Gulez Nesrin, Aksu Guzide, Berdeli Afig, Karaca Neslihan, Tanrıverdi Sema, Kutukculer Necil, Azarsiz Elif
Department of Pediatric Immunology, Ege University Medical School, 35100 Izmir, Turkey.
Case Rep Med. 2011;2011:121258. doi: 10.1155/2011/121258. Epub 2011 Apr 12.
The X-linked lymphoproliferative syndrome (XLP) is a rare, inherited immunodeficiency characterized by recurrent episodes of hemophagocytic lymphohistiocytosis, hypogammaglobulinemia, and/or lymphomas. Recently, X-linked inhibitor of apoptosis (XIAP/BIRC4) gene defects, in families with XLP but without SH2D1A gene defects, has been defined. The distinction from primary immunodeficiencies with a defined genetic cause is mandatory. A six-year-old male patient was admitted with the complaints of persistent general lymphadenopathy, for two years had fever, bilateral cervical multiple microlymphadenopathy, hepatic/splenic enlargement with laboratory findings as decreased serum immunoglobulins, negative EBV VCA IgM (viral capsid antigen) and anti-EBV EA (antibody to early D antigen), positive EBV VCA IgG (viral capsid antigen) and EBV EBNA (antibody to nuclear antigen). SH2D1A gene analysis was negative. XIAP/BIRC4 sequencing revealed two novel single nucleotide variants (exon 7, 1978G > A, and 1996T > A) in the 3'UTR of the gene in both patient and mother which were not disease causing. XIAP protein expression was found to be normal. The clinical and laboratory resemblance, no gene mutations, and normal XIAP protein expression led us to think that there may be another responsible gene for XLP. The patient will to be followed up as CVID until he presents new diagnostic signs or until the identification of a new gene.
X连锁淋巴增殖综合征(XLP)是一种罕见的遗传性免疫缺陷病,其特征为噬血细胞性淋巴组织细胞增生症反复发作、低丙种球蛋白血症和/或淋巴瘤。最近,在无SH2D1A基因缺陷的XLP家族中,已明确了X连锁凋亡抑制蛋白(XIAP/BIRC4)基因缺陷。必须将其与具有明确遗传病因的原发性免疫缺陷区分开来。一名6岁男性患者因持续性全身淋巴结肿大入院,发热两年,双侧颈部多发微小淋巴结病,肝脾肿大,实验室检查发现血清免疫球蛋白降低,EBV VCA IgM(病毒衣壳抗原)和抗EBV EA(早期D抗原抗体)阴性,EBV VCA IgG(病毒衣壳抗原)和EBV EBNA(核抗原抗体)阳性。SH2D1A基因分析为阴性。XIAP/BIRC4测序显示患者及其母亲的该基因3'UTR中有两个新的单核苷酸变体(外显子7,1978G>A和1996T>A),均不致病。XIAP蛋白表达正常。临床和实验室表现相似、无基因突变以及XIAP蛋白表达正常,使我们认为可能存在另一个导致XLP的相关基因。该患者将按普通变异型免疫缺陷病(CVID)进行随访,直至出现新的诊断体征或鉴定出新基因。