Inflammatory bowel disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract and is associated with higher risks for complications, surgeries that affect the quality of life, and frequent hospitalizations. It has been stated in studies that more research is needed to measure the extent of inflammatory bowel disease at the appropriate time and to evaluate its effectiveness with one-on-one trials. With timely assessments and treatments, these quality improvement efforts will ultimately improve the quality of care and contribute to the reduction of preventable hospitalizations and healthcare costs from delayed inflammatory bowel disease treatment. Our study is one of the preliminary studies which is conducted to detect the severity and extent of the disease in patients with ulcerative colitis by noninvasive methods with a serum marker such as endocan [3, 8].
Studies conducted in many centers in both infection and inflammatory conditions have revealed that endocan is a strong marker. Wu et al. [9] determined the acid endocan level in patients with decompensated cirrhosis with spontaneous bacterial peritonitis compared to patients with ascites without peritonitis, likewise in Zuwala-Jagiello et al. [10] as a mediator of the inflammatory state associated with a bacterial infection in liver cirrhosis, Omma et al. [11] showed that endocan was significantly higher in colchicine-resistant Familial Mediterranean Fever patients compared to colchicine responders.
In a study by Voiosu et al. [12] in 33 patients with inflammatory bowel disease, endocan levels were significantly higher in the IBD group when compared with both the healthy control group and cancer patients. The coexistence of both Crohn’s patients and ulcerative colitis patients in the study indicates that our study may be more valuable. Considering that the endocan level is high in patients with IBD, the fact that this elevation mostly indicates patients with common colitis adds value to our study. Considering that the endocan level is high in patients with IBD, the fact that this elevation mostly indicates patients with common colitis adds value to our study.
As the prevalence and severity of ulcerative colitis increase, inflammatory markers in serum and stool increase. In important diseases such as acute pancreatitis with similar inflammation, studies have shown that the level of endocan increases as the severity of the disease increases [13]. In particular, the study of Çakır et al. [14] in infants with necrotizing enterocolitis showed that the endocan increased significantly in showing the severity of the disease, opening a new window. The most important finding in the study of Sakuraba et al. [15] in 133 patients with ulcerative colitis was that the extent of the disease may affect the correlation between fecal biomarker values. Especially in patients with proctitis, the low correlation between stool biomarkers and endoscopic findings, just as in our study, shows that both endocan and fecal calprotectin are more valuable in cases of extensive disease.
In the study of Kyle et al. [16], the fecal marker was used instead of the serum marker to determine the extent of the disease. They found that fecal calprotectin was significantly elevated in a concentration-dependent manner, which correlated with the number of sites of active inflammation reported in colon biopsy from inflammatory bowel patients. As in our study, a comparison was made with CRP. Although CRP and leukocyte measurements showed an upward trend in line with inflammation reported from biopsy, results were highly variable, underscoring the poor reliability of these biomarkers in demonstrating IBD inflammation. In addition, CRP may be elevated due to many factors unrelated to IBD, such as infection, rheumatoid arthritis, and autoimmune diseases. Current blood and serological laboratory tests such as total leukocyte count, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR), provide indirect, objective but non-specific markers for UC. Few studies have shown relatively poor sensitivity and specificity for the use of these biomarkers in diagnosing IBD and monitoring treatment [17, 18].
Colonoscopy is the gold standard to characterize ulcerative colitis and is used to directly evaluate ongoing mucosal inflammation. Colonoscopy should be performed every 1–5 years to track the flare-ups. This procedure is expensive, invasive, and associated with patient preparation, waiting times, and discomfort while carrying a small but significant risk of complications. Because of these parameters, colonoscopy in patients with ulcerative colitis is a burden for patients and physicians and is not an appropriate procedure for monitoring the disease. Therefore, a serum marker such as endocan or a stool marker such as fecal calprotectin can be used both to monitor patients and to decide on hospitalization for severe disease [6, 19].
The missing aspect of our study is that endocan cannot be evaluated in exact comparison with fecal calprotectin because of the cost.
In conclusion, serum endocan level can be a useful test in determining the extent and severity of ulcerative colitis, making hospitalization decisions, and planning treatment. Stool markers may not always be available due to patient compliance. It would be appropriate to conduct a large-scale study with a larger number of patients.