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master's thesis
Patogeneza sindroma posteriorne reverzibilne encefalopatije uzrokovanog citotoksičnom terapijom
Zagreb: University of Zagreb, School of Medicine, 2018. urn:nbn:hr:105:437766
Pozaić, Antonio
University of Zagreb
School of Medicine
Department of Pathophysiology

Institutional repository: Dr Med - University of Zagreb School of Medicine Digital Repository

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Pozaić, A. (2018). Patogeneza sindroma posteriorne reverzibilne encefalopatije uzrokovanog citotoksičnom terapijom (Master's thesis). Zagreb: University of Zagreb, School of Medicine. Retrieved from https://urn.nsk.hr/urn:nbn:hr:105:437766

Pozaić, Antonio. "Patogeneza sindroma posteriorne reverzibilne encefalopatije uzrokovanog citotoksičnom terapijom." Master's thesis, University of Zagreb, School of Medicine, 2018. https://urn.nsk.hr/urn:nbn:hr:105:437766

Pozaić, Antonio. "Patogeneza sindroma posteriorne reverzibilne encefalopatije uzrokovanog citotoksičnom terapijom." Master's thesis, University of Zagreb, School of Medicine, 2018. https://urn.nsk.hr/urn:nbn:hr:105:437766

Pozaić, A. (2018). 'Patogeneza sindroma posteriorne reverzibilne encefalopatije uzrokovanog citotoksičnom terapijom', Master's thesis, University of Zagreb, School of Medicine, accessed 05 November 2024, https://urn.nsk.hr/urn:nbn:hr:105:437766

Pozaić A. Patogeneza sindroma posteriorne reverzibilne encefalopatije uzrokovanog citotoksičnom terapijom [Master's thesis]. Zagreb: University of Zagreb, School of Medicine; 2018 [cited 2024 November 05] Available at: https://urn.nsk.hr/urn:nbn:hr:105:437766

A. Pozaić, "Patogeneza sindroma posteriorne reverzibilne encefalopatije uzrokovanog citotoksičnom terapijom", Master's thesis, University of Zagreb, School of Medicine, Zagreb, 2018. Available at: https://urn.nsk.hr/urn:nbn:hr:105:437766

Metadata
TitlePatogeneza sindroma posteriorne reverzibilne encefalopatije uzrokovanog citotoksičnom terapijom
Title (english)Pathogenesis of Posterior Reversible Encephalopathy Syndrome (PRES) caused by cytotoxic therapies
AuthorAntonio Pozaić
MentorNatalija Dedić Plavetić (mentor)
Committee memberBranko Malojčić (predsjednik povjerenstva)
Committee memberJasenka Markeljević (član povjerenstva)
Committee memberNatalija Dedić Plavetić (član povjerenstva)
GranterUniversity of Zagreb
School of Medicine
(Department of Pathophysiology)
Zagreb
Defense date and country2018-07-13, Croatia
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Clinical Medical Sciences
Pathophysiology
Abstract
Sindrom posteriorne reverzibilne encefalopatije (PRES) je kliničko-radiološki sindrom obilježen glavoboljom, epileptičnim napadima, promijenjenim stanjem svijesti i smetnjama vida. Nespecifičnu kliničku sliku tipično prate radiološki nalazi simetričnog edema hemisfera u posterio-okcipitalnim regijama najbolje uočljivog pretragom magnetskom rezonancom (MR-om). Iako naziv sindroma ukazuje na reverzibilnost simptoma, moguća su trajna neurološka oštećenja i smrtni, prilikom čega letalitet može biti 15%. Najčešća stanja koja se povezuju s PRES-om su preeklampsija/eklampsija, transplantacija solidnih organa i koštane srži, autoimunosne bolesti, hipertenzija te imunosupresivna terapija i citotoksični lijekovi. Cilj ovog rada je ponuditi moguće mehanizme kojima citotoksični lijekovi uzrokuju PRES. Nijedna grupa citotoksičnih lijekova se nije konstantno povezivala sa nastankom PRES-a. Smatra se kako je endotelna disfunkcija glavni mehanizam kojim citotoksični lijekovi dovode do disrupcije krvno-moždane barijere i posljedičnog moždanog edema, a endotelna disfunkcija nastaje kao posljedica izravnog ili neizravnog djelovanja lijekova. Neki citotoksični lijekovi uzrokuju endotelnu disfunkciju uglavnom preko oksidativnog stresa. Osim endotelne disfunkcije, opisat ćemo kako drugi čimbenici rizika inducirani citotoksičnom terapijom, poput hipertenzije, hipoalbuminemije, hipomagnezemije i hiponatremije, doprinose nastanku PRES-a. Iako se smatralo kako je hipertenzija najvažniji pojedinačni čimbenik za nastanak PRES-a, ona bi u slučaju PRES-a induciranog citotoksičnim lijekovima bila posljedica endotelne disfunkcije, a ne njen uzrok. Hipomagnezemija se povezuje s povećanom endotelnom permeabilnošću, moguće zbog povećane ekspresije akvaporina 4, vodopropusnog transmembranskog proteina, a liječenje magnezijevim sulfatom smanjuje propusnost krvnomoždane barijere za 41% na životinjskim modelima. Hiponatremija smanjuje osmolalnost plazme, a hipoalbuminemija onkotski tlak, uzrokujući prijelaz tekućine iz vaskularnog u ekstravaskularni prostor. Navedeni čimbenici rizika naglašavaju važnost regulacije elektrolitnog disbalansa pri liječenju PRES-a, kao i regulaciju tlaka i plazmatske razine albumina.
Abstract (english)
Posterior reversible encephalopathy syndrome (PRES) is a clinico-radiological syndrome characterized by headache, seizures, altered consciousness, and visual disturbance. Nonspecific symptoms are typically coupled with symmetric hemispheric edema in the posterio-occipital regions, best seen on MR. Although the name of the syndrome indicates it is reversible, permanent neurologic injury or death are possible. Lethality by PRES is 15%. Most frequent conditions associated with PRES are preeclampsia/eclampsia, solid organ and bone marrow transplantation, autoimmune diseases, hypertension and immunosupressive and cytotoxic drugs. The aim of this study is to propose a mechanism by which cytotoxic drugs cause PRES. No single antineoplastic class or agent has been consistently associated with PRES. It is believed that endothelial dysfunction is the main mechanism by which cytotoxic drugs lead to disruption of the blood-brain barrier and consequently to brain edema. Some cytotoxic drugs cause endothelial dysfunction, mostly by oxidative stress. Here we will also discuss how other risk factors, induced by cytotoxic drugs, such as hypertension, hypoalbuminemia, hypomagnesemia and hyponatremia, contribute to the development of PRES. Althought hypertension is the single most important risk factor for developing PRES, she is a consequence of endothelial dysfunction and not it's cause. Hypomagnesemia is associated with increased endothelial permeability, possibly because of an increased expression of aquaporin 4, a water-permeabile transmembrane protein. Not only that, magnesium sulphate reduces the blood-brain permeabilityby 41% in animal models. Hyponatremia decerases plasma osmolality and hypoalbuminemia decreases oncotic pressure, allowing fluid to leak out from the intravascular to extravascular space. These risk factors point out the importance of the correction of electroyite imbalance, as well as the blood pressure and plasma albumin levels.
Keywords
Keywords (english)
Languagecroatian
URN:NBNurn:nbn:hr:105:437766
Study programmeTitle: Medicine
Study programme type: university
Study level: integrated undergraduate and graduate
Academic / professional title: doktor/doktorica medicine (doktor/doktorica medicine)
Type of resourceText
File originBorn digital
Access conditionsOpen access
Terms of useLicence In copyright icon
Created on2019-03-21 13:13:01