Parasites & Helicobacter Pylori in Egyptian Children with or without Diabetes with Gastrointestinal Manifestations & High Calprotectin Level
Background and Objective
This study highlighted the prevalence of parasitic infection in type-1 diabetes mellitus children and evaluated the effect of intestinal parasites on fecal calprotectin as a part of innate mucosal immunity. A total of 431 children with gastrointestinal manifestations attended the outpatients clinics, Aboul-Reesh Pediatric Teaching Hospital, Cairo University were randomly selected. Medical sheets were filled out on each patient. Stool samples were collected in labeled covered cartoon boxes and macroscopically examined for adult worms and segments, and microscopically for ova and protozoa by Lugol’s iodine1% smears and formol-ether concentration method, also, MZN was used for Cryptosporidium oocysts.
Besides, stool samples were examined for Helicobacter pylori. The results showed that 171/431 (39.67%) were type-1DM (p=0.000) and 260 (60.32%) were nondiabetic used as positive control. The overall intestinal parasitosis was (45.26%), H. pylori was (39.47%), irritable bowel syndrome was (25.78%), inflammatory bowel disease was (3.96%). Treatment of the causative agents diminished the gastrointestinal troubles.
Fecal calprotectin was measured quantitatively (Radin et al, 2014). DRG: HYBRiD XL Calprotectin Kit, which is a solid phase sandwich ELISA (Calprest1, Eurospital, Trieste, Italy). Wells of reagent cartridges were antibody-coated ones. Murine monoclonal antibody captured an exclusive antigenic site in the chemical composition of the calprotectin molecule. Aliquots from the collected samples and enzyme conjugate were incubated together in the coated well. The used enzyme conjugate was a monoclonal anti-calprotectin antibody impregnated with horse-radish peroxidase enzyme. Wells were washed off to remove unbound conjugate. Bound peroxidase conjugate amount was measured by color intensity. Calprotectin concentration measure higher than 200μg/g was considered positive. The Ethical Committee of Cairo University was followed and written informed agreement was obtained from the parents of the participated patients who joined.
Intestinal parasitic infections were high in diabetic children than in non-diabetic ones. H. pylori co-infection with intestinal parasites was highly prevalent. Pathogenicity of intestinal parasites induce symptoms mimic irritable bowel syndrome. Intestinal protozoans induce fecal calprotectin while intestinal helminths evade innate mucosal immunity. Parasites infection and H. pylori must be considered with low hygiene style and impaired immunity as diabetic children. Symptoms related to some parasites mimic irritable bowel syndrome due to their intercalated pathogenesis. Protozoan infections and H. pylori may induce high calprotectin values. The low values of fecal calprotectin in intestinal helminths were a model for immune evasion. Confusing parasitic causes that induce high calprotectin values with IBD may expose children to immune compromising treatment, especially those with type-1 DM. Children treatment will be published in due time by the first author.