Anemia and iron deficiency in compensated and decompensated cirrhosis: Prevalence and impact on clinical outcomes.


Journal

Journal of gastroenterology and hepatology
ISSN: 1440-1746
Titre abrégé: J Gastroenterol Hepatol
Pays: Australia
ID NLM: 8607909

Informations de publication

Date de publication:
Sep 2020
Historique:
received: 15 04 2019
revised: 19 12 2019
accepted: 22 01 2020
pubmed: 24 1 2020
medline: 5 11 2020
entrez: 24 1 2020
Statut: ppublish

Résumé

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. 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. 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). 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.

Sections du résumé

BACKGROUND AND AIM OBJECTIVE
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 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 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 CONCLUSIONS
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.

Identifiants

pubmed: 31972057
doi: 10.1111/jgh.14988
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1619-1627

Informations de copyright

© 2020 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.

Références

Camaschella C. Iron-deficiency anemia. N Engl J MedThe New England journal of medicine 2015; 372: 1832-1843.
Polin V, Coriat R, Perkins G et al. Iron deficiency: from diagnosis to treatment. Digestive and liver disease: official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver 2013; 45: 803-809.
Qamar AA, Grace ND, Groszmann RJ et al. Incidence, prevalence, and clinical significance of abnormal hematologic indices in compensated cirrhosis. Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 2009; 7: 689-695.
Cirera I, Elizalde JI, Pique JM et al. Anemia worsens hyperdynamic circulation of patients with cirrhosis and portal hypertension. Dig Dis SciDigestive diseases and sciences 1997; 42: 1697-1702.
Cirera I, Panes J, Bordas JM et al. Anemia increases gastric blood flow in noncirrhotic and cirrhotic patients. Gastrointest EndoscGastrointestinal endoscopy 1995; 42: 403-407.
Gonzalez-Casas R, Jones EA, Moreno-Otero R. Spectrum of anemia associated with chronic liver disease. World J Gastroenterol: WJGWorld journal of gastroenterology: WJG 2009; 15: 4653-4658.
Stein J, Connor S, Virgin G, Ong DE, Pereyra L. Anemia and iron deficiency in gastrointestinal and liver conditions. World J Gastroenterol: WJGWorld journal of gastroenterology: WJG 2016; 22: 7908-7925.
Maiwall R, Kumar S, Chaudhary AK et al. Serum ferritin predicts early mortality in patients with decompensated cirrhosis. J HepatolJournal of hepatology 2014; 61: 43-50.
Walker NM, Stuart KA, Ryan RJ et al. Serum ferritin concentration predicts mortality in patients awaiting liver transplantation. Hepatology (Baltimore, Md) 2010; 51: 1683-1691.
Viveiros A, Finkenstedt A, Schaefer B et al. Transferrin as a predictor of survival in cirrhosis. Liver transplantation: official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society 2017.
Bruns T, Nuraldeen R, Mai M et al. Low serum transferrin correlates with acute-on-chronic organ failure and indicates short-term mortality in decompensated cirrhosis. Liver international: official journal of the International Association for the Study of the Liver 2017; 37: 232-241.
Zareifar S, Dehghani SM, Rahanjam N, Farahmand Far MR. Prevalence of iron deficiency anemia in children with liver cirrhosis: a cross-sectional study. International journal of hematology-oncology and stem cell research 2015; 9: 128-132.
Intragumtornchai T, Rojnukkarin P, Swasdikul D, Israsena S. The role of serum ferritin in the diagnosis of iron deficiency anaemia in patients with liver cirrhosis. J Intern MedJournal of internal medicine 1998; 243: 233-241.
Ryan JD, Chin JL, Crowe J. Ferritin in decompensated cirrhosis: iron or inflammation? J HepatolJournal of hepatology 2015; 62: 499-500.
Pietrangelo A. Iron and the liver. Liver international: official journal of the International Association for the Study of the Liver 2016; 36: 116-123.
EASL. clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. J Hepatol 2010; 53: 397-417.
Vilstrup H, Amodio P, Bajaj J et al. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver. Hepatology (Baltimore, Md) 2014; 60: 715-735.
Reiberger T, Puspok A, Schoder M et al. Austrian consensus guidelines on the management and treatment of portal hypertension (Billroth III). Wien Klin WochenschrWiener klinische Wochenschrift 2017; 129: 135-158.
de Franchis R. Expanding consensus in portal hypertension: report of the Baveno VI Consensus Workshop: stratifying risk and individualizing care for portal hypertension. J HepatolJournal of hepatology 2015; 63: 743-752.
D'Amico G, Garcia-Tsao G, Pagliaro L. Natural history and prognostic indicators of survival in cirrhosis: a systematic review of 118 studies. J HepatolJournal of hepatology 2006; 44: 217-231.
Child CTJ. Surgery and portal hypertension. In: Child C, ed. The Liver and Portal Hypertension. Philadelphia: Saunders, 1964.
Kamath PS, Kim WR. The model for end-stage liver disease (MELD). Hepatology (Baltimore, Md) 2007; 45: 797-805.
https://optn.transplant.hrsa.gov/media/1575/policynotice_20151101.pdf.
Kalaitzakis E, Josefsson A, Castedal M et al. Hepatic encephalopathy is related to anemia and fat-free mass depletion in liver transplant candidates with cirrhosis. Scand J GastroenterolScandinavian journal of gastroenterology 2013; 48: 577-584.
Tandon P, Raman M, Mourtzakis M, Merli M. A practical approach to nutritional screening and assessment in cirrhosis. Hepatology (Baltimore, Md) 2017; 65: 1044-1057.
Lai JC, Covinsky KE, McCulloch CE, Feng S. The liver frailty index improves mortality prediction of the subjective clinician assessment in patients with cirrhosis. Am J GastroenterolThe American journal of gastroenterology 2018; 113: 235-242.
Durand F, Buyse S, Francoz C et al. Prognostic value of muscle atrophy in cirrhosis using psoas muscle thickness on computed tomography. J HepatolJournal of hepatology 2014; 60: 1151-1157.
Paternostro R, Lampichler K, Bardach C et al. The value of different CT-based methods for diagnosing low muscle mass and predicting mortality in patients with cirrhosis. Liver international: official journal of the International Association for the Study of the Liver 2019.
Nahon P, Nuraldeen R, Rufat P, Sutton A, Trautwein C, Strnad P. In alcoholic cirrhosis, low-serum hepcidin levels associate with poor long-term survival. Liver international: official journal of the International Association for the Study of the Liver 2016; 36: 185-188.
Weismuller TJ, Kirchner GI, Scherer MN et al. Serum ferritin concentration and transferrin saturation before liver transplantation predict decreased long-term recipient survival. Hepatology (Baltimore, Md) 2011; 54: 2114-2124.
Piano S, Tonon M, Vettore E et al. Incidence, predictors and outcomes of acute-on-chronic liver failure in outpatients with cirrhosis. J HepatolJournal of hepatology 2017; 67: 1177-1184.
Bernardi M, Moreau R, Angeli P, Schnabl B, Arroyo V. Mechanisms of decompensation and organ failure in cirrhosis: from peripheral arterial vasodilation to systemic inflammation hypothesis. J HepatolJournal of hepatology 2015; 63: 1272-1284.
Moller S, Bendtsen F. The pathophysiology of arterial vasodilatation and hyperdynamic circulation in cirrhosis. Liver international: official journal of the International Association for the Study of the Liver 2017.

Auteurs

Rafael Paternostro (R)

Vienna Hepatic Hemodynamic Lab, Divison of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Lea Kapzan (L)

Vienna Hepatic Hemodynamic Lab, Divison of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Mattias Mandorfer (M)

Vienna Hepatic Hemodynamic Lab, Divison of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Remy Schwarzer (R)

Vienna Hepatic Hemodynamic Lab, Divison of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Schaefer Benedikt (S)

Division for Internal Medicine I, Medical University of Innsbruck, Innsbruck, Austria.

André Viveiros (A)

Division for Internal Medicine I, Medical University of Innsbruck, Innsbruck, Austria.

David Bauer (D)

Vienna Hepatic Hemodynamic Lab, Divison of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Monika Ferlitsch (M)

Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Heinz Zoller (H)

Division for Internal Medicine I, Medical University of Innsbruck, Innsbruck, Austria.

Michael Trauner (M)

Vienna Hepatic Hemodynamic Lab, Divison of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Arnulf Ferlitsch (A)

Vienna Hepatic Hemodynamic Lab, Divison of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Department of Internal Medicine I, KH Barmherzige Brüder Vienna, Vienna, Austria.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH