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[PMID]: 29524409
[Au] Autor:Norris PC; Serhan CN
[Ad] Address:Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Road, BTM 3016, Boston, MA, 02115, USA.
[Ti] Title:Metabololipidomic profiling of functional immunoresolvent clusters and eicosanoids in mammalian tissues.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Metabolomics enables a systems approach to interrogate the bioactive mediators, their pathways and further metabolites involved in the physiology and pathophysiology of human and animal tissues. New metabololipidomic approaches with mass spectrometry presented in this brief review can now be utilized for the identification and profiling of lipid mediator networks that control inflammation-resolution in human blood and healthy and diseased solid tissues. Coagulation of blood is a protective response that prevents excessive bleeding on injury of blood vessels. Here, we review novel approaches to understand the relationship(s) between coagulation and resolution of inflammation and infection. To determine whether coagulation is involved in host-protective actions by lipid mediators, we used a metabololipidomic-based profiling approach with human whole blood (WB) during coagulation. We identified recently temporal clusters of endogenously produced pro-thrombotic and proinflammatory lipid mediators (eicosanoids), as well as specialized proresolving mediators (SPMs) in this vital process. In addition to the classic eicosanoids (prostaglandins, thromboxanes and leukotrienes), a specific SPM cluster was identified that consists of resolvin E1 (RvE1), RvD1, RvD5, lipoxin B , and maresin 1, each of which present at bioactive concentrations (0.1-1 nM). The removal of adenosine from coagulating blood samples significantly enhances SPM amounts and unleashes the biosynthesis of RvD3, RvD4, and RvD6 evident following rapid snap freezing with centrifugation before extraction and LC-MS-MS. The classic cyclooxygenase inhibitors, celecoxib and indomethacin, that block thromboxanes and prostanoids do not block production of the clot-driven SPM cluster. Unbiased mass cytometry analysis demonstrated that the SPM cluster produced in human blood targets leukocytes at the single-cell level, directly activating extracellular signaling in human neutrophils and monocytes. Human whole blood treated with the components of this SPM cluster enhanced both phagocytosis and killing of Escherichia coli by leukocytes. Thus, we identified a pro-resolving lipid mediator circuit and specific SPM cluster that promotes host defense. This new lipid mediator (LM)-SPM metabololipidomic approach now provides accessible metabolomic profiles in healthy and diseased human tissues, including cancer, for precision and personalized medicine.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 40958 MEDLINE  
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[PMID]: 29463696
[Au] Autor:Zhang H; Li HS; Hillmer EJ; Zhao Y; Chrisikos TT; Hu H; Wu X; Thompson EJ; Clise-Dwyer K; Millerchip KA; Wei Y; Puebla-Osorio N; Kaushik S; Santos MA; Wang B; Garcia-Manero G; Wang J; Sun SC; Watowich SS
[Ad] Address:Department of Immunology, University of Texas MD Anderson Cancer Center, Houston, TX 77030.
[Ti] Title:Genetic rescue of lineage-balanced blood cell production reveals a crucial role for STAT3 antiinflammatory activity in hematopoiesis.
[So] Source:Proc Natl Acad Sci U S A;115(10):E2311-E2319, 2018 Mar 06.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Blood cell formation must be appropriately maintained throughout life to provide robust immune function, hemostasis, and oxygen delivery to tissues, and to prevent disorders that result from over- or underproduction of critical lineages. Persistent inflammation deregulates hematopoiesis by damaging hematopoietic stem and progenitor cells (HSPCs), leading to elevated myeloid cell output and eventual bone marrow failure. Nonetheless, antiinflammatory mechanisms that protect the hematopoietic system are understudied. The transcriptional regulator STAT3 has myriad roles in HSPC-derived populations and nonhematopoietic tissues, including a potent antiinflammatory function in differentiated myeloid cells. STAT3 antiinflammatory activity is facilitated by STAT3-mediated transcriptional repression of , which encodes the E2 ubiquitin-conjugating enzyme Ubc13 involved in proinflammatory signaling. Here we demonstrate a crucial role for STAT3 antiinflammatory activity in preservation of HSPCs and lineage-balanced hematopoiesis. Conditional removal from the hematopoietic system led to depletion of the bone marrow lineage Sca-1 c-Kit CD150 CD48 HSPC subset (LSK CD150 CD48 cells), myeloid-skewed hematopoiesis, and accrual of DNA damage in HSPCs. These responses were accompanied by intrinsic transcriptional alterations in HSPCs, including deregulation of inflammatory, survival and developmental pathways. Concomitant /Ubc13 deletion from -deficient hematopoietic cells enabled lineage-balanced hematopoiesis, mitigated depletion of bone marrow LSK CD150 CD48 cells, alleviated HSPC DNA damage, and corrected a majority of aberrant transcriptional responses. These results indicate an intrinsic protective role for STAT3 in the hematopoietic system, and suggest that this is mediated by STAT3-dependent restraint of excessive proinflammatory signaling via Ubc13 modulation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1713889115

  3 / 40958 MEDLINE  
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[PMID]: 29505518
[Au] Autor:Zhang S; Huang Q; Xu B; Ma J; Cao G; Pei F
[Ad] Address:Department of Orthopaedics, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
[Ti] Title:Effectiveness and safety of an optimized blood management program in total hip and knee arthroplasty: A large, single-center, retrospective study.
[So] Source:Medicine (Baltimore);97(1):e9429, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Little has been published on blood management in total hip and knee arthroplasty (THA and TKA, respectively) patients focusing on both hematopoiesis and hemostasis. Our aim was to explore the effectiveness and safety of an optimized blood management program in THA and TKA patients in a large, single-center, retrospective study.We retrospectively reviewed consecutive primary unilateral THA and TKA patients' data at our institution through the National Health Database. They were divided into 3 groups according to an optimized blood management program: group A-combined use of intravenous and topical tranexamic acid (TXA); group B-use of recombinant human erythropoietin (rHuEPO) and iron supplements in addition to treatments in group A; group C-use of additional multiple boluses of TXA in addition to treatments in group B. The primary outcomes were hemoglobin (Hb) drop and calculated total blood loss (TBL). Other outcome measurements such as transfusion rate, postoperative length of stay (PLOS), venous thromboembolism (VTE), and mortality were also compared.From 2014 to 2016, a total of 1907 unilateral THA (986 in group A, 745 in group B, and 176 in group C) and 1505 unilateral TKA (795 in group A, 556 in group B, and 154 in group C) procedures were conducted at our institution. The Hb drop, calculated TBL, and PLOS in group C were significantly lower than those in groups A and B for THA and TKA patients. The transfusion rate in group C was also significantly less than in groups A and B for THA patients, while it was similar in groups A and B for TKA patients. No patients in group C received a transfusion. A significant difference was not detected in the incidence of deep vein thrombosis. No episode of symptomatic pulmonary embolism or all-cause mortality occurred within 30 days postoperatively.The current retrospective study suggests that for patients receiving primary unilateral THA or TKA, multiple boluses of intravenous TXA combined with topical TXA, rHuEPO, and iron supplements can reduce the calculated TBL, Hb drop, transfusion rate, and PLOS without increasing the incidence of VTE or mortality.
[Mh] MeSH terms primary: Anemia/drug therapy
Antifibrinolytic Agents/administration & dosage
Blood Loss, Surgical/prevention & control
Erythropoietin/therapeutic use
Iron/therapeutic use
Trace Elements/therapeutic use
Tranexamic Acid/administration & dosage
[Mh] MeSH terms secundary: Administration, Intravenous
Administration, Topical
Adult
Aged
Anemia/etiology
Arthroplasty, Replacement, Hip/adverse effects
Arthroplasty, Replacement, Knee/adverse effects
Female
Humans
Male
Middle Aged
Recombinant Proteins/therapeutic use
Retrospective Studies
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antifibrinolytic Agents); 0 (Recombinant Proteins); 0 (Trace Elements); 11096-26-7 (Erythropoietin); 6T84R30KC1 (Tranexamic Acid); E1UOL152H7 (Iron)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180306
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009429

  4 / 40958 MEDLINE  
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[PMID]: 29488682
[Au] Autor:Mirramezani M; Herbig BA; Stalker TJ; Nettey L; Cooper M; Weisel JW; Diamond SL; Sinno T; Brass LF; Shadden SC; Tomaiuolo M
[Ad] Address:Department of Mechanical Engineering, University of California, Berkeley.
[Ti] Title:Platelet packing density is an independent regulator of the hemostatic response to injury.
[So] Source:J Thromb Haemost;, 2018 Feb 28.
[Is] ISSN:1538-7836
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Hemostasis studies performed in vivo have shown that hemostatic plugs formed after penetrating injuries are characterized by a core of highly-activated densely-packed platelets near the injury site, covered by a shell of less-activated and loosely-packed platelets. Thrombin production occurs near the injury site, further activating platelets and starting the process of platelet mass retraction. Tightening of interplatelet gaps may then prevent the escape and exchange of solutes. OBJECTIVES: To reconstruct the hemostatic plug macro- and micro-architecture and examine how platelet mass contraction regulates solute transport and solute concentration in the gaps between platelets. METHODS: Our approach consisted of three parts. First, platelet aggregates formed in vitro under flow were analyzed using scanning electron microscopy to extract data on porosity and gap size distribution. Second, a 3-dimensional model was constructed with features matching the platelet aggregates formed in vitro. Finally, the 3D model was integrated with volume and morphology measurements of hemostatic plugs formed in vivo to determine how solutes move within the platelet plug microenvironment. RESULTS: The results show that the hemostatic mass is characterized by extremely narrow gaps, porosity values even smaller than previously estimated, and stagnant plasma velocity. Importantly, the concentration of a chemical species released within the platelet mass increases as the gaps between platelets shrink. CONCLUSIONS: Platelet mass retraction provides a physical mechanism to establish steep chemical concentration gradients that determine the extent of platelet activation and account for the core and shell architecture observed in vivo. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1111/jth.13986

  5 / 40958 MEDLINE  
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[PMID]: 29475063
[Au] Autor:Hu X; Xiao Y; Yu C; Zuo Y; Yang W; Wang X; Gu B; Li J
[Ad] Address:Department of Pharmacology & Toxicology, Sunshine Lake Pharma Co., Ltd, Dong Yang Guang Park, Chang'an, Dongguan, Guangdong Province, China.
[Ti] Title:Characterization of a novel selective factor Xa inhibitor, DJT06001, which reduces thrombus formation with low risk of bleeding.
[So] Source:Eur J Pharmacol;825:85-91, 2018 Feb 21.
[Is] ISSN:1879-0712
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Factor Xa (FXa) is a serine protease that plays key roles in linking the intrinsic and extrinsic coagulation pathways to the final common pathway. DJT06001 is an oral, highly specific and direct FXa inhibitor for the prevention and treatment of thromboembolic diseases. We characterized the compound in vitro and studied its in vivo activity in rat thrombosis models, as well as bleeding risk and Pharmacokinetics and Pharmacodynamics (PK/PD) relationship. DJT06001 inhibited free FXa with an inhibitory constant (Ki) of 0.99 nM, and exhibited >10000-fold selectivity for FXa than for other related serine proteases. DJT06001 concentration-dependently inhibited FXa activity in the prothrombinase complex with an IC of 2.53 nM. The concentrations for DJT06001 to double the prothrombin time (PT) and activated partial thromboplastin time (APTT) were 0.74 and 0.57 M, respectively. Importantly, DJT06001 did not impair platelet aggregation induced by ADP, platelet activating factor (PAF) and collagen. Furthermore, DJT06001 inhibited thrombus formation in rat thrombosis models in a dose dependent manner. And in rat tail bleeding risk test, it caused less bleeding than rivaroxaban at doses that achieve the same antithrombotic effect. PK/PD studies further demonstrated that there was a good correlation between the plasma concentrations of DJT06001and its inhibition of plasma FXa activity and prolongation of PT. In conclusion, DJT06001 was shown to be a potent and specific FXa inhibitor with excellent PK/PD profiles and it could be developed as a new anticoagulant for the management of thromboembolic diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  6 / 40958 MEDLINE  
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[PMID]: 29352103
[Au] Autor:Zhang J; Huang Y; Chen J; Zhu H; Whiteheart SW
[Ad] Address:From the Department of Molecular and Cellular Biochemistry, University of Kentucky College of Medicine, Lexington, Kentucky 40536.
[Ti] Title:Dynamic cycling of t-SNARE acylation regulates platelet exocytosis.
[So] Source:J Biol Chem;293(10):3593-3606, 2018 Mar 09.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Platelets regulate vascular integrity by secreting a host of molecules that promote hemostasis and its sequelae. Given the importance of platelet exocytosis, it is critical to understand how it is controlled. The t-SNAREs, SNAP-23 and syntaxin-11, lack classical transmembrane domains (TMDs), yet both are associated with platelet membranes and redistributed into cholesterol-dependent lipid rafts when platelets are activated. Using metabolic labeling and hydroxylamine (HA)/HCl treatment, we showed that both contain thioester-linked acyl groups. Mass spectrometry mapping further showed that syntaxin-11 was modified on cysteine 275, 279, 280, 282, 283, and 285, and SNAP-23 was modified on cysteine 79, 80, 83, 85, and 87. Interestingly, metabolic labeling studies showed incorporation of [ H]palmitate into the t-SNAREs increased although the protein levels were unchanged, suggesting that acylation turns over on the two t-SNAREs in resting platelets. Exogenously added fatty acids did compete with [ H]palmitate for t-SNARE labeling. To determine the effects of acylation, we measured aggregation, ADP/ATP release, as well as P-selectin exposure in platelets treated with the acyltransferase inhibitor cerulenin or the thioesterase inhibitor palmostatin B. We found that cerulenin pretreatment inhibited t-SNARE acylation and platelet function in a dose- and time-dependent manner whereas palmostatin B had no detectable effect. Interestingly, pretreatment with palmostatin B blocked the inhibitory effects of cerulenin, suggesting that maintaining the acylation state is important for platelet function. Thus, our work shows that t-SNARE acylation is actively cycling in platelets and suggests that the enzymes regulating protein acylation could be potential targets to control platelet exocytosis .
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.RA117.000140

  7 / 40958 MEDLINE  
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[PMID]: 29522245
[Au] Autor:Barratclough A; Floyd RF; Reep RL; Ball RL; Conner BJ
[Ad] Address:Tampa's Lowry Park Zoo, Tampa, FL, USA.
[Ti] Title:Thromboelastography in wild Florida manatees (Trichechus manatus latirostris).
[So] Source:Vet Clin Pathol;, 2018 Mar 09.
[Is] ISSN:1939-165X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Thromboelastography (TEG) provides a comprehensive evaluation of blood clot formation. This test can be used to identify abnormalities in coagulation by assessing multiple aspects of the clotting cascade, including the speed of clot initiation and formation, clot strength, and ultimately fibrinolysis. Thromboembolic disease has been hypothesized to play a role in the pathophysiology of cold stress syndrome (CSS), an important cause of mortality in the threatened Florida manatee (Trichechus manatus latirostris). OBJECTIVES: The objective of this study was to establish thromboelastography RIs using the TEG 5000 with citrated whole blood samples and kaolin activation in wild, healthy manatees. METHODS: In December 2014 and January 2015, 29 wild manatees (17 male and 12 female) were blood sampled as part of the annual wild manatee health assessments organized by United States Geological Survey (USGS). TEG was performed using citrated kaolin-activated samples. RESULTS: The samples were obtained from manatees caught in Crystal River, Citrus County, and used to identify the meanSD of normal TEG parameters: R=reaction time 2.1minutes (0.8), K=clot formation time 0.8min (0), α angle=83.1 (2), MA=maximum amplitude 75mm (7.6), and LY30=clot lysis 0.41% (0.68). No significant differences were found between manatee size, sex, or time between sampling and running the test. CONCLUSIONS: Manatee TEG parameters demonstrate a relatively hypercoagulable condition when compared to other mammals. This information will facilitate detection of changes in hemostasis during injury and disease and provide a valuable reference range.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1111/vcp.12599

  8 / 40958 MEDLINE  
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[PMID]: 29519941
[Au] Autor:Adam F; Kauskot A; Kurowska M; Goudin N; Munoz I; Bordet JC; Huang JD; Bryckaert M; Fischer A; Borgel D; de Saint Basile G; Christophe OD; Mnasch G
[Ad] Address:From the INSERM, UMR_S 1176, Paris-Sud University, Universit Paris-Saclay, Le Kremlin-Bictre, France (F.A., A.K., M.B., D.B., O.D.C.); INSERM, UMR_S 1163, Laboratory of Normal and Pathological Homeostasis of the Immune System, Paris, France (M.K., I.M., A.F., G.d.S.B., G.M.); Imagine Institute (M.
[Ti] Title:Kinesin-1: A New Actor Involved in Platelet Secretion and Thrombus Stability.
[So] Source:Arterioscler Thromb Vasc Biol;, 2018 Mar 08.
[Is] ISSN:1524-4636
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Platelet secretion is crucial for many physiological platelet responses. Even though several regulators of the fusion machinery for secretory granule exocytosis have been identified in platelets, the underlying mechanisms are not yet fully characterized. APPROACH AND RESULTS: By studying a mouse model (cKO [conditional knockout] ) lacking Kif5b (kinesin-1 heavy chain) in its megakaryocytes and platelets, we evidenced unstable hemostasis characterized by an increase of blood loss associated to a marked tendency to rebleed in a tail-clip assay and thrombus instability in an in vivo thrombosis model. This instability was confirmed in vitro in a whole-blood perfusion assay under blood flow conditions. Aggregations induced by thrombin and collagen were also impaired in cKO platelets. Furthermore, P-selectin exposure, PF4 (platelet factor 4) secretion, and ATP release after thrombin stimulation were impaired in cKO platelets, highlighting the role of kinesin-1 in α-granule and dense granule secretion. Importantly, exogenous ADP rescued normal thrombin induced-aggregation in cKO platelets, which indicates that impaired aggregation was because of defective release of ADP and dense granules. Last, we demonstrated that kinesin-1 interacts with the molecular machinery comprising the granule-associated Rab27 protein and the Slp4 (synaptotagmin-like protein 4/SYTL4) adaptor protein. CONCLUSIONS: Our results indicate that a kinesin-1-dependent process plays a role for platelet function by acting into the mechanism underlying α-granule and dense granule secretion.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  9 / 40958 MEDLINE  
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[PMID]: 29519806
[Au] Autor:Xu XR; Yousef GM; Ni H
[Ad] Address:Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science, St. Michael's Hospital, University of Toronto, Canada.
[Ti] Title:Cancer and Platelet Crosstalk: Opportunities and challenges for aspirin and other anti-platelet agents.
[So] Source:Blood;, 2018 Mar 08.
[Is] ISSN:1528-0020
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Platelets have long been recognized as key players in hemostasis and thrombosis; however, growing evidence suggests that they are also significantly involved in cancer, the second leading cause of mortality worldwide. Preclinical and clinical studies showed that tumorigenesis and metastasis can be promoted by platelets through a wide variety of crosstalk between platelets and cancer cells. For example, cancer changes platelet behavior by directly inducing tumor-platelet aggregates, triggering platelet granule and extracellular vesicle release, altering platelet phenotype and platelet RNA profiles, and enhancing thrombopoiesis. Reciprocally, platelets reinforce tumor growth with proliferation signals, anti-apoptotic effect, and angiogenic factors. Platelets also activate tumor invasion and sustain metastasis inducing an invasive epithelial-mesenchymal transition phenotype of tumor cells, promoting tumor survival in circulation, tumor arrest at the endothelium, and extravasation. Furthermore, platelets assist tumors in evading immune destruction. Hence, cancer cells and platelets maintain a complex, bidirectional communication. Recently, aspirin (acetylsalicylic acid) has been recognized as a promising cancer-preventative agent. It is recommended at daily low-dose by the United States Preventive Services Task Force for primary prevention of colorectal cancer. The exact mechanisms of action of aspirin in chemoprevention are not very clear, but evidence has emerged that suggests a platelet-mediated effect. In this article, we will introduce how cancer changes platelets to be more cancer-friendly, and highlight advances in the modes of action for aspirin in cancer prevention. We also discuss the opportunities, challenges, and opposing viewpoints on applying aspirin and other anti-platelet agents for cancer prevention and treatment.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  10 / 40958 MEDLINE  
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[PMID]: 29517984
[Au] Autor:Wander P; Castaneda D; D'Souza L; Singh S; Serouya S; Velazquez AI; Mamun R; Voaklander R; Benias P; Carr-Locke DL
[Ad] Address:Department of Internal Medicine, Mount Sinai St Luke's and West Hospital.
[Ti] Title:Single Center Experience of a New Endoscopic Clip in Managing Nonvariceal Upper Gastrointestinal Bleeding.
[So] Source:J Clin Gastroenterol;52(4):307-312, 2018 Apr.
[Is] ISSN:1539-2031
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: To assess the safety and efficacy of the Instinct clip in the acute endoscopic treatment of upper gastrointestinal bleeding (UGIB). MATERIALS AND METHODS: This is the first large series reporting this clip in achieving hemostasis. A retrospective descriptive chart review was performed on patients presenting with recent overt GI bleeding treated with endoclip therapy at Mount Sinai Beth Israel Medical Center between May 2013 and January 2016. Results are expressed in absolute numbers, percentages, and trends. RESULTS: In total, 178 consecutive patients with UGIB were included. Source of bleeding was identified as duodenal ulcer (29.2%), gastric ulcer (22.5%), gastro-esophageal junction tear (8.4%), anastomosis (5.6%), erosive gastropathy (5.6%), Dieulafoy (5.1%), gastric polyp (4.5%), postendoscopic procedure (3.9%), angioectasia (3.4%), esophageal ulcer (2.8%), benign duodenal mass (2.8%), peg tube site (2.3%), gastric neoplasm (1.7%), esophagitis (1.1%), and small bowel ulcer (1.1%). Lesions demonstrated active bleeding in 47.5% (11.3% spurting and 36.2% oozing) and nonbleeding lesions in 52.5% (25.0% visible vessel, 11.9% hematin in ulcer base, 10.0% adherent clot, 5.6% flat spot). Initial hemostasis was achieved in 96.6%. Additional methods were used in 24.1% (argon plasma coagulation and epinephrine injection in 21.3%, surgery in 0.6%, and interventional radiology in 2.2%). There were no adverse events. In-hospital rebleeding was 7.3% and 3.9% presented with rebleeding within 30 days. Average procedure duration was 22.9 minutes and average length of hospital stay was 11.3 days. CONCLUSIONS: The Instinct clip, when used for UGIB, seems to be safe and effective with similar rebleeding rates compared with other modalities.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1097/MCG.0000000000000785


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