OBEZ ADOLESANLARDA YAĞLI KARACİĞER HASTALIĞININ PORTAL VEN AKIMINA ETKİSİ

Abstract

Amaç Çocuklarda obezitenin artması, nonalkolik yağlı karaciğer hastalığının pediatrik yaş grubunda en önemli kronik karaciğer hastalığı haline gelmesine neden olmuştur. Bu çalışmada alkolik olmayan karaciğer yağlanması (NAFLD) olan obez çocuklarda portal ven çapı ve kan akım hızını değerlendirmesi ve normal sağlıklı çocuklarla karşılaştırması amaçlanmıştır. Gereç ve Yöntem 10-18 yaş arası 71 obez adolesan hasta, transaminaz yüksekliği ve ultrasonda hepatosteatoz (NAFLD grubu ve NAFLD olmayan grup) varlığına göre iki gruba ayrıldı. Kontrol grubu olarak 30 sağlıklı ergen çalışmaya dahil edildi. Her hastadan açlık glukozu, insülin, transaminaz düzeyleri ve tiroid fonksiyonları için kan örnekleri alındı. İnsülin direnci HOMA indeksi kullanılarak hesaplandı. Portal ven ölçümleri, bifurkasyon öncesi ana portal venden yapıldı. Bulgular NAFLD grubunda portal ven çapı (8.5 ± 0.9 mm) hem kontrol grubuna (7.8 ± 2.0 mm) hem de NAFLD olmayan obez gruba (7.6 ± 1.1 mm) göre istatistiksel olarak anlamlı derecede geniş olarak saptandı (p= 0.004) ve (p=0.002). NAFLD olmayan obez grup ile kontrol grubu arasında anlamlı fark yoktu (p=0.460, p=0.214). Portal ven Vmax, Vmin, RI, S/D açısından gruplar arasında anlamlı fark yoktu. İnsülin direncine göre sınıflandırılan obez gruplarda portal ven çaplarında farklılık olmamasına rağmen, Vmax (33.9 ± 10.3 ve 28.6 ± 10.6 cm/sn, p= 0.03) ve Vmin (24.8 ± 6.2 ve 20.5 ± 5.5 cm/sn) insülin direnci grubunda önemli ölçüde farklıydı. Sonuç Bu çalışmada NAFLD olan obez adolesanlarda portal ven çapı ve akım hızlarının (Vmax ve Vmin) arttığı belirlendi. Bu nedenle özellikle ergenlik döneminde insülin direnci olan obez hastalarda hepatik portal ven steatozuna bağlı hepatik venöz akımda direnç geliştiği düşünüldü. Bu bulgu, karaciğer yağlanmasının devam etmesi durumunda erişkin dönemde portal çapının artacağını ve bunun da portal hipertansiyona yol açacağını düşündürmektedir.

Keywords

• obezite
• hepatosteatoz
• doppler ultrasonografi

THE EFFECT OF FATTY LIVER DISEASE ON PORTAL VEIN FLOW IN OBESE ADOLESCENTS

Abstract

Objective The increase in obesity in children has caused nonalcoholic fatty liver disease to become the most important chronic liver disease in the pediatric age group. In this study, we aimed to evaluate the portal diameter and blood flow velocity in obese children with fatty liver (NAFLD) and to compare them with normal healthy children. Material and Method 71 obese adolescent patients aged 10-18 years were divided into two groups (NAFLD group and non- NAFLD group) according to the presence of elevated transaminases and the presence of hepatosteatosis on ultrasound. 30 healthy adolescents were included in the study as the control group. Blood samples were taken from each patient for fasting glucose, insulin, transaminases, and thyroid functions. Insulin resistance was calculated using the HOMA index. Portal vein measurements were performed from the main portal vein before bifurcation. Results The portal vein diameter (8.5 ± 0.9 mm) of the NAFLD group was statistically significantly wide compared to both the control group (7.8 ± 2.0 mm) and the non-NAFLD obese group (7.6 ± 1.1 mm) (p= 0.004) and (p= 0.002). There was no significant difference between the non-NAFLD obese group and the control group (p=0.460, p=0.214). There was no significant difference between the groups in terms of portal vein Vmax, Vmin, RI, S/D. Although there was no difference in portal vein diameter in the obese groups classified according to insulin resistance, Vmax (33.9 ± 10.3 and 28.6 ± 10.6 cm/sec, p= 0.03) and Vmin (24.8 ± 6.2 and 20.5 ± 5.5 cm/sec) were significantly different in the insulin resistance group. Conclusion In this study, it was determined that portal vein diameter and flow velocities (Vmax and Vmin) increased in obese adolescents with NAFLD. Thus, we suggest that resistance develops in hepatic venous flow due to hepatic portal vein steatosis, especially in obese patients with insulin resistance in adolescence. This finding suggests that when fatty liver continues, portal diameter will increase in adulthood, leading to portal hypertension.

Keywords

• obesity
• hepatosteatosis
• doppler ultrasonography

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