The Incidence of Inflammatory Bowel Disease in the Paediatric Population in the District of Lower Silesia, Poland

Krzesiek, Elżbieta; Kofla-Dłubacz, Anna; Akutko, Katarzyna; Stawarski, Andrzej

doi:10.3390/jcm10173994

Cited by 8 publications

(4 citation statements)

References 14 publications

(27 reference statements)

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“…Inflammatory bowel disease (IBD) is a chronic, non-specific intestinal inflammatory illness that mostly includes Crohn’s disease (CD) and ulcerative colitis (UC) [ 1 ]. The incidence of IBD has increased globally in recent years, particularly in Europe and developing countries, posing a significant clinical challenge [ 2 – 5 ]. Although its probable causes are unknown, the immune impairment viewpoint gives a full picture of the disease’s multi-factor origin [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Impact of insomnia upon inflammatory digestive diseases and biomarkers: a two-sample mendelian randomization research on Europeans

Dai,

Ye,

Mugaanyi

et al. 2024

BMC Gastroenterol

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Background A number of observational studies indicate that insomnia is linked to inflammatory digestive diseases (IDDs). However, the definite relationship between insomnia and IDDs remains unclear. Methods We obtained the publicly available data from genome-wide association studies (GWAS) to conduct two-sample Mendelian randomization (MR) for association assessment. Five MR analysis methods were used to calculate the odds ratio (OR) and effect estimate, and the heterogeneity and pleiotropy tests were performed to evaluate the robustness of the variable instruments (IVs). Results One exposure and twenty outcome datasets based on European populations were included in this study. Using the inverse variance weighted method, we found insomnia was closely correlated with esophageal ulcer (OR = 1.011, 95%CI = 1.004–1.017, p = 0.001) and abdominal pain (effect estimate = 1.016, 95%CI = 1.005–1.026, p = 0.003). Suggestive evidence of a positively association was observed between insomnia and duodenal ulcer (OR = 1.006, 95%CI = 1.002–1.011, p = 0.009), gastric ulcer (OR = 1.008, 95%CI = 1.001–1.014, p = 0.013), rectal polyp (OR = 1.005, 95%CI = 1.000-1.010, p = 0.034), haemorrhoidal disease (OR = 1.242, 95%CI = 1.004–1.535, p = 0.045) and monocyte percentage (effect estimate = 1.151, 95%CI = 1.028–1.288, p = 0.014). No correlations were observed among other IDDs, phenotypes and biomarkers. Conclusions Our MR study assessed the relationship between insomnia and IDDs/phenotypes/biomarkers in depth and revealed potential associations between insomnia and ulcers of the esophagus and abdominal pain.

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Section: Introductionmentioning

confidence: 99%

Impact of insomnia upon inflammatory digestive diseases and biomarkers: a two-sample mendelian randomization research on Europeans

Dai,

Ye,

Mugaanyi

et al. 2024

BMC Gastroenterol

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“…However, over the past three decades, the incidence of IBD in low-income countries has steadily risen. [ 26 , 28 , 29 , 30 , 31 , 32 , 33 ]. The burden/implication of IBD is discrete in various countries and locations, especially when contrasted/matched between low-income [ 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 ] and wealthy nations [ 50 , 51 ].…”

Section: Introductionmentioning

confidence: 99%

Inflammatory Bowel Disease-Associated Colorectal Cancer: Translational and Transformational Risks Posed by Exogenous Free Hemoglobin Alpha Chain, a By-Product of Extravasated Erythrocyte Macrophage Erythrophagocytosis

Bragg,

Breaux,

M’Koma

2023

Medicina

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Colonic inflammatory bowel disease (IBD) encompasses ulcerative colitis (UC) and Crohn’s colitis (CC). Patients with IBD are at increased risk for colitis-associated colorectal cancer (CACRC) compared to the general population. CACRC is preceded by IBD, characterized by highly heterogenous, pharmacologically incurable, pertinacious, worsening, and immune-mediated inflammatory pathologies of the colon and rectum. The molecular and immunological basis of CACRC is highly correlated with the duration and severity of inflammation, which is influenced by the exogenous free hemoglobin alpha chain (HbαC), a byproduct of infiltrating immune cells; extravasated erythrocytes; and macrophage erythrophagocytosis. The exogenous free HbαC prompts oxygen free radical-arbitrated DNA damage (DNAD) through increased cellular reactive oxygen species (ROS), which is exacerbated by decreased tissue antioxidant defenses. Mitigation of the Fenton Reaction via pharmaceutical therapy would attenuate ROS, promote apoptosis and DNAD repair, and subsequently prevent the incidence of CACRC. Three pharmaceutical options that attenuate hemoglobin toxicity include haptoglobin, deferoxamine, and flavonoids (vitamins C/E). Haptoglobin’s clearance rate from plasma is inversely correlated with its size; the smaller the size, the faster the clearance. Thus, the administration of Hp1-1 may prove to be beneficial. Further, deferoxamine’s hydrophilic structure limits its ability to cross cell membranes. Finally, the effectiveness of flavonoids, natural herb antioxidants, is associated with the high reactivity of hydroxyl substituents. Multiple analyses are currently underway to assess the clinical context of CACRC and outline the molecular basis of HbαC-induced ROS pathogenesis by exposing colonocytes and/or colonoids to HbαC. The molecular immunopathogenesis pathways of CACRC herein reviewed are broadly still not well understood. Therefore, this timely review outlines the molecular and immunological basis of disease pathogenesis and pharmaceutical intervention as a protective measure for CACRC.

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“…A slightly smaller population lives in North America, where it reaches 248/100,000 for UC and 318/100,000 CD. In developing countries, the number of new cases has been growing dynamically [ 2 , 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

Etiology of IBD—Is It Still a Mystery?

Kofla-Dłubacz

Pytrus

Akutko

et al. 2022

IJMS

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Inflammatory bowel diseases (IBD), including colitis ulcerosa and Crohn’s disease, are chronic diseases of the gastrointestinal tract for which the cause has not been fully understood. However, it is known that the etiology is multifactorial. The multidirectional network of interactions of environmental, microbiological and genetic factors in predisposed persons lead to an excessive and insufficiently inhibited reaction of the immune system, leading to the development of chronic inflammation of the gastrointestinal walls, the consequence of which is the loss of the function that the intestine performs, inter alia, through the process of fibrosis. Detailed knowledge of the pathways leading to chronic inflammation makes it possible to pharmacologically modulate disorders and effectively treatthese diseases. In this review, we described the primary and adaptive immune system response in the gut and the known immune pathogenetic pathways leading to the development of IBD. We also described the process leading to intestinal tissue fibrosis, which is an irreversible consequence of untreated IBD.

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The Incidence of Inflammatory Bowel Disease in the Paediatric Population in the District of Lower Silesia, Poland

Cited by 8 publications

References 14 publications

Impact of insomnia upon inflammatory digestive diseases and biomarkers: a two-sample mendelian randomization research on Europeans

Impact of insomnia upon inflammatory digestive diseases and biomarkers: a two-sample mendelian randomization research on Europeans

Inflammatory Bowel Disease-Associated Colorectal Cancer: Translational and Transformational Risks Posed by Exogenous Free Hemoglobin Alpha Chain, a By-Product of Extravasated Erythrocyte Macrophage Erythrophagocytosis

Etiology of IBD—Is It Still a Mystery?

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