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Anemia and iron deficiency in compensated and decompensated cirrhosis: Prevalence and impact on clinical outcomes
Author(s) -
Paternostro Rafael,
Kapzan Lea,
Mandorfer Mattias,
Schwarzer Remy,
Benedikt Schaefer,
Viveiros André,
Bauer David,
Ferlitsch Monika,
Zoller Heinz,
Trauner Michael,
Ferlitsch Arnulf
Publication year - 2020
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.14988
Subject(s) - medicine , anemia , cirrhosis , gastroenterology , decompensation , transferrin saturation , model for end stage liver disease , cohort , retrospective cohort study , liver disease , hemoglobin , iron deficiency , liver transplantation , transplantation
Background and Aim 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. Methods Consecutive cirrhotic patients from a prospective registry study were included. Anemia was defined as hemoglobin concentration ≤ 12 g/dL. IDA was defined as Hb ≤ 12 g/dL + transferrin‐saturation < 20%. 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. Results Two hundred forty‐two patients with compensated ( n  = 53 [21.9%]) and decompensated (n = 189 [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–Pugh Score (CPS; A: 26.5%, B: 59.2%, C: 69%; P  < 0.001) and with decompensated cirrhosis(62.4% vs 18.8%, P  < 0.001). Within anemic patients, a higher proportion of patients in CPS A/B vs C (73% vs 35%; P  = 0.025) and in compensated cirrhosis (80% vs 46.6%; P  = 0.043) were found with IDA. Model for End‐Stage Liver Disease (MELD) scores were significantly lower in patients with IDA (14.4 vs 17.9 non‐ID‐anemia; P  = 0.005). Similar results were found in the validation cohort: median MELD (16[8–28]non‐IDA vs 12 [7–23] IDA; P  < 0.001) and within anemic patients IDA was more common in patients with MELD <15 (58%) versus >15 (24%, P  < 0.001). Anemia was associated with a significant risk for hepatic decompensation and/or mortality both in the validation (aSHR: 1.65, P  = 0.008) and in the derivation cohort (aSHR: 2.11, P < 0.001) and an independent risk factor for hepatic decompensation and/or mortality in compensated patients (aHR: 4.91, P  = 0.004). Conclusion 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‐term follow up.

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