# Observations on the effect of enteral nutrition support on serum nutritional proteins, proinflammatory cytokines and immunoglobulins in patients with cerebral hemorrhage **Authors:** Wenjun Tan, Xiaoqiang Li, Xiaolu Tang PMC · DOI: 10.5937/jomb0-58247 · Journal of Medical Biochemistry · 2025-11-05 ## TL;DR This study shows that enteral nutrition support improves nutrition and immune markers in patients with cerebral hemorrhage. ## Contribution The study reveals that intermittent enteral nutrition better reduces inflammation and boosts immunity compared to continuous feeding. ## Key findings - Both groups showed improved serum nutrient proteins and immunoglobulins after enteral nutrition. - Intermittent feeding reduced proinflammatory cytokines more effectively than continuous feeding. - No significant difference in adverse reactions between the two feeding methods. ## Abstract This study will analyse the changes in serum nutrient protein, a proinflammatory cytokine, and immunoglobulins before and after enteral nutrition support (ENS) in patients with intracerebral haemorrhage (ICH), which will serve as a reference for future clinics when performing ENS. This retrospective observational study included 160 patients with ICH (76 in the intermittent group and 84 in the continuous group), and changes in indicators before and after EN intervention were retrospectively analysed in both groups, including serum nutrient protein (albumin ALB, transferrin TRF, prealbumin PAB), proinflammatory cytokine (IL-1 b, IL-6, TNF-a), immunoglobulins (IgA, IgG, IgM) and gastrointestinal tolerance. There was no difference in adverse reactions between the two groups during ENS (P>0.05). After ENS, ALB, TRF PAB, IgA, IgG, and IgM were significantly increased in both groups, while IL-1 b, IL-6, and TNF-a were decreased (P<0.05). After ENS, there was no difference in serum nutrient protein between the two groups (P>0.05). Still, proinflammatory cytokines were lower in the intermittent group than in the continuous group, while immunoglobulins were higher than in the intermittent group (P<0.05). ENS exerts neuroprotection through the "intestinal barrier repair-immune remodeling-inflammation inhibition axis". ## Linked entities - **Proteins:** CD79A (CD79a molecule), IGG (Immunoglobulin G level), CD40LG (CD40 ligand), IL1B (interleukin 1 beta), IL6 (interleukin 6), TNF (tumor necrosis factor) ## Full-text entities - **Genes:** CCK (cholecystokinin) [NCBI Gene 885], CD79A (CD79a molecule) [NCBI Gene 973] {aka IGA, IGAlpha, MB-1, MB1}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, HDAC9 (histone deacetylase 9) [NCBI Gene 9734] {aka HD7, HD7b, HD9, HDAC, HDAC7B, HDAC9B}, TF (transferrin) [NCBI Gene 7018] {aka HEL-S-71p, PRO1557, PRO2086, TFQTL1}, PPARA (peroxisome proliferator activated receptor alpha) [NCBI Gene 5465] {aka NR1C1, PPAR, PPAR-alpha, PPARalpha, hPPAR}, NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, RBP4 (retinol binding protein 4) [NCBI Gene 5950] {aka MCOPCB10, RDCCAS}, TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, TJP1 (tight junction protein 1) [NCBI Gene 7082] {aka ZO-1}, IKBKB (inhibitor of nuclear factor kappa B kinase subunit beta) [NCBI Gene 3551] {aka IKK-2, IKK-beta, IKK2, IKKB, IMD15, IMD15A}, CYGB (cytoglobin) [NCBI Gene 114757] {aka HGB, NOD, STAP}, PRKAB1 (protein kinase AMP-activated non-catalytic subunit beta 1) [NCBI Gene 5564] {aka AMPK, HAMPKb}, TREM1 (triggering receptor expressed on myeloid cells 1) [NCBI Gene 54210] {aka CD354, TREM-1}, MYD88 (MYD88 innate immune signal transduction adaptor) [NCBI Gene 4615] {aka IMD68, MYD88D, WM1}, FOXP3 (forkhead box P3) [NCBI Gene 50943] {aka AIID, DIETER, IPEX, JM2, PIDX, XPID}, CHRNA7 (cholinergic receptor nicotinic alpha 7 subunit) [NCBI Gene 1139] {aka CHRNA7-2, NACHRA7, a7nAChR, nAChR7}, IL5 (interleukin 5) [NCBI Gene 3567] {aka EDF, IL-5, TRF}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1} - **Diseases:** intracranial space-occupying lesion (MESH:D020765), cerebrovascular diseases (MESH:D002561), vascular rupture (MESH:D012421), gastrointestinal tolerance (MESH:D005767), oedema (MESH:C536897), SIRS (MESH:D018746), infection (MESH:D007239), ICH (MESH:D002543), brain damage (MESH:D001925), pain (MESH:D010146), hypertension (MESH:D006973), Brain parenchymal injury (MESH:D001930), hematoma (MESH:D006406), haematological diseases (MESH:D004194), inflammation (MESH:D007249), vomiting (MESH:D014839), gastrointestinal bleeding (MESH:D006471), hemangioma (MESH:D006391), inflammatory storm (MESH:C566109), cerebral hernia (MESH:D004677), strokes (MESH:D020521), diarrhoea (MESH:D003967), Hypoalbuminemia (MESH:D034141), system (MESH:D015619), gastrointestinal feeding intolerance (MESH:D001068), arteriolosclerosis (MESH:D050379), vascular malformation (MESH:D054079), Organ Failure (MESH:D009102), gastric retention (MESH:C565114), abdominal distension (MESH:D000007), bleeding (MESH:D006470), cerebral oedema (MESH:D001929) - **Chemicals:** fatty acid (MESH:D005227), nitrogen (MESH:D009584), heme (MESH:D006418), thiol (MESH:D013438), midazolam (MESH:D008874), ENS (-), ROS (MESH:D017382), DHA (MESH:C027493), BCAAs (MESH:D000597), LPS (MESH:D008070), iron (MESH:D007501), arachidonic acid (MESH:D016718), glutamine (MESH:D005973), butyric acid (MESH:D020148) - **Species:** Homo sapiens (human, species) [taxon 9606] - **Mutations:** G12D ## Full text _Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12967174/full.md ## Figures 3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12967174/full.md ## References 24 references — full list in the complete paper: https://tomesphere.com/paper/PMC12967174/full.md --- Source: https://tomesphere.com/paper/PMC12967174