Clinicopathological Correlation of Stool Microscopy, Fecal Calprotectin, and Helicobacter pylori Status in Patients with Gastrointestinal Symptoms

Author(s): Bhazan Chandra Majumder, Fariya Khan Sharna, Md Jakir Hossain, Saiful Islam, Mohammad Abdus Salam, Tamanna Khondokar Imu, Mst. Papiya Sultana, Md Shafiul Azam, Debash Chandra Poddar, Aunip Kumar Biswas

Background: Gastrointestinal disorders are a major global health burden, particularly in low- and middle-income countries where diagnostic resources are limited. Stool microscopy remains a commonly used first-line investigation; however, it has limited ability to differentiate functional disorders from inflammatory conditions. Fecal calprotectin is a reliable non-invasive marker of intestinal inflammation, but its clinicopathological correlation with stool microscopy findings and Helicobacter pylori infection has not been well studied in Bangladesh.

Objective: To assess the clinicopathological correlation between stool microscopy findings, fecal calprotectin levels, and Helicobacter pylori status among patients presenting with gastrointestinal symptoms.

Methods: This cross-sectional study was conducted at Dhaka General Hospital, Bangladesh, from October to December 2024. A total of 328 symptomatic patients were enrolled. Stool samples underwent macroscopic and microscopic examination, including assessment of pus cells, red blood cells (RBCs), mucus, yeast, and occult blood. Fecal calprotectin was measured using immunoassay and categorized as normal (≤50 μg/g), mild (>50–200 μg/g), or severe (>200 μg/g). H. pylori status, stool rotavirus antigen, and systemic biochemical markers were evaluated. Statistical analyses included Mann–Whitney U tests, correlation analysis, and multinomial logistic regression.

Results: The study population comprised 179 males (54.57%) and 149 females (45.43%), with a mean age of 34.30 ± 21.82 years. H. pylori infection was detected in 32.62% of patients. Median fecal calprotectin levels were significantly higher in H. pylori–positive patients compared with negatives (165.2 vs. 46.0 μg/g; p < 0.001). Elevated FC levels were also associated with positive stool occult blood tests (315 vs. 48.8 μg/g; p < 0.001), presence of RBCs on microscopy (233 vs. 55 μg/g; p < 0.001), and stool rotavirus positivity (146.5 vs. 40.1 μg/g; p < 0.001). In multinomial logistic regression, H. pylori positivity independently increased the odds of mild FC elevation by 2.40-fold (95% CI: 1.17–4.91; p = 0.017) and severe elevation by 5.94-fold (95% CI: 2.73–12.93; p < 0.001). Pancreatic enzymes, particularly lipase (r = 0.400; p < 0.001), showed the strongest positive correlation with fecal calprotectin.

Conclusion: This study demonstrates a strong, dose-dependent association between Helicobacter pylori infection and fecal calprotectin elevation, suggesting that H. pylori contributes to intestinal inflammation beyond its gastric effects. Biochemical and pathogen-specific markers were more reliable indicators of inflammatory severity than stool morphology alone.