Background: Metabolic instability, encompassing fluctuations in body weight, glucose, insulin, and sex hormones, may create a pro-inflammatory and proliferative endometrial microenvironment even in women with normal BMI. Methods: A systematic literature review was performed in PubMed, Embase, and Google Scholar, including studies assessing the relationship between metabolic, endocrine, and inflammatory factors and the risk of endometrial cancer in non-obese women. Results: Variability in body weight and hormonal parameters was associated with chronic subclinical inflammation, altered leptin/adiponectin secretion, decreased sex hormone-binding globulin, and increased estrogen bioavailability. These changes disrupt the homeostatic rhythm of endometrial cell regeneration and increase the likelihood of neoplastic transformation. Conclusions: Metabolic instability represents a novel integrated risk factor for endometrial cancer among women without obesity and should be incorporated into future risk stratification and prevention models.

Gallbladder stones are present in 10-20 % of the population of Western countries, and the incidence rate has almost tripled over the past 30 years. Asymptomatic cholecystitis is more common than it is mentioned in the literature. Approximately 80 % of the GI have no clinical manifestations. In most cases, the disease will remain asymptomatic throughout life. The problem of asymptomatic cholecystitis is often hushed up and ignored. Surgeons try to avoid examining this pathology. Works on asymptomatic cholecystitis are not only few, but also scattered. At the same time, there is no uniformity in the literature. Since the tactics of treating such patients still does not have an unambiguous approach. Many surgeons doubt the decision on surgical treatment, a smaller part chooses cholecystectomy at the same time, without substantiating the indications for it. That is why most cases of postcholecystectomy syndrome occur in patients operated on for asymptomatic cholecystitis. The unwillingness to discover the secret of stone formation and asymptomatic cholecystitis in humans when concretions in the gallbladder are detected without reference to surgery, to indicate the trajectory of the examination, leads to a number of tactical errors, preserving the risk of PES, and erasing practical recommendations for the management of such patients. The solution to this issue lies in a thorough study of each stage of the tactical search in patients with asymptomatic cholecystitis, which will determine a new strategy in biliary surgery.

Background and Objectives: Severe chronic postoperative inguinal pain (CPIP) affects 2–5% of patients after hernia repair, yet most published explanations remain neuropathic. The pubic periosteum, including the tubercle and adjacent symphyseal zone, lies within the operative field and may be engaged by medial mesh fixation. Its contribution to CPIP has not been tested. This narrative review brings together anatomical, imaging and clinical evidence and defines a hypothesis that can be examined prospectively. Materials and Methods: PubMed/MEDLINE, Embase and the Cochrane Library were searched without date restriction, with the final search run in April 2026. Thirty-three publications met the eligibility criteria. Evidence was classified using the 2011 OCEBM Levels of Evidence, with indirectness recorded when the population, exposure or outcome did not match the review question. The review was narrative, so no PRISMA flow diagram or formal risk-of-bias assessment was undertaken. Results: Direct evidence is limited. Among 1633 patients in one retrospective study, six underwent reoperation for severe late pain, and two had a staple placed in the periosteum. Pain resolved after staple removal. Two further cases of MRI-confirmed osteitis pubis followed laparoscopic repair with a titanium tacker. CT found pubic spurs in 17 of 20 patients, although their clinical meaning was uncertain. Fixation trials, CPIP reviews and groin-pain imaging studies repeatedly examined adjacent outcomes but did not define a periosteal endpoint. Conclusions: Pubic periosteal pathology is a plausible and testable pain generator, not an established cause of CPIP. Prospective studies should pair preoperative MRI and standardised pain mapping with explicit recording of fixation at the pubic tubercle. This design would show whether periosteal findings identify a distinct pain phenotype and whether penetrating fixation modifies its course.

Colorectal cancer (CRC) is traditionally viewed as the result of the sequential accumulation of molecular alterations and the clonal expansion of transformed cells. However, the state of morphologically non-neoplastic mucosa preceding the development of neoplasia remains considerably less well characterized. This narrative review aims to integrate evidence on biliary and lipid metabolism, intestinal transit, microbial metabolism, and field cancerization and to formulate a testable model of early metabolic remodeling in the distal colon. We propose that a chronically altered biliary–metabolic environment, combined with prolonged luminal and mucosa-associated exposure, may promote lipid–metabolic remodeling of morphologically non-neoplastic mucosa. This state is considered not as a new disease entity but as a potential tissue phenotype capable of altering the barrier, metabolic, and regenerative properties of the epithelium. Subsequent exposure to nitrogen-containing products of microbial metabolism may sustain repeated cycles of injury and regeneration, thereby creating conditions for clonal selection. Following the emergence of a neoplastic clone, the same local environment may potentially assume a different biological role and become part of a metabolic niche that supports further clonal expansion. The proposed model extends the concept of field cancerization by incorporating a metabolic dimension and generates a series of spatial and temporal predictions amenable to experimental and prospective clinical testing. Validation of this model may provide a basis for investigating morphologically non-neoplastic mucosa as potential tissue at risk and for developing earlier preventive and diagnostic approaches.

The mutually aggravating role of endocrine glands and metabolic disorders in the process of carcinogenesis is well known, but it is underestimated in modern oncological practice. The study of the manifestations of thyroid dysfunction, its effect on carcinogenesis in patients with metabolic syndrome and the possibility of improvement should become an important direction in refining patient outcomes in colorectal cancer (CRC). The aim of our review was to study the issue of thyroid dysfunction as a key link in the concept of colorectal carcinogenesis in metabolic syndrome. Current research data demonstrate a link between hypothyroidism and metabolic syndrome, suggesting that they mutually exacerbate each other, thereby worsening the condition of patients. Metabolic syndrome not only contributes to the development and progression of cancer, but also affects patient outcomes. In clinical practice, an imbalance of thyroid hormones occurs in various types of cancer and is regarded as a confounding factor. Existing data regarding the influence of thyroid hormones on tumors are inconsistent. While hypothyroidism appears to play a role in promoting cancer progression, the underlying mechanisms of this association remain poorly understood and necessitate further research. Despite conflicting evidence regarding the impact of thyroid hormones on colorectal cancer development, their significance in influencing a patient’s overall condition should not be overlooked. Therefore, it is important to integrate strategies for controlling the endocrine profile and correcting its changes into standard cancer treatment protocols. Moreover, some publications report the effect of levothyroxine replacement therapy on reducing the risk of developing CRC. Investigating the interplay between metabolic syndrome and cancer, particularly through the lens of thyroid dysfunction, may contribute to the development of novel approaches to colorectal cancer management and improve patient outcomes.