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What Is Crohn's Disease And How Does It Affect You

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What Is Crohn's Disease And How Does It Affect You – Mid- to long-term survival of geriatric patients with primary septic arthritis of the shoulder: a retrospective study over a 20-year period.

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What Is Crohn's Disease And How Does It Affect You

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Alternative Treatment For Crohn’s Disease And Diet In Crohn’s Disease

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By Ioanna Aggeletopoulou Ioanna Aggeletopoulou Scilit Preprints.org Google Scholar 1, 2, Efthymios P. Tsounis Efthymios P. Tsounis Scilit Preprints.org Google Scholar 1, Athanasia Mouzaki Athanasia Mouzaki Athanasia Mouzantoski Triprints. os org Google Scholar 1, *

A Review Of The Therapeutic Management Of Crohn’s Disease

Received: 23 May 2023 / Revised: 16 June 2023 / Accepted: 19 June 2023 / Published: 21 June 2023

During Crohn’s disease, the response of mesenteric adipose tissues to the production of inflammatory mediators and the invasion of bacteria through the intestinal mucosa leads to the formation of creeping fat. Creeping fat describes the finger-like protrusions that surround the inflamed intestines. In this review, microscopic and macroscopic features of reptilian fat and histological evidence for the importance of this tissue are discussed. Additionally, updated insights into the radiological assessment of creeping fat in Crohn’s disease patients are reported. Advances in imaging techniques have revolutionized the possibility of visualizing and quantifying adipose tissue depots with excellent accuracy. Visceral fat is significantly associated with several Crohn’s disease-related outcomes. Despite difficulties in distinguishing physiologic parenteral fat from creeping fat, increased interest in fat packing in Crohn’s disease has renewed radiologic research. Regarding noninvasive fat envelope assessment, a new CT enterography-based mesenteric crepe fat index was developed to reduce the confounding effect of normal retroperitoneal and perienteric adipose tissue. Research in conjunction with machine learning algorithms and computational radiomics studies may be the key to elucidating the complex role of fat creep in Crohn’s disease.

Crohn’s disease is a chronic inflammatory bowel disease that can affect any part of the digestive system and is characterized by periods of flares and remissions [ 1 ]. It is considered to be a heterogeneous multifactorial disease in which genetic, environmental, immunological and microbial factors contribute to the pathogenesis of the disease. At the same time, research is ongoing on possible gender differences and biases related to certain aspects of the disease [2, 3, 4, 5, 6, 7]. Management of patients with Crohn’s disease depends on disease severity, patient risk assessment, patient preferences and clinical parameters [8]. Treatment options include a variety of interventions, including steroids, monoclonal antibody therapy, immunomodulators, and surgical procedures [ 8 ]. In addition, adequate nutritional management affects the overall treatment and well-being of individuals with Crohn’s disease [9, 10, 11, 12, 13, 14].

The phenomenon of hypertrophic adipose tissue surrounding inflamed intestinal segments in Crohn’s disease was first described by Burril Crohn and colleagues in 1932 [ 15 ]. Nearly a century later, the function of this pathological entity, known as “creeping fat” or “fat packaging,” and the mechanisms mediating its formation are still not fully understood. Emerging evidence suggests multiple functions of adipose tissue beyond energy storage, bringing reptilian fat to the forefront of scientific research. Adipose tissue constitutes a complex and highly functional endocrine and metabolic organ that plays an important role in immune regulation and mediates inflammatory signaling cascades [ 16 ]. Adipose tissue is composed of a wide variety of cell types, including fat cells, immune cells, endothelial cells, preadipocytes, fibroblasts and stem cells [ 17 ]. Although adipocytes account for the vast majority of fat pad volume (>90%), they constitute approximately 20–40% of the cellular content [ 18 ].

Harnessing Murine Models Of Crohn’s Disease Ileitis To Advance Concepts Of Pathophysiology And Treatment

In Crohn’s disease, dysbiosis and transmural injury compromise the integrity of the intestinal barrier, resulting in excessive influx of intraluminal microbiota and xenobiotics [ 19 ]. Intestinal and peri-intestinal fat present a close physiological relationship, implying a direct mutual immunological association, while adipocytes are equipped with a large number of innate immune sensors that respond to invasive stimuli [ 20 ]. As a result, adipocytes and their progenitor cells undergo major immunophenotypic changes, leading to adipose tissue remodeling and creeping fat formation (Figure 1) [21].

Although reptilian fat has historically been considered an innocent bystander, it is actually an active player during inflammation and immunity [22]. Reptile fat is an immunologically active organ that produces various pro- and anti-inflammatory cytokines, pro-fibrotic factors and adipokines, which act as regulators of paracrine/autocrine signaling and modulators of immune responses [ 23 ]. At the same time, crepe-fat-derived adipocytes in Crohn’s disease produce higher levels of total, saturated, and polyunsaturated free fatty acids compared to mesenteric fat in ulcerative colitis and healthy individuals, which produce intestinal smooth muscle cells. significantly increase the prevalence [24].

The role of lipids in inflammatory signaling partially explains why it is associated with more progressive Crohn’s disease or a more complex disease phenotype [25, 26, 27]. Ha etc. [28] revealed that in Crohn’s disease, an increase in mucosa-associated gut bacteria migrates to the mesenteric adipose tissue, leading to the expansion of this adipose tissue, suggesting that creeping fat promotes systemic bacterial proliferation. can limit In parallel, data suggest an alternative immune role of creeping fat as a second barrier that hinders the development of a systemic inflammatory response at the expense of a slowly proliferating profibrotic environment [ 24 , 29 , 30 ]. Additional insights from previously published single-cell RNA-seq data provided by Ha et al. was provided by Shu et al. [31], describing cellular heterogeneity in the mesenteric adipose tissue of patients with Crohn’s disease. In reptilian fat, a specific stromal vascular cell reaction was found, showing high expression of lipoprotein lipase [ 31 ]. This subpopulation exhibits high transcriptional activity of peroxisome proliferator-activated receptor γ (PPARγ) and is intimately involved in the upregulation of the PPAR signaling pathway in the metabolism of lipids and antibacterial responses [ 31 ]. Another abundant subpopulation also described in this study is the fibroblast subpopulation (FC3); This cell subset is closely related to the inflammatory response and intestinal fibrosis. Finally, several macrophage subclusters within the myeloid compartment have also been reported [ 31 ].

The present review describes in detail the microscopic and macroscopic features of reptilian fat and the histological evidence for the importance of this tissue. At the same time, emphasis is placed on the latest insights into the radiological evaluation of rectal fat in patients with Crohn’s disease.

Trichosporon Montevideense Isolated From The Descending Colon Of A Patient With Active Severe Crohn Disease: A Case Report

The mesentery is formed by a double fold of the peritoneum and connects the alimentary canal to the posterior abdominal wall. It provides topographical stability and flexibility necessary for normal bowel movements [32]. The major histological components of the mesentery include the superficial mesothelium, which is supported by a thin layer of loose, fibrous connective tissue augmented by adipocytes [ 33 ]. Traditional assumptions about the fragmented nature of the mesentery are now considered outdated, as recent advances have shown that the mesentery is a unique sheet-like structure that extends in continuity from the duodenal flexure to the rectum [32, 34]. . The mesentery and intestine have a close anatomical relationship that is established in the early stages of embryogenesis. While the epithelial component of the gut originates from the endoderm, the mesenchymal cells originate from the mesentery [24, 32, 33]. The mesothelium of the mesentery fuses with the serosa and contributes to the cell population of this layer [34]. In parallel, bundles of connective tissues extend from the mesentery to the underlying outer layers of the gut wall, including the muscularis mucosa and submucosa, forming a continuum at their intersection [ 32 , 33 ]. Lymphatic and blood vessels crossing this boundary allow unimpeded transport of immune cells and signaling molecules from the mesentery to the gut and vice versa. This partially explains the phenomenon of polarized ulceration, which predominantly affects the mesenteric rather than the antimesenteric border of the intestine in Crohn’s disease [ 35 ]. Conversely, complex cross-talk may promote remodeling of proximal adipose tissue mediated by neuropeptides, adipokines and vascular/lymphatic endothelia.

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