronic abdominal pain (CAP) in children.
- Disaccharidase deficiencies may underlie CAP in a subset of pediatric patients.
Purpose of the Study:
- To investigate the prevalence of disaccharidase deficiencies in children experiencing functional CAP.
- To determine if specific clinical features correlate with the presence of these deficiencies.
Main Methods:
- A cohort of 203 pediatric patients with CAP (symptoms ≥1 month) was studied.
- Disaccharidase activity was assessed retrospectively from endoscopic biopsies with normal histology.
- Clinical data, including demographics and symptoms, were collected prospectively.
Main Results:
- Significant percentages of patients exhibited low disaccharidase levels: lactase (37%), sucrase (21%), glucoamylase (25%), and palatinase (8%).
- A notable overlap existed between lactase and sucrase deficiencies (39% of low lactase also had low sucrase; 67% of low sucrase also had low lactase).
- No significant associations were found between disaccharidase activity and patient age, stool consistency, stool frequency, or pain location.
Conclusions:
- Disaccharidase deficiencies are common in children with chronic abdominal pain.
- Clinical symptoms such as bowel frequency, vomiting, or pain location are not reliable predictors of disaccharidase deficiencies in this population.
Objectives:
Carbohydrate intolerance or malabsorption has been suggested as a cause of chronic abdominal pain (CAP) in a subset of patients. We aimed to evaluate disaccharidase deficiencies in children with functional CAP and to correlate deficiencies with clinical features.
Method:
Patients presenting to the gastroenterology clinic at Children's Hospital of Wisconsin with abdominal pain prospectively completed a detailed demographic, history, and symptom questionnaire. The CAP cohort included those with at least 1 month of symptoms. Data on disaccharidase activity and histology of endoscopic biopsies were collected retrospectively. Only patients with normal histology were included in the study. The association between groups with low disaccharidases and clinical features was examined.
Results:
A total of 203 pediatric patients with CAP were included. The mean (SD) age was 11.5 (3.1) years, and 32.5% were male. The percentages of abnormally low disaccharidase levels using the standard laboratory cutoffs were lactase, 37%; sucrase, 21%; glucoamylase, 25%; and palatinase, 8%. Thirty-nine percent of the patients with low lactase also had low sucrase, and 67% of the patients with low sucrase had low lactase. There was no significant difference in the activities of any of the disaccharidases or sucrase/lactase ratio in relation to age. Also, no association was found between stool consistency, stool frequency, or location of pain and low disaccharidase activity.
Conclusions:
A large proportion of patients with CAP have deficiencies in disaccharidases. Bowel frequency, vomiting, or location of pain was no different between groups, suggesting that these clinical features cannot be used to predict disaccharidase deficiencies.
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