Constipation is one of the major gastrointestinal disorders diagnosed in clinical practice in Western countries. Almost 20% of population suffer from this disorder, which means constipation is a substantial utilization of healthcare. Pathophysiology of constipation is complex and multifactorial, where aspects like disturbance in colonic transit, genetic predisposition, lifestyle habits, psychological distress, and many others need to be taken into consideration. Diagnosis of constipation is troublesome and requires thorough accurate examination. A nonpharmacological approach, education of the patient about the importance of lifestyle changes like diet and sport activity state, are the first line of therapy. In case of ineffective treatment, pharmacological treatments such as laxatives, secretagogues, serotonergic agonists, and many other medications should be induced. If pharmacologic treatment fails, the definitive solution for constipation might be surgical approach. Commonness of this disorder, costs of medical care and decrease in quality life cause constipation is a serious issue for many specialists. The aim of this review is to present current knowledge of chronic constipation and management of this disorder.

Irritable bowel syndrome (IBS) is a functional heterogenous disease with a multifactorial pathogenesis. It is characterized by abdominal pain, discomfort, and alteration in gut motility. The occurrence of similar symptoms was observed in patients in clinical remission of inflammatory bowel diseases (IBD) that is Crohn’s disease (CD) and ulcerative colitis (UC), which pathogenesis is also not fully understood. Hence, arose the question if these symptoms are “true IBS” imposed on IBD, or is it a subclinical form of IBD or even pre-IBD? In this article, based on a narrative overview of the literature, we try to find an answer to this query by discussing the pathogenesis and overlaps between these conditions.

Background: Despite the fact that colorectal cancer (CRC) is one of the most commonly diagnosed cancers in men and women, its current treatment remains unsatisfactory and therefore novel studies proposing new approaches are necessary. A high sugar diet is believed to promote carcinogenesis. Fructose is absorbed from the gastrointestinal tract by members of the glucose transporter family—GLUT. The aim of the study was to characterize the expression of GLUT5 at mRNA level in CRC patients. Moreover, our goal was to elucidate the molecular role of GLUT5 in CRC and assess whether GLUT5 inhibitor may affect the viability of colon cancer cells. Methods: The expression of GLUT5 at mRNA level was characterized based on 30 samples from resected colorectal cancers and 30 healthy colonic mucosa specimens from surgical margins. The inhibitory effect of N-[4-(methylsulfonyl)-2-nitrophenyl]-1,3-benzodioxol-5-amine (MSBNA) was assessed on a colon cancer cell line, HT-29, and normal colon epithelium cells—CCD 841 CoN Cells. Results: GLUT5 expression was found in 96.7% of cancer specimens and only in 53.3% of healthy mucosa fragments. In cancer tissue, real-time PCR analysis showed almost 2, fivefold (p< 0.001) increase of GLUT5 mRNA expression level compared with the healthy intestinal mucosa. GLUT5 inhibitor, MSNBA (10 µM) significantly decreased the viability of colon cancer cells, while barely affected the viability of normal colon epithelium cells. Conclusions: Our study suggests that a strong focus should be put on GLUT5 and its inhibitors for both diagnostic and therapeutic purposes in CRC.

The novel coronavirus disease (COVID-19) still remains a major challenge to the health-care systems worldwide, inciting ongoing search for pharmaceutical and non-pharmaceutical interventions which could benefit patients already infected with SARS-CoV-2 or at increased risk thereof. Although SARS-CoV-2 primarily affects the respiratory system, it may also infect other organs and systems, including gastrointestinal tract, where it results in microbial dysbiosis. There is an emerging understanding of the role the gut microbiota plays in maintaining immune homeostasis, both inside the gastrointestinal tract and beyond (i.e. through gut–lung and gut–brain axes). One family of compounds with recognized immunomodulatory and anti-inflammatory properties are short chain fatty acids (SCFAs). SCFAs are believed that they have a protective effect in case of gastrointestinal diseases. Moreover, they are responsible for maintaining proper intestinal barrier and they take part in relevant immune functions. This review presents mechanisms of action and potential benefits of SCFA-based probiotics and direct SCFA supplementation as a strategy to support immune function amid the COVID-19 pandemic.

Inflammatory bowel diseases (IBD) are chronic and relapsing gastrointestinal disorders, where a significant proportion of patients are unresponsive or lose response to traditional and currently used therapies. In the current study, we propose a new concept for anti-inflammatory treatment based on a selective acidic mammalian chitinase (AMCase) inhibitor. The functions of chitinases remain unclear, but they have been shown to be implicated in the pathology of various inflammatory disorders regarding the lung (asthma, idiopathic pulmonary fibrosis) and gastrointestinal tract (IBD and colon cancer). The aim of the study is to investigate the impact of AMCase inhibitor (OAT-177) on the dextran sulfate sodium (DSS)-induced models of colitis. In the short-term therapeutic protocol, OAT-177 given intragastrically in a 30 mg/kg dose, twice daily, produced a significant (p < 0.001) anti-inflammatory effect, as shown by the macroscopic score. Additionally, OAT-177 significantly decreased TNF-α mRNA levels and MPO activity compared to DSS-only treated mice. Intraperitoneal administration of OAT-177 at a dose of 50 mg/kg caused statistically relevant reduction of the colon length. In the long-term therapeutic protocol, OAT-177 given intragastrically in a dose of 30 mg/kg, twice daily, significantly improved colon length and body weight compared to DSS-induced colitis. This is the first study proving that AMCase inhibitors may have therapeutic potential in the treatment of IBD.

Background: Inflammatory bowel disease (IBD) is a risk factor in developing colitis-associated colorectal cancer (CA-CRC). CA-CRC causes the death of about 15% IBD patients and the risk is 1.5–2.4 fold higher among IBD sufferers than in the general population. The dysplasia CA-CRC develops in a different mechanism in comparison to sporadic colorectal cancer (CRC). This study aimed at evaluating the surgical treatment and its outcomes as well as 5-year survival rates in the CA-CRC and sporadic CRC patients. Materials and methods: This single-center, retrospective, propensity score-matched case-control study was conducted with 2204 patients operated on due to primary CRC, who were hospitalized from 2003 to 2019. The CA-CRC group consisted of 49 patients with CRC in the course of IBD. The sporadic CRC group was selected with the propensity score matching technique and comprised 98 patients with sporadic CRC who did not have clinical or histopathological features characteristic for IBD. Results: CA-CRC is characterized by a more aggressive clinical course. Surgical treatment of CA-CRC involves more palliative operations and is related with a higher risk of perioperative and postoperative complications. Further studies of CA-CRC risk factor stratification and the development of molecular markers hold promise in reducing CRC in IBD patients in the future were warranted.