YKL-40 or Chitinase-3-Like Protein 1 (CHI3L1) is a highly conserved glycoprotein that binds heparin and chitin in a non-enzymatic manner. It is a member of the chitinase protein family 18, subfamily A, and unlike true chitinases, YKL-40 is a chitinase-like protein without enzymatic activity for chitin. Although its accurate function is yet unknown, the pattern of its expression in the normal and disease states suggests its possible engagement in apoptosis, inflammation and remodeling or degradation of the extracellular matrix. During an inflammatory response, YKL-40 is involved in a complicated interaction between host and bacteria, both promoting and attenuating immune response and potentially being served as an autoantigen in a vicious circle of autoimmunity. Based on its pathophysiology and mechanism of action, the aim of this review was to summarize research on the growing role of YKL-40 as a persuasive biomarker for inflammatory diseases’ early diagnosis, prediction and follow-up (e.g., cardiovascular, gastrointestinal, endocrinological, immunological, musculoskeletal, neurological, respiratory, urinary, infectious) with detailed structural and functional background of YKL-40.

As the burden of liver disease in the general populace steadily increases, so does the need for both advanced diagnostic and treatment options. Endoscopic ultrasound is a reliable diagnostic and therapeutic method that has an established role, foremost in pancreatobiliary pathology. This paper aims to summarize the growing role of endoscopic ultrasound in hepatology based on the search of the current literature. A number of applications of endoscopic ultrasound are reviewed, including both noninvasive methods and tissue acquisition in focal and diffuse liver disease, portal hypertension measurement, detection and management of gastric and esophageal varices, treatment of focal liver lesions and staging of pancreatobiliary malignancies, treatment of cystic and solid liver lesions, as well as liver abscess drainage. Both hepatologists and endoscopists should be aware of the evolving role of endoscopic ultrasound in liver disease. The inherent invasive nature of endoscopic examination limits its use to a targeted population identified using noninvasive methods. Endoscopic ultrasound is one the most versatile methods in gastroenterology, allowing immediate access with detection, sampling, and treatment of digestive tract pathology. Further expansion of its use in hepatology is immanent.

Introduction: Pancreatic exocrine insufficiency (PEI) is seen in primary pancreatic disease but has also been seen in extrapancreatic conditions including celiac disease (CeD). The symptoms of PEI and CeD often overlap, which makes diagnostics challenging. In this systematic review and meta‐analysis, we aimed to investigate the prevalence of PEI in CeD. Methods: With the assistance of a professional librarian, we searched five databases: PubMed, Embase, Cochrane, Web of Science Core Collection, and Google Scholar, up until October 21, 2024. The pooled prevalence of PEI in biopsy‐confirmed CeD was estimated, and the quality of studies appraised. Results: We identified and screened the titles and abstracts of 1432 publications, of which 60 were reviewed in full text and 12 were included in the analyses. The overall pooled weighted prevalence of PEI in CeD was 13.5% (95% CI 7.2–21.0). The prevalence was similar among children (14.2%; 95% CI 2.0–32.8) and adults (12.8%; 95% CI 7.8–18.7) with CeD. The prevalence in studies that used secretory testing to define PEI was 13.1% (95% CI 6.4–21.3) and in those requiring digestive tests 17.1% (95% CI 5.8–32.1). The weighted prevalence of PEI was significantly higher among untreated CeD patients (18.2%) than patients on a gluten‐free diet (6.9%) ( p = 0.03), in both adults and children. Conclusion: One in eight individuals with CeD may suffer from PEI. The prevalence was particularly high in untreated CeD. PEI should be considered in patients who do not respond to a gluten‐free diet.

Background/Objectives: Melanoma-associated antigen A3 (MAGEA3) is a cancer–testis antigen with potential biological and prognostic relevance in pancreatic ductal adenocarcinoma (PDAC). This study evaluated the association between OTI1H1-defined MAGEA3-directed immunoreactivity and clinicopathological characteristics and overall survival after pancreatic resection for PDAC. Methods: This retrospective cohort included 76 patients with histologically confirmed PDAC. Patients who died within 30 postoperative days were excluded, and all tumors were retrospectively restaged according to the eighth edition of the AJCC TNM classification. Immunohistochemical staining was assessed using the mouse monoclonal anti-MAGE3 antibody clone OTI1H1 (ab140678, Abcam) by a single experienced pathologist blinded to clinical and outcome data. The percentage of immunoreactive tumor cells was retained as the principal exploratory quantitative measure; the prespecified <10% versus ≥10% classification was evaluated secondarily. Results: Thirty-six of 76 tumors (47.4%) had ≥10% OTI1H1-reactive tumor cells. When staining was modeled continuously, the adjusted HR per 10-percentage-point increase was 0.969 (95% CI 0.898–1.046; p = 0.420). For the secondary binary classification, the adjusted HR for ≥10% versus <10% staining was 0.745 (95% CI 0.417–1.331; p = 0.320). No statistically clear association with overall survival was observed; however, the confidence intervals do not exclude potentially clinically relevant associations in either direction. Conclusions: No statistically clear association between OTI1H1-defined immunoreactivity and overall survival was observed in this cohort. Because OTI1H1 has known cross-reactivity with selected MAGE-A family proteins and no orthogonal molecular validation was performed, these findings should be interpreted as assay-specific and do not establish biological inactivity of MAGEA3 or related MAGE-A proteins.

Background: There are known associations between periodontitis and colorectal cancer, but knowledge on the connections existing between the two are not fully understood. The aim of our study was to assess prevalence and clinical severity of periodontitis in patients with localized colorectal cancer. Secondly, the dynamics of metabolic derangements, particularly glucose metabolism, insulin resistance, and diabetes mellitus were studied as well. Methods: Diagnostic procedures included endoscopies with patohistology, laboratory exams, the insulin resistance homeostatic model assessment method (HOMA index), anthropometrics, and radiology imaging. Periodontal status was evaluated by full-mouth periodontal examination. Results: A total of 79 patients with localized colorectal carcinoma, with slight male predominance of 55.7%, and an age of 65.7 ± 12.4 years participated in this study. Three-quarters of patients (73.4%; 95% CI: 63.0–82.2%) were diagnosed with periodontitis. Patients with periodontitis and colorectal cancer had significantly increased glucose levels (fasting and after oral glucose challenge), (both p < 0.05). Also, increased values of the HOMA index were found in patients with periodontitis vs. controls (without periodontitis) and colorectal cancer; 6.38 ± 5.74 vs. 3.58 ± 2.6 (p = 0.012); Spearman’s Rho correlation coefficient = 0.271 (p = 0.039). There were significant differences in high-density cholesterol in patients with periodontitis vs. controls, 1.41 ± 0.28 vs. 1.23 ± 0.35 mmol/L (p = 0.016), but correlations were insignificant; Rho c.c. = 0.045 (p = 0.738). Conclusions: The most consorted connections between periodontitis and colorectal cancer were found among parameters of metabolic domain, especially glucose concentrations and insulin resistance. Further studies, which would include novel and emerging antidiabetic treatments and their effects on the prevention or control of both diseases, would be warranted.