Risk of impaired nutritional status and flare occurrence in IBD outpatients

Spooren, Corinne E.G.M.; Wintjens, Dion S J; Jong, Marin J de; Jong, Andrea E. van der Meulen-de; Romberg-Camps, Mariëlle; Becx, Marco C.; Maljaars, Jeroen; Bodegraven, Ad A. van; Mahmmod, Nofel; Markus, Tineke; Hameeteman, W.; Masclee, Ad A.M.; Winkens, Bjorn; Jonkers, Daisy; Pierik, Marie J.

doi:10.1016/j.dld.2019.05.024

Cited by 12 publications

(6 citation statements)

References 44 publications

(57 reference statements)

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“…Patients with polypharmacy or malnutrition have a higher chance of developing an IBD flare. 17,32 The association between depression and disease activity has been established before, 33 but a link between IBD disease activity and cognitive function has also been described previously. 34 Also, mechanisms related to inflammation contribute to muscle wasting.…”

Section: Discussionmentioning

confidence: 81%

Deficits in Geriatric Assessment Associate With Disease Activity and Burden in Older Patients With Inflammatory Bowel Disease

Asscher

Waars

Jong

et al. 2022

Clinical Gastroenterology and Hepatology

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Section: Discussionmentioning

confidence: 81%

Deficits in Geriatric Assessment Associate With Disease Activity and Burden in Older Patients With Inflammatory Bowel Disease

Asscher

Waars

Jong

et al. 2022

Clinical Gastroenterology and Hepatology

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“…Recently, Szilagyi's review greatly described the pro-inflammatory pathogenic mechanism between obesity and IBD and noted specific possible interactions in both IBD and obesity [31] that can merit further investigation. A low BMI is associated with several nutritional deficiencies, micronutrients (iron, calcium, zinc, copper, magnesium, and selenium) and vitamins, such as A, D, K, B12, and folic acid, which are the main determinants for the development of IBD [4,32,33]. Thereby, both low and high BMI may introduce a two-fold challenge to the increasing IBD burden.…”

Section: Discussionmentioning

confidence: 99%

Impact of Body Mass Index on the Development of Inflammatory Bowel Disease: A Systematic Review and Dose-Response Analysis of 15.6 Million Participants

et al. 2021

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Background: A growing trove of literature describes the effect of malnutrition and underweight on the incidence of inflammatory bowel disease (IBD). However, evidence regarding the association between underweight or obesity and IBD is limited. The study aimed to assess the association of body mass index (BMI) with a risk of IBD (Crohn’s disease (CD) and ulcerative colitis (U.C.)) incidence. Methods: We systematically searched PubMed/Medline, Cochrane, Web of Science, and Scopus for observational studies assessing the association between BMI and IBD that were published up to 30 June 2020. We estimated pooled hazard ratios (HR) with corresponding 95% confidence intervals (CI). Random effect dose-response meta-analysis was performed using the variance weighted least-squares regression (VWLS) models to identify non-linear associations. Results: A total of ten studies involving 15.6 million individuals and 23,371 cases of IBD were included. Overall, obesity was associated with an increased IBD risk (HR: 1.20, 95% CI: 1.08–1.34, I2 = 0%). Compared to normal weight, underweight (BMI < 18.5 kg/m2) and obesity (BMI ≥ 30 kg/m2) were associated with a higher risk of CD, and there was no difference in the risk of U.C. among those with BMI < 18.5 kg/m2 and BMI ≥ 30 kg/m2. There was a significant non-linear association between being underweight and obesity and the risk of development of CD (Coef1 = −0.0902, p1 < 0.001 Coef2 = 0.0713, p2 < 0.001). Conclusions: Obesity increases the risk of IBD development. Underweight and obesity are independently associated with an increased risk of CD, yet there is no evident association between BMI and the risk of U.C. Further studies are needed to clarify the underlying mechanism for these findings, particularly in CD.

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“…These cytokines bind to their respective receptors, which causes increased activation of the p 38 mitogen-activated protein kinase (MAPK), nuclear factor kappa B (NF- κ B), and c-Jun N-terminal kinase (JNK) pathways, resulting in excessive bone loss and reduced BMD [ 35 ]. On the other hand, digestive system diseases lead to malabsorption of trace elements such as calcium, vitamin C, and vitamin D [ 36 ]. Studies suggest that insufficient calcium intake leads to excessive parathyroid hormone production and decreased BMD.…”

Section: Discussionmentioning

confidence: 99%

QiangGuYin Modulates the OPG/RANKL/RANK Pathway by Increasing Secretin Levels during Treatment of Primary Type I Osteoporosis

Cui

Chen

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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QiangGuYin (QGY) is a common Traditional Chinese medicine prescription for the treatment of osteoporosis. Previous clinical studies have found that QGY effectively improves bone mineral density (BMD) in postmenopausal women, but its underlying mechanism remains unclear. The osteoprotegerin (OPG)/receptor activator of nuclear factor kappa B ligand (RANKL)/receptor activator of nuclear factor kappa B (RANK) pathway is a classic pathway involved in osteoporosis. Secretin levels are a serum marker of osteoporosis, but their effect on the OPG/RANKL/RANK pathway has not been reported. Hence, we investigated the relationship between the OPG/RANKL/RANK pathway and secretin and further revealed the mechanism underlying the effect of QGY in the treatment of osteoporosis. Mice were divided into secretin knockdown, secretin overexpression, and corresponding control groups. Micro-computed tomography was used to detect BMD in different groups, and the results show that QGY significantly improved BMD in mice of the secretin knockdown group. To further verify this, the serum levels of OPG, RANKL, RANK, and secretin were measured by enzyme-linked immunosorbent assays, and femur levels of OPG, RANKL, RANK, and secretin were evaluated by real-time quantitative PCR and western blotting. The results show that the expression of OPG was inhibited and that of RANKL and RANK was increased in mice from the secretin knockdown group, whereas the expression of OPG was upregulated and that of RANKL and RANK was downregulated after QGY intervention. Therefore, QGY inhibited bone resorption by promoting the expression of secretin and modulating the OPG/RANKL/RANK pathway. In addition to the effect of QGY, we also revealed the general regulatory effect of secretin on the OPG/RANKL/RANK pathway. We conclude that QGY modulates the OPG/RANKL/RANK pathway by increasing secretin levels during treatment of primary type I osteoporosis. This work provides a theoretical basis for the clinical use of QGY in the treatment of osteoporosis.

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Risk of impaired nutritional status and flare occurrence in IBD outpatients

Cited by 12 publications

References 44 publications

Deficits in Geriatric Assessment Associate With Disease Activity and Burden in Older Patients With Inflammatory Bowel Disease

Deficits in Geriatric Assessment Associate With Disease Activity and Burden in Older Patients With Inflammatory Bowel Disease

Impact of Body Mass Index on the Development of Inflammatory Bowel Disease: A Systematic Review and Dose-Response Analysis of 15.6 Million Participants

QiangGuYin Modulates the OPG/RANKL/RANK Pathway by Increasing Secretin Levels during Treatment of Primary Type I Osteoporosis

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