Çocukluk çağında tromboz
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Date
2016
Authors
Kuzucu, Teslime Ersoy
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Publisher
Uludağ Üniversitesi
Abstract
Bu çalışma Çocuk Sağlığı ve Hastalıkları Anabilim Dalı kliniklerinde çeşitli nedenler ile yatışı yapılan ve tromboz saptanan çocuk hastalarda; yaş, cinsiyet, aile öyküsü, başvuru yakınmaları, tromboz yeri, atak sayısı, kullanılan tedaviler, kazanılmış ve genetik risk faktörlerini incelemek amacı ile yapıldı. Çalışma 2005-2015 yılları arasında tromboz tanısı alan 150 hastanın klinik ve laboratuvar bulguları elektronik dosya sisteminden retrospektif olarak incelendi. Herhangi bir nedenle hastaneye yatan hastalar arasında tromboz sıklığı 40 /10 000 olarak bulundu. Olgulardan 90'ı erkek (%60), 60'ı kız (%40) cinsiyetteydi. Ortalama yaş 83 ay (0-338) olup %8,6 (n:13) olgu yenidoğan dönemindeydi. Ven kaynaklı tromboz %88,7 (n:133) iken arteryel kaynaklı tromboz %11,3 (n:17) olarak saptandı. Tromboz lokalizasyonu açısından incelendiğinde ilk üç sırada; kraniyal %48,7 (n:73), alt ekstremite %26,7 (n:40) ve kardiyak %10,7 (n:16) trombozlar saptandı. En sık saptanan çevresel risk faktörlerinden ilk üç sırada; enfeksiyon 37,6 (n:32), kateter %34,1 (n:29) ve konjenital kalp hastalığı %32,9 (n:28) yer alıyordu. Enfeksiyonlarda ise ilk sırada sepsis %46,8 (n:15) oranında saptanmıştı. Genetik açıdan 129 hastadan gönderilen mutasyon analizi incelendi. FVL mutasyonu %20,2 (n:26), MTHFR mutasyonu homozigot %25,6 (n:33), PAI gen mutasyonu homozigot pozitifliği %18,6 (n:24) ve protrombin gen mutasyonu %1,6 (n:2) saptandı. FVL mutasyonu ve homozigot MTHFR mutasyonlu olgular %4,7 (n:6) olarak saptandı. Konjenital ve çevresel faktör açısından pozitif hasta 39 (%30,2) iken negatif hasta sayısı 27 (%20,9) olarak saptandı. Herhangi bir trombofilik mutasyon saptanmayan olgu %8,5 (n:11) oranında idi. Tedavi başlanan 111 olgunun 90'ında (%81,1) düşük molekül ağırlıklı heparin ve 10'unda (%9) klasik heparin uygulandı. Diğer hastaların 4'ünde (%3,6) rekombinant doku plazminojen aktivatörü, 3'ünde (%2,7) asetilsalisilik asit, 3'ünde (%2,7) trombektomi ve 1'inde (%0,9) ise düşük molekül ağırlıklı heparin ile birlikte trombektomi uygulandı. Tedaviye bağlı komplikasyon hastaların %6'sında (n:9), trombozun oluştuğu yere bağlı komplikasyon ise %16'sında (n:24) gelişti. Tromboza bağlı mortalite saptanmadı. Ancak izlemde 5 hastamızı altta yatan hastalıklarına bağlı olarak kaybettik. Hastanemizdeki tromboz insidansı ülkemizdeki literatür ile uyumlu olarak yüksek bulundu. Tromboz tanılı 150 olgunun %56,7'sinde (n:85) kazanılmış risk faktörü varken genetik risk faktörü değerlendirmeye alınan 129 hastanın %55,8'inde (n:72) saptandı. Tromboz saptanan tüm hastalarda kazanılmış risk faktörü olsa dahi mutlaka genetik açıdan tetkik edilmesi gerektiğini düşünmekteyiz.
This study was performed in pediatric patients who were admitted to Child Health and Disease Department due to various reasons and detected for thrombosis in order to examine age, gender, family history, presenting symptoms, thrombosis location, number of attacks, treatments used, acquired and genetic risk factors. In this study, clinical and laboratory results of 150 patients diagnosed with thrombosis between 2005-2015 were retrospectively examined from the electronic file system. The frequency of thrombosis among patients who were hospitalized for any reason was found to be 40/10 000. 90 patients (60%) of the study were male, and 60 patients (40%) were female. The mean age was 83 months (0-338), and 8.6% (n:13) was in neonatal period. Vein-induced thrombosis was present in 88.7% (n:133) of the patients, and arterial-induced thrombosis was detected as 11.3% (n:17). When examined in terms of localization of thrombosis, first three were detected as cranial 48.7% (n:73), lower extremities 26.7% (n:40) and cardiac 10.7% (n:16) thrombosis. First three of the most frequently detected environmental risk factors were infection 37.6% (n:32), catheter 34.1% (n:29) and congenital heart disease 32.9% (n:28). In infections, sepsis was determined for the first place with 46.8% (n:15) rate. Mutation analysis sent from 129 patients was examined genetically. FVL mutation was detected as 20.2% (n:26), MTHFR mutation was detected as 25.6% (n:33) in homozygous individuals, PAI gene mutation homozygous positivity was detected as 18.6% (n:24), and prothrombin gene mutation was detected as 1.6% (n:2). Cases with FVL mutation and homozygous MTHFR mutation was detected as 4.7% (n:6). While the number of patients who were positive in terms of congenital and environmental factors was 39 (30.2%), number of negative patients was detected as 27 (20.9%). Rate of the patients without any thrombophilic mutation was 8.5% (n:11). 90 (81.1%) of 111 cases started to treatment were treated with low molecular weight heparin, and 10 of them (9%) were treated with classical heparin. 4 of other patients (3.6%) were treated with recombinant tissue plasminogen activator, 3 of them (2.7%) were treated with acetylsalicylic acid, 3 of them (2.7%) were treated with thrombectomy, and 1 of them (0.9%) was treated with thrombectomy together with low molecular weight heparin. Treatment-related complication occurred in 6% (n:9) of the patients, and complication related with the place of the thrombosis occurred in 16% (n:24) of the patients. Thrombosis-related mortality was not detected. However, our 5 patients were lost due to the underlying disease during follow-up. The incidence of thrombosis in our hospital was significantly high in accordance with the literature of our country. While there was acquired risk factor in 56.7% (n:85) of 150 cases diagnosed with thrombosis, it was detected as 55.8% (n:72) of 129 patients whose genetic risk factors were assessed. Although there was acquired risk factor in all patients with thrombosis, we believe that it needs to be examined genetically.
This study was performed in pediatric patients who were admitted to Child Health and Disease Department due to various reasons and detected for thrombosis in order to examine age, gender, family history, presenting symptoms, thrombosis location, number of attacks, treatments used, acquired and genetic risk factors. In this study, clinical and laboratory results of 150 patients diagnosed with thrombosis between 2005-2015 were retrospectively examined from the electronic file system. The frequency of thrombosis among patients who were hospitalized for any reason was found to be 40/10 000. 90 patients (60%) of the study were male, and 60 patients (40%) were female. The mean age was 83 months (0-338), and 8.6% (n:13) was in neonatal period. Vein-induced thrombosis was present in 88.7% (n:133) of the patients, and arterial-induced thrombosis was detected as 11.3% (n:17). When examined in terms of localization of thrombosis, first three were detected as cranial 48.7% (n:73), lower extremities 26.7% (n:40) and cardiac 10.7% (n:16) thrombosis. First three of the most frequently detected environmental risk factors were infection 37.6% (n:32), catheter 34.1% (n:29) and congenital heart disease 32.9% (n:28). In infections, sepsis was determined for the first place with 46.8% (n:15) rate. Mutation analysis sent from 129 patients was examined genetically. FVL mutation was detected as 20.2% (n:26), MTHFR mutation was detected as 25.6% (n:33) in homozygous individuals, PAI gene mutation homozygous positivity was detected as 18.6% (n:24), and prothrombin gene mutation was detected as 1.6% (n:2). Cases with FVL mutation and homozygous MTHFR mutation was detected as 4.7% (n:6). While the number of patients who were positive in terms of congenital and environmental factors was 39 (30.2%), number of negative patients was detected as 27 (20.9%). Rate of the patients without any thrombophilic mutation was 8.5% (n:11). 90 (81.1%) of 111 cases started to treatment were treated with low molecular weight heparin, and 10 of them (9%) were treated with classical heparin. 4 of other patients (3.6%) were treated with recombinant tissue plasminogen activator, 3 of them (2.7%) were treated with acetylsalicylic acid, 3 of them (2.7%) were treated with thrombectomy, and 1 of them (0.9%) was treated with thrombectomy together with low molecular weight heparin. Treatment-related complication occurred in 6% (n:9) of the patients, and complication related with the place of the thrombosis occurred in 16% (n:24) of the patients. Thrombosis-related mortality was not detected. However, our 5 patients were lost due to the underlying disease during follow-up. The incidence of thrombosis in our hospital was significantly high in accordance with the literature of our country. While there was acquired risk factor in 56.7% (n:85) of 150 cases diagnosed with thrombosis, it was detected as 55.8% (n:72) of 129 patients whose genetic risk factors were assessed. Although there was acquired risk factor in all patients with thrombosis, we believe that it needs to be examined genetically.
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Keywords
Çocukluk çağında tromboz, Risk faktörleri, Genetik mutasyon, Childhood thrombosis, Risk factors, Genetic mutations
Citation
Kuzucu, T. E. (2016). Çocukluk çağında tromboz. Yayınlanmamış uzmanlık tezi. Uludağ Üniversitesi Tıp Fakültesi.