{"id":2959,"date":"2019-08-19T13:52:28","date_gmt":"2019-08-19T10:52:28","guid":{"rendered":"http:\/\/blog.ulubat.org\/?p=2959"},"modified":"2019-08-19T13:52:30","modified_gmt":"2019-08-19T10:52:30","slug":"akut-romatizmal-ates-ara-eklemi-yalar-kalbi-isirir-lasegue-1884","status":"publish","type":"post","link":"https:\/\/blog.ulubat.org\/index.php\/tip-egitimi\/akut-romatizmal-ates-ara-eklemi-yalar-kalbi-isirir-lasegue-1884\/","title":{"rendered":"Akut Romatizmal Ate\u015f (ARA) \u2013 \u2018Eklemi yalar, kalbi \u0131s\u0131r\u0131r (Lasegue-1884)\u2019"},"content":{"rendered":"\n
\"\"<\/figure>\n\n\n\n

Giri\u015f<\/h2>\n\n\n\n

Akut romatizmal ate\u015f (ARA); duyarl\u0131 ki\u015filerde Streptococcus\npyogenes \u00fcyesi olan A grubu beta hemolitik Streptokok\u2019un (GABS) neden oldu\u011fu\nfarenjitten 1-5 hafta (latent d\u00f6nem) sonra ortaya \u00e7\u0131kan otoimmun bir\nhastal\u0131kt\u0131r (1). Kalp ve eklem tutulumu yayg\u0131n g\u00f6r\u00fcl\u00fcp beyin, deri ve deri alt\u0131\nba\u011f dokusunu da tutabilen sistemik bir rahats\u0131zl\u0131kt\u0131r (2). <\/p>\n\n\n\n

\u00c7ocukluk ya\u015flar\u0131nda farenjit g\u00f6r\u00fclme s\u0131kl\u0131\u011f\u0131 fazla\noldu\u011fundan ARA ataklar\u0131 daha \u00e7ok 5-15 ya\u015flar\u0131nda g\u00f6r\u00fclmeye ba\u015flar. Te\u015fhis edilemez\nveya yeterli penisilin tedavisi verilmez ise ARA ataklar\u0131 zamanla \u015fiddetlenir.\nAtaklar \u015fiddetlendik\u00e7e hastal\u0131\u011f\u0131n sebep oldu\u011fu komplikasyonlar da a\u011f\u0131rla\u015f\u0131r. Bu\nsebeple mortalitesi ve morbisitesi y\u00fcksek olan \u2018romatizmal kalp hastal\u0131\u011f\u0131 (RKH)\u2019\ndedi\u011fimiz ARA\u2019n\u0131n karditi daha \u00e7ok 25-45 ya\u015flar\u0131nda ortaya \u00e7\u0131kabilir (2).<\/p>\n\n\n\n

\u00a0Geli\u015fmi\u015f \u00fclkelerde erken te\u015fhis ve yeterli tedavi imk\u00e2n\u0131 ile ya\u015fam ko\u015fullar\u0131n\u0131n iyile\u015fmesi sebebiyle ARA\u2019n\u0131n s\u0131kl\u0131\u011f\u0131 azalmakta; az geli\u015fmi\u015f ve geli\u015fmekte olan \u00fclkelerde ise ARA hastal\u0131\u011f\u0131 edinilmi\u015f kalp hastal\u0131klar\u0131n\u0131n en \u00f6nemli sebebini olu\u015fturmaktad\u0131r (3). <\/p>\n\n\n\n

<\/p>\n\n\n\n

Patofizyoloji<\/h2>\n\n\n\n

Hastal\u0131\u011f\u0131n patogenezi bug\u00fcne kadar tam olarak\nayd\u0131nlat\u0131lamam\u0131\u015ft\u0131r. Ama son y\u0131llarda ARA hastal\u0131\u011f\u0131 i\u00e7in \u00fc\u00e7 ana hipotez\nolu\u015fturulmu\u015ftur (4-6).<\/p>\n\n\n\n

  1. GABS\u2019\u0131n\nolu\u015fturdu\u011fu direk enfeksiyon<\/li>
  2. Streptekokal\ntoksinler (\u00f6zellikle streptolizin O)<\/li>
  3. Anormal\nimmun yan\u0131ta sebep olan konak-GABS antijenik benzerlik (\u00e7apraz reaksiyon)<\/li><\/ol>\n\n\n\n

    Yap\u0131lan \u00e7al\u0131\u015fmalarda GABS antijenleri ile konak (insan) antijenleri aras\u0131nda benzerlikler g\u00f6sterilmi\u015f (\u015eekil 1<\/strong>) ve hasta serumlar\u0131nda bu antijenlere kar\u015f\u0131 otoantikorlara rastlan\u0131lm\u0131\u015ft\u0131r (\u00e7apraz reaksiyon). Bu sebeple \u2018antijenik benzerlik\u2019 hipotezi \u00fczerine daha fazla \u00e7al\u0131\u015fmalar yap\u0131lm\u0131\u015ft\u0131r (7-9).<\/p>\n\n\n\n

    <\/p>\n\n\n\n

    \u015eekil 1<\/strong><\/p>\n\n\n\n

    \"\"<\/figure>\n\n\n\n

    Ara\u015ft\u0131rmalarda GABS enfeksiyonu sonras\u0131 b\u00fct\u00fcn\nhastalarda ARA geli\u015fmedi\u011fi duyarl\u0131 konak dedi\u011fimiz belli HLA antijenlerine\nsahip konaklarda ARA geli\u015fti\u011fi g\u00f6zlemlenmi\u015ftir (10-13). Ek olarak da A grubu\nbeta hemolitik streptokoklar\u0131n romatojenik su\u015flar\u0131n\u0131n (M 1, 3, 5, 6, 18, 19,\n24) olu\u015fturdu\u011fu farenjitten sonra ARA olu\u015ftu\u011fu da g\u00f6zlemlenmi\u015ftir (14).<\/p>\n\n\n\n

    Sonu\u00e7 olarak GABS\u2019\u0131n belli romatolojik su\u015flar\u0131n\u0131n duyarl\u0131 konakta farenjit enfeksiyonu yapmas\u0131 ve yeterli tedavi g\u00f6rmemesi sonucunda GABS antijenleri \u2013 konak antijenleri aras\u0131nda \u00e7apraz reaksiyon (\u015eekil 1<\/strong>) olu\u015fur ve latent d\u00f6nemin ard\u0131ndan kardit, artrit, korea, subkutan nod\u00fcl, eritema marginatum gibi klinik tablolar meydana gelir (\u015eekil 2<\/strong>).<\/p>\n\n\n\n

    <\/p>\n\n\n\n

    \u015eekil 2 \u00a0<\/strong><\/p>\n\n\n\n

    • \"\"<\/figure><\/li><\/ul>\n\n\n\n

      Klinik Bulgular ve Tan\u0131<\/h2>\n\n\n\n

      Akut romatizmal ate\u015f tan\u0131s\u0131n\u0131 kesinle\u015ftiren klinik\nveya laboratuvar bulgusu yoktur. \u0130lk kez 1944 y\u0131l\u0131nda T. Duckett Jones\ntaraf\u0131ndan tan\u0131mlanm\u0131\u015f Jones kriterleri ARA tan\u0131s\u0131nda kullan\u0131lmaktayd\u0131 (15,16).\nJones kriterleri, d\u00fc\u015f\u00fck riskli toplumlarda* gereksiz ARA tan\u0131s\u0131 konulmas\u0131n\u0131\n\u00f6nlemek ve orta-y\u00fcksek riskli toplumlarda** ise ARA hastal\u0131\u011f\u0131n\u0131 ka\u00e7\u0131rmamak i\u00e7in\n2015 y\u0131l\u0131nda modifiye edilerek \u20182015- Modifiye Jones Kriterleri\u2019\nolu\u015fturulmu\u015ftur (Tablo 1-2<\/strong>) (17).<\/p>\n\n\n\n

      *D\u00fc\u015f\u00fck riskli toplum: ARA\n<2\\100.000\\y\u0131l, RKH <1\\1000<\/p>\n\n\n\n

      **Orta-y\u00fcksek riskli toplum: ARA >2\\100.000\\y\u0131l, RKH>1\\1000<\/p>\n\n\n\n

      <\/p>\n\n\n\n

      Tablo 1 (D\u00fc\u015f\u00fck Riskli B\u00f6lgeler i\u00e7in\nJones Kriterleri)<\/strong><\/p>\n\n\n\n
      \n Major\n Bulgular<\/strong>\n  <\/strong>\n <\/td>\n Min\u00f6r\n Bulgular<\/strong>\n <\/td><\/tr>
      \n Poliartrit\n  \n <\/td>\n Ate\u015f> 38.5\n <\/td><\/tr>
      \n Kardit (klinik ve\\veya subklinik)\n  \n <\/td>\n Poliartralji\n <\/td><\/tr>
      \n Sydenham korea\n  \n <\/td> Akut faz reaktanlar\u0131nda art\u0131\u015f
      – CRP \u2265 3 mg\\dl
      – ESR \u2265 60 mm\\h <\/td><\/tr>
      \n Eritema marginatum\n  \n <\/td>\n PR uzamas\u0131 veya tedaviyle k\u0131salmas\u0131\n <\/td><\/tr>
      \n Subkutan nod\u00fcller\n  \n <\/td>\n  \n <\/td><\/tr><\/tbody><\/table>\n\n\n\n

      Tablo 2 (Orta-Y\u00fcksek Riskli B\u00f6lgeler\ni\u00e7in Jones Kriterleri)<\/strong><\/p>\n\n\n\n
      \n Major\n Bulgular<\/strong>\n  <\/strong>\n <\/td>\n Min\u00f6r\n Bulgular<\/strong>\n <\/td><\/tr>
      \n Monoartrit\n  \n <\/td>\n Ate\u015f > 38\n <\/td><\/tr>
      \n Poliartralji\n  \n <\/td>\n Monoartralji\n <\/td><\/tr>
      \n  \n <\/td>\n ESR \u2265 30 mm\\h\n  \n <\/td><\/tr><\/tbody><\/table>\n\n\n\n

      Ge\u00e7irilmi\u015f GABS Enfeksiyonu Kan\u0131t\u0131<\/strong><\/p>\n\n\n\n

      • Bo\u011faz K\u00fclt\u00fcr\u00fc:\n%25 etken \u00fcretilme olas\u0131l\u0131\u011f\u0131 vard\u0131r<\/li>
      • H\u0131zl\u0131 Antijen\nTesti: Yeni enfeksiyon ve ta\u015f\u0131y\u0131c\u0131l\u0131k aras\u0131nda ayr\u0131m yap\u0131lamaz<\/li>
      • Streptokokal\nAntikor Testleri: ASO (anti-streptolizin O), anti-DNAse B, antihyaluronidaz.\nY\u00fcksek bulunmas\u0131 veya artmakta olmas\u0131 anlaml\u0131d\u0131r<\/li><\/ul>\n\n\n\n

        G\u00fcn\u00fcm\u00fczde ARA tan\u0131s\u0131 koyabilmemiz i\u00e7in ge\u00e7irilmi\u015f GABS enfeksiyonu kan\u0131t\u0131 olmas\u0131 \u015fart\u0131yla 2 major veya 1 major + 2 min\u00f6r bulguyu kar\u015f\u0131lamas\u0131 laz\u0131md\u0131r.<\/p>\n\n\n\n

        1.Artrit<\/strong><\/p>\n\n\n\n

        Artrit, kelime anlam\u0131yla\neklem yang\u0131s\u0131 demektir ve ARA\u2019da en s\u0131k g\u00f6r\u00fclen bulgudur. Eklemlerde \u015fi\u015flik,\na\u011fr\u0131, k\u0131zar\u0131kl\u0131k ve tutukluk ile kar\u015f\u0131m\u0131za \u00e7\u0131kar. Genellikle diz, dirsek, ayak\nbile\u011fi, el bile\u011fi gibi b\u00fcy\u00fck eklemleri tek tarafl\u0131 (asimetrik) tutar ve gezici\ntarzdad\u0131r (12). Tek eklem tutulumu (monoartrit) veya birden fazla eklem\ntutulumu (poliartrit) g\u00f6r\u00fclebilir. Daha \u00e7ok b\u00fcy\u00fck ya\u015ftaki hastalarda g\u00f6r\u00fcl\u00fcr ve\n5 ya\u015f alt\u0131nda nadirdir (1). <\/p>\n\n\n\n

        ARA artriti salisilatlara (NSA\u0130\u0130) \u00e7ok iyi yan\u0131t verir ve uygun dozda tedavi ile 24-48 saatte gerileyip bir haftadan k\u0131sa s\u00fcrede ge\u00e7er. Tedavisiz b\u0131rak\u0131lsa bile 2-3 haftada kendili\u011finden gerileyip sekel b\u0131rakmadan 4 haftadan uzun s\u00fcrmez (18-23). Ama ARA \u015f\u00fcphenilen hastada kesin tan\u0131 konulmadan NSA\u0130\u0130 verilemez \u00e7\u00fcnk\u00fc hem klinik hem de laboratuvar bulgular\u0131n\u0131 etkileyebilir. Bu sebeple ARA\u2019dan \u015f\u00fcphelenilen hastalarda tan\u0131 konulana kadar ate\u015f d\u00fc\u015f\u00fcr\u00fcc\u00fc ve a\u011fr\u0131 kesici olarak NSA\u0130\u0130 yerine parasetamol verilmesi \u00e7ok \u00f6nemlidir (24).<\/p>\n\n\n\n

        <\/p>\n\n\n\n

        2. Kardit<\/strong><\/p>\n\n\n\n

        Artritten sonra ikinci\ns\u0131kl\u0131kta ve artritten farkl\u0131 olarak k\u00fc\u00e7\u00fck ya\u015flarda daha g\u00f6r\u00fcl\u00fcr (24). Prognozu\nbelirlemede kardit tek ba\u015f\u0131na en \u00f6nemli komponenttir ve ARA\u2019da kal\u0131c\u0131 sakatl\u0131\u011fa\nyol a\u00e7an tek bulgudur.  Kardiyovask\u00fcler\nmortalite ve morbiditenin yayg\u0131n bir nedenidir. Kardiyovask\u00fcler hastal\u0131\u011fa ba\u011fl\u0131\nhastane ba\u015fvurular\u0131n\u0131n% 35 ila 40’\u0131n\u0131 olu\u015fturur (25-29). ARA perikard, endokard\nve miyokard\u0131 tutabilir. Tutulumlar \u00f6zellikle \u015fiddetli veya yeterli tedavi\nedilmemesi sebebiyle tekrarlayan ARA ataklar\u0131 sebebiyle g\u00f6r\u00fcl\u00fcr. \u0130\u00e7eriden\nd\u0131\u015far\u0131ya bir tutulum vard\u0131r. Endokard tutulmadan miyokard veya perikard\ntutulumu olmaz (30). <\/p>\n\n\n\n

        Endokard tutulumu<\/em> kapak yetersizlikleri ile kar\u015f\u0131m\u0131za \u00e7\u0131kar. En \u00e7ok mitral kapak ard\u0131ndan\naort kapak tutulumu g\u00f6r\u00fcl\u00fcr. Akut hastal\u0131k s\u0131ras\u0131nda kapak yetersizlikleri\ng\u00f6r\u00fcl\u00fcrken ilerleyen y\u0131llarda tekrarlayan ARA ataklar\u0131 sebebiyle kapaklarda\nfibrozisler olu\u015fur ve kapak stenozlar\u0131 (daralmalar) meydana gelir (31). <\/p>\n\n\n\n

        Miyokard tutulumu<\/em> spesifik g\u00f6stergesi ate\u015ften ba\u011f\u0131ms\u0131z uykuda dahil olu\u015fan sin\u00fcs\nta\u015fikardisi ile kar\u015f\u0131m\u0131za \u00e7\u0131kar. Romatizmal miyokardit, ileri kapak\nbozukluklar\u0131 ile beraber ciddi kalp yetersizli\u011fine sebep olabilir. Miyokardit\nileti sistemini de tutabilir ve atriyoventrik\u00fcler (AV) bloklar veya ventrik\u00fcler\naritmiler g\u00f6r\u00fclebilir (32,33).<\/p>\n\n\n\n

        Perikard tutulumu <\/em>g\u00f6\u011f\u00fcs a\u011fr\u0131s\u0131, kalp seslerinin derinden gelmesi, frotman veya s\u00fcrt\u00fcnme\nsesinin duyulmas\u0131 ile kar\u015f\u0131m\u0131za \u00e7\u0131kar. Kardit tutulumu i\u00e7ten d\u0131\u015fa oldu\u011fu i\u00e7in\nkarditli hastalarda sistol veya diyastolde duyulabilen s\u00fcrt\u00fcnme sesi hemen her\nzaman pankardit (endokard + miyokard + perikard) oldu\u011funu g\u00f6sterir (32,33). <\/p>\n\n\n\n

        Klinik olarak kardit bulgusu vermeyen ama EKO (ekokardiyografi) yap\u0131ld\u0131\u011f\u0131 zaman kardit ile uyumlu bulgular saptanan hastalara sessiz kardit veya subklinik kardit denir. Subklinik kardit ile ilgili bir metaanalizde ARA\u2019l\u0131 hastalarda %0-53, ortalama %16,8 oran\u0131nda subklinik kardit saptand\u0131\u011f\u0131 bildirilmi\u015ftir (34). Ekokardiyografi kullan\u0131lmad\u0131\u011f\u0131 takdirde bu hastalar\u0131n tan\u0131s\u0131 g\u00f6zden ka\u00e7abilir ve sonu\u00e7ta yenileyen ARA ataklar\u0131 sebepli kardiyovask\u00fcler mortalite ve morbidite oran\u0131 artabilir. Bu nedenle, subklinik kardit tan\u0131s\u0131 son derece \u00f6nemlidir (35).<\/p>\n\n\n\n

        <\/p>\n\n\n\n

        3. Sydenham Korea<\/strong><\/p>\n\n\n\n

        K\u0131zlarda ve ergenlikte\ndaha fazla g\u00f6r\u00fcl\u00fcr. Bazal ganglionlar\u0131n \u00f6zellikle caudat \u00e7ekirde\u011fin\ninflamasyonu nedeniyle meydana gelir. Latent d\u00f6nemi di\u011fer ARA bulgular\u0131n\u0131n\nd\u00f6nemine g\u00f6re daha uzundur (1-6 ay). <\/p>\n\n\n\n

        Duygusal bozukluklar, g\u00f6vde ve ekstremitelerde (\u00f6zellikle \u00fcst ekstremitelerde) istemsiz, h\u0131zl\u0131, d\u00fczensiz, ama\u00e7s\u0131z hareketler ile koordinasyon bozukluklar\u0131 \u015feklinde kar\u015f\u0131m\u0131za \u00e7\u0131kar (36). Kore ile sessiz kardit \u00e7ok s\u0131k birlikte g\u00f6r\u00fcl\u00fcr bu sebeple kore g\u00f6r\u00fclen ARA hastalar\u0131n\u0131 mutlaka EKO ile takip etmek gerekir (37,38).<\/p>\n\n\n\n

        <\/p>\n\n\n\n

        4.Eritema Marginatum<\/strong><\/p>\n\n\n\n

        \u00d6zellikle g\u00f6vde ve ekstremitelerin proksimal i\u00e7 y\u00fcz\u00fcnde g\u00f6r\u00fcl\u00fcr. Ka\u015f\u0131nt\u0131s\u0131z, kenarlar\u0131 dantel \u015feklinde, koyu pembe renkli, ortas\u0131 soluk ve basmakla solmayan mak\u00fcler lezyonlard\u0131r. Kardit ile beraber s\u0131k g\u00f6r\u00fcl\u00fcr (39). <\/p>\n\n\n\n

        <\/p>\n\n\n\n

        Tedavi\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 <\/strong> <\/h2>\n\n\n\n

        ARA\u2019ya \u00f6zel bir tedavi\nyoktur. Tedavi antimikrobiyal, antiinflamatuvar, destekleyici ve cerrahi tedavi\nolmak \u00fczere d\u00f6rt b\u00f6l\u00fcmden olu\u015fur. Ama\u00e7; streptekok enfeksiyonunu ortadan\nkald\u0131rmak, yak\u0131nmalar\u0131 d\u00fczeltmek ve \u00f6zellikle kalbin hasar g\u00f6rmesini\nengellemektir.<\/p>\n\n\n\n

        1. Antimikrobiyal Tedavi <\/strong><\/p>\n\n\n\n

        Antibiyotik tedavisi\nprimer ve sekonder profilaksi (korunma) amac\u0131yla verilmektedir. Primer\nprofilakside (Tablo 3<\/strong>) ama\u00e7; streptokoklara ba\u011fl\u0131 farenjitin tedavisi ve\nbo\u011fazda var olabilecek streptokoklar\u0131n temizlenmesidir. Bo\u011faz k\u00fclt\u00fcr\u00fc negatif\nolsa bile tedavi uygulan\u0131r.<\/p>\n\n\n\n

        Sekonder profilakside (Tablo 4<\/strong>) ise ama\u00e7; streptokoklar\u0131n yeniden \u00fcremesini ve b\u00f6ylece ARA\u2019n\u0131n tekrarlamas\u0131n\u0131 \u00f6nlemektir. Amerika Kalp Birli\u011fi taraf\u0131ndan sekonder profilaksi s\u00fcreleri belirlenmi\u015ftir (Tablo 5<\/strong>) (40-43).<\/p>\n\n\n\n

        <\/p>\n\n\n\n

        Tablo 3 (Primer Profilaksi)<\/strong><\/p>\n\n\n\n
        \n Antibiyotik<\/strong>\n  <\/strong>\n <\/td>\n Doz<\/strong>\n <\/td>\n Uygulama<\/strong>\n <\/td><\/tr>
        \n Benzatin\n Penisilin G\n <\/td>\n \u226427 kg\n 600.000 \u00dc\n >27 kg 1.200.000 \u00dc \n <\/td>\n IM, Tek doz\n <\/td><\/tr>
        \n Penisilin V\n <\/td>\n \u00c7ocuk 250 mg\n x 2-3\\g\u00fcn\n Eri\u015fkin 500\n mg x 2-3\\g\u00fcn\n <\/td>\n PO, 10 g\u00fcn\n <\/td><\/tr>
        \n Amoxilin\n <\/td>\n 50 mg\\kg\\g\u00fcn\n (max 1 gr)\n <\/td>\n PO, 10 g\u00fcn\n <\/td><\/tr>
        \n Azitromisin*\n <\/td>\n 12 mg\\kg\\g\u00fcn\n (max 500 mg)\n <\/td>\n PO, 5 g\u00fcn\n <\/td><\/tr>
        \n Kloritromisin*\n <\/td>\n 15 mg\\kg\\g\u00fcn\n (max 500 mg)\n <\/td>\n PO, 10 g\u00fcn\n <\/td><\/tr>
        \n Klindamisin*\n <\/td>\n 20 mg\\kg\\g\u00fcn\n (max 600mg)\n <\/td>\n PO, 10 g\u00fcn\n <\/td><\/tr><\/tbody><\/table>\n\n\n\n

        *Penisiline alerjisi varsa<\/p>\n\n\n\n

        <\/p>\n\n\n\n

         Tablo 4 (Sekonder Profilaksi)<\/strong><\/p>\n\n\n\n
        \n Antibiyotik<\/strong>\n  <\/strong>\n <\/td>\n Doz<\/strong>\n <\/td>\n Uygulama<\/strong>\n <\/td><\/tr>
        \n Benzatin Penisilin G\n <\/td>\n \u226427 kg 600.000 \u00dc\n >27 kg 1.200.000 \u00dc\n <\/td>\n IM\n <\/td><\/tr>
        \n Penisilin V\n <\/td>\n 250 mg x 2\\g\u00fcn\n <\/td>\n PO\n <\/td><\/tr>
        \n Sulfadiazin\n <\/td>\n \u226427 kg 0.5 gr\\g\u00fcn\n >27 kg 1 gr\\g\u00fcn\n <\/td>\n PO\n <\/td><\/tr>
        \n Azitromisin*\n <\/td>\n 5 mg\\kg\\g\u00fcn (max 250 mg)\n <\/td>\n PO\n <\/td><\/tr><\/tbody><\/table>\n\n\n\n

        \u00a0*Penisilin veya sulfadiazin alerjisi varsa<\/p>\n\n\n\n

        <\/p>\n\n\n\n

         Tablo 5 (Sekonder Profilaksi S\u00fcresi)*<\/strong><\/p>\n\n\n\n
        \n Klinik\n Durum<\/strong>\n  <\/strong>\n <\/td>\n S\u00fcre<\/strong>\n <\/td><\/tr>
        \n Ge\u00e7irilmi\u015f ARA \u2013 Kardit, RKH (+)\n <\/td>\n 10 y\u0131l\\40 ya\u015f\\\u00f6m\u00fcr boyu\n <\/td><\/tr>
        \n Ge\u00e7irilmi\u015f ARA – \n Kardit, RKH (-)\n <\/td>\n 10 y\u0131l veya 21 ya\u015f\n <\/td><\/tr>
        \n Ge\u00e7irilmi\u015f ARA – Artrit\n <\/td>\n 5 y\u0131l veya 21 ya\u015f\n <\/td><\/tr><\/tbody><\/table>\n\n\n\n

        *Hangisi daha uzunsa<\/p>\n\n\n\n

        <\/p>\n\n\n\n

        2. Antiinflamatuvar Tedavi <\/strong><\/p>\n\n\n\n

        ARA tan\u0131s\u0131 kesin olmadan hastal\u0131\u011f\u0131n seyrini bozmamas\u0131 i\u00e7in NSA\u0130\u0130 yerine parasetamol kullan\u0131labilir. Tan\u0131dan emin oldu\u011fumuz zaman NSA\u0130\u0130 ba\u015flan\u0131labilir (24).<\/p>\n\n\n\n

        <\/p>\n\n\n\n

        3. Destek Tedavisi <\/strong><\/p>\n\n\n\n

        \u015eiddetli veya tekrarlayan\nARA ataklar\u0131na ba\u011fl\u0131 kalp yetersizli\u011fi olan hastalara ACE-i, beta bloker,\ndi\u00fcretik gibi destek tedavileri verilebilir.<\/p>\n\n\n\n

        ARA ge\u00e7iren her hastada yatak istirahati zorunludur. Hastalar \u00f6zellikle istirahat a\u015famas\u0131nda kardit a\u00e7\u0131s\u0131ndan yak\u0131ndan takip edilmelidir. Karditi olmayan hastaya klinik ve laboratuvar\u0131 d\u00fczelene kadar; karditi olan hastaya ise en az 4 hafta yatak istirahati verilir (44-46).<\/p>\n\n\n\n

        <\/p>\n\n\n\n

        4. Cerrahi Tedavi<\/strong><\/p>\n\n\n\n

        Karditi a\u011f\u0131r olan ve kalp yetersizli\u011fine medikal tedavi cevap vermeyen ARA hastalar\u0131nda valv\u00fcloplasti veya kapak replasman\u0131 yap\u0131labilir (47).<\/p>\n\n\n\n

        <\/p>\n\n\n\n

        Yazar: Nilay Nur \u00d6nder \\ Stajyer Doktor<\/h2>\n\n\n\n

        <\/p>\n\n\n\n

        <\/p>\n\n\n\n

        Kaynaklar<\/h2>\n\n\n\n
        1. \u0130.\nLevent Salt\u0131k. Akut Romatizmal Ate\u015f. The Journal of Current Pediatrics. G\u00fcncel\nPediatri. March 2007 cilt:5 say\u0131:1<\/li>
        2. Lawrence\nJG, Carapetis JR, Griffiths K, Edwards K, Condon JR. Acute rheumatic fever and\nrheumatic heart disease: incidence and progression in the Northern Territory of\nAustralia, 1997 to 2010. Circulation. 2013; 128:492\u2013501. [PubMed: 23794730]<\/li>
        3. Figen\nAkal\u0131n. Akut Romatizmal Ate\u015f ve Yenilikler. T\u00fcrk Pediatri Ar\u015fivi. 2007. 85-93<\/li>
        4. Cunningham\nMW. Pathogenesis of group A streptococcal infections. Clin Microbiol Rev\n2000;13:470\u2013511. [PMC free article] [PubMed] [Google Scholar]<\/li>
        5.  Minick CR, Fabricant CG, Fabricant J.\nAtheroarteriosclerosis induced by infection with a herpes virus. Am J Pathol\n1979;96:673\u2013706. [PMC free article] [PubMed] [Google Scholar]<\/li>
        6.  Maisch B, Ristic AD, Portig I, et al. Human\nviral cardiomyopathy. Frontiers in Bioscience 2003;8:s39\u201367. [PubMed] [Google\nScholar]<\/li>
        7. Quinn\nA, Kosanke S, Fichetti VA, Factor SM, Cunningham MW. Induction of autoimmune\nvalvular heart disease by recombinant streptococcal M protein. Infect Immun\n2001;69:4072-8.<\/li>
        8. Quinn\nA, Kosanke S, Fichetti VA, Factor SM, Cunningham MW. Induction of autoimmune\nvalvular heart disease by recombinant streptococcal M protein. Infect Immun\n2001;69:4072-8.<\/li>
        9. Fae\nKC, Oshiro SE, Toubert A, Charron D, Kalil J, Guilherme L. How an autoimmune\nreaction triggered by molecular mimicry between streptococcal M protein and\ncardiac tissue proteins leads to heart lesions in rheumatic heart disease. J\nAutoimmun 2005;24:101-9.<\/li>
        10. Salt\u0131k\n\u0130L. Akut romatizmal ate\u015f. The Journal of Current Pediatrics 2007;5 \u00d6zel say\u0131\n1:156-9.<\/li>
        11. Ayoub\nEM. Acute rheumatic fever. In: Allen HD, Gutgesel HP, Clark EB, Driscoll DJ\n(eds). Moss and Adams\u2019 Heart Disease in Infants, Children and Adolescents, 6th\ned. Philadelphia: Lippincott Williams and Wilkins, 2001:1226-41.<\/li>
        12. Anita\nKM, Zaidi and Donald A. Goldman. Rheumatic fever in the Nelson textbook of\npediatrics. Kliegman RM, Behrman RE, Jenson HB, Stanton BF (eds). 18 th\nedition. Philadelphia: WB Saunders Company, 2007:1140-5.<\/li>
        13. Bryant\nPA, Robins- Browne R, Carapetis JR, Curtis N. Some of the people, some of the\ntime: Susceptibility to acute rheumatic fever. Circulation 2009;119:742-53.<\/li>
        14. Galvin\nJE, Hemric ME, Ward K, Cunningham MW. Cytotoxic mAb from rheumatic carditis\nrecognizes heart valves and laminin. J Clin Invest. 2000;106:217\u201324. doi:\n10.1172\/JCI7132<\/li>
        15. No\nauthors listed. Jones criteria (revised) for guidance in the diagnosis of\nrheumatic fever. Circulation 1965;32:664\u20138. <\/li>
        16. Jones\nTD. The diagnosis of rheumatic fever. JAMA 1944;126:481\u2013 4.<\/li>
        17. Gewitz\nMH, Baltimore RS, Tani LY, et al. American Heart Association Committee on\nRheumatic Fever, Endocarditis and Kawasaki Disease of the Council on\nCardiovascular Disease in the Young. Revision of the Jones criteria for the\ndiagnosis of the rheumatic fever in the era of Doppler echocardiography: a\nscientific statement of the American Heart Association. Circulation 2015; 131:\n1806-18. <\/li>
        18. Galal\nME, Medhat ME, Khalid AS, Howaida GE. Rheumatic fever and rheumatic heart\ndisease. In: Garson A, Bricker JT, Fisher DJ, Neish SR (eds). The Science and\nPractice of Pediatric Cardiology, 2nd ed. Baltimore: Williams and Wilkins,\n1998:1691-724. <\/li>
        19.  Ayoub EM. Acute rheumatic fever. In: Allen HD,\nGutgesel HP, Clark EB, Driscoll DJ (eds). Moss and Adams\u2019 Heart Disease in\nInfants, Children and Adolescents, 6th ed. Philadelphia: Lippincott Williams\nand Wilkins, 2001:1226-41. <\/li>
        20.  Bernstein D. Acquired heart disease In: Behr-\nman RE, Kliegman RM, Jenson HB (eds). Nelson Textbook of Pediatrics, 17th ed.\nPhiladelphia: WB Saunders, 2004:1565-72. <\/li>
        21.  Cilliers AM. Rheumatic fever and its\nmanagement. BMJ 2006;333:1153-6. <\/li>
        22.  Carapetis JR, Mc Donald M, Wilson N. Acute\nrheumatic fever. Lancet 2005;366:155-66. <\/li>
        23.  Dajani AS. Rheumatic fever in braunwald heart\ndisease. In: Braunwald E (ed). A Textbook of Cardiovascular Medicine. 5th ed.\nPhiladelphia: WB Saunders Co, 1997:1769-75.<\/li>
        24. Ero\u011flu\nAG. Akut romatizmal ate\u015f 2015 Jones \u00f6l\u00e7\u00fctleri Turk Pediatri Ars 2016; 51: 1-7<\/li>
        25. WHO\nStudy Group. Rheumatic Fever and Rheumatic Heart Disease<\/em>. WHO Technical\nReport Series No. 764. Geneva: World Health Organization; 1988.<\/li>
        26. Vijaykumar\nM, Narula J, Reddy KS, Kaplan EL. Incidence of rheumatic fever and prevalence\nof rheumatic heart disease in India. Int J Cardiol<\/strong>.<\/em>1994; 43<\/em>:221\u2013228.<\/li>
        27. Murray\nCJ, Lopez AD, eds. Global Health Statistics: A Compendium of Incidence,\nPrevalence and Mortality Estimates for Over 200 Conditions<\/em>. Global\nBurden of Disease and Injury Series<\/em>. Vol 2. Cambridge, Mass: Harvard School\nof Public Health; 1996:132\u2013140.<\/li>
        28. Padmavati\nS. Rheumatic fever and rheumatic heart disease in developing countries. Bull\nWorld Health Organ<\/strong>.<\/em>1978; 56<\/em>:543\u2013550.<\/li>
        29. Rutstein\nDD, Bauer W, Dorfman A, Gross RE, Lichty JA, Taussig HB, Whittemore R. Report\nof the Committee on Standards and Criteria for Programs of Care of the Council\nof Rheumatic Fever and Congenital Heart Disease of American Heart Association.\nJones Criteria (Modified) for guidance in the diagnosis of rheumatic fever. Circulation<\/strong>.<\/em>1956;\n13<\/em>:617\u2013620.<\/li>
        30. Narula\nJ, Chandrasekhar Y, Rahimtoola. Diagnosis of active rheumatic carditis. The\nechoes of change. Circulation 1999;100:157681.<\/li>
        31. Galal\nME. Medhat ME. Khalid AS.Howaida GE. Rheumatic fever and rheumatic  heart disease. In The science and practice of\nPediatric Cardiology. Garson A. Bricker JT. Fisher DJ. Neish SR (eds). 2nd ed.\nBaltimore: Williams and Wilkins; 1998: 1691- 1724<\/li>
        32. Veasy\nLG. Rheumatic fever. T. Duckett Jones and the rest of the story. Cardiol Young\n1995;5:293-391<\/li>
        33. Narula\nJ, Chopra P, Talwar KK, Reddy KS, Vasan RS, Tandon R, et al. Does\nendomyocardial biopsy aid in the diagnosis of active rheumatic carditis.\nCirculation 1993;88:2198-205.<\/li>
        34. Tubridy-Clark\nM, Carapedis JR. Subclinical carditis in rheumatic fever: a systematic review.\nInt J Cardiol 2007; 119: 54-8.<\/li>
        35. Carapetis\nJR. Rheumatic heart disease in developing countries. N Engl J Med\n2007;357:439-41.<\/li>
        36. Owlia\nM, Mirza M. Acute rheumatic fever: Over Estimation or misconception? Int J\nCardiol 2013;174:53-8.<\/li>
        37. Vijayalakshmi\nIB, Mithravinda J, Deva ANP. The role of echocardiography in diagnosing\ncarditis in the setting of rheumatic fever. Cardiol Young 2005;15:583-86.<\/li>
        38. El\nSaid GM, Sanour KA. Acute rheumatic fever. In: Garson A, Bricker JT, Mcnamara\nDG (eds). The Science and Practice of Pediatric Cardiology. Lea and Febiger.\nLondon:Philadelphia, 1990:1485-500.<\/li>
        39. Guidelines\nfor the diagnosis of rheumatic fever. Jones criteria, 1992 update. Special\nWriting Group of the Committee on rheumatic fever, endocarditis, and Kawasaki\ndisease of the council on cardiovascular disease in the young of the American\nHeart Association. JAMA 1992;268:2069\u201373<\/li>
        40. Ay\u015fe\nG\u00fcler Ero\u011flu. Akut Romatizmal Ate\u015f. Klinik Geli\u015fim \u00c7ocuk ve Ergenlik \u00c7a\u011f\u0131\nRomatizmal Hastal\u0131klar \u00f6zel say\u0131s\u0131 2006; cilt: 19 say\u0131:1  <\/li>
        41. Rosenthal\nA. Czaniczer G. Massel BF. Rheumatic fever under 3 years age: A report of\ncases. Pediatrics 1968; 41: 612 <\/li>
        42.  Binotto MA. Guillherme L. Tanaka AC. Rheumatic\nFever. Images Pediatr Cardiol 2002; 11: 12-25 \n<\/li>
        43.  Lue HC. Wu MH. Wang JK. Wu FF. Wu YN. Longterm\noutcome of patients with rheumatic fever recieving benzathine peniciline G\nprophylaxis every three weeks versus every four weeks. J Pediatr 1994; 125:\n812-816<\/li>
        44. Brandt\nER, Good MF. Vaccine strategies to prevent rheumatic fever. Immunol Res\n1999;19:89-103.<\/li>
        45. Ciliers\nAM, Manyemba J, Saloojee HH. Anti-inflammatory treatment for carditis in acute\nrheumatic fever. Cochrane Database Syst Rev 2003;2:CD 00 3176<\/li>
        46. Akal\u0131n\nF. Akut romatizmal ate\u015f ve yenilikler. T\u00fcrk Ped Ar\u015f 2007;42:85-93.<\/li>
        47. \u00d6zer\nS, Halkao\u011flu O, Ozkutlu S, \u00c7eliker A, Alehan D, Karag\u00f6z T. Childhood acute\nrheumatic fever in Ankara, Turkey. Turk J Pediatr 2005;47:120-4.<\/li><\/ol>\n\n\n\n

          <\/p>\n","protected":false},"excerpt":{"rendered":"

          Giri\u015f Akut romatizmal ate\u015f (ARA); duyarl\u0131 ki\u015filerde Streptococcus pyogenes \u00fcyesi olan A grubu beta hemolitik Streptokok\u2019un (GABS) neden oldu\u011fu farenjitten<\/p>\n","protected":false},"author":149,"featured_media":2970,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":[],"categories":[23],"tags":[452,450,449,451],"acf":[],"views":4444,"_links":{"self":[{"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/posts\/2959"}],"collection":[{"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/users\/149"}],"replies":[{"embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/comments?post=2959"}],"version-history":[{"count":4,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/posts\/2959\/revisions"}],"predecessor-version":[{"id":2972,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/posts\/2959\/revisions\/2972"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/media\/2970"}],"wp:attachment":[{"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/media?parent=2959"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/categories?post=2959"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/blog.ulubat.org\/index.php\/wp-json\/wp\/v2\/tags?post=2959"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}