Bile acid homeostasis in gastrointestinal and metabolic complications of cystic fibrosis

Peppel, Ivo P van de; Bodewes, Frank; Verkade, Henkjan J.; Jonker, Johan W.

doi:10.1016/j.jcf.2018.08.009

Cited by 25 publications

(22 citation statements)

References 120 publications

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“…Interestingly, we observed a significant increase of vitamin E levels after the treatment and the Vitamin E was positively correlated with the months of treatment. These findings may suggest a significant effect of drug on intestinal digestion/absorption of lipids [25] .…”

Section: Discussionmentioning

confidence: 83%

“…After the treatment with lumacaftor/ivacaftor, the levels of plasma cholestanol, a surrogate marker of intestinal absorption [12] , were significantly increased, suggesting that the drug improves the mechanism of intestinal cholesterol absorption in patients with CF [25] , although phytosterols levels did not increase after the treatment. Jakulj et al [26] questioned the role of phy-tosterols as marker of intestinal cholesterol absorption.…”

Section: Discussionmentioning

confidence: 97%

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Lumacaftor/ivacaftor improves liver cholesterol metabolism but does not influence hypocholesterolemia in patients with cystic fibrosis

Gelzo¹,

Iacotucci²,

Caputo³

et al. 2021

Journal of Cystic Fibrosis

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 97%

Lumacaftor/ivacaftor improves liver cholesterol metabolism but does not influence hypocholesterolemia in patients with cystic fibrosis

Gelzo¹,

Iacotucci²,

Caputo³

et al. 2021

Journal of Cystic Fibrosis

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“…Exocrine pancreatic function is needed for appropriate digestion and absorption of fat and fat‐soluble vitamins, and to a lesser extent, carbohydrates and protein . Fat malabsorption leads to impairment in fat‐soluble vitamin absorption, which may be exacerbated in CF‐related liver disease because of decreased and/or abnormal intestinal bile acids …”

Section: Cystic Fibrosismentioning

confidence: 99%

Malnutrition in Children With Chronic Disease

Larson‐Nath

Goday

2019

Nut in Clin Prac

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Malnutrition occurs when nutrient intake does not meet the needs for normal body functions and as a consequence leads to alterations of growth and development in children. Chronic illness puts children at risk for developing malnutrition. Because of children's rapid periods of growth and development, early diagnosis, prevention, and management of malnutrition are paramount. The reasons for malnutrition in children with chronic disease are multifactorial and are related to the underlying disease and nonillness-associated factors. This review addresses the causes, evaluation, and management of malnutrition in pediatric congenital heart disease, chronic kidney disease, liver disease, and cystic fibrosis. (Nutr Clin Pract. 2019;34:349-358)

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“…Bile acid pro les were determined in plasma isolated from whole blood collected at termination (by cardiac puncture). Plasma bile acids were quanti ed using an Ultra High Performance Liquid Chromatography system (SHIMADZU, Kyoto, Japan), coupled to a SCIEX QTRAP 4500 MD triple quadruple mass spectrometer (SCIEX, Framingham, MA, USA) (UHPLC-MS/MS) as previously described (21,22). Gene expression analysis was performed in on distal ileal segments which were stored in RNAlater at -20 o C. Total RNA was isolated using TRI-reagent (Sigma, St. Louis, MO, USA) and quanti ed by NanoDrop (NanoDrop Technologies, Wilmington, DE, USA).…”

Section: Bile Acids and Ileal Gene Expressionmentioning

confidence: 99%

Host Microbiome Dictates Infection Risk after Chemotherapy Revealing New Avenues for Antibiotic Stewardship in Oncology

Wardill¹,

Mooij²,

Ferreira³

et al. 2020

Preprint

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Background: Mucosal barrier injury (MBI) is a recognized risk factor for blood stream infection (BSI) in people undergoing chemotherapy, permitting expansion and translocation of enteric pathobionts; a phenomenon now clinically referred to as MBI-associated laboratory-confirmed BSI. Although recognized to originate from endogenous gastrointestinal sources, MBI-associated BSI continue to be treated with antibiotics; a counterintuitive approach that may increase infection risk by depletion of the host microbiome. While this point has been argued in numerous clinical studies and opinion pieces, there are few data describing mechanistic strategies to decrease MBI-associated BSI, reflecting a lack of translationally robust preclinical models. Here, we report on a new translational model of MBI caused by the chemotherapeutic drug, melphalan. We aimed to identify candidate pathways to strengthen the mucosal barrier and prevent infection, prompting new antibiotic stewardship initiatives. Results: Melphalan caused dose-dependent, systemic toxicity characterized by severe neutropenia, self-limiting intestinal injury, inflammation and biphasic fever, all of which were clinically and molecularly consistent with the dynamics of melphalan conditioning. The fecal microbiome following melphalan was depleted in richness and commensal taxa, impairing colonization resistance and the microbial metabolome and prompting expansion of enteric pathogens. Breakdown of the intestinal barrier was initiated by melphalan and exacerbated by mucotoxic bile acids.Conclusions: MBI-associated BSI is simply a form of collateral damage resulting from breakdown of the gastrointestinal microenvironment and self-perpetuating injury. Efforts to intervene early in these sequelae are therefore of great clinical significance to restrict antibiotic use and mitigate their detrimental consequences on treatment outcomes and antibiotic resistance. Our data support interventions targeting the host microbiome and metabolome due to its ubiquitous control of inflammation, mucosal injury, bile acid transformation; all of which contribute to infection risk in cancer.

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Bile acid homeostasis in gastrointestinal and metabolic complications of cystic fibrosis

Cited by 25 publications

References 120 publications

Lumacaftor/ivacaftor improves liver cholesterol metabolism but does not influence hypocholesterolemia in patients with cystic fibrosis

Lumacaftor/ivacaftor improves liver cholesterol metabolism but does not influence hypocholesterolemia in patients with cystic fibrosis

Malnutrition in Children With Chronic Disease

Host Microbiome Dictates Infection Risk after Chemotherapy Revealing New Avenues for Antibiotic Stewardship in Oncology

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