Understanding and Managing Thrombotic Risks in Medical Conditions: One Size Does Not Fit All

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Fältnamn	Indikatorer	Metadata
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003		SwePub
008		240820s2024 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
020		a 9789180756396q print
020		a 9789180756402q electronic
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-2065582 URI
024	7	a https://doi.org/10.3384/97891807564022 DOI
040		a (SwePub)liu
041		a engb eng
042		9 SwePub
072	7	a vet2 swepub-contenttype
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100	1	a Heenkenda, Menikae Kanchena,d 1982-u Linköpings universitet,Avdelningen för klinisk kemi och farmakologi,Medicinska fakulteten,Region Östergötland, Laboratoriemedicin sjukhus4 aut0 (Swepub:liu)menhe81
245	1 0	a Understanding and Managing Thrombotic Risks in Medical Conditions :b One Size Does Not Fit All
264	1	a Linköping :b Linköping University Electronic Press,c 2024
300		a 109 s.
338		a electronic2 rdacarrier
490	0	a Linköping University Medical Dissertations,x 0345-0082 ;v 1915
520		a Hemostasis is a critical physiological process that stops bleeding at the site of an injury while ensuring normal blood flow elsewhere, thereby preventing excessive clot formation that could lead to dangerous conditions like thrombosis. This delicate balance is influenced by genetics, medical conditions such as cancer, and various medications. When a blood vessel is damaged, platelets adhere to the exposed area, become activated, and aggregate to form an initial plug. Coagulation factors, particularly thrombin, create a strong fibrin network to stabilize the clot. Disruptions in this process can result in significant bleeding or dangerous clot formation.This thesis aims to explore and understand the factors affecting coagulation and the risks of thrombotic events in different medical contexts. This includes studying genetic variability in the protease-activated receptor 4 (PAR4) gene (specifically the Ala120Thr variant) among sub-Saharan African populations, identifying genetic and non-genetic risk factors for venous thromboembolism (VTE) in patients with the brain cancer glioblastoma multiforme (GBM), and investigating the impact of intravenous morphine on platelet activity in patients with ST-elevation myocardial infarction (STEMI) treated with ticagrelor, a P2Y12 inhibitor. The A allele of the rs773902 single-nucleotide polymorphism (SNP) in the PAR4 gene (F2RL3) substitutes threonine for alanine at the 120th protein position (Thr120). This allele is more prevalent in African populations compared to Caucasian populations, although previous studies did not specify the geographic ancestry of participants. Thr120 is associated with higher PAR4-induced human platelet aggregation and Ca2+ flux. Our study found that the frequency of the A allele in the Somali population is significantly lower than previously reported for African Americans. The A allele frequency in Somalis is 38%, compared to 63% for African Americans. The A allele frequency in Somalis is closer to that of the Maasai population in Kenya (41%), but vastly different from the Esan population in Nigeria (68%). Certain cancers, such as GBM, are associated with a higher risk of VTE, including deep vein thrombosis (DVT) and pulmonary embolism (PE). Our research identified blood group B as a significant risk factor for patients with GBM (OR=6.91; 95% CI=2.2–24.1; P =0.001). Also, GBM tumors in the frontal lobe are associated with an increased risk of VTE (OR=3.14; 95% CI=1.1–10.7; P =0.05). Our study on morphine, commonly used for pain management in STEMI patients, found that morphine is associated with increased platelet aggregation one hour after percutaneous coronary intervention (PCI), impacting the efficacy of ticagrelor. Morphine delays platelet inhibition by affecting the pharmacodynamics of antiplatelet therapy, likely by delaying gastric emptying. However, this effect is short-lived, as platelet reactivity returns to similar levels in both groups 12 hours post-PCI. Despite this immediate impact on platelet function, our research found no significant differences in biomarkers of platelet activity, coagulation, or inflammation between the morphine and non-morphine groups. Additionally, all patients in our study were administered unfractionated heparin injections or bivalirudin infusion during primary PCI, which may help control the risk of blood clot formation. These studies collectively emphasize the need for individualized strategies to manage thrombotic risks and coagulation. The significant genetic variability among sub-Saharan African populations highlights the need for precise genetic research to understand how genetics influence coagulation and develop personalized medical strategies. The increased risk of cancer-associated thrombosis, particularly in patients with GBM, calls for individualized anticoagulant therapies based on unique risk profiles, such as blood group typing and tumor location. Incorporating these insights into clinical practice can help healthcare providers better identify high-risk patients and tailor thromboprophylaxis strategies accordingly. Similarly, the impact of morphine on patients with STEMI treated with ticagrelor requires careful consideration. In conclusion, these findings underscore the importance of a personalized approach in managing coagulation and thrombotic risks. The studies show that genetic variability, specific medical conditions, and medication effects are crucial in thrombotic risk. Therefore, customized strategies based on individual patient profiles and contexts are essential for effectively managing and preventing thrombotic events.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Hematologi0 (SwePub)302022 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Hematology0 (SwePub)302022 hsv//eng
653		a Hemostasis
653		a Coagulation
653		a Thrombosis
653		a Genetic variability
653		a Venous thromboembolism
653		a Glioblastoma multiforme
700	1	a Lindahl, Tomas,c Professor emeritus,d 1954-u Linköpings universitet,Avdelningen för klinisk kemi och farmakologi,Medicinska fakulteten,Region Östergötland, Klinisk kemi4 ths0 (Swepub:liu)tomli13
700	1	a Aardal, Elisabeth,c PhD,d 1959-u Linköpings universitet,Avdelningen för klinisk kemi och farmakologi,Medicinska fakulteten,Region Östergötland, Klinisk kemi4 ths0 (Swepub:liu)eliaa63
700	1	a Boknäs, Niklas,c Associate Professor,d 1979-u Linköpings universitet,Avdelningen för klinisk kemi och farmakologi,Medicinska fakulteten,Region Östergötland, Hematologiska kliniken US4 ths0 (Swepub:liu)nikbo14
700	1	a Gimm, Oliver,c Professor,d 1967-u Linköpings universitet,Avdelningen för kirurgi, ortopedi och onkologi,Medicinska fakulteten,Region Östergötland, Kirurgiska kliniken US4 ths0 (Swepub:liu)oligi51
700	1	a Loitto, Vesa-Matti,c PhD,d 1970-u Linköpings universitet,Avdelningen för inflammation och infektion,Medicinska fakulteten4 ths0 (Swepub:liu)veslo07
700	1	a Szanto, Timea,c Adjunct Professoru Coagulation Disorders Unit, Department of Hematology, Comprehensive Cancer Centre, Comprehensive Care Centre of Hemophilia and Allied Disorders (EAHAD), Helsinki University Hospital, Helsinki, Finland; Research Program Unit in Systems Oncology, Faculty of Medicine, University of Helsinki, Helsinki, Finland4 opn
710	2	a Linköpings universitetb Avdelningen för klinisk kemi och farmakologi4 org
856	4	u https://doi.org/10.3384/9789180756402y Fulltext
856	4	u https://liu.diva-portal.org/smash/get/diva2:1890588/FULLTEXT01.pdfx primaryx Raw objecty fulltext
856	4	u https://liu.diva-portal.org/smash/get/diva2:1890588/PREVIEW01.pngx Previewy preview image
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-206558
856	4 8	u https://doi.org/10.3384/9789180756402

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