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端粒生物学障碍疾病的进展和临床结局。

Disease progression and clinical outcomes in telomere biology disorders.

机构信息

Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD.

出版信息

Blood. 2022 Mar 24;139(12):1807-1819. doi: 10.1182/blood.2021013523.

Abstract

Dyskeratosis congenita related telomere biology disorders (DC/TBDs) are characterized by very short telomeres caused by germline pathogenic variants in telomere biology genes. Clinical presentations can affect all organs, and inheritance patterns include autosomal dominant (AD), autosomal recessive (AR), X-linked (XLR), or de novo. This study examined the associations between mode of inheritance with phenotypes and long-term clinical outcomes. Two hundred thirty-one individuals with DC/TBDs (144 male, 86.6% known genotype, median age at diagnosis 19.4 years [range 0 to 71.6]), enrolled in the National Cancer Institute's Inherited Bone Marrow Failure Syndrome Study, underwent detailed clinical assessments and longitudinal follow-up (median follow-up 5.2 years [range 0 to 36.7]). Patients were grouped by inheritance pattern, considering AD-nonTINF2, AR/XLR, and TINF2 variants separately. Severe bone marrow failure (BMF), severe liver disease, and gastrointestinal telangiectasias were more prevalent in AR/XLR or TINF2 disease, whereas pulmonary fibrosis developed predominantly in adults with AD disease. After adjusting for age at DC/TBD diagnosis, we observed the highest cancer risk in AR/XLR individuals. At last follow-up, 42% of patients were deceased with a median overall survival (OS) of 52.8 years (95% confidence interval [CI] 45.5-57.6), and the hematopoietic cell or solid organ transplant-free median survival was 45.3 years (95% CI 37.4-52.1). Significantly better OS was present in AD vs AR/XLR/TINF2 disease (P < .01), while patients with AR/XLR and TINF2 disease had similar survival probabilities. This long-term study of the clinical manifestations of DC/TBDs creates a foundation for incorporating the mode of inheritance into evidence-based clinical care guidelines and risk stratification in patients with DC/TBDs. This trial was registered at www.clinicaltrials.gov as #NCT00027274.

摘要

先天性角化不良相关端粒生物学疾病(DC/TBDs)的特征是端粒非常短,这是由端粒生物学基因的种系致病性变异引起的。临床表现可影响所有器官,遗传模式包括常染色体显性(AD)、常染色体隐性(AR)、X 连锁(XLR)或新生。本研究探讨了遗传方式与表型和长期临床结局之间的关系。231 名患有 DC/TBDs 的个体(144 名男性,86.6%已知基因型,诊断时的中位年龄为 19.4 岁[范围 0 至 71.6 岁]),参加了国家癌症研究所的遗传性骨髓衰竭综合征研究,接受了详细的临床评估和纵向随访(中位随访时间为 5.2 年[范围 0 至 36.7 年])。根据遗传模式将患者分组,分别考虑 AD-非 TINF2、AR/XLR 和 TINF2 变异。严重骨髓衰竭(BMF)、严重肝病和胃肠道毛细血管扩张症在 AR/XLR 或 TINF2 疾病中更为常见,而肺纤维化主要发生在 AD 疾病的成年人中。在调整 DC/TBD 诊断时的年龄后,我们观察到 AR/XLR 个体的癌症风险最高。在最后一次随访时,42%的患者死亡,中位总生存期(OS)为 52.8 年(95%置信区间[CI]45.5-57.6),造血细胞或实体器官移植无失败的中位生存时间为 45.3 年(95%CI 37.4-52.1)。AD 与 AR/XLR/TINF2 疾病相比,OS 显著更好(P<.01),而 AR/XLR 和 TINF2 疾病患者的生存概率相似。本研究对 DC/TBD 临床表现进行了长期研究,为将遗传方式纳入 DC/TBD 患者基于证据的临床护理指南和风险分层奠定了基础。该试验在 www.clinicaltrials.gov 注册,编号为 NCT00027274。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0701/8952184/abb254e2ef53/bloodBLD2021013523absf1.jpg

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