Introduction:InfectionwithHelicobacter pylori is accepted as a main cause of gastritis and gastritis-associated diseases. Giardia lambliaparasite is considered the most common protozoal infection in human. Concomitant H. pyloriand Giardiainfection is common for their similar mode of transmission and strong correlation to socioeconomic levels, but only few reports had described gastric giardiasis. In this work, H. pyloriand Giardia lambliawere detected by PCR in gastric antral mucosal biopsies from a random sample of patients complaining from dyspepsia, in Sohag University Hospital, Egypt. Results were compared with a control group of patients undergoing EGD for other reasons rather than dyspepsia. The impact of H. pyloriand Giardia lambliainfection whether singularly or concert, on clinical, endoscopic or histopathogical changes was studied.

Patients and methods: 48 patients (26 males and 22 females) with dyspepsia and 28 controls (26 males and 2 females), were subjected to esophagogastroduodenoscopy (EGD). Endoscopic data were reported and gastric biopsy specimens were obtained for subsequent PCR assay for H. pyloriand Giardia lamblia, histopathological and electron microscopic examination.

Results:Endoscopicantral gastritis and duodenal lesions were found in both patients and controls. Both lesions occurred significantly more frequently in patients group (p= 0.002 & 0.0005 respectively). Esophageal lesions, nodular antral gastritis, gastric ulcers and superficial corpal gastritis were found only in patients group.

   PCR detected H. pyloriinfection in 28 out of the 48 patients (about 58%) and in 18 out of 28 (64%) control subjects while Giardia lambliainfection was present in 32 out of 48 patients (67%) compared to 12 out of 28 controls (64%). In the latter, the results were statistically significant (P=0.0003, Odd ratio=2.6). Co-infection with H. pyloriand Giardiawas present in 33% of patients compared to 36% of controls.

   Abnormal histologic findings were found in both patients and control groups, however, gastric atrophy occurred significantly more frequently in symptomatizing patients (P=0.027) with an odd ratio = 2.6. Intestinal metaplasia was found only in the patients group.

   Electron microscopic study; cellular abnormalities in the form of cytoplasmic vacuoles, mitochondrial destruction or nuclear abnormalities were found in infected subjects (H.pylori, Giardiaor both).

Conclusion:H. pyloriis not the only gastric pathogen in our community, gastric giardiasis is quite common. Its contribution to symptoms or pathological changes couldn't be confirmed in our study but it might be a factor in persistent epigastric pain after H. pylorieradication.