Budd-Chiari Sendromu (BCS) karacigerin venöz drenajinin çesitli nedenlerle bozulmasi sonucu hepatik venlerin vena cava inferiora (VCI) açilim seviyesinde tikanmasi sonucunda olusan bir sendromdur. Nedenleri arasinda nadiren viral enfeksiyonlarin oldugu bilinmektedir. Ebstein-Barr virüs (EBV) multisistemik klinik tablolar olusturabilen bir virüstur. 29 yasindaki bayan hasta karinda sislik, bas dönmesi, bulanti, karin ve sirt bölgesinde yaygin makulopapüler döküntü ile klinigimize yatirildi. Fizik bakisinda ates, servikal bilateral multipl, en büyügü 1x1 cm’lik lenfadenopatiler, agrili hepatomegali, splenomegali ve yaygin assiti mevcut idi. Laboratuvar sonuçlarinda dissemine intravasküler koagülopati düsündüren hematolojik parametrelerle birlikte, EBV için monospot testi (+), EBV viral kapsid antijen (VCA) IgG 1/320 titrede bulundu. Portal doppler US’de hepatik ven trombozu, splenomegali, hepatomegali ve kaudat lob hipertrofisi saptanan olgu BCS olarak kabul edildi. Hastanin nörolojik ve KBB muayenesiyle vestibüler nörit, cilt lezyonlarindan alinan biyopside Lichen Planus tanisi kondu. Literatürler degerlendirildiginde EBV’nin olguda bulunan semptom ve bulgulara yol açabilecek klinik tablo yaratabilecegi ve DIC olusturma potansiyeli ile BCS’ye neden olabilecegi düsünüldü. Sonuç olarak, olgumuzu EBV’nin DIC, vestibüler nörit, lichen planus gibi genis klinik spektrumda BCS’ ye neden olmasi açisindan sunmayi uygun bulduk.
Budd-Chiari Syndrome (BCS) is a disorder resulting from the obstruction of hepatic veins at the level of junction with the vena cava inferior because of the disruption of venous drainage of the liver from various reasons. The etiology rarely involves viral infections. Epstein-Barr virus (EBV) is a virus which may cause multi-systemic clinic disorders. A 29- year-old female with complaints of dizziness, nausea, widespread maculopapular rash in abdominal and dorsal regions was hospitalized. Physical examination revealed fever, cervical bilateral multiple lymphadenopathy (largest was 1x1 cm in size), painful hepatomegaly, splenomegaly and massive ascites. Laboratory results showed hematologic parameters suggesting disseminated intravascular coagulopathy (DIC). Monospot test for EBV was positive and EBV viral capsular antigen (VCA) IgG was found at a titer of 1/320. Portal Doppler ultrasonography revealed hepatic vein thrombosis, splenomegaly, hepatomegaly and hypertrophy of caudate lobe, and the patient was accepted as BCS. The patient was given the diagnosis of vestibular neuritis after neurologic and otologic examination and the biopsy taken from the skin lesions suggested the diagnosis of lichen planus. After review of the literature, it was considered that EBV infection may cause a clinical picture as seen in our case and may result in BCS with its potential to form DIC. In conclusion we found it worthwhile to present our case in regard to EBV’s potential to cause a wide clinical spectrum including DIC, vestibular neuritis, lichen planus and finally BCS.