Fecal Calprotectin Is Increased in Stroke

Park, Shin Young; Lee, Sang Pyung; Kim, Woo Jin

doi:10.3390/jcm11010159

Cited by 4 publications

(5 citation statements)

References 25 publications

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“…We have reported increase in stroke patients of fecal calprotectin [33], which binds to and sequesters Zn, Mn, Ni, Cu, and Fe in the extracellular milieu through the action of metal-binding sites [56], and our present study showed that gut microbiome in stroke patients became enriched in the nickel transport system and the iron transport system.…”

Section: Discussionsupporting

confidence: 65%

“…We have previously collected blood samples from stroke patients and analyzed various parameters; a notable finding is low levels of albumin and lymphocytes [ 33 ]. Albumin and lymphocytes serve as markers of prognostic nutritional index (PNI), and depletion of both markers is associated with poor functional outcome [ 52 ].…”

Section: Discussionmentioning

confidence: 99%

“…We have previously measured fecal calprotectin (FC), a gut nutritional immunity marker of host, in stroke and reported two meaningful findings: (1) there was a significant increase in FC levels in stroke patients compared to those in controls; (2) FC in stroke patients had negative correlation with levels of albumin and lymphocyte but positive correlation with C-reactive protein (CRP) [ 33 ]. This study aimed further to explore the gut microbiota, the other side of host and microbe interaction, in stroke patients with comparison to control group.…”

Section: Introductionmentioning

confidence: 99%

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Gut Dysbiosis: A New Avenue for Stroke Prevention and Therapeutics

Park,

Lee,

Kim

et al. 2023

Biomedicines

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A stroke is a serious life-threatening condition and a leading cause of death and disability that happens when the blood vessels to part of the brain are blocked or burst. While major advances in the understanding of the ischemic cascade in stroke was made over several decades, limited therapeutic options and high mortality and disability have caused researchers to extend the focus toward peripheral changes beyond brain. The largest proportion of microbes in human body reside in the gut and the interaction between host and microbiota in health and disease is well known. Our study aimed to explore the gut microbiota in patients with stroke with comparison to control group. Fecal samples were obtained from 51 subjects: 25 stroke patients (18 hemorrhagic, 7 ischemic) and 26 healthy control subjects. The variable region V3–V4 of the 16S rRNA gene was sequenced using the Illumina MiSeq platform. PICRUSt2 was used for prediction of metagenomics functions. Our results show taxonomic dysbiosis in stroke patients in parallel with functional dysbiosis. Here, we show that stroke patients have (1) increased Parabacteroides and Escherichia_Shigella, but decreased Prevotella and Fecalibacterium; (2) higher transposase and peptide/nickel transport system substrate-binding protein, but lower RNA polymerase sigma-70 factor and methyl-accepting chemotaxis protein, which are suggestive of malnutrition. Nutrients are essential regulators of both host and microbial physiology and function as key coordinators of host–microbe interactions. Manipulation of nutrition is expected to alleviate gut dysbiosis and prognosis and improve disability and mortality in the management of stroke.

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Gut Dysbiosis: A New Avenue for Stroke Prevention and Therapeutics

Park,

Lee,

Kim

et al. 2023

Biomedicines

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“…According to the Korean study, 27 stroke patients had significantly higher levels of fecal calprotectin in their feces than in the controls. This finding raises the possibility that elevated fecal calprotectin is linked to consciousness and systemic response in stroke patients [36].…”

Section: Discussionmentioning

confidence: 96%

Releasing Dynamic of Serum ST2 and Calprotectin in Patients with Acute Ischemic Stroke

Sruk,

Budinčević,

Šimundić

et al. 2024

Diagnostics

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This study investigated the releasing dynamics of serum ST2 and calprotectin in patients with acute IS. The study included acute IS patients (N = 20) with an NIH Stroke Scale score ≥8. Sampling was performed at seven time points: after admission (T0) and at the following 24 h consecutive intervals (T1–T6). Primary outcome at 90 days was evaluated using the modified Rankin scale: 0–2 for good and 3–6 for poor functional outcome. The secondary outcome was all-cause mortality after 90 days. Fifteen patients had a poor outcome, and eight died. Results showed a statistically significant difference in ST2 concentrations between good and poor outcomes at T0 (p = 0.04), T1 (p = 0.006), T2 (p = 0.01), T3 (p = 0.021), T4 (p = 0.007), T5 (p = 0.032), and for calprotectin T6 (p = 0.034). Prognostic accuracy was highest for ST2 at T1 for a cut-off > 18.9 µg/L (sensitivity 80% and specificity 100.0%) and for calprotectin at T5 for a cut-off > 4.5 mg/L (sensitivity 64.3% and specificity 100.0%). Serum ST2 and calprotectin-releasing dynamics showed a valuable prognostic accuracy for IS outcomes.

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“…Stroke patients show increased levels of fecal calprotectin which positively correlates with high concentrations of serum inflammatory C-reactive protein. Moreover, fecal calprotectin amounts negatively correlate with serum albumin levels and the Glasgow Coma Scale which is suggested as an indicator of intestinal inflammation ( 43 ). Thus, activated neutrophils after stroke can increase intestinal inflammation and fecal calprotectin can be a promising biomarker for diagnosing intestinal inflammation.…”

Section: Stroke Changes Intestinal Microflora and Increases Inflammat...mentioning

confidence: 99%

Ischemic stroke and concomitant gastrointestinal complications- a fatal combination for patient recovery

et al. 2022

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Stroke is primarily a neurodegenerative disease but can also severely impact the functions of other vital organs and deteriorate disease outcomes. A malfunction of the gastrointestinal tract (GIT), commonly observed in stroke patients, is often characterized by severe bowel obstruction, intestinal microbiota changes and inflammation. Over-activated immune cells after stroke are the major contributors to endorse intestinal inflammation and may induce damage to single-layer epithelial cell barriers. The post-stroke leakage of intestinal barriers may allow the translocation and dissemination of resident microflora to systemic organs and cause sepsis. This overshooting systemic immune reaction fuels ongoing inflammation in the degenerating brain and slows recovery. Currently, the therapeutic options to treat these GIT-associated anomalies are very limited and further research is required to develop novel treatments. In this mini-review, we first discuss the current knowledge from clinical studies and experimental stroke models that provide strong evidence of the existence of post-stroke GIT complications. Then, we review the literature regarding novel therapeutic approaches that might help to maintain GIT homeostasis and improve neurological outcomes in stroke patients.

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Fecal Calprotectin Is Increased in Stroke

Cited by 4 publications

References 25 publications

Gut Dysbiosis: A New Avenue for Stroke Prevention and Therapeutics

Gut Dysbiosis: A New Avenue for Stroke Prevention and Therapeutics

Releasing Dynamic of Serum ST2 and Calprotectin in Patients with Acute Ischemic Stroke

Ischemic stroke and concomitant gastrointestinal complications- a fatal combination for patient recovery

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