Instituto de Medicina Integral Professor Fernando Figueira, Recife, PE, Brazil.
Hospital Israelita Albert Einstein, São Paulo, SP, Brazil.
Einstein (Sao Paulo). 2022 Sep 12;20:eRC0048. doi: 10.31744/einstein_journal/2022RC0048. eCollection 2022.
Gain-of-function mutations in the STAT1 gene have been initially associated with chronic mucocutaneous candidiasis. However, further research has shown that STAT1 GOF variants may increase susceptibility to infection by other intracellular pathogens. This report describes the first case of disseminated leishmaniasis associated with a STAT1 GOF mutation in a pediatric patient who did not have chronic mucocutaneous candidiasis. The patient was a four-year-old boy presenting with fever, severe asthenia, hepatosplenomegaly, pancytopenia, and liver failure. Bone marrow aspirate revealed hemophagocytosis and Leishmania parasites. Treatment consisted primarily of liposomal amphotericin B, as per the Hemophagocytic Lymphohistiocytosis 2004 protocol. After eight weeks of treatment, the patient did not improve and was submitted to diagnostic splenectomy. Activated macrophages and nodular spleen necrosis secondary to the visceral leishmaniasis were detected. Unfortunately, the patient died in the second week after splenectomy due to overwhelming systemic infection. DNA sequencing revealed a pathogenic (p. R274Q) GOF mutation in STAT1.
STAT1 基因的功能获得性突变最初与慢性黏膜皮肤念珠菌病有关。然而,进一步的研究表明,STAT1 功能获得性变异可能会增加对其他细胞内病原体感染的易感性。本报告描述了首例与 STAT1 功能获得性突变相关的播散性利什曼病的儿科病例,该患者无慢性黏膜皮肤念珠菌病。该患者为 4 岁男孩,表现为发热、严重乏力、肝脾肿大、全血细胞减少和肝功能衰竭。骨髓抽吸显示噬血细胞现象和利什曼原虫。治疗主要包括两性霉素 B 脂质体,按照噬血细胞性淋巴组织细胞增生症 2004 年方案。治疗 8 周后,患者病情未见改善,并进行了诊断性脾切除术。检测到巨噬细胞活化和结节性脾坏死继发于内脏利什曼病。不幸的是,患者在脾切除术后第二周因全身感染而死亡。DNA 测序显示 STAT1 存在致病性(p.R274Q)功能获得性突变。