Display options
Cite
Trilianos P, Agnihotri A, Ucbilek E, et al. Greater Biosynthetic Liver Dysfunction in Primary Sclerosing Cholangitis Suggests Co-existent or Impending Cholangiocarcinoma. J Clin Transl Hepatol. 2016;4(1):1-4doi: 10.14218/JCTH.2015.00048.
Trilianos, P., Agnihotri, A., Ucbilek, E., & Gurakar, A. (2016). Greater Biosynthetic Liver Dysfunction in Primary Sclerosing Cholangitis Suggests Co-existent or Impending Cholangiocarcinoma. Journal of clinical and translational hepatology, 4(1), 1-4. https://doi.org/10.14218/JCTH.2015.00048
Trilianos, Panagiotis, et al. "Greater Biosynthetic Liver Dysfunction in Primary Sclerosing Cholangitis Suggests Co-existent or Impending Cholangiocarcinoma." Journal of clinical and translational hepatology vol. 4,1 (2016): 1-4. doi: https://doi.org/10.14218/JCTH.2015.00048
Trilianos P, Agnihotri A, Ucbilek E, Gurakar A. Greater Biosynthetic Liver Dysfunction in Primary Sclerosing Cholangitis Suggests Co-existent or Impending Cholangiocarcinoma. J Clin Transl Hepatol. 2016 Mar 28;4(1):1-4. doi: 10.14218/JCTH.2015.00048. Epub 2016 Mar 15. PMID: 27047765; PMCID: PMC4807136.
Copy Download .nbib Format: NLM
Share it on

J Clin Transl Hepatol. 2016 Mar 28;4(1):1-4. doi: 10.14218/JCTH.2015.00048. Epub 2016 Mar 15.

Greater Biosynthetic Liver Dysfunction in Primary Sclerosing Cholangitis Suggests Co-existent or Impending Cholangiocarcinoma.

Journal of clinical and translational hepatology

Panagiotis Trilianos, Abhishek Agnihotri, Enver Ucbilek, Ahmet Gurakar

Affiliations

  1. Department of Gastroenterology & Hepatology, Section of Transplant Hepatology, The Johns Hopkins School of Medicine, Baltimore MD, USA; Department of Medicine, MetroWest Medical Center, Framingham, MA, USA.
  2. Department of Gastroenterology & Hepatology, Section of Transplant Hepatology, The Johns Hopkins School of Medicine, Baltimore MD, USA.

PMID: 27047765 PMCID: PMC4807136 DOI: 10.14218/JCTH.2015.00048

Abstract

Background and Aim : Patients with primary sclerosing cholangitis (PSC) who develop cholangiocarcinoma (CCA) have a median survival of less than 6 months. In half of cases, PSC and CCA will be diagnosed either concurrently or within a year of one another. The aim of the present study is to demonstrate that the degree of biochemical liver dysfunction is associated with concomitant or impending CCA. Methods : We did a chart review of patients diagnosed with PSC and CCA up to 18 months from presentation ("CCA" group) as well as patients with PSC that underwent transplantation with no sign of CCA in their explanted liver ("nCCA" group). Along with demographic data and follow-up length, we recorded their presenting liver function tests, including alanine and aspartate aminotransferases (ALT, AST), total bilirubin (TBil), alkaline phosphatase (ALP), international normalization ratio (INR), and serum Ca 19-9 levels. Differences between mean values of the two groups were analyzed with a student's t-test. Results : Twenty-four patients were included. The "CCA" group consisted of eight patients, and the "non-CCA" group had 16 patients. There was no significant difference between the two groups in their presenting values of ALT, ALP, or serum Ca 19-9. However, the "CCA" group had significantly higher levels of AST, TBil, and INR. Conclusion : Patients with PSC and concurrent or impending CCA appear to exhibit significantly greater biochemical liver dysfunction than those who do not develop CCA. Therefore, newly-diagnosed PSC patients presenting with these findings may warrant more rigorous evaluation.

Keywords: Cholestatic disease; Liver function tests; Liver transplantation; Malignancy

References

  1. Hepatology. 2011 Mar;53(3):875-84 - PubMed
  2. Scand J Gastroenterol. 2002 Oct;37(10):1205-11 - PubMed
  3. J Hepatobiliary Pancreat Surg. 2000;7(4):426-31 - PubMed
  4. Hepatology. 2014 Sep;60(3):896-907 - PubMed
  5. Gastroenterology. 2002 Oct;123(4):1090-8 - PubMed
  6. J Hepatol. 2000 Mar;32(3):374-80 - PubMed
  7. Liver. 1999 Dec;19(6):501-8 - PubMed
  8. Gut. 1996 Apr;38(4):610-5 - PubMed
  9. Hepatology. 2000 Jan;31(1):7-11 - PubMed
  10. Hepatology. 2008 Jan;47(1):90-6 - PubMed
  11. Br J Cancer. 2011 Oct 25;105(9):1370-8 - PubMed
  12. Clin Gastroenterol Hepatol. 2011 May;9(5):434-9.e1 - PubMed
  13. Digestion. 2014;89(2):165-73 - PubMed
  14. Am J Gastroenterol. 2004 Mar;99(3):523-6 - PubMed
  15. Hepatogastroenterology. 2014 May;61(131):567-73 - PubMed
  16. Gut. 2013 Jan;62(1):122-30 - PubMed
  17. Hepatology. 1998 Feb;27(2):311-6 - PubMed

Publication Types