Published online Dec 6, 2020. doi: 10.12998/wjcc.v8.i23.6130
Peer-review started: June 28, 2020
First decision: September 29, 2020
Revised: October 13, 2020
Accepted: October 27, 2020
Article in press: October 27, 2020
Published online: December 6, 2020
Processing time: 159 Days and 7.4 Hours
Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening hyper-inflammatory syndrome caused by many genetic defects. STAT1 is a DNA-binding factor that regulates gene transcription. HLH caused by STAT1 gain-of-function (GOF) mutations has rarely been reported and its clinical manifestations and mechanisms are not clearly defined.
A 2-year-old boy presented to our hospital with recurrent fever for > 20 d. The patient had a personal history of persistent oral candidiasis and inoculation site infection during the past 2 years. Hepatosplenomegaly was noted. Complete blood cell count showed severe anemia, thrombocytopenia and neutropenia. Other laboratory tests showed liver dysfunction, hypertriglyceridemia and decreased fibrinogen. Hemophagocytosis was found in the bone marrow. Chest computed tomography showed a cavitary lesion. Tests for fungal infection were positive. Serum T helper (Th) 1/Th2 cytokine determination demonstrated moderately elevated levels of interleukin (IL)-6 and IL-10 with normal interferon (IFN)-γ concentration. Mycobacterium bovis was identified in bronchoalveolar lavage fluid by polymerase chain reaction. Genetic testing identified a heterozygous mutation of c.1154C>T causing a T385M amino acid substitution in STAT1. Despite antibacterial and antifungal therapy, the febrile disease was not controlled. The signs of HLH were relieved after HLH-94 protocol administration, except fever. Fever was not resolved until he received anti-tuberculosis therapy. Hematopoietic stem cell transplantation was refused and the patient died six months later due to severe pneumonia.
Patients with STAT1 GOF mutation have broad clinical manifestations and may develop HLH. This form of HLH presents with normal IFN-γ level without cytokine storm.
Core Tip: Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening hyperinflammatory syndrome caused by many genetic defects. Cytokine storm is frequent and interferon (IFN)-γ is considered to play a key role. We present a case of HLH caused by STAT1 gain-of-function (GOF) mutation. The cytokine profile showed moderately elevated interleukin (IL)-6 and IL-10 and normal IFN-γ. In STAT1 GOF mutation, although inhibition of IL-12R/IL-23R signaling leads to diminished T helper (Th) 1/Th17 and IL-12 response, which then prevent a cytokine storm, overactivity of phagocytic cells due to hyperphosphorylation of STAT1 can lead to HLH.