PO5 GIARDIASIS IN SUSPECTED CELIAC DISEASE

Abstract

Background and Objectives: Celiac disease (CD) is an immunemediated enteropathy induced by gluten ingestion in a genetically susceptible patient. Giardia lamblia is the most common human parasite with a worldwide distribution and fecal-oral way of transmission. Giardia lamblia has a cosmopolitan distribution. Infected children may have acute or chronic diarrhea, crampy abdominal pain, anorexia, malasorption and poor weight gain and may be misdiagnosed as celiac disease. Diagnosis is usually made by finding the characteristic cysts in stool specimens or by duodenal aspiration. In most cases histology reveals a dense accumulation of the parasites on the surface of the duodenal mucosa with no or only slight inflammation. In rare cases, a dense inflammatory infiltrate with severe mucosal atrophy and increased count of intraepithelial lymphocytes may be seen. If in such cases the amount of parasites is low, the histological picture may mimic celiac disease. We report the case of a child 2 years old who presented poor growth, recurrent aphtous stomatitis, abdominal pain and recurrent diarrhea. No family history of CD. Material and Methods: In suspected CD, were assayed the IgA anti-endomysium antibodies (EmA-IgA) that resulted doubt and the IgA anti-tissue transglutaminase antibodies (TgA-IgA) that were found weakly positive (17.50UA; normal value 16UA). He was referred to our hospital for further diagnostic. We performed the search for genetic susceptibility of CD; the antibodies assay was repeated after 3 months. These investigations documented the presence of HLADQ2, positivity of EmA-IgA and an increase value of TgA-IgA (20.70UA). In the meantime symptoms worsened, so we proceeded performing the esophagogastroduodenoscopy and duodenal biopsies. The macroscopic appearance of duodenal mucosa was of villous atrophy, but microscopic examination showed a parasitic duodenitis, with the presence of microorganisms like Giardia lamblia. Then was started medical therapy with metronidazole per os for 10 days, and the child continued to eat gluten. Results: Abdominal pain and diarrhea disappeared gradually but rapidly; the parasitological examination was negative on 3 consecutive samples (at 3 weeks after eradication therapy); EmA-IgA and TgAIgA were negative at 1 month after eradication. The follow up to 1 year had confirmed that the increase in IgA was secondary to giardiasis, and that the symptoms were due to the histological damage of the parasite. Conclusions: When investigating a patient with suspected celiac disease (CD), several other conditions must be considered, including potential infection with Giardia lamblia. In doubtful cases like our patient, are of fundamental support an accurate assessment and appropriate follow up.