{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:15:15Z","timestamp":1787015715300,"version":"build-2736575974"},"reference-count":34,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2021,6,8]],"date-time":"2021-06-08T00:00:00Z","timestamp":1623110400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Liver International"],"published-print":{"date-parts":[[2021,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Aims<\/jats:title>\n                    <jats:p>Relative adrenal insufficiency (RAI) in patients with cirrhosis is associated with increased mortality. Although the pathogenesis of RAI remains unclear, disordered cholesterol metabolism may contribute.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We performed a prospective cohort study of 96 non\u2010critically ill subjects with decompensated cirrhosis at a tertiary care centre. Subjects were administered 250\u00a0\n                      <jats:italic>\u00b5<\/jats:italic>\n                      cg cosyntropin, with RAI defined as an increase in total cortisol &lt;9\u00a0\u00b5g\/dL. High\u2010density lipoprotein (HDL) levels and serum cholesterol esterification percentage (%CE), a validated surrogate marker of lecithin\u2010cholesterol acyltransferase (LCAT) activity, were measured to assess the relationship between disordered cholesterol metabolism and the presence of RAI. Subjects were followed until death, liver transplantation or a maximum of 6\u00a0months.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Subjects with RAI had decreased levels of HDL (18 vs 29\u00a0mg\/dL,\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a0.01) and %CE (64% vs 66%,\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a0.03). Correlation was seen between HDL and %CE (\n                      <jats:italic>r<\/jats:italic>\n                      \u00a0=\u00a00.7,\n                      <jats:italic>R<\/jats:italic>\n                      <jats:sup>2<\/jats:sup>\n                      \u00a0=\u00a00.49;\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a0.01) and each integer decrease in %CE predicted an approximately 2% increase in the probability of RAI. Transplant\u2010free survival was reduced in subjects with RAI at both 6\u00a0months (43% vs 71%,\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a0.01) and 90\u00a0days (54% vs 81%,\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a0.01).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Disruption in cholesterol metabolism contributes to the development of RAI in cirrhosis, as decreased LCAT activity leads to reduced HDL trafficking to the adrenal gland.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/liv.14970","type":"journal-article","created":{"date-parts":[[2021,5,24]],"date-time":"2021-05-24T07:25:38Z","timestamp":1621841138000},"page":"1913-1921","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Abnormal cholesterol metabolism underlies relative adrenal insufficiency in decompensated cirrhosis"],"prefix":"10.1111","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3642-887X","authenticated-orcid":false,"given":"Brian J.","family":"Wentworth","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology University of Virginia Health System Charlottesville VA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebecca M.","family":"Haug","sequence":"additional","affiliation":[{"name":"Department of Medicine University of Virginia Health System Charlottesville VA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick G.","family":"Northup","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology University of Virginia Health System Charlottesville VA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen H.","family":"Caldwell","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology University of Virginia Health System Charlottesville VA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zachary H.","family":"Henry","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology University of Virginia Health System Charlottesville VA 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