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IntroductionVisceral pain is a symptom reported by over 70% of inflammatory bowel disease (IBD) sufferers. So far, a single, specific cause of this debilitating state has not been established. Chronic pain is one of the most important factors decreasing the quality of life in IBD course. Concurrently, management of pain is the most challenging issue encountered by clinicians in IBD treatment.Areas coveredThis review focuses on pathophysiology of inflammatory bowel disease-caused visceral pain and explores currently available approaches to its management. We also covered recent pharmacological developments in the field.ConclusionsPain-related disability has major effects on quality of life and on functional and social outcomes in IBD patients. Currently, there is no one standardized method of managing chronic visceral pain in IBD. Therefore, future development, focusing primarily on alleviating the pain, but also on reducing inflammation, is essential.

Long-term fluoroquinolone-associated disability (FQAD) after fluoroquinolone (FQ) antibiotic therapy appears in recent years as a significant medical and social problem, because patients suffer for many years after prescribed antimicrobial FQ treatment from tiredness, concentration problems, neuropathies, tendinopathies, and other symptoms. The knowledge about the molecular activity of FQs in the cells remains unclear in many details. The effective treatment of this chronic state remains difficult and not effective. The current paper reviews the pathobiochemical properties of FQs, hints the directions for further research, and reviews the research concerning the proposed treatment of patients. Based on the analysis of literature, the main directions of possible effective treatment of FQAD are proposed: (a) reduction of the oxidative stress, (b) restoring reduced mitochondrion potential ΔΨm, (c) supplementation of uni- and bivalent cations that are chelated by FQs and probably ineffectively transported to the cell (caution must be paid to Fe and Cu because they may generate Fenton reaction), (d) stimulating the mitochondrial proliferation, (e) removing FQs permanently accumulated in the cells (if this phenomenon takes place), and (f) regulating the disturbed gene expression and enzyme activity.

Introduction Presacral tumors are a rare group of heterogeneous lesions located in a potential space referred to as the retrorectal or presacral space. Lack of characteristic symptomatology and difficult anatomical localization make the diagnosis and management challenging for a surgeon. The aim of this study was to analyze cases of presacral tumors that underwent surgical treatment with regard to diagnostics, methods and outcomes. Material and methods The study enrolled patients who underwent surgical treatment at the Department of General and Colorectal Surgery, Medical University of Lodz. The data was analyzed for age, gender, clinical symptoms, type of diagnostic procedures conducted, histopathology results, type of treatment implemented, intra- and perioperative complications as well as early and long-term treatment outcomes. Results The study enrolled 29 patients who underwent surgical treatment for presacral tumors. Malignant tumors accounted for 34% of all cases ( n = 10), and 80% of them occurred in men. Benign cases accounted for 66% of cases ( n = 19), and they occurred predominantly in women (58%). Malignant lesions were more common in men ( p < 0.05). The average age of patients with benign tumors was lower than that of patients with malignant tumors ( p < 0.05). The transsacral approach was used in 51% of patients, abdominal laparotomy in 41% and a combined approach in 7%. Cure was achieved in 72% of patients, including 67% who were cured after their initial surgery. Conclusions Presacral tumors are more common in men and more commonly are malignant tumors in this group. The success rate of surgical treatment is 72%, and selection of the surgical approach does not affect the final treatment outcome.

Skin lesions in CD patients during biological therapy may result from significantly increased concentrations of IL-17A and IL-23, which are strongly associated with TNF-α/Th1 immune pathways.