{"id":13849,"date":"2025-11-09T17:21:20","date_gmt":"2025-11-09T15:21:20","guid":{"rendered":"https:\/\/www.kliinikum.ee\/yhendlabor\/?page_id=13849"},"modified":"2025-11-09T17:21:25","modified_gmt":"2025-11-09T15:21:25","slug":"antitrombiin-iii-p-at-iii","status":"publish","type":"page","link":"https:\/\/www.kliinikum.ee\/yhendlabor\/kasiraamat\/huubimisuuringud\/antitrombiin-iii-p-at-iii\/","title":{"rendered":"Antitrombiin III (P-AT III)"},"content":{"rendered":"\n<p><em>Kliinilise keemia ja laboratoorse hemaotoloogia osakond<\/em><\/p>\n\n\n\n<p><strong>Antitrombiin III (AT III)<\/strong> on maksas s\u00fcnteesitav gl\u00fckoproteiin, mis inhibeerib trombiini, faktorit Xa ja v\u00e4hemal m\u00e4\u00e4ral faktoreid IXa, XIa, XIIa ning plasmiini ja kallikreiini. Hepariin v\u00f5imendab AT III inhibeerivat toimet h\u00fc\u00fcbimisfaktoritele.<\/p>\n\n\n\n<p>AT III defitsiidi levimus \u00fcldpopulatsioonis on 1:2000 kuni 1:3000, venoosse trombembooliaga (VTE) patsientide hulgas aga 1:20 kuni 1:200. AT III defitsiit suurendab VTE riski 5\u201350 korda.<\/p>\n\n\n\n<p class=\"has-medium-font-size\"><strong>Uuritav materjal, selle v\u00f5tmine, saatmine ja s\u00e4ilitamine<\/strong><\/p>\n\n\n\n<figure class=\"wp-block-table is-style-stripes\"><table width=\"100%\"><tbody><tr><td width=\"1%\"><\/td><td width=\"15%\"><strong>Katsuti<\/strong><\/td><td width=\"84%\">9NC-katsuti (helesinine kork)<\/td><\/tr><tr><td><\/td><td><strong>S\u00e4ilivus<\/strong><\/td><td>Plasma toatemperatuuril kaheksa tundi, -20 \u00b0C \u00fcks kuu. Plasma tuleb eraldada nelja tunni jooksul peale proovi v\u00f5tmist (tsentrifuugida 2000\u20132500 x g juures 15 min).<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<p>Proovimaterjal hemostaasi uuringuteks v\u00f5etakse esimese katsutina (v.a juhul, kui v\u00f5etakse ka verek\u00fclv).<\/p>\n\n\n\n<p>NB! Proovin\u00f5u peab olema t\u00e4itunud katsutil oleva m\u00e4rgini!<\/p>\n\n\n\n<p>Mistahes kliiniliste erijuhtude (nt hematokrit &gt; 0,55) puhul ja s\u00e4ilitamise\/saatmisega seotud k\u00fcsimuste korral tuleb n\u00f5u pidada laboriga.<\/p>\n\n\n\n<p class=\"has-medium-font-size\"><strong>Anal\u00fc\u00fcsi tegemise aeg: <\/strong>\u00f6\u00f6p\u00e4evaringselt<\/p>\n\n\n\n<p class=\"has-medium-font-size\"><strong>Anal\u00fc\u00fcsimeetod: <\/strong>kolorimeetriline meetod<\/p>\n\n\n\n<p class=\"has-medium-font-size\"><strong>Referentsv\u00e4\u00e4rtused<\/strong><\/p>\n\n\n\n<figure class=\"wp-block-table\"><table width=\"100%\"><tbody><tr><td width=\"1%\"><\/td><td width=\"30%\"><strong>0 p \u2013 &lt; 3 p<\/strong><\/td><td width=\"69%\">58\u201390%<\/td><\/tr><tr><td><\/td><td><strong>3 p \u2013 &lt; 1 k<\/strong><\/td><td>60\u201389%<\/td><\/tr><tr><td><\/td><td><strong>1 k \u2013 &lt; 1 a<\/strong><\/td><td>72\u2013134%<\/td><\/tr><tr><td><\/td><td><strong>1 a \u2013 &lt; 6 a<\/strong><\/td><td>101\u2013131%<\/td><\/tr><tr><td><\/td><td><strong>6 a \u2013 &lt; 11 a<\/strong><\/td><td>95\u2013134%<\/td><\/tr><tr><td><\/td><td><strong>11 a \u2013 &lt; 18 a<\/strong><\/td><td>96\u2013126%<\/td><\/tr><tr><td><\/td><td><strong>\u2265 18 a<\/strong><\/td><td>80\u2013120%<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<p class=\"has-medium-font-size\"><strong>N\u00e4idustus ja kliiniline t\u00e4hendus<\/strong><\/p>\n\n\n\n<p>Trombofiilia diferentsiaaldiagnostika, p\u00e4riliku v\u00f5i omandatud AT III defitsiidi kahtlus.<\/p>\n\n\n\n<p>Kongenitaalne AT III defitsiit jaguneb j\u00e4rgnevalt:<\/p>\n\n\n\n<figure class=\"wp-block-table\"><table width=\"100%\"><tbody><tr><td width=\"1%\"><\/td><td width=\"15%\"><strong>Alat\u00fc\u00fcp<\/strong><\/td><td width=\"15%\"><strong>AT III hulk<\/strong><\/td><td width=\"69%\"><strong>AT III bioloogiline aktiivsus<\/strong><\/td><\/tr><tr><td><\/td><td>I<\/td><td>\u2193<\/td><td>\u2193<\/td><\/tr><tr><td><\/td><td>II RS<\/td><td>N<\/td><td>\u2193<\/td><\/tr><tr><td><\/td><td>II HBS<\/td><td>N<\/td><td>\u2193 ainult hepariini juuresolekul, muidu N<\/td><\/tr><tr><td><\/td><td>II PE<\/td><td>\u2193<\/td><td>\u2193<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<p>\u00dchendlabori AT III anal\u00fc\u00fcsi tulemus on langenud k\u00f5igi AT III defitsiidi alat\u00fc\u00fcpide korral, kuid ei v\u00f5imalda neid omavahel eristada. Haiguse raskusaste s\u00f5ltub alat\u00fc\u00fcbist ja sellest, kas tegemist on homos\u00fcgootse v\u00f5i heteros\u00fcgootse muutusega.<\/p>\n\n\n\n<p>Omandatud AT III defitsiit esineb s\u00fcnteesi puudulikkuse (maksahaigused), suurenenud valgukaotusega seotud seisundite (nefrootiline s\u00fcndroom), Crohni t\u00f5ve, haavandilise koliidi, suurenenud tarbimise (sepsis, DIK, \u00e4ge trombemboolia, trombootilised mikroangiopaatiad, \u00e4ge m\u00fceloidne leukeemia, preeklampsia) v\u00f5i lahjendusefekti (hemodial\u00fc\u00fcs, plasmaferees, kardiopulmonaarne <em>bypass<\/em>) korral. Lisaks on AT III tase langenud pikaajalise ravi korral fraktsioneerimata hepariiniga ja L-asparaginaasiga. AT III madalate v\u00e4\u00e4rtuste puhul ei anna hepariinravi soovitud tulemust.<\/p>\n\n\n\n<p>AT III ei ole soovitav m\u00e4\u00e4rata kolme kuu jooksul peale tromboosi v\u00f5i tormbemboolia episoodi, kuna v\u00f5ivad esineda valemadalad tulemused.<\/p>\n\n\n\n<p>Valek\u00f5rged AT III tulemused v\u00f5ivad esineda varfariin- ja dabigatraanravi korral.<\/p>\n\n\n\n<p>Koostaja: Kaja Vaagen<br>Muudetud 03.08.2022<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Kliinilise keemia ja laboratoorse hemaotoloogia osakond Antitrombiin III (AT III) on maksas s\u00fcnteesitav gl\u00fckoproteiin, mis inhibeerib trombiini, faktorit Xa ja v\u00e4hemal m\u00e4\u00e4ral faktoreid IXa, XIa, XIIa ning plasmiini ja kallikreiini. Hepariin v\u00f5imendab AT III inhibeerivat toimet h\u00fc\u00fcbimisfaktoritele. AT III defitsiidi levimus \u00fcldpopulatsioonis on 1:2000 kuni 1:3000, venoosse trombembooliaga (VTE) patsientide hulgas aga 1:20 kuni 1:200. [&hellip;]<\/p>\n","protected":false},"author":38,"featured_media":0,"parent":7274,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_uag_custom_page_level_css":"","footnotes":""},"class_list":["post-13849","page","type-page","status-publish","hentry"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.3 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Antitrombiin III (P-AT III) - \u00dchendlabor<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.kliinikum.ee\/yhendlabor\/kasiraamat\/huubimisuuringud\/antitrombiin-iii-p-at-iii\/\" \/>\n<meta property=\"og:locale\" content=\"et_EE\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Antitrombiin III (P-AT III) - \u00dchendlabor\" \/>\n<meta property=\"og:description\" content=\"Kliinilise keemia ja laboratoorse hemaotoloogia osakond Antitrombiin III (AT III) on maksas s\u00fcnteesitav gl\u00fckoproteiin, mis inhibeerib trombiini, faktorit Xa ja v\u00e4hemal m\u00e4\u00e4ral faktoreid IXa, XIa, XIIa ning plasmiini ja kallikreiini. Hepariin v\u00f5imendab AT III inhibeerivat toimet h\u00fc\u00fcbimisfaktoritele. AT III defitsiidi levimus \u00fcldpopulatsioonis on 1:2000 kuni 1:3000, venoosse trombembooliaga (VTE) patsientide hulgas aga 1:20 kuni 1:200. 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Hepariin v\u00f5imendab AT III inhibeerivat toimet h\u00fc\u00fcbimisfaktoritele. AT III defitsiidi levimus \u00fcldpopulatsioonis on 1:2000 kuni 1:3000, venoosse trombembooliaga (VTE) patsientide hulgas aga 1:20 kuni 1:200. 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Hepariin v\u00f5imendab AT III inhibeerivat toimet h\u00fc\u00fcbimisfaktoritele. AT III defitsiidi levimus \u00fcldpopulatsioonis on 1:2000 kuni 1:3000, venoosse trombembooliaga (VTE) patsientide hulgas aga 1:20 kuni 1:200.&hellip;","_links":{"self":[{"href":"https:\/\/www.kliinikum.ee\/yhendlabor\/wp-json\/wp\/v2\/pages\/13849","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.kliinikum.ee\/yhendlabor\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/www.kliinikum.ee\/yhendlabor\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/www.kliinikum.ee\/yhendlabor\/wp-json\/wp\/v2\/users\/38"}],"replies":[{"embeddable":true,"href":"https:\/\/www.kliinikum.ee\/yhendlabor\/wp-json\/wp\/v2\/comments?post=13849"}],"version-history":[{"count":0,"href":"https:\/\/www.kliinikum.ee\/yhendlabor\/wp-json\/wp\/v2\/pages\/13849\/revisions"}],"up":[{"embeddable":true,"href":"https:\/\/www.kliinikum.ee\/yhendlabor\/wp-json\/wp\/v2\/pages\/7274"}],"wp:attachment":[{"href":"https:\/\/www.kliinikum.ee\/yhendlabor\/wp-json\/wp\/v2\/media?parent=13849"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}