Galectins represent a family of widely expressed lectins that have the ability to bind β-galactoside in modulating “cell-to-cell” and “cell-to-matrix” interactions in all organisms. These proteins are expressed in many inflammatory cells, such as macrophages, and depending on the inflammatory environment, they promote pro-inflammatory or anti-inflammatory responses. Galectin-3 (Gal-3) is predominantly located in the cytoplasm, but, as noted, it has also been detected in the nucleus, on the cell surface and in the extracellular environment, which indicates the multifunctionality of this molecule. It has been shown in many studies that Gal-3 is involved in immune regulation, fibrosis, and tissue remodeling, making it an important player in disorders such as inflammatory bowel disease (IBD), non-alcoholic steatohepatitis (NASH), and liver fibrosis. In IBD, this protein is associated with activation of the NLRP3 inflammasome, contributing to chronic intestinal inflammation. Also, in primary biliary cholangitis and autoimmune hepatitis, Gal-3 potentiate development of fibrosis through fibroblast-to-myofibroblast transition and extracellular matrix deposition, while in liver fibrosis, it is upregulated in hepatic stellate cells and macrophages, promoting fibrosis and inflammation. Studies show that Gal-3 inhibition reduces fibrosis and inflammation, making it a promising therapeutic target.

Background and Objectives: Metabolic syndrome (MetS) is characterized by a cluster of metabolic abnormalities, including abdominal obesity, hyperglycemia, insulin resistance, dyslipidemia, and hypertension. Growing evidence suggests that these components may contribute to the development of gastrointestinal (GI) malignancies. This review aims to explore the association between MetS and GI cancers, including esophageal, gastric, pancreatic, and colorectal cancers. Materials and Methods: A narrative literature review was conducted using PubMed, incorporating 22 sources published between 1991 and 2024. Search terms included “gastrointestinal malignant tumors”, “metabolic syndrome”, “diabetes mellitus”, and “obesity”. Priority was given to large-scale studies from Europe, America, and Asia. Case reports, commentaries, and conference abstracts were excluded. Results: By analyzing the available literature data, this study determined that hyperinsulinemia (IGF-1 pathway), hyperglycemia, and obesity (>102 cm in men and >88 cm in women) are highly associated with the development of esophageal cancer (primarily with Barret’s long and short segment as precancerosis), gastric cancer (through reactive oxygen species), and both pancreatic (1.5–2.4 higher risk) and colorectal cancer (30% higher risk). Patients with a high BMI (>40 kg/m²) show a 20%- or 1.18-times greater risk of developing colorectal cancer and a 1.72-times higher risk of developing pancreatic cancer. There is not enough evidence on the specific influence of hypertriglyceridemia, low HDL cholesterol, and high blood pressure on the development of gastrointestinal malignancy. However, those three conditions have shown a low to moderate association (from 6% to 12%) with the development of colorectal cancer. Conclusions: Metabolic syndrome (MetS) is increasingly being recognized as a significant risk factor for the development and progression of gastrointestinal cancers. Key components such as obesity, hyperglycemia, insulin resistance, and type 2 diabetes mellitus appear to contribute to carcinogenesis through mechanisms involving chronic inflammation, oxidative stress, and immune dysregulation. Further research is needed to clarify the biological pathways linking MetS to gastrointestinal malignancies and to inform effective prevention strategies.

Background: Sepsis is a leading cause of mortality in intensive care units, with liver dysfunction representing a critical determinant of poor outcome, mainly associated with excessive inflammation and oxidative stress. Lycopene, a carotenoid with potent antioxidant and anti-inflammatory properties, has been proposed as a potential therapeutic agent. This study investigated whether lycopene supplementation mitigates lipopolysaccharide-induced oxidative and inflammatory liver injury in rats. Methods: Male Wistar rats, divided into four groups, were exposed to either lipopolysaccharide or a combination of lipopolysaccharide (10 mg/kg) and lycopene (6 mg/kg). In order to assess liver damage induced by lipopolysaccharide, hepatocellular injury markers, oxidative stress indices, nitric oxide metabolism, glutathione redox status, apoptotic enzyme activity, and inflammatory mediators were assessed in serum and liver tissue. Results: Lipopolysaccharide induced marked hepatocellular damage, characterized by elevated serum liver-cell damage parameters, and liver tissue xanthine oxidase, myeloperoxidase, thiobrabituric reactive substances, protein carbonyl content, deoxyribonuclease I/II activity, nuclear factor kappa B, tumor necrosis factor-α, and interleukin-6, alongside depletion of reduced glutathione and reduced glutathione reductase and glutathione peroxidase activities. Lyc pretreatment significantly attenuated liver enzyme leakage, oxidative damage, and cytokine release while restoring reduced glutathione and glutathione reductase activity. In contrast, lycopene had limited effects on glutathione peroxidase activity, nitric oxide/inducible nitric oxide synthase signaling, and nuclear factor erythroid 2-related factor 2 expression. Conclusions: These findings demonstrate that lycopene confers partial hepatoprotection in endotoxemic rats, primarily through suppression of oxidative damage and nuclear factor kappa B-mediated inflammation. Further studies are needed to clarify tissue-specific mechanisms and optimize dosing strategies in order to increase the efficacy of this carotenoid.

Introduction. One of the more uncommon etiological factors responsible for the development of acute pancreatitis (AP) is hypercalcemia. Hyperparathyroidism (HPT), as a cause of hypercalcemia, is responsible, according to a number of studies, for 1.5 to 13% of AP. A mechanism of the development of AP in hyperparathyroidism is still unclear. Case report. We presented a 47-year-old female patient, who had five episodes of AP in total before the etiological factors were finally determined. The patient had certain comorbidities which were considered to be potential causes of AP. She had chronic renal insufficiency (she was on a regular hemodialysis program), Systemic lupus erythematosus and mioma of uterus. She has regularly taken an antiepileptic drug Eftil. During the fifth episode of AP, serum levels of calcium was for the first time elevated to twice the normal value. Parathyroid hormone was several times higher. A static scintigraphy was found hyperplasia or hyperfunctional adenoma of the right inferior and superior parathyroid glands. Abdominal multislice computed tomography (MSCT) scan verified the enlargement of the entire pancreas, as well as the presence of heterogeneous structures with diffuse amorphous calcifications. The lytic lesions in the pelvic bones could be seen in both sides. Parathyroidectomy was being postponed by an endocrine surgeon because of the poor overall condition of the patient. In the next period the patient had five more episodes of AP. The condition was significantly contributed by increasingly more frequent and longer episodes of metrorrhagia. Despite all therapeutic measures that were taken, Systemic Inflammatory Response Syndrome (SIRS) have been developed, and lethal outcome occurred. Conclusion. In a case of recurrent pancreatitis, hyperparathyroidism is to be considered even if a significant elevation of serum calcium is not present. This is especially the case for patients with chronic renal insufficiency or impaired vitamin D metabolism, who have a higher risk of secondary hyperthyroidism.

Background/Objectives: Colorectal cancer (CRC) is a major global health concern, with rising incidence across age groups. Early detection via colonoscopy and identification of precancerous polyps are crucial for prevention and improved outcomes. The objectives were to evaluate the epidemiology, anatomical distribution, morphology, and histopathology of CRC, and its association with synchronous colorectal polyps. Methods: In 2023, a retrospective study was conducted on 1973 patients undergoing colonoscopy due to symptoms like blood in the stool, changes in bowel habits, abdominal pain, weight loss, anemia, or as CRC follow-up. Complete colonoscopies were performed, and suspicious lesions were biopsied or resected for histological evaluation. Statistical analysis was performed using SPSS 11.0. Results: CRC was diagnosed in 78 patients (3.95%), with a male predominance (70.51%, p < 0.05) and a mean age of 65.1 ± 8.9 years. The most affected age group was 61–70 years (43.58%). Tumors were most commonly located in the rectum (32.05%) and sigmoid colon (26.92%). Polypoid morphology was observed in 67.95% of cases. Adenocarcinoma was the predominant histological type (93.59%), followed by mucinous adenocarcinoma (6.41%), with significant differences between right and left colon (p < 0.001). Synchronous polyps were detected in 47.43% of CRC cases, primarily adenomas (60.22%). In 37.84%, the tumor and polyp were in the same colon segment. Men had a higher rate of synchronous polyps than women (p < 0.05). Conclusions: CRC is more common in older males and typically affects the rectosigmoid region. Adenocarcinoma is the leading type. Nearly half of patients had synchronous adenomas, highlighting the importance of full colonoscopy for early CRC detection and prevention.