{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,6]],"date-time":"2026-11-06T21:52:14Z","timestamp":1794001934748,"version":"4.8.0"},"reference-count":33,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2020,2,26]],"date-time":"2020-02-26T00:00:00Z","timestamp":1582675200000},"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":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2020,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Aim<\/jats:title>\n                    <jats:p>Iron deficiency anemia (IDA)is the leading cause of anemia worldwide. Data on prevalence and clinical impact of anemia in cirrhosis are scarce. Aim was to report on the following:(i) prevalence of anemia and IDA in cirrhosis and (ii) its possible impact on clinical outcomes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Consecutive cirrhotic patients from a prospective registry study were included. Anemia was defined as hemoglobin concentration \u2264\u00a012\u00a0g\/dL. IDA was defined as Hb\u00a0\u2264\u00a012\u00a0g\/dL\u00a0+\u00a0transferrin\u2010saturation\u00a0&lt;\u00a020%. Follow up for hepatic decompensation and mortality started with study inclusion and terminated in December 2017. A retrospective validation cohort of 1244 patients was used to validate our findings.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Two hundred forty\u2010two patients with compensated (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a053 [21.9%]) and decompensated (n\u00a0=\u00a0189 [78.1%]) cirrhosis were included. Anemia was present in 128 patients (52.9%); of those, 63 (49.2%) had IDA. Prevalence of anemia increased with Child\u2013Pugh Score (CPS; A: 26.5%, B: 59.2%, C: 69%;\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.001) and with decompensated cirrhosis(62.4%\n                      <jats:italic>vs<\/jats:italic>\n                      18.8%,\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.001). Within anemic patients, a higher proportion of patients in CPS A\/B\n                      <jats:italic>vs<\/jats:italic>\n                      C (73%\n                      <jats:italic>vs<\/jats:italic>\n                      35%;\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.025) and in compensated cirrhosis (80%\n                      <jats:italic>vs<\/jats:italic>\n                      46.6%;\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.043) were found with IDA. Model for End\u2010Stage Liver Disease (MELD) scores were significantly lower in patients with IDA (14.4\n                      <jats:italic>vs<\/jats:italic>\n                      17.9 non\u2010ID\u2010anemia;\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.005). Similar results were found in the validation cohort: median MELD (16[8\u201328]non\u2010IDA\n                      <jats:italic>vs<\/jats:italic>\n                      12 [7\u201323] IDA;\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.001) and within anemic patients IDA was more common in patients with MELD &lt;15 (58%)\n                      <jats:italic>versus<\/jats:italic>\n                      &gt;15 (24%,\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.001).\n                    <\/jats:p>\n                    <jats:p>\n                      Anemia was associated with a significant risk for hepatic decompensation and\/or mortality both in the validation (aSHR: 1.65,\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.008) and in the derivation cohort (aSHR: 2.11, P\u00a0&lt;\u00a00.001) and an independent risk factor for hepatic decompensation and\/or mortality in compensated patients (aHR: 4.91,\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.004).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Anemia is highly prevalent in cirrhosis. In compensated cirrhosis, CPS A\/B, and low MELD, IDA seems to be the most likely reason for anemia. Furthermore, anemia is associated with a significant risk for hepatic decompensation or mortality during long\u2010term follow up.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jgh.14988","type":"journal-article","created":{"date-parts":[[2020,1,23]],"date-time":"2020-01-23T12:24:17Z","timestamp":1579782257000},"page":"1619-1627","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["Anemia and iron deficiency in compensated and decompensated cirrhosis: Prevalence and impact on clinical outcomes"],"prefix":"10.1111","volume":"35","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1813-5769","authenticated-orcid":false,"given":"Rafael","family":"Paternostro","sequence":"first","affiliation":[{"name":"Vienna Hepatic Hemodynamic Lab, Divison of Gastroenterology and Hepatology, Department of Internal Medicine III Medical University of Vienna  Vienna Austria"},{"name":"Division of Gastroenterology and Hepatology, 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