Published online Nov 6, 2018. doi: 10.12998/wjcc.v6.i13.659
Peer-review started: August 7, 2018
First decision: August 24, 2018
Revised: September 10, 2018
Accepted: October 9, 2018
Article in press: October 9, 2018
Published online: November 6, 2018
Processing time: 92 Days and 0 Hours
A previously healthy 16-year-old boy developed acute liver failure (ALF) and hemophagocytic lymphohistiocytosis (HLH) soon after varicella infection.
Generalized skin rash with various stages of development including maculopapules, vesicles, pustules, and crusts were typical features of chickenpox [primary infection of varicella-zoster virus(VZV)].
The differential diagnosis for extremely high level of ferritin (> 50000 ng/mL) could be limited to few clinical circumstances, such as Still’s disease, HLH, and systemic histoplasmosis.
A sudden onset of liver injury with soared transaminases and decreased prothrombin activity pointed to ALF. Pancytopenia, hypofibrinogenemia, and hyperferritinemia were clues for HLH. The polymerase chain reaction (PCR) amplifications of VZV confirmed varicella infection.
An ultrasound of the abdomen showed splenomegaly, but neither hepatomegaly nor ascites.
Not applicable.
The patient underwent a combination therapy of acyclovir (10 mg/kg every 8 h), supportive care, and immunosuppression with dexamethasone and etoposide.
ALF associated with HLH is extremely fatal and rarely reported. In recent years, HLH first presenting as ALF was becoming increasingly noticed while the mortality remained high.
HLH, also known as hemophagocytic syndrome, is a devastating disorder characterized by fever, splenomegaly, cytopenia and the finding of activated macrophages in hemopoietic organs.
Accumulating evidence pointed towards a similar immune dysregulation pattern in ALF and HLH. It is important to maintain a high suspicion for HLH in ALF with or without an identified trigger. Patients might benefit from therapies targeted to halt any underlying trigger and control the overactive immune system.