File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: Prevalence of graft steatosis after liver transplantation using controlled attenuation parameter measurements: a large cohort study

TitlePrevalence of graft steatosis after liver transplantation using controlled attenuation parameter measurements: a large cohort study
Authors
Issue Date2017
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
The 68th Annual Meeting of the American Association for the Study of Liver Diseases: The Liver Meeting 2017, Washington DC, USA, 20-24 October 2017. In Hepatology, 2017, v. 66 n. Suppl. 1, p. 914A-915A, abstract no. 1710 How to Cite?
AbstractBackground: Liver steatosis is a cause of graft dysfunction after liver transplantation. The current study aims to determine the prevalence of steatosis in a large cohort of liver transplant recipients from a single center. Methods: Consecutive patients transplanted from 2003 to 2014 underwent liver stiffness (LS) and controlled attenuation parameter (CAP) measurements using transient elastography. Liver biochemistry and fasting lipid profile and glucose were taken. Results: A total of 554 patients underwent valid transient elastography, of which 396 (71.5%) were male, with a median age of 59 (range, 19-78) years, and median time to transient elastography of 77 months (range, 6-167) after transplantation. The majority (71.8%) was transplanted for hepatitis B related complications. The prevalence of no, mild, moderate, and severe steatosis was 49.1%, 6.3%, 25.8%, and 18.8% respectively. A higher CAP score was observed in males vs. females (229 vs 212 dB/m respectively, p=0.007) and in living vs. deceased donor transplant (229 vs 215 dB/m respectively, p=0.004). Steatosis, as diagnosed by CAP score of ≥222 dB/m, was observed in 282 (50.9%) patients, of which 35 (6.3%) had mild steatosis, 143 (25.8%) had moderate steatosis, and 104 (18.8%) had severe steatosis. Patients with steatosis had older age at transplant (53 vs. 51 years, p=0.005), older age at transient elastography (60 vs 57 years, p=0.001), and higher BMI (25.4 vs 23.2 kg/m2, p<0.001), ALT (24 vs 22 U/L, p=0.026), GGT (35 vs 28 U/L, p=0.041), platelets (181 vs 168, p=0.001), fasting glucose (5.8 vs 5.3, p=0.002), total cholesterol (4.3 vs 4.2, p=0.037), LDL-cholesterol (2.5 vs 2.2, p<0.001), triglyceride (1.3 vs 1.0, p<0.001). A lower HDL-cholesterol was observed in steatotic patients (1.2 vs 1.5, p<0.001). There was no significant difference in LS measurements between those with and without graft steatosis (4.9 vs 5.0 kPa, p=0.635). Hypertension, diabetes, and hyperlipidemia were present in 324 (58.5%), 190 (34.3%), and 124 (22.4%) patients respectively. A higher CAP score was observed in patients with hypertension (237 vs 204 dB/m, p<0.001), diabetes (233 vs 217 dB/m, p=0.008), and hyperlipidemia (239 vs 217 dB/m, p<0.001). The highest CAP scores was observed for those transplanted for alcoholic liver disease (254 dB/m) and cryptogenic cirrhosis (261 dB/m), with lowest scores seen in patients with biliary atresia (161 dB/m) and polycystic liver disease (188 dB/m)(p=0.019). Conclusion: Graft steatosis is common after liver transplantation, and is associated with higher baseline BMI, and higher rates of hypertension, diabetes, and hyperlipidemia. However, there is no significant increase in LS.
DescriptionPoster presentation
Persistent Identifierhttp://hdl.handle.net/10722/262552
ISSN
2021 Impact Factor: 17.298
2020 SCImago Journal Rankings: 5.488

 

DC FieldValueLanguage
dc.contributor.authorFung, JYY-
dc.contributor.authorWong, CLT-
dc.contributor.authorChok, KSH-
dc.contributor.authorDai, WC-
dc.contributor.authorChan, ACY-
dc.contributor.authorSin, SL-
dc.contributor.authorShe, WH-
dc.contributor.authorMak, KW-
dc.contributor.authorNg, K-
dc.contributor.authorSeto, WKW-
dc.contributor.authorLai, CL-
dc.contributor.authorYuen, RMF-
dc.contributor.authorLo, CM-
dc.date.accessioned2018-09-28T05:01:17Z-
dc.date.available2018-09-28T05:01:17Z-
dc.date.issued2017-
dc.identifier.citationThe 68th Annual Meeting of the American Association for the Study of Liver Diseases: The Liver Meeting 2017, Washington DC, USA, 20-24 October 2017. In Hepatology, 2017, v. 66 n. Suppl. 1, p. 914A-915A, abstract no. 1710-
dc.identifier.issn0270-9139-
dc.identifier.urihttp://hdl.handle.net/10722/262552-
dc.descriptionPoster presentation-
dc.description.abstractBackground: Liver steatosis is a cause of graft dysfunction after liver transplantation. The current study aims to determine the prevalence of steatosis in a large cohort of liver transplant recipients from a single center. Methods: Consecutive patients transplanted from 2003 to 2014 underwent liver stiffness (LS) and controlled attenuation parameter (CAP) measurements using transient elastography. Liver biochemistry and fasting lipid profile and glucose were taken. Results: A total of 554 patients underwent valid transient elastography, of which 396 (71.5%) were male, with a median age of 59 (range, 19-78) years, and median time to transient elastography of 77 months (range, 6-167) after transplantation. The majority (71.8%) was transplanted for hepatitis B related complications. The prevalence of no, mild, moderate, and severe steatosis was 49.1%, 6.3%, 25.8%, and 18.8% respectively. A higher CAP score was observed in males vs. females (229 vs 212 dB/m respectively, p=0.007) and in living vs. deceased donor transplant (229 vs 215 dB/m respectively, p=0.004). Steatosis, as diagnosed by CAP score of ≥222 dB/m, was observed in 282 (50.9%) patients, of which 35 (6.3%) had mild steatosis, 143 (25.8%) had moderate steatosis, and 104 (18.8%) had severe steatosis. Patients with steatosis had older age at transplant (53 vs. 51 years, p=0.005), older age at transient elastography (60 vs 57 years, p=0.001), and higher BMI (25.4 vs 23.2 kg/m2, p<0.001), ALT (24 vs 22 U/L, p=0.026), GGT (35 vs 28 U/L, p=0.041), platelets (181 vs 168, p=0.001), fasting glucose (5.8 vs 5.3, p=0.002), total cholesterol (4.3 vs 4.2, p=0.037), LDL-cholesterol (2.5 vs 2.2, p<0.001), triglyceride (1.3 vs 1.0, p<0.001). A lower HDL-cholesterol was observed in steatotic patients (1.2 vs 1.5, p<0.001). There was no significant difference in LS measurements between those with and without graft steatosis (4.9 vs 5.0 kPa, p=0.635). Hypertension, diabetes, and hyperlipidemia were present in 324 (58.5%), 190 (34.3%), and 124 (22.4%) patients respectively. A higher CAP score was observed in patients with hypertension (237 vs 204 dB/m, p<0.001), diabetes (233 vs 217 dB/m, p=0.008), and hyperlipidemia (239 vs 217 dB/m, p<0.001). The highest CAP scores was observed for those transplanted for alcoholic liver disease (254 dB/m) and cryptogenic cirrhosis (261 dB/m), with lowest scores seen in patients with biliary atresia (161 dB/m) and polycystic liver disease (188 dB/m)(p=0.019). Conclusion: Graft steatosis is common after liver transplantation, and is associated with higher baseline BMI, and higher rates of hypertension, diabetes, and hyperlipidemia. However, there is no significant increase in LS.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/-
dc.relation.ispartofHepatology-
dc.relation.ispartofThe 68th Annual Meeting of the American Association for the Study of Liver Diseases: The Liver Meeting 2017-
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.-
dc.titlePrevalence of graft steatosis after liver transplantation using controlled attenuation parameter measurements: a large cohort study-
dc.typeConference_Paper-
dc.identifier.emailFung, JYY: jfung@hkucc.hku.hk-
dc.identifier.emailWong, CLT: wongtcl@hku.hk-
dc.identifier.emailChok, KSH: chok6275@hku.hk-
dc.identifier.emailDai, WC: daiwc@hku.hk-
dc.identifier.emailChan, ACY: acchan@hku.hk-
dc.identifier.emailShe, WH: brianshe@hku.hk-
dc.identifier.emailSeto, WKW: wkseto@hku.hk-
dc.identifier.emailLai, CL: hrmelcl@hkucc.hku.hk-
dc.identifier.emailYuen, RMF: mfyuen@hku.hk-
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hk-
dc.identifier.authorityFung, JYY=rp00518-
dc.identifier.authorityWong, CLT=rp01679-
dc.identifier.authorityChok, KSH=rp02110-
dc.identifier.authorityChan, ACY=rp00310-
dc.identifier.authoritySeto, WKW=rp01659-
dc.identifier.authorityLai, CL=rp00314-
dc.identifier.authorityYuen, RMF=rp00479-
dc.identifier.authorityLo, CM=rp00412-
dc.identifier.hkuros292161-
dc.identifier.volume66-
dc.identifier.issueSuppl. 1-
dc.identifier.spage914A-
dc.identifier.epage915A-
dc.publisher.placeUnited States-
dc.identifier.issnl0270-9139-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats