Minerva gastroenterology最新文献

Acute severe ulcerative colitis is a potentially life-threatening condition that requires hospitalization with early and aggressive intervention to prevent complications. Mirikizumab (an anti-IL-23 monoclonal antibody) is recommended for the treatment of adult patients with moderate-to-severe ulcerative colitis. Currently, there is lack of evidence supporting its use in acute severe colitis, and no evidence has been produced on the use of this medication in pregnant women. A 30-year-old pregnant woman, with a 4-year history of corticosteroid-refractory pancolitis, who had failure to respond to multiple biological therapies, including infliximab, adalimumab, and vedolizumab, presented with acute severe ulcerative colitis and suspected threatened preterm rupture of membranes at 18 weeks' gestation. After administering five days of intravenous corticosteroids, the patient showed an unfavorable clinical and endoscopic response. Given the corticosteroid-refractory ASUC and the significant obstetric and neonatal risks associated with colectomy, Mirikizumab was initiated as a rescue therapy. Remarkably, within one day of receiving the first dose, the patient exhibited significant clinical improvement. One month after Mirikizumab initiation, the patient maintained clinical remission with improved markers. At 35 weeks and 4 days of gestation, the patient underwent an urgent cesarean section, delivering a preterm female infant. This is the first reported case regarding the efficacy and safety of Mirikizumab as a rescue therapy in a pregnant woman with severe acute ulcerative colitis. Further research is needed to confirm its efficacy in ASUC and the safety of this drug during pregnancy.

Sarcopenia, characterized by the progressive loss of skeletal muscle mass and function, represents a significant yet underrecognized extraintestinal manifestation of inflammatory bowel disease (IBD). Imaging techniques such as dual-energy X-ray absorptiometry (DXA), computed tomography (CT), magnetic resonance imaging (MRI), and ultrasound, combined with functional performance tests, offer promising strategies for early diagnosis. However, elucidating the molecular drivers of muscle wasting remains crucial. In IBD, chronic systemic inflammation, gut microbiota dysbiosis, and malnutrition synergistically disrupt muscle homeostasis by activating catabolic pathways and suppressing anabolic signals. Key molecular mechanisms involve NF-κB and JAK/STAT3 activation, inhibition of the IGF-1/mTOR axis, and alterations in microbiota-derived metabolites. Emerging evidence supports the existence of a gut-muscle axis, mediating the systemic effects of intestinal dysbiosis on skeletal muscle integrity. This review provides a comprehensive analysis of the molecular drivers of IBD-associated sarcopenia and explores potential therapeutic interventions targeting the gut-muscle interplay to improve clinical outcomes.

Introduction: The worldwide increase in acute diverticulitis (AD) prevalence and the resulting growing economic burden on the healthcare system have driven the scientific community towards standardizing a methodological approach to obtain a prompt diagnosis, optimized treatment, and thus containing costs. By the analysis of currently available evidence, this review could provide effective strategies for efficient AD clinical management and highlights possible innovative therapeutic strategies.

Evidence acquisition: A systematic literature search was conducted from October 2014 to October 2024 according to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines.

Evidence synthesis: The accurate collection of the medical history with investigation of preexisting diverticulosis and known AD risk factors, in combination with careful physical examination, permits a direct AD diagnosis but with proper accuracy. The contextual integration of laboratory data and the use of clinical scores may discourage the use of radiology, which, despite this, remains the only available methodology to exclude complications requiring hospitalization. CT scan with intravenous contrast remains the gold standard both for diagnosis and staging. However, the principal purpose is to prevent AD onset and recurrence (primary and secondary prevention) to reduce the health burden. The intervention on modifiable risk factors reduced AD incidence, whereas the currently available therapeutic options, such as non-absorbable antibiotics, probiotics, and mesalazine, have proven disappointing results. Breakthroughs may arise from recent evidence of a pathogenic role of a transmural colonic oxidative imbalance, likely ascribed to chronic ischemia-reperfusion injuries, that could contribute to reduced colonic wall compliance and represent a new possible therapeutic target.

Conclusions: Although progress has been made in the last decade towards more efficient AD management, further efforts are needed to impact its management and healthcare costs efficiently.

Crohn's disease (CD) is a chronic inflammatory disorder of the gastrointestinal tract, characterized by heterogeneous manifestations with significant morbidities. Diagnosing and managing CD remains challenging due to its variable clinical presentation, complexities in assessing disease extent and activity, and lack of a definitive diagnostic marker. Over the last years, there has been a switch towards a treat-to-target approach in the management of inflammatory bowel disease (IBD). Capsule endoscopy (CE) has emerged as a non-invasive, complementary tool for CD diagnosis and monitoring. CE is patient friendly being wireless and enables direct visualization of the entire small bowel in one sitting. CE plays a role in the diagnostic workup of suspected CD and in cases of in IBD unclassified (IBDU). In established CD, CE plays a role in monitoring mucosal healing, a key therapeutic target linked to improved long-term outcomes. CE findings significantly influence treatment strategies, leading to therapy escalation, adjustment, or avoidance of unnecessary surgical interventions. Moreover, CE disease activity assessment by means of the Lewis score is able to predict disease flares, thus having also a prognostic role. In conclusion, the non-invasive nature of CE, combined with its diagnostic, prognostic, and therapeutic implications, establishes it as an essential tool in the comprehensive management of CD across all disease stages. This review provides a comprehensive update on CE's evolving role in optimizing care of patients with CD.

Background: Medication adherence, defined as the extent to which a patient's behaviour aligns with medical recommendations, is crucial in managing chronic diseases. Despite its importance, global adherence rates are suboptimal, with non-adherence leading to poor clinical outcomes and increased healthcare costs. The General Medication Adherence Scale (GMAS) is a self-report tool widely used to assess adherence across cultural contexts. However, no validated Italian version exists. This study aimed to translate and validate the GMAS in Italian, ensuring its reliability and cultural relevance for Italian patients with chronic conditions.

Methods: A multicenter observational study was conducted across three Italian hospitals. The translation adhered to international guidelines, encompassing initial translation, synthesis, back-translation, and expert review. A test was conducted with 30 patients. The psychometric properties of the Italian GMAS were assessed using Cronbach's alpha, intraclass correlation coefficients (ICC), and construct validity.

Results: A total of 389 patients participated, demonstrating acceptable internal consistency (Cronbach's alpha = 0.758) and good test-retest reliability (ICC=0.859). The GMAS effectively differentiated adherence levels across various demographic and clinical factors, thereby confirming its construct validity.

Conclusions: The Italian GMAS is a feasible and preliminarily valid tool for assessing medication adherence. It provides a standardized approach for clinical and research settings in Italy. Its use can enhance chronic disease management by enabling healthcare professionals to identify and address adherence barriers effectively.

Background: The optimal timing of endoscopy in cirrhotic patients with acute variceal bleeding (AVB) remains uncertain. The study aimed to determine whether the timing of endoscopy affects short-term outcomes in patients with AVB.

Methods: Cirrhotic patients with AVB who underwent endoscopy within 24 hours of admission between 2016-2022 were evaluated. Patients were categorized into two group: the urgent endoscopy group (<12 hours) and the early endoscopy group (12-24 hours). The primary outcome was 30-day mortality. Secondary outcomes included the incidence of treatment failure, the need for intensive care unit (ICU) and the length of hospital stay (LOS). A multivariate analysis was performed to identify risk factors for 30-day mortality.

Results: A total of 183 patients were enrolled. Of them, 89 patients (48.6%) underwent urgent endoscopy, while 94 patients (51.4%) underwent early endoscopy. There were no significant differences between the urgent and early endoscopy groups, in terms of short-term mortality (6.7% vs. 7.4%, P=0.541), treatment failure (12.4% vs. 10.6%, P=0.445) or the incidence of ICU admission (3.4% vs. 6.4%, P=0.075). However, the LOS was longer in patients in the urgent endoscopy group compared to the early endoscopy group (14.1 vs. 11.9, P=0.001). In the multivariate analysis, MELD-Na score (aHR 1.21, 95% CI 1.12-1.48) and Glasgow-Blatchford score (aHR 2.71, 95% CI 1.45-5.08) were identified as independent risk factors for 30-day mortality.

Conclusions: Performing urgent endoscopy within 12 hours of admission in patients with cirrhosis and AVB, rather than within 12 to 24 hours, did not improve short-term outcomes.

Background: High rates of migration and invasiveness are crucial factors contributing to the elevated mortality associated with liver cancer. Peptidyl-prolyl isomerase A (PPIA) has emerged as a key player in the progression of various human cancers, although its specific role in the advancement of liver cancer has not been fully elucidated. Previous research revealed that PPIA dictated nuclear factor E2-related factor 2 (Nrf2) stability to promote cancer progression. To clarify this by exploring the biological effects of PPIA and Nrf2 in liver cancer.

Methods: First, PPIA and Nrf2 expression in normal hepatocyte cells and human hepatoma cells were quantitatively analyzed using RT-qPCR and western blot. Then, to assess effects of PPIA on migration and invasion of hepatoma cells, the study employed the scratch assay and the transwell invasion assay. Further, PPIA and Nrf2 were knock-downed, and ferroptotic cell death was assessed in erastin-treated hepatoma cells to clarify effect mechanism of PPIA in liver cancer progression. The interaction between PPIA and Nrf2 by conducting Co-IP experiments.

Results: The findings of our research indicate that PPIA is overexpressed, and promotes proliferation, migration and invasion in human hepatoma cells. The knockdown of PPIA and Nrf2 significantly enhances ferroptosis, which subsequently leads to a marked decrease in both migration and invasion of human hepatoma cells. Furthermore, our investigation revealed that PPIA interacts with Nrf2 in hepatoma cells, suggesting a complex relationship between these two proteins in the progression of liver cancer.

Conclusions: This study highlights the potential role of PPIA as a critical oncogenic driver in liver cancer, suggesting that targeting PPIA could offer therapeutic advantages in the treatment of this malignancy.