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病例报告:腺苷脱氨酶 2 缺乏症表现为自身免疫性淋巴增生综合征和骨髓衰竭的重叠特征。

Case Report: Deficiency of Adenosine Deaminase 2 Presenting With Overlapping Features of Autoimmune Lymphoproliferative Syndrome and Bone Marrow Failure.

机构信息

Hematology Unit, Istituto di Ricerca e Cura a Carattere Scintifico (IRCCS) Istituto Giannina Gaslini, Genoa, Italy.

Unitá Operativa Semplice Dipartimentale (UOSD) Genetics and Genomics of Rare Diseases, Istituto di Ricerca e Cura a Carattere Scintifico (IRCCS) Istituto Giannina Gaslini, Genoa, Italy.

出版信息

Front Immunol. 2021 Oct 14;12:754029. doi: 10.3389/fimmu.2021.754029. eCollection 2021.

Abstract

Deficiency of adenosine deaminase 2 (DADA2) is an autosomal recessive disease associated with a highly variable clinical presentation, such as vasculitis, inflammation, and hematologic manifestations. Some associations of clinical features can mimic autoimmune lymphoproliferative syndrome (ALPS). We report a case of a female patient who fulfilled the 2009 National Institute of Health revised criteria for ALPS and received a delayed diagnosis of DADA2. During her childhood, she suffered from autoimmune hemolytic anemia, immune thrombocytopenia, and chronic lymphoproliferation, which partially responded to multiple lines of treatments and were followed, at 25 years of age, by pulmonary embolism, septic shock, and bone marrow failure with myelodysplastic evolution. The patient died from the progression of pulmonary disease and multiorgan failure. Two previously unreported variants of gene ADA2/CECR1 were found through next-generation sequencing analysis, and a pathogenic role was demonstrated through a functional study. A single somatic STAT3 mutation was also found. Clinical phenotypes encompassing immune dysregulation and marrow failure should be evaluated at the early stage of diagnostic work-up with an extended molecular evaluation. A correct genetic diagnosis may lead to a precision medicine approach consisting of the use of targeted treatments or early hematopoietic stem cell transplantation.

摘要

腺苷脱氨酶 2(DADA2)缺乏症是一种常染色体隐性疾病,其临床表现具有高度可变性,如血管炎、炎症和血液学表现。一些临床特征的关联可能类似于自身免疫性淋巴增生综合征(ALPS)。我们报告了一例女性患者,该患者符合 2009 年美国国立卫生研究院修订的 ALPS 标准,并被延迟诊断为 DADA2。在儿童时期,她患有自身免疫性溶血性贫血、免疫性血小板减少症和慢性淋巴增生,这些疾病对多种治疗方法有部分反应,并在 25 岁时出现肺栓塞、感染性休克和骨髓衰竭伴骨髓增生异常演变。患者死于肺病和多器官衰竭的进展。通过下一代测序分析发现了两个先前未报道的 ADA2/CECR1 基因突变,并通过功能研究证明了其致病性作用。还发现了一个单一的体细胞 STAT3 突变。在诊断工作的早期阶段,应通过扩展的分子评估来评估包含免疫失调和骨髓衰竭的临床表型。正确的基因诊断可能会导致采用靶向治疗或早期造血干细胞移植的精准医疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/596f/8552009/13f9c9208e66/fimmu-12-754029-g001.jpg

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