Febril ve afebril konvülziyon ile başvuran çocuk hastalarda nöronal hasarın belirlenmesinde serum tau protein düzeyinin yeri ve risk belirlemede önemi
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Dosyalar
Tarih
2011
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Yayıncı
Trakya Üniversitesi Tıp Fakültesi
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Febril ve afebril nöbetlerde hekim ve aile için en büyük kaygı nöronal hasar oluşturmasıdır. Nöronal hasarı belirlemede radyolojik görüntüleme yöntemleri kullanılmaktadır. Ancak bu tetkiklerin yapılması uzun zaman almakta, uzman eleman gerektirmekte, pahalı olmakta ve radyasyona maruziyet söz konusu olmaktadır. Bunun yerine kolay, hızlı, tekrarlanabilir, objektif, kullanıcı yorumundan bağımsız ve ucuz olan nöron spesifik enolaz, beyin tipi kreatin kinaz, miyelin bazik protein, serum 100 ß protein, glial fibril asidik protein, Tau proteini gibi serum biyobelirteçleri kullanıma girmiştir. Bu çalışmanın amacı afebril ve febril konvülziyon geçiren çocuklarda nöbet sırasında oluşan hipoksiye bağlı olabilecek nöronal hasar belirteci olarak serum Tau protein düzeyinin yerini ve risk belirlemedeki önemini araştırmaktır. Bu çalışmada afebril konvülziyon tanısı alan 30 çocuk Grup A, febril konvülziyon tanısı alan 30 çocuk Grup B, kontrol grubunu oluşturan 26 çocuk Grup C olarak tanımladı. A grubu bir kez nöbet geçiren (A1), tekrarlayan nöbet geçiren (A2), B grubu basit febril konvülziyon (B1), komplike febril konvülziyon geçiren (B2) olarak alt gruplara ayrıldı. Gruplar yaş, cinsiyet, konvülziyon tipi, konvülziyon süresi, ailede epilepsi öyküsü gibi veriler ve Tau protein açısından karşılaştırıldı. Grup A, Grup B ve alt grupları kontrol grubu ile karşılaştırıldığında çalışma gruplarında serum Tau protein düzeyi kontrol grubuna göre yüksek bulundu. Bunun yanında yaş, cinsiyet, konvülziyon tipi, konvülziyon süresi, ailede epilepsi öyküsü ve nöbetin idiopatik veya semptomatik olmasından etkilenmiyordu. Tau proteini için `cut-off' düzeyi 124.83 pg/ml olarak kullanıldığında, duyarlılığı %66.67 ve özgüllüğü %92.31 olarak tespit edildi. Sonuç olarak konvülziyonlarda nöronal hasara yol açan mekanizmalar serum Tau protein düzeyini artırmaktadır. Ama bu durumun nöbetin febril veya afebril olması, bir kez veya tekrarlayan şekilde geçirilmesi, febril konvülziyonun basit veya komplike olması, konvülziyon klinik tipi, konvülziyon süresi, ailede epilepsi ve febril konvülziyon öyküsü, nöbetin idiopatik veya semptomatik olması gibi risk ve prognoz belirleyici parametrelerden etkilenmediği saptanılmıştır. Daha farklı biyobelirteçlerin karşılaştırılmalı olarak çalışılması ve tekrarlayan şekilde düzeyinın bakılmasını araştıran daha ileri klinik çalışmalara ihtiyaç olduğunu düşünmekteyiz. Anahtar kelimeler: Afebril konvülziyon, febril konvülziyon, nörolojik hasar, Tau protein
Abstract
With patients having febrile or afebrile seizures, the greatest concern for both physician and family is the risk of neuronal injury. Radiologic screening methods are used for detecting neuronal injury. However, while such techniques induce exposure to radiation, they are also time-consuming, costly and labor intensive. Therefore, serum bio-markers such as neuron specific enolase, brain type creatine kinase, myelin basic protein, serum 100 ß protein glial fibrillary protein and Tau protein were suggested as alternative screening methods since they are less time and resource consuming, simple, reproducible, objective and independent of user interpretation. The objective of this study is to investigate the use of serum Tau protein levels as a marker to determine the possible neuronal injury which might be caused by hypoxia that occurs in children during febrile and afebrile seizures. In this study, 30 children diagnosed with afebrile convulsion defined as Group A, 30 children diagnosed with febrile convulsion as Group B and 26 children forming the control group as Group C. Group A were divided into subgroups as history of having seizure for once (A1) or having multiple seizures (A2) and Group B were divided into subgroups as having simple febrile seizures (B1) or having complex febrile seizures (B2). The groups were compared regarding to age, sex, type of seizure, duration of seizure, epilepsy history in family and Tau protein levels. Serum Tau protein levels were found to be higher in Group A, Group B and their subgroups compared to the control group. Meanwhile Tau levels were not effected by age, sex, type of seizure, duration of seizure, family history or the seizure type being idiopathic or symptomatic. When 124.83 pg/ml was taken as a`cut-off level for Tau protein, the sensitivity and specificity of the marker found to be %66,67 and %92,31 respectively. In a conclusion, mechanisms leading to neuronal injury in convulsions result with an increase in serum Tau protein levels. However, it was detected that this situation is not effected by risk factors or prognosis determining parameters such as seizures being febrile or afebrile, having single or multiple seizures, febrile seizures being simple or complex, clinical type and duration of seizure, family history of epilepsy or febrile seizure, and type of seizure as idiopathic or symptomatic. In our opinion, further clinical trials that might study different bioindicators comparatively and measuring their levels repetitiously are needed to be performed for better judgement. Key words: Afebrile convulsion, febrile convulsion, neurological damage, Tau protein
Abstract
With patients having febrile or afebrile seizures, the greatest concern for both physician and family is the risk of neuronal injury. Radiologic screening methods are used for detecting neuronal injury. However, while such techniques induce exposure to radiation, they are also time-consuming, costly and labor intensive. Therefore, serum bio-markers such as neuron specific enolase, brain type creatine kinase, myelin basic protein, serum 100 ß protein glial fibrillary protein and Tau protein were suggested as alternative screening methods since they are less time and resource consuming, simple, reproducible, objective and independent of user interpretation. The objective of this study is to investigate the use of serum Tau protein levels as a marker to determine the possible neuronal injury which might be caused by hypoxia that occurs in children during febrile and afebrile seizures. In this study, 30 children diagnosed with afebrile convulsion defined as Group A, 30 children diagnosed with febrile convulsion as Group B and 26 children forming the control group as Group C. Group A were divided into subgroups as history of having seizure for once (A1) or having multiple seizures (A2) and Group B were divided into subgroups as having simple febrile seizures (B1) or having complex febrile seizures (B2). The groups were compared regarding to age, sex, type of seizure, duration of seizure, epilepsy history in family and Tau protein levels. Serum Tau protein levels were found to be higher in Group A, Group B and their subgroups compared to the control group. Meanwhile Tau levels were not effected by age, sex, type of seizure, duration of seizure, family history or the seizure type being idiopathic or symptomatic. When 124.83 pg/ml was taken as a`cut-off level for Tau protein, the sensitivity and specificity of the marker found to be %66,67 and %92,31 respectively. In a conclusion, mechanisms leading to neuronal injury in convulsions result with an increase in serum Tau protein levels. However, it was detected that this situation is not effected by risk factors or prognosis determining parameters such as seizures being febrile or afebrile, having single or multiple seizures, febrile seizures being simple or complex, clinical type and duration of seizure, family history of epilepsy or febrile seizure, and type of seizure as idiopathic or symptomatic. In our opinion, further clinical trials that might study different bioindicators comparatively and measuring their levels repetitiously are needed to be performed for better judgement. Key words: Afebrile convulsion, febrile convulsion, neurological damage, Tau protein
Açıklama
Tıpta Uzmanlık Tezi
Anahtar Kelimeler
Afebril Konvülziyon, Febril Konvülziyon, Nörolojik Hasar, Tau Protein, Afebrile Convulsion, Febrile Convulsion, Neurological Damage