Kafa travmasının akut döneminde hipofiz fonksiyonlarının değerlendirilmesi
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Dosyalar
Tarih
2012
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
AMAÇ: Travmatik beyin hasarı sonrası hipofiz bezinin fonksiyonlarını değerlendirmek ve olası etkenleri ayırt etmek için travmanın akut döneminde hipofiz fonksiyonlarını sunmak. YÖNTEM: Çalı?mada Eylül 2009 ve Temmuz 2010 arası kayıtları olan 30 hasta (22 erkek ve 8 kadın) yer aldı. Glasgow Koma Skorlarına göre hastalar ağır, orta ve hafif travma olmak üzere üç gruba ayrıldılar. Ya?, cinsiyet, etiyoloji, hastanede kalma süresi ve hipofiz hormon seviyelerini içeren veri incelendi. p değerinin <0,05’ten küçük olması anlamlı kabul edildi. BULGULAR: Kafa travması olan erkek hastalar (40,5±21,76) belirgin olarak kadın hastalardan (49,13±27,93) daha gençtiler. Kafa travmasının akut döneminde büyüme hormonu, ACTH ve LH/FSH eksiklikleri sırasıyla %36,6, %20 ve %20 hastada vardı. Travmatik beyin hasarlarının önde gelen sebepleri yüksekten dü?me (%46,6) ve motorlu araç kazalarıydı (%33,3). ACTH seviyelerinin yüksekliği, Glasgow coma skoru ve prolaktin seviyesinin dü?üklüğü daha uzun hastanede kalma süresine sebep oldu. SONUÇ: Travma sonrası hipopitüiterizm geli?mesi açısından ?iddetli travmatik beyin hasarı en önemli risk faktörü sayılsa da, daha hafif bir hasar da hipopitüiterizme yol açabilir. Post travmatik hipopitüiterizm tanısından uzakla?mak için bütün kafa travması hastaları yeterince uzun süre izlenmelidir.
AIM: To evaluate the functional outcome of the pituitary gland after the traumatic brain injury and to present the pituitary functional changes during the acute phase of the trauma in order to identify the possible factors. METHODS: The study included records of 30 patients (22 male and 8 female) between September 2009 and July 2010. The patients were allocated into three groups according to their Glasgow Coma Scale as severe, moderate and mild traumas. Data including the age, gender, aetiology, hospital stay time and the pituitary hormone levels was analyzed. A p value <0.05 was considered signifi cant. RESULTS: The male patients (40.5±21.76) with head injury were signifi cantly younger than the female patients (49.13±27.93). During the acute phase of the head injury, there were growth hormone, ACTH and LH/FSH defi ciencies in 36.6%, 20% and 20% of the patients, respectively. The leading causes of the traumatic brain injuries were falling from high altitude (46.6%) and motor vehicle accidents (33.3%). Higher ACTH levels, and lower Glasgow Coma Score and lower prolactin levels caused longer hospital stay times. CONCLUSION: Although the severity of traumatic brain injury is considered as the major risk factor leading to the development of post-traumatic hypopituitarism, a milder injury may also cause hypopituitarism. All head trauma patients should be followed up long enough in order to rule out the posttraumatic hypopituitarism.
AIM: To evaluate the functional outcome of the pituitary gland after the traumatic brain injury and to present the pituitary functional changes during the acute phase of the trauma in order to identify the possible factors. METHODS: The study included records of 30 patients (22 male and 8 female) between September 2009 and July 2010. The patients were allocated into three groups according to their Glasgow Coma Scale as severe, moderate and mild traumas. Data including the age, gender, aetiology, hospital stay time and the pituitary hormone levels was analyzed. A p value <0.05 was considered signifi cant. RESULTS: The male patients (40.5±21.76) with head injury were signifi cantly younger than the female patients (49.13±27.93). During the acute phase of the head injury, there were growth hormone, ACTH and LH/FSH defi ciencies in 36.6%, 20% and 20% of the patients, respectively. The leading causes of the traumatic brain injuries were falling from high altitude (46.6%) and motor vehicle accidents (33.3%). Higher ACTH levels, and lower Glasgow Coma Score and lower prolactin levels caused longer hospital stay times. CONCLUSION: Although the severity of traumatic brain injury is considered as the major risk factor leading to the development of post-traumatic hypopituitarism, a milder injury may also cause hypopituitarism. All head trauma patients should be followed up long enough in order to rule out the posttraumatic hypopituitarism.
Açıklama
Anahtar Kelimeler
Hypopituitarism, Craniocerebral Trauma, Head Injury, Growth Hormone, Hypogonadism, Traumatic Brain Injury, Hipopitüitarizm, Kraniyoserebral Travma, Kafa Travması, Büyüme Hormonu, Hipogonadizm, Travmatik Beyin Hasarı
Kaynak
Kafkas Tıp Bilimleri Dergisi
WoS Q Değeri
Scopus Q Değeri
Cilt
2
Sayı
2
