Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD.
Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Hepatology. 2019 Jun;69(6):2579-2585. doi: 10.1002/hep.30578. Epub 2019 Apr 10.
Loss-of-function mutations in genes that encode for components of the telomere repair complex cause accelerated telomere shortening. Hepatic involvement has been recognized as a cause of morbidity in telomere diseases, but very few studies have characterized the nature and extent of liver involvement in affected patients. We report the prevalence and characteristics of liver involvement in a large cohort of patients with telomere disease evaluated serially at the National Institutes of Health. One hundred twenty-one patients with known or suspected telomere disease were screened; 40 patients with liver involvement were included in the current study. Median follow-up was 2.4 years. Data were collected regarding their demographic information, laboratory analysis, imaging, and histopathology. Forty patients (40% of the cohort) with a median age of 42 years were found to have liver involvement. Liver enzyme elevation was cholestatic in pattern; 8 (21%) had drug-related enzyme elevations. The most common imaging finding was increased hepatic echogenicity on ultrasound in 39% (9) of patients, followed by hepatomegaly in 26% (6). Biopsies were infrequent because of risk associated with thrombocytopenia, but in 6 patients, there were varying findings: nodular regenerative hyperplasia, steatohepatitis, hemosiderosis, cholestasis, and cirrhosis with hepatic steatosis. Almost half the cohort had pulmonary diffusion abnormalities, and 25% died during the follow-up period. Conclusion: In patients with telomere disease, hepatic involvement is common and can present in diverse ways, including elevated liver enzymes as well as histopathologic and imaging abnormalities. Liver disease has important implications for morbidity and mortality in patients with telomere disease.
端粒修复复合物成分相关基因的功能丧失性突变可导致端粒缩短加速。肝受累已被认为是端粒疾病发病的原因之一,但很少有研究对受累患者的肝脏受累性质和程度进行特征描述。我们报告了在国立卫生研究院进行连续评估的一组大型端粒疾病患者中肝脏受累的患病率和特征。对 121 名已知或疑似端粒疾病的患者进行了筛查;本研究纳入了 40 名有肝脏受累的患者。中位随访时间为 2.4 年。收集了有关其人口统计学信息、实验室分析、影像学和组织病理学的数据。发现 40 名(队列的 40%)中位年龄为 42 岁的患者有肝脏受累。肝酶升高呈胆汁淤积模式;8 名(21%)有药物相关的酶升高。最常见的影像学表现是 39%(9 名)患者的超声检查显示肝脏回声增强,其次是肝肿大(26%,6 名)。由于血小板减少相关风险,活检并不常见,但在 6 名患者中发现了不同的表现:结节性再生性增生、脂肪性肝炎、血色素沉着症、胆汁淤积和伴有肝脂肪变性的肝硬化。近一半的队列有肺弥散功能异常,25%的患者在随访期间死亡。结论:在端粒疾病患者中,肝脏受累很常见,可表现为多种方式,包括肝酶升高以及组织病理学和影像学异常。肝脏疾病对端粒疾病患者的发病率和死亡率有重要影响。