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Telomere length in patients with alcohol-associated liver disease: a brief report
  1. Nazmul Huda1,
  2. Praveen Kusumanchi1,
  3. Kristina Perez1,
  4. Yanchao Jiang1,
  5. Nicholas J Skill2,
  6. Zhaoli Sun3,
  7. Jing Ma1,
  8. Zhihong Yang1,
  9. Suthat Liangpunsakul1,4
  1. 1 Division of Gastroenterology and Hepatology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA
  2. 2 Department of Surgery, Louisiana State University Health Science Center, New Orleans, LA, USA
  3. 3 Department of Surgery, Johns Hopkins University School of Medicine, Baltiore, MD, USA
  4. 4 Roudebush Veterans Administration Medical Center, Indianapolis, IN, USA
  1. Correspondence to Dr. Suthat Liangpunsakul, Division of Gastroenterology and Hepatology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA; sliangpu{at}


The intact telomere structure is essential for the prevention of the chromosome end-to-end fusions and maintaining genomic integrity. The maintenance of telomere length is critical for cellular homeostasis. The shortening of telomeres has been reported in patients with chronic liver diseases. The telomere length has not been systemically studied in patients with alcohol-associated liver disease (ALD) at different stages, such as alcoholic hepatitis and alcoholic cirrhosis. In this brief report, we observed evidence of telomere shortening without changes in the telomerase activity in the liver of patients with alcoholic hepatitis and alcoholic cirrhosis when compared with controls. The alterations in the genes associated with telomere binding proteins were only observed in patients with alcoholic cirrhosis. Future studies are required to determine the mechanism of how alcohol affects the length of the telomere and if the shortening impacts the disease progression in ALD.

  • liver diseases, alcoholic

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  • Contributors NH and SL: Study concept and design. NH: Acquisition of data, analysis, and interpretation of data. PK, KP, YJ, and JM: Critical revision of the manuscript. NJS and ZS: Providing human liver samples. NH, ZY, and SL: Drafting and finalizing the manuscript. All authors have read and approved the manuscript for submission.

  • Funding ZY is supported by NIH K01AA26385 and the Ralph W. and Grace M. Showalter Research Trust and the Indiana University School of Medicine; SL is supported in part by R01 AA025208, U01 AA026917, UH2/UH3 AA026903, VA Merit Award 1I01CX000361, and Dean’s Scholar in Medical Research, Indiana University School of Medicine.

  • Competing interests SL is a Journal of Investigative Medicine Editorial Board member. All other authors declare no competing interests.

  • Provenance and peer review Not commissioned; externally peer reviewed.