Department of Pediatrics, Division of Hematology/Oncology/Stem Cell Transplant, Ann and Robert H. Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Department of Pathology & Laboratory Medicine, Ann and Robert H. Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Mol Genet Genomic Med. 2021 Mar;9(3):e1494. doi: 10.1002/mgg3.1494. Epub 2021 Feb 17.
Homozygous or compound heterozygous pathogenic variants in the thromboxane A synthase 1 (TBXAS1) gene are associated with Ghosal hematodiaphyseal dysplasia (GHDD) which is characterized by defective hematopoiesis and increased bone density of long bones.
Patients 1 and 2 are identical twins, who presented with red blood cell transfusion-dependent normocytic anemia and thrombocytopenia with bone marrow fibrosis and cortical bone thickening of long bones on plain radiograph. To clarify the etiology of their anemia and thrombocytopenia, whole blood was used for the DNA extraction and analyzed using next-generation sequencing (NGS) on an in-house bone marrow failure syndrome panel.
The NGS results indicated that these two patients carried two heterozygous variants in TBXAS1, exon7, c.583_584del, p.Ala195Leufs*12, and exon12, c.1420G>T, p.Gly474Trp, which were inherited from their mother and father, respectively. Patients 1 and 2 have been on chronic oral steroids with normalization of hemoglobin and platelet count after steroid initiation. Patient 3 is their sister who has normal blood counts but also has the same variants in TBXAS1 as her brothers. Radiographs showed cortical bone thickening and she has not required any treatment or transfusion.
We report three Caucasian siblings from non-consanguineous parents with novel compound heterozygous variants of TBXAS1 presenting with the phenotypes of GHDD. These three cases illustrate the variable clinical expressivity of the GHDD from two-compound heterozygous pathogenic variants of TBXAS1.
血栓素合酶 1(TBXAS1)基因中的纯合子或复合杂合致病性变异与 Ghosal 骨血液发育不良(GHDD)有关,其特征为造血功能缺陷和长骨骨密度增加。
患者 1 和 2 是同卵双胞胎,表现为红细胞依赖输血的正细胞性贫血和血小板减少症,骨髓纤维化和长骨皮质骨增厚。为阐明其贫血和血小板减少症的病因,使用全血进行 DNA 提取,并在内部骨髓衰竭综合征面板上进行下一代测序(NGS)分析。
NGS 结果表明,这两名患者携带 TBXAS1 外显子 7,c.583_584del,p.Ala195Leufs*12 和外显子 12,c.1420G>T,p.Gly474Trp 的两个杂合变异,分别从母亲和父亲遗传而来。患者 1 和 2 一直接受慢性口服类固醇治疗,类固醇治疗开始后血红蛋白和血小板计数正常。患者 3 是他们的妹妹,她的血常规正常,但也有与她的兄弟相同的 TBXAS1 变异。影像学检查显示皮质骨增厚,她无需任何治疗或输血。
我们报告了来自非近亲父母的三个白种人兄弟姐妹,他们具有 TBXAS1 的新型复合杂合变异,表现为 GHDD 的表型。这三个病例说明了 GHDD 从 TBXAS1 的两个复合杂合致病性变异的不同临床表现。