Evidence map›Paper›PMID 37027066›Full record

ArticleClinical and experimental medicine2023

Fecal levels of SCFA and BCFA during capecitabine in patients with metastatic or unresectable colorectal cancer.

Janine Ziemons, Romy Aarnoutse, Anne Heuft, Lars Hillege, Janneke Waelen, Judith de Vos-Geelen, Liselot Valkenburg-van Iersel, Irene E G van Hellemond, Geert-Jan M Creemers, Arnold Baars and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Clinical and experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 1 country.

Janine ZiemonsGROW - School for Oncology and Reproduction, Maastricht University, Maastricht, The Netherlands. j.ziemons@maastrichtuniversity.nl.ORCID https://orcid.org/0000-0002-4559-5488
Romy AarnoutseGROW - School for Oncology and Reproduction, Maastricht University, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0002-8713-9747
Anne HeuftDepartment of Internal Medicine, Division of Medical Oncology, Maastricht University Medical Centre, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0001-5860-9319
Lars HillegeGROW - School for Oncology and Reproduction, Maastricht University, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0001-7010-7610
Janneke WaelenGROW - School for Oncology and Reproduction, Maastricht University, Maastricht, The Netherlands.
Judith de Vos-GeelenGROW - School for Oncology and Reproduction, Maastricht University, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0003-2578-1766
Liselot Valkenburg-van IerselGROW - School for Oncology and Reproduction, Maastricht University, Maastricht, The Netherlands.
Irene E G van HellemondDepartment of Medical Oncology, Catharina Hospital, Eindhoven, The Netherlands.ORCID https://orcid.org/0000-0001-6775-7364
Geert-Jan M CreemersDepartment of Medical Oncology, Catharina Hospital, Eindhoven, The Netherlands.
Arnold BaarsDepartment of Medical Oncology, Hospital Gelderse Vallei, Ede, The Netherlands.ORCID https://orcid.org/0000-0002-5196-4358
Johanna H M J VestjensDepartment of Internal Medicine, VieCuri Medical Centre, Venlo, The Netherlands.ORCID https://orcid.org/0000-0002-1114-083X
John PendersNUTRIM - School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0001-9146-5919
Koen VenemaEuregional Microbiome Center, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0001-7046-5127
Marjolein L SmidtGROW - School for Oncology and Reproduction, Maastricht University, Maastricht, The Netherlands.ORCID https://orcid.org/0000-0002-8328-1869
Maastricht University Medical Centre · NLRadboud University Nijmegen · NLQiagen (Netherlands) · NLVieCuri Medisch Centrum · NLZiekenhuis Gelderse Vallei · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGut bacteria-derived short-chain fatty acids (SCFA) and branched-chain fatty acids (BCFA) are considered to have beneficial metabolic, anti-inflammatory as well as anti-carcinogenic effects. Previous preclinical studies indicated bidirectional interactions between gut bacteria and the chemotherapeutic capecitabine or its metabolite 5-FU. This study investigated the effect of three cycles of capecitabine on fecal SCFA and BCFA levels and their associations with tumor response, nutritional status, physical performance, chemotherapy-induced toxicity, systemic inflammation and bacterial abundances in patients with colorectal cancer (CRC).

methodsForty-four patients with metastatic or unresectable CRC, scheduled for treatment with capecitabine (± bevacizumab), were prospectively enrolled. Patients collected a fecal sample and completed a questionnaire before (T1), during (T2) and after (T3) three cycles of capecitabine. Tumor response (CT/MRI scans), nutritional status (MUST score), physical performance (Karnofsky Performance Score) and chemotherapy-induced toxicity (CTCAE) were recorded. Additional data on clinical characteristics, treatment regimen, medical history and blood inflammatory parameters were collected. Fecal SCFA and BCFA concentrations were determined by gas chromatography-mass spectrometry (GC-MS). Gut microbiota composition was assessed using 16S rRNA amplicon sequencing.

resultsFecal levels of the SCFA valerate and caproate decreased significantly during three cycles of capecitabine. Furthermore, baseline levels of the BCFA iso-butyrate were associated with tumor response. Nutritional status, physical performance and chemotherapy-induced toxicity were not significantly associated with SCFA or BCFA. Baseline SCFA correlated positively with blood neutrophil counts. At all time points, we identified associations between SCFA and BCFA and the relative abundance of bacterial taxa on family level.

conclusionsThe present study provided first indications for a potential role of SCFA and BCFA during capecitabine treatment as well as implications for further research.

trial registrationThe current study was registered in the Dutch Trial Register (NTR6957) on 17/01/2018 and can be consulted via the International Clinical Trial Registry Platform (ICTRP).

Indexed as

Antineoplastic AgentsColorectal NeoplasmsBacteriaCapecitabineFatty AcidsFatty Acids, VolatileHumansRNA, Ribosomal, 16SAntineoplastic AgentsCapecitabineFatty AcidsFatty Acids, VolatileRNA, Ribosomal, 16SChemotherapy toxicityGut microbiotaInflammationPalliative chemotherapyTumor response

Identifiers

PMID37027066
PMCPMC10618330
OpenAlexW4362692064

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.