• community-acquired pneumonia
• health care–associated pneumonia
• hemoglobin
• mortality

• Humans
• Community-Acquired Infections/mortality
• Community-Acquired Infections/blood
• Community-Acquired Infections/epidemiology
• Pneumonia/mortality
• Pneumonia/blood
• Pneumonia/complications
• Pneumonia/epidemiology
• Hemoglobins/analysis
• Male
• Female
• Middle Aged
• Aged
• Prospective Studies
• Risk Factors
• Adult
• Aged, 80 and over
• Anemia/epidemiology
• Community-Acquired Pneumonia

• 20232BAB216039 Jiangxi Provincial Natural Science Foundation

• ESA resistance
• anemia
• chronic kidney disease
• gut dysbiosis
• inflammation
• uremic toxins

• Humans
• Dysbiosis
• Renal Insufficiency, Chronic/microbiology
• Renal Insufficiency, Chronic/metabolism
• Renal Insufficiency, Chronic/complications
• Gastrointestinal Microbiome/drug effects
• Anemia/drug therapy
• Anemia/etiology
• Anemia/microbiology
• Animals
• Probiotics/therapeutic use
• Prebiotics

• Fenton Reaction
• Iron Chelator
• Iron Metabolism
• Nanotechnology
• Sepsis-associated Encephalopathy

• Humans
• Iron/metabolism
• Animals
• Sepsis-Associated Encephalopathy/metabolism
• Iron Chelating Agents/therapeutic use
• Iron Chelating Agents/pharmacology

• 82160364 National Natural Science Foundation of China
• 20202ACBL206007 Project of the Jiangxi Provincial Department of Science and Technology

• Humans
• Erythrocytes/metabolism
• Neoplasms/therapy
• Neoplasms/diagnosis
• Neoplasms/pathology
• Precision Medicine
• Animals
• Drug Delivery Systems
• Erythrocyte Membrane/chemistry
• Erythrocyte Membrane/metabolism
• Biomimetic Materials/chemistry

• anemia
• chronic kidney disease
• end-stage kidney disease
• iron overload
• magnet resonance imaging

• anemia
• chronic kidney disease
• erythropoietin
• ferritin
• hemoglobin
• iron

• Adrenergic Beta-Antagonists
• anaemia
• angiotensin receptor antagonists
• angiotensin-converting enzyme inhibitors
• heart failure
• mineralocorticoid receptor antagonists
• sodium-glucose transporter 2 inhibitors

• CRP
• Kawasaki disease
• Z scores of Hb
• age
• bacteremia
• children
• hemoglobin

• CMRPG8M1441 Chang Gung Memorial Hospital

• CKD
• SGLT2i
• low protein diet
• low sodium diet
• nutrition
• phosphate
• proteinuria

• HIF-PH inhibitors
• anemia
• cardiorenal syndrome
• erythropoiesis-stimulating agents
• hepcidin antagonists
• iron therapy

• Anemia
• Chronic kidney disease
• Hepcidin
• Iron
• Vitamin D

• bone marrow microenvironment (BMME)
• hematopoietic stem cell (HSC)
• hematopoietic stem cell transplantation
• poor graft function
• prognosis

This study aimed to investigate whether serum indicators related to iron stores in the body are associated with clinical and endoscopic disease severity. Eighty-four patients with Crohn’s disease (CD) and twenty-four healthy volunteers were included. The indicators related to iron stores were detected within one week after endoscopic and CT enterography examinations. Patients were divided into three groups according to the CDAI(Crohn's disease activity index)scores. Serum iron levels were decreased in all groups (p < 0.05), and the values of remission group were higher than those of moderate group (p < 0.001). The total iron binding capacity(TIBC)values of the moderate group were lower than those of the controls and the other groups (p < 0.05). None of the indicators differed significantly among the patients classified by SES-CD (p > 0.05). Underweight, decreased serum iron and TIBC were independent risk factors for moderate clinical disease. Combined detection of decreased serum iron and TIBC was helpful in differentiating severe patients. The sensitivity and specificity were 32.7% and 100%, respectively (AUC = 0.812, p < 0.01). Decreases in serum iron and TIBC were associated with the clinical activity of CD. Combined detection of the two indicators was conducive to screening serious disease.

• COVID 19
• HIF prolyl-hydroxylase inhibitor
• HIF stabilizer
• anemia
• chronic kidney disease
• erythropoiesis-stimulating agents
• hepcidin
• iron

Anemia is a significant comorbidity for older adults not fully attributable to iron deficiency. Low-grade inflammation and other micronutrient deficiencies also contribute. This cross-sectional study examined the relationships between nutrient and non-nutrient factors with hemoglobin and anemia in 285 residents (>65 years) of 16 New Zealand aged-care facilities. Blood samples were analyzed for hemoglobin, ferritin, sTfR, hepcidin, zinc, selenium, and interleukin-6 (IL-6), (with ferritin, sTfR, zinc and selenium adjusted for inflammation). Linear regression models examined the relationships between micronutrient biomarkers (iron, zinc, selenium, vitamin B-12 and D), age, sex, and health factors with hemoglobin. Thirty-two percent of participants exhibited anemia, although <2% had either depleted iron stores or iron deficiency. Plasma zinc and selenium deficiencies were present in 72% and 38% of participants, respectively. Plasma zinc and total body iron (TBI) were positively associated (p < 0.05) with hemoglobin, while gastric acid suppressing medications, hepcidin, and interleukin-6 were inversely associated. These relationships were maintained after the application of anemia cut-offs. These findings emphasize the importance of considering multiple micronutrient deficiencies as risk factors for anemia.

• anemia
• anti-secretory medications
• inflammation
• interleukin-6
• nursing home
• proton pump inhibitors
• soluble transferrin receptor
• total body iron

• Aged
• Cardiovascular Diseases/blood
• Cardiovascular Diseases/diagnosis
• Cardiovascular Diseases/etiology
• Cerebrovascular Disorders/blood
• Cerebrovascular Disorders/diagnosis
• Cerebrovascular Disorders/etiology
• Female
• Ferritins/blood
• Humans
• Iron/blood
• Male
• Middle Aged
• Prognosis
• Proportional Hazards Models
• Renal Dialysis/adverse effects
• Risk Factors
• Transferrin/analysis

• Astellas Pharma
• Chugai Pharmaceutical

Anemia is frequently observed in the course of chronic kidney disease (CKD) and it is associated with diminishing the quality of a patient’s life. It also enhances morbidity and mortality and hastens the CKD progression rate. Patients with CKD frequently suffer from a chronic inflammatory state which is related to a vast range of underlying factors. The results of studies have demonstrated that persistent inflammation may contribute to the variability in Hb levels and hyporesponsiveness to erythropoietin stimulating agents (ESA), which are frequently observed in CKD patients. The understanding of the impact of inflammatory cytokines on erythropoietin production and hepcidin synthesis will enable one to unravel the net of interactions of multiple factors involved in the pathogenesis of the anemia of chronic disease. It seems that anti-cytokine and anti-oxidative treatment strategies may be the future of pharmacological interventions aiming at the treatment of inflammation-associated hyporesponsiveness to ESA. The discovery of new therapeutic approaches towards the treatment of anemia in CKD patients has become highly awaited. The treatment of anemia with erythropoietin (EPO) was associated with great benefits for some patients but not all.

• ESA hyporesponsiveness
• anemia
• anemia of inflammation
• chronic kidney disease
• inflammation

Anemia is one of the most common complications of sepsis. Sepsis-related anemia is associated mainly with inflammation. We aimed to observe the changes in the inflammatory anemia-associated parameters of patients with sepsis in the early stage of intensive care unit (ICU) admission and to evaluate their association with 28-day mortality.

A total of 198 patients with sepsis were divided into survivor (n = 110) and non-survivor (n = 88) groups on the basis of 28-day survival. Healthy volunteers (n = 20) were enrolled as a control group. Plasma levels of iron, ferritin, erythropoietin (EPO), soluble transferrin receptor (sTfR), hepcidin, interleukin-6 (IL-6), hemoglobin and the red blood cell distribution width (RDW) were measured on days 1, 3 and 7 of ICU admission. Clinical data and laboratory findings were collected, and the Sequential Organ Failure Assessment (SOFA) score was calculated.

Patients with sepsis showed significant decreases in hemoglobin, plasma iron and sTfR/log ferritin and significant increases in plasma EPO, sTfR, hepcidin, ferritin and IL-6 on days 1, 3 and 7 of ICU admission compared with healthy volunteers. Hemoglobin was correlated negatively with plasma IL-6 and hepcidin. In patients with sepsis, non-survivors had significantly lower plasma iron, EPO and sTfR/log ferritin, but higher plasma hepcidin, ferritin and IL-6 than survivors on days 1, 3 and 7 of ICU admission. Plasma EPO, hepcidin, ferritin, IL-6, sTfR/log ferritin, the RDW and SOFA score were associated significantly with 28-day mortality but to a varying extent. In particular, in predicting 28-day mortality, plasma hepcidin had an area under the receiver operating curve of 0.808 and 87.3% specificity, which was the highest among the inflammatory anemia-associated parameters tested.

Inflammatory anemia-associated parameters changed significantly in patients with sepsis in the first week of ICU admission. Plasma EPO, hepcidin, ferritin, IL-6, sTfR/log ferritin, the RDW and SOFA score were associated significantly with 28-day mortality. Plasma hepcidin might have a superior predictive value, with high specificity, compared with other inflammatory anemia-associated parameters for 28-day mortality of sepsis patients in the ICU.

The online version of this article (10.1186/s13613-019-0542-7) contains supplementary material, which is available to authorized users.

• Erythropoietin
• Hepcidin
• Iron metabolism
• Mortality
• Sepsis

The aim of this study was to assess the influence of active tobacco smoke exposure in utero on the concentration of hepcidin and selected iron markers in umbilical cord blood and to evaluate the relationships between these parameters. Newborns of smoking mothers had significantly lower concentrations of serum hepcidin (p < 0.001), iron, and ferritin (p = 0.043; p = 0.042, respectively), but higher levels of erythropoietin (EPO, p < 0.001) and soluble transferrin receptor (sTfR, p = 0.011) compared with newborns of non-smoking women. Negative correlations between cotinine and the number of cigarettes smoked per day with hepcidin serum level (r = −0.33, p = 0.033, r = −0.32, p = 0.041, respectively) and EPO (r = 0.47, p = 0.002; r = 0.46, p = 0.003, respectively) were found. Univariate analysis defined for the whole group of children revealed significant associations between the concentration of hepcidin and other iron status parameters. In the models estimated separately for smokers and non-smokers, we found relations between the level of hepcidin and erythropoietin (B = −0.23, p = 0.004; B = −0.46, p = 0.01, respectively). In the multivariate regression model, a negative association between hepcidin and EPO concentrations in the whole group of newborns (β = −0.53; p = 0.001) and in the group of smokers (β = −0.57; p = 0.011) was confirmed. The present study shows significant relations between smoking during pregnancy and hepcidin levels in children born at term. Decreased cord serum concentrations of hepcidin associated with high erythropoietin levels suggest induced fetal erythropoiesis, probably due to the hypoxic effects imposed by maternal smoking.

• cord blood
• erythropoietin
• hepcidin
• iron
• soluble transferrin receptor
• tobacco smoke

• Indonesia
• anemia
• hemoglobin
• infants
• iron
• micronutrient biomarkers
• retinol-binding protein

To specify the type and prevalence of anemia along with a treatment approach for inflammatory bowel disease (IBD).

We conducted a retrospective study on 465 patients who were diagnosed with IBD and followed up at our hospital from June 2015 to June 2016 [male: 254, female: 211; average age: 47 ± 14.4; Crohn’s disease (CD): 257, Ulcerative Colitis (UC): 208]. Epidemiological and clinical data, such as sex, age, age of diagnosis, type of IBD, disease extension, disease behavior and duration, treatments for IBD and anemia, and surgical history were obtained for each patient. Per World Health Organization guidelines, anemia was diagnosed for males if hemoglobin values were less than 13 g/dL and for females if hemoglobin values were less than 12 g/dL.

We determined that 51.6% of the patients had anemia, which was more frequent in women then men (64% vs 41.3%, P < 0.001). Anemia frequency was higher in CD cases (57.6%) than in UC cases (44.2%) (P = 0.004). CD involvements were as follows: 48.2% in ileal involvement, 19% in colonic involvement, and 32.8% in ileocolonic involvement. Furthermore, 27.5% of UC patients had proctitis (E1) involvement, 41% of them had involvement in left colitis (E2), and 31.5% had pancolitis involvement. There was no significant relationship between anemia frequency and duration of disease (P = 0.55). Iron deficiency anemia (IDA) was the most common type of anemia in this cohort. Moreover, because anemia parameters have not been evaluated during follow-up of 15.3% of patients, the etiology of anemia has not been clarified. Fifty percent of patients with anemia received treatment. Twenty-three percent of IDA patients had oral iron intake and forty-one percent of IDA patients had parenteral iron treatment. Fifty-three percent of patients who were suffering from megaloblastic anemia received B₁₂/folic acid treatment.

We found out that almost half of all IBD patients (51.6%) had anemia, the most frequent of which was IDA. Almost half of these patients received treatment. We should increase the treatment rate in our IBD patients that have anemia.

• Anemia
• Inflammatory bowel disease
• Anemia of iron deficiency

• Adolescent
• Adult
• Aged
• Aged, 80 and over
• Anemia/blood
• Anemia/epidemiology
• Anemia/etiology
• Anemia/therapy
• C-Reactive Protein/analysis
• Colitis, Ulcerative/blood
• Colitis, Ulcerative/complications
• Colitis, Ulcerative/therapy
• Crohn Disease/blood
• Crohn Disease/complications
• Crohn Disease/therapy
• Female
• Gastrointestinal Agents/therapeutic use
• Hematinics/therapeutic use
• Hemoglobins/analysis
• Humans
• Male
• Middle Aged
• Prevalence
• Retrospective Studies
• Sex Factors
• Turkey/epidemiology
• Young Adult

• Hospitalized heart failure
• Iron deficiency
• Prognosis

• Aged
• Aged, 80 and over
• Anemia, Iron-Deficiency/blood
• Anemia, Iron-Deficiency/diagnosis
• Anemia, Iron-Deficiency/mortality
• Cohort Studies
• Female
• Ferritins/blood
• Follow-Up Studies
• Heart Failure/blood
• Heart Failure/diagnosis
• Heart Failure/mortality
• Hospitalization/trends
• Humans
• Male
• Prospective Studies
• Registries
• Time Factors
• Transferrin/metabolism
• Treatment Outcome

Kawasaki disease (KD) is an autoimmune-like disease and acute childhood vasculitis syndrome that affects various systems but has unknown etiology. In addition to the standard diagnostic criteria, anemia is among the most common clinical features of KD patients and is thought to have a more prolonged duration of active inflammation. In 2001, the discovery of a liver-derived peptide hormone known as hepcidin began revolutionizing our understanding of anemia’s relation to a number of inflammatory diseases, including KD. This review focuses on hepcidin-induced iron deficiency’s relation to transient hyposideremia, anemia, and disease outcomes in KD patients, and goes on to suggest possible routes of further study.

• Kawasaki disease
• anemia
• hepcidin
• iron deficiency

• Age Factors
• Anemia/diagnosis
• Anemia/etiology
• Anemia, Iron-Deficiency/diagnosis
• Anemia, Iron-Deficiency/etiology
• Animals
• Biomarkers
• Coronary Vessels/metabolism
• Coronary Vessels/pathology
• Hepcidins/blood
• Humans
• Iron/metabolism
• Macrophages/immunology
• Macrophages/metabolism
• Mucocutaneous Lymph Node Syndrome/blood
• Mucocutaneous Lymph Node Syndrome/complications
• Mucocutaneous Lymph Node Syndrome/epidemiology
• Mucocutaneous Lymph Node Syndrome/therapy

We aim to review the literature and provide guidance on preventive health measures in inflammatory bowel disease (IBD). Structured searches were performed in PubMed, MEDLINE, EMBASE, Web of Science and Cochrane Library from January 1976 to June 2016 using the following keywords: (inflammatory bowel disease OR Crohn’s disease OR ulcerative colitis) AND (health maintenance OR preventive health OR health promotion). Abstracts of the articles selected from each of these multiple searches were reviewed, and those meeting the inclusion criteria (that is, providing data regarding preventive health or health maintenance in IBD patients) were recorded. Reference lists from the selected articles were manually reviewed to identify further relevant studies. Patients with IBD are at increased risk of developing adverse events related to the disease course, therapeutic interventions, or non-adherence to medication. Recent studies have suggested that IBD patients do not receive preventive services with the same thoroughness as patients with other chronic diseases. Preventive health measures can avert morbidity and improve the quality of life of patients with IBD. Gastroenterologists and primary care physicians (PCPs) should have an up to date working knowledge of preventive health measures for IBD patients. A holistic approach and better communication between gastroenterologists and PCPs with explicit clarification of roles will prevent duplication of services and streamline care.

• Health maintenance
• Prevention
• Ulcerative colitis
• Crohn’s disease

• Adrenal Cortex Hormones/therapeutic use
• Anemia/diagnosis
• Bone Diseases, Metabolic/prevention & control
• Cardiovascular System
• Chronic Disease
• Colitis, Ulcerative/therapy
• Communication
• Crohn Disease/therapy
• Dietary Supplements
• Exercise
• Humans
• Inflammatory Bowel Diseases/therapy
• Neoplasms/complications
• Neoplasms/prevention & control
• Nutritional Sciences
• Osteoporosis/prevention & control
• Patient Compliance
• Preventive Health Services/methods
• Quality of Life
• Sleep Wake Disorders
• Smoking Cessation
• Vaccination
• Venous Thromboembolism/prevention & control
• Vitamin D/therapeutic use

• Inflammatory bowel disease
• anemia
• iron deficiency

• Kawasaki disease
• anemia
• hepcidin
• iron

• Adolescent
• Anemia, Iron-Deficiency/blood
• Anemia, Iron-Deficiency/complications
• Case-Control Studies
• Female
• Hemoglobins/metabolism
• Hepcidins/blood
• Hepcidins/urine
• Humans
• Immunoglobulins, Intravenous/therapeutic use
• Interleukin-6/blood
• Iron/blood
• Iron Deficiencies
• Male
• Mucocutaneous Lymph Node Syndrome/blood
• Mucocutaneous Lymph Node Syndrome/complications
• Mucocutaneous Lymph Node Syndrome/drug therapy

Stunting, anemia and inflammation are frequently observed in children with end-stage renal disease (ESRD).

To assess anthropometric, hematological and inflammatory data and to study their potential interrelationship in Guatemalan juveniles undergoing hemodialysis (HD) and peritoneal dialysis (PD).

54 juveniles 7–20 years of age were recruited in FUNDANIER, Guatemala City: 27 on HD and 27 PD. Hemoglobin, serum iron, transferrin, serum transferrin receptor (sTfR), serum ferritin, transferrin saturation and iron-binding capacity, white blood cell count (WBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), as well as IL-6, IL-1 and TNF-α, weight and height were determined by standard methods. Hepcidin–25 (Hep-25) was assessed by weak cation exchange time-of-flight mass-spectrometry.

92% and 55% of HD and PD children, respectively, were stunted and 95% and 85% were anemic. Among iron status biomarkers, serum ferritin was massively increased and significantly higher in the HD group compared to the PD group. Hep-25 was also greatly elevated in both groups. 41% of HD patients showed increments in three or more inflammatory biomarkers, while it was 2 or less in all PD subjects.

The degree of stunting, the prevalence and severity of anemia in Guatemalan juvenile ESRD far exceed the national statistics for this low-income Central American country. Ferritin and Hep-25 concentrations were elevated, with the latter to an extraordinary magnitude. Additional biomarkers of inflammation not directly related to iron status were elevated as well. The role of both disease- and environment-related factors in combination best explains the magnitude of the biomarker abnormalities.

• Ferritin
• Hepcidin
• Inflammatory bowel disease
• Intravenous iron
• Iron deficiency anemia
• Oral iron

Anemia is a common extraintestinal manifestation of inflammatory bowel disease (IBD) and is frequently overlooked as a complication. Patients with IBD are commonly found to have iron deficiency anemia (IDA) secondary to chronic blood loss, and impaired iron absorption due to tissue inflammation. Patients with iron deficiency may not always manifest with signs and symptoms; so, hemoglobin levels in patients with IBD must be regularly monitored for earlier detection of anemia. IDA in IBD is associated with poor quality of life, necessitating prompt diagnosis and appropriate treatment. IDA is often associated with inflammation in patients with IBD. Thus, commonly used laboratory parameters are inadequate to diagnose IDA, and newer iron indices, such as reticulocyte hemoglobin content or percentage of hypochromic red cells or zinc protoporphyrin, are required to differentiate IDA from anemia of chronic disease. Oral iron preparations are available and are used in patients with mild disease activity. These preparations are inexpensive and convenient, but can produce gastrointestinal side effects, such as abdominal pain and diarrhea, that limit their use and patient compliance. These preparations are partly absorbed due to inflammation. Non-absorbed iron can be toxic and worsen IBD disease activity. Although cost-effective intravenous iron formulations are widely available and have improved safety profiles, physicians are reluctant to use them. We present a review of the pathophysiologic mechanisms of IDA in IBD, improved diagnostic and therapeutic strategies, efficacy, and safety of iron replacement in IBD.

• Iron deficiency anemia
• Inflammatory bowel disease
• Hepcidin
• Ferritin
• Oral iron
• Intravenous iron

Approximately 10% of patients treated with erythropoiesis‐stimulating agents (ESAs) for the anemia of chronic kidney disease are unresponsive or relatively resistant to therapy. The etiology of this is usually linked to iron deficiency or an independent underlying illness. We describe a hemodialysis patient with a failed renal transplant 1.5 years earlier, who developed progressive erythropoietin resistance and anemia without an apparent cause. He simultaneously developed nonspecific malaise and fatigue. By exclusion, the only possible cause of these signs and symptoms was inflammation from acute and chronic rejection in the retained failed renal allograft. Following pulse steroids and transplant nephrectomy, the patient's symptoms resolved and both his hemoglobin improved and his erythropoietin requirements decreased significantly. The patient never required a blood transfusion and was successfully relisted for a deceased donor renal transplant. Hence, inflammation from a retained transplant allograft may be an under‐recognized cause of erythropoietin resistance in dialysis patients. Although transplant nephrectomy remains a controversial practice due to concerns of alloantibody production, it may be considered in patients with failed renal allografts and anemia refractory to treatment with ESAs.

In patients undergoing maintenance hemodialysis (HD), hyporesponsiveness to erythropoiesis stimulating agents (ESAs) is associated with adverse clinical outcomes. Systemic inflammation is highly prevalent in HD patients and is associated with ESA hyporesponsiveness. Oxidative stress is also highly prevalent in HD patients, but no previous study has determined its association with ESA response. This study assessed the association of plasma markers of oxidative stress and inflammation with ESA resistance in patients undergoing maintenance HD.

We analyzed data from 165 patients enrolled in the Provision of Antioxidant Therapy in Hemodialysis study, a randomized controlled trial evaluating antioxidant therapy in prevalent HD patients. Linear and mixed-effects regression were used to assess the association of baseline and time-averaged high sensitivity F2-isoprostanes, isofurans, C-reactive protein (hsCRP), and interleukin-6 (IL-6) with ESA resistance index (ERI), defined as the weekly weight-adjusted ESA dose divided by blood hemoglobin level. Unadjusted models as well as models adjusted for potential confounders were examined. Predicted changes in ERI per month over study follow-up among baseline biomarker quartiles were also assessed.

Patients with time-averaged isofurans in the highest quartile had higher adjusted mean ERI compared with patients in the lowest quartile (β = 14.9 ng/ml; 95 % CI 7.70, 22.2; reference group <0.26 ng/ml). The highest quartiles of hsCRP and IL-6 were also associated with higher adjusted mean ERI (β = 10.8 mg/l; 95 % CI 3.52, 18.1 for hsCRP; β = 10.2 pg/ml; 95 % CI 2.98, 17.5 for IL-6). No significant association of F2-isoprostanes concentrations with ERI was observed. Analyses restricted to baseline exposures and ERI showed similar results. Baseline hsCRP, IL-6, and isofurans concentrations in the highest quartiles were associated with greater predicted change in ERI over study follow-up compared to the lowest quartiles (P = 0.008, P = 0.004, and P = 0.04, respectively). There was no association between baseline F2-isoprostanes quartile and change in ERI.

In conclusion, higher concentrations of isofurans, hsCRP and IL-6, but not F2-isoprostanes, were associated with greater resistance to ESAs in prevalent HD patients. Further research is needed to test whether interventions that successfully decrease oxidative stress and inflammation in patients undergoing maintenance HD improve ESA responsiveness.

The online version of this article (doi:10.1186/s12882-015-0074-9) contains supplementary material, which is available to authorized users.

Elevated iron stores as indicated by hyperferritinemia with normal or mildly elevated transferrin saturation and mostly mild hepatic iron deposition are a characteristic finding in subjects with non-alcoholic fatty liver disease (NAFLD). Excess iron is observed in approximately one third of NAFLD patients and is commonly referred to as the “dysmetabolic iron overload syndrome”. Clinical evidence suggests that elevated body iron stores aggravate the clinical course of NAFLD with regard to liver-related and extrahepatic disease complications which relates to the fact that excess iron catalyses the formation of toxic hydroxyl-radicals subsequently resulting in cellular damage. Iron removal improves insulin sensitivity, delays the onset of type 2 diabetes mellitus, improves pathologic liver function tests and likewise ameliorates NAFLD histology. Several mechanisms contribute to pathologic iron accumulation in NAFLD. These include impaired iron export from hepatocytes and mesenchymal Kupffer cells as a consequence of imbalances in the concentrations of iron regulatory factors, such as hepcidin, cytokines, copper or other dietary factors. This review summarizes the knowledge about iron homeostasis in NAFLD and the rationale for its therapeutic implications.

• Dysmetabolic iron overload syndrome
• Hepcidin
• Iron overload
• Metabolic syndrome
• Non-alcoholic fatty liver disease
• Nonalcoholic steatohepatitis

• Anemia
• Epoetin beta pegol
• Ferritin
• Hemodialysis
• Hepcidin-25

• ferritin and hemosiderin
• iron deficiency and overload
• serum ferritin kinetics
• storage iron turnover

Most chronically-infected hepatitis C virus (HCV) patients have increased levels of iron in the liver. Iron overload reduces sustained responses to antiviral therapy, leading to more rapid progression to liver cirrhosis and the development of hepatocellular carcinoma. However, it is still unclear how HIV-1 infection affects iron status in patients chronically infected with HCV. The present study recruited 227 patients from a village in central China. These patients were either monoinfected with HCV (n = 129) or coinfected with HCV/HIV-1 (n = 98). Healthy controls (n = 84) were also recruited from the same village. Indicators of iron status, such as serum levels of iron, ferritin, and transferrin, total iron-binding capacity (TIBC), transferrin saturation (Tfs), and hepcidin, were analyzed and compared across the three groups. The results showed that serum levels of iron (p = 0.001) and ferritin (p = 0.009) and the Tfs (p = 0.002) were significantly higher in HCV-monoinfected patients than in the healthy controls; however, there were no differences in iron levels and Tfs between HCV/HIV-1 coinfected patients and healthy controls. Additionally, although serum hepcidin levels in HCV-monoinfected and HCV/HIV-1-coinfected patients were lower (p<0.001) than those in health controls, the levels in coinfected patients were higher (p = 0.025) than those in HCV-monoinfected patients. Serum iron and ferritin levels in HCV-monoinfected patients were positively correlated with serum ALT/AST. Serum transferrin levels were negatively correlated with ALT/AST levels. The levels of iron in the serum of coinfected patients with a CD4+T-cell count <500/µl were lower than those in patients with a CD4+T-cell count ≥500/µl, whereas serum hepcidin levels showed the opposite trend. Taken together, these results suggest that coinfection with HIV-1 alleviates iron accumulation caused by chronic HCV infection. Our study indicated that determining the status of serum iron and other iron-associated parameters will be helpful to understand the complexity of alternations in iron distribution in HCV/HIV-1-coinfected patients.

• Adult
• China
• Coinfection
• Female
• HIV/immunology
• HIV Infections/blood
• HIV Infections/complications
• HIV Infections/virology
• Hepacivirus/immunology
• Hepatitis C, Chronic/blood
• Hepatitis C, Chronic/complications
• Hepatitis C, Chronic/virology
• Hepcidins/blood
• Humans
• Iron/blood
• Iron-Binding Proteins/blood
• Male
• Middle Aged

Anemia, a common complication associated with inflammatory bowel disease (IBD), is frequently overlooked in the management of IBD patients. Unfortunately, it represents one of the major causes of both decreased quality of life and increased hospital admissions among this population. Anemia in IBD is pathogenically complex, with several factors contributing to its development. While iron deficiency is the most common cause, vitamin B₁₂ and folic acid deficiencies, along with the effects of pro-inflammatory cytokines, hemolysis, drug therapies, and myelosuppression, have also been identified as the underlying etiology in a number of patients. Each of these etiological factors thus needs to be identified and corrected in order to effectively manage anemia in IBD. Because the diagnosis of anemia in IBD often presents a challenge, combinations of several hematimetric and biochemical parameters should be used. Recent studies underscore the importance of determining the ferritin index and hepcidin levels in order to distinguish between iron deficiency anemia, anemia due to chronic disease, or mixed anemia in IBD patients. With regard to treatment, the newly introduced intravenous iron formulations have several advantages over orally-administered iron compounds in treating iron deficiency in IBD. In special situations, erythropoietin supplementation and biological therapies should be considered. In conclusion, the management of anemia is a complex aspect of treating IBD patients, one that significantly influences the prognosis of the disease. As a consequence, its correction should be considered a specific, first-line therapeutic goal in the management of these patients.

• Anemia
• Inflammatory bowel disease
• Iron deficiency
• Anemia of chronic disease
• Erythropoietin

• Anemia/complications
• Anemia, Iron-Deficiency/complications
• Cytokines/metabolism
• Dietary Supplements
• Erythropoietin/therapeutic use
• Ferritins/blood
• Folic Acid Deficiency/complications
• Hemolysis
• Hepcidins/blood
• Humans
• Inflammatory Bowel Diseases/complications
• Iron/administration & dosage
• Prognosis
• Quality of Life
• Vitamin B 12 Deficiency/complications

• Anemia
• Chronic disease
• Hepcidin
• Inflammation
• Iron metabolism

• Anemia/metabolism
• Cell Proliferation
• Cell Survival
• Chronic Disease
• Cytokines/metabolism
• Erythroid Precursor Cells
• Erythropoiesis/physiology
• Hepcidins/metabolism
• Humans
• Inflammation/metabolism
• Iron/metabolism
• Up-Regulation

• hepatocyte growth factor
• hepcidin
• iron
• liver regeneration

• Animals
• Antibodies/immunology
• Antibodies/pharmacology
• Cell Proliferation
• Gene Expression/drug effects
• Gene Expression/genetics
• Hepatectomy/methods
• Hepatocyte Growth Factor/blood
• Hepatocyte Growth Factor/immunology
• Hepatocytes/cytology
• Hepatocytes/metabolism
• Hepcidins/genetics
• Hepcidins/physiology
• Immunohistochemistry
• Interleukin-6/blood
• Iron/blood
• Liver Regeneration/genetics
• Liver Regeneration/physiology
• Male
• Mice, Inbred BALB C
• Proliferating Cell Nuclear Antigen/metabolism
• Reverse Transcriptase Polymerase Chain Reaction
• Time Factors

• Adult
• Antitubercular Agents/therapeutic use
• CD4 Lymphocyte Count
• CD4-Positive T-Lymphocytes/immunology
• CD4-Positive T-Lymphocytes/pathology
• Case-Control Studies
• Disease Progression
• Female
• Ferritins/blood
• HIV Infections/blood
• HIV Infections/complications
• HIV Infections/drug therapy
• HIV Infections/immunology
• Hemoglobins/metabolism
• Hepatitis C/blood
• Hepatitis C/complications
• Hepatitis C/drug therapy
• Hepatitis C/immunology
• Hepcidins/blood
• Humans
• Indonesia
• Iron/blood
• Male
• Prospective Studies
• Tuberculosis, Pulmonary/blood
• Tuberculosis, Pulmonary/complications
• Tuberculosis, Pulmonary/drug therapy
• Tuberculosis, Pulmonary/immunology