Serum hepcidin levels and iron parameters in children with iron deficiency

Choi, Hyoung Soo; Song, Sang Hoon; Lee, Jae Hee; Kim, Hee Jin; Yang, Hye Ran

doi:10.5045/kjh.2012.47.4.286

Cited by 63 publications

(66 citation statements)

References 30 publications

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“…They increase the pro- trols (220.44±49.52ng/mL). This result is not compatible with the literature [1]. This finding can be attributed to the small number of patients with iron-deficiency anemia.…”

Section: Discussioncontrasting

confidence: 56%

“…Although commercial tests are available, the absolute values of hepcidin have not been established. It has been reported that reference values changed according to age, gender and the method used [1,6,11]. Although there are large-scale population studies in adults; there are no studies on children on this scale [6].…”

Section: Discussionmentioning

confidence: 99%

“…It takes place in oxygen transport, protein synthesis, and function of enzymes. Adequate iron stores are necessary for normal childhood growth and development [1,2]. Although the biological importance of iron has been known since ancient times, there have been new developments in the field of absorption and storage of the iron during the the last decade, especially in the last 2-3 years.…”

Section: Introductionmentioning

confidence: 99%

“…However, there are not enough studies investigating the effectiveness of serum hepcidin levels in iron-deficiency anemia and anemia of inflammation in children [1,2,[8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

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Serum hepcidin, iron metabolism and infection parameters in children with anemia of inflammation and with iron deficiency anemia

Duru¹

2014

Turk J Bioch

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Objective: Hepcidin is a key regulator of iron homeostasis. Increased hepcidin concentrations cause iron sequestration in enterocytes and macrophages. The role of hepcidin in children with iron-deficiency anemia and anemia of inflammation is unclear. In this study, we aimed to evaluate the use of serum hepcidin level as an index for iron deficiency and inflammation anemia in pediatric population. Furthermore, hepcidin is also known to be an acute-phase reactant induced by interleukin-6 (IL-6) during infection. Therefore, we investigated the relationships between hepcidin and inflammatory markers. Methods: This study included 50 children with anemia (13 with iron deficiency and 37 with inflammation) and 17 age-and gender-matched healthy children (control group). Parameters related to iron metabolism (ferritin, serum iron and total iron binding capacity), infection (Creactive protein, white blood cell count and neutrophil percentage) and hepcidin levels were measured. Results: Serum hepcidin levels in patients with anemia of inflammation (362.63±132.27 ng/ mL) were significantly higher than in patients with iron-deficiency anemia (234.10±93.59 ng/ mL) and healthy controls (220.44±49.52 ng/mL) (p=0.002, p<0.001, respectively). Serum hepcidin levels were positively correlated with ferritin (r=0.246, p=0.045), leucocytes (r=0.259, p=0.034) and CRP (r=0.426, p<0.001) levels in all children. Conclusion: This study suggested that hepcidin may have the potential advantage of being able to distinguish between anemia of inflammation and iron-deficiency anemia. In addition, serum hepcidin levels are significantly correlated with acute phase reactants and can be more useful marker than CRP which decreases quickly after the onset of an infection. Key Words: Anemia, ferritin, hepcidin, infection, inflammation, iron deficiency Conflict of Interest: Authors have no conflict of interest. ÖZETAmaç: Hepsidin demir metabolizmasının düzenlenmesinde anahtar rol oynar ve enterositlerde ve makrofajlarda demirin sekestrasyonuna yol açar. Demir eksikliği ve inflamasyon anemisi olan çocuklarda hepsidinin rolü açık değildir. Bu çalışmada serum hepsidin düzeylerinin demir eksikliği ve inflamasyon anemisinde bir belirleyici olarak kullanımı pediyatrik popülasyonda çalışıldı. Ayrıca hepsidinin infeksiyonlarda interlökin-6 (IL-6) tarafından indüklenen bir akut faz reaktanı olduğu bilinir. Bu nedenle serum hepsidin düzeyleri ile inflamatuar markerlar arasındaki ilişkiyi araştırdık. Metod: Bu çalışmaya 50 anemili (37'si inflamasyon, 13'ü demir eksikliği) çocuk ve onlarla benzer yaş grubunda ve cinsiyette 17 sağlıklı çocuk (kontrol grubu) alındı. Serum hepsidin düzeyleri, demir metabolizması ile ilgili olarak ferritin, demir ve demir bağlama kapasitesi parametreleri ve infeksiyon belirteçleri olarak da CRP, lökosit sayısı ve nötrofil oranları belirlendi. Bulgular: Serum hepsidin düzeyleri inflamasyon anemili grupta (362,63±132,27 ng/mL) demir eksikliği anemisi (234,10±93,59 ng/mL) ve sağlıklı kontrol grubundan (220,44±49,52 ng/mL) anlamlı ...

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Section: Discussioncontrasting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…However, there are not enough studies investigating the effectiveness of serum hepcidin levels in iron-deficiency anemia and anemia of inflammation in children [1,2,[8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

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Serum hepcidin, iron metabolism and infection parameters in children with anemia of inflammation and with iron deficiency anemia

Duru¹

2014

Turk J Bioch

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“…This phenomenon has also been observed in children with iron deficiency (Choi et al 2012), the most common form of iron deficiency anemia, which is characterized by a reduction of hepcidin. In contrast, Hb concentrations in LC patients correlated negatively with hepcidin levels, which is a type of anemia characterized by induction of hepcidin.…”

Section: Anemia and Hepcidin In Hf Patientsmentioning

confidence: 87%

Liver Congestion in Heart Failure Contributes to Inappropriately Increased Serum Hepcidin despite Anemia

Ohno¹,

Hanawa²,

Jiao³

et al. 2015

Tohoku J. Exp. Med.

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Hepcidin is a key regulator of mammalian iron metabolism and mainly produced by the liver. Hepcidin excess causes iron deficiency and anemia by inhibiting iron absorption from the intestine and iron release from macrophage stores. Anemia is frequently complicated with heart failure. In heart failure patients, the most frequent histologic appearance of liver is congestion. However, it remains unclear whether liver congestion associated with heart failure influences hepcidin production, thereby contributing to anemia and functional iron deficiency. In this study, we investigated this relationship in clinical and basic studies. In clinical studies of consecutive heart failure patients (n = 320), anemia was a common comorbidity (41%). In heart failure patients without active infection and ongoing cancer (n = 30), log-serum hepcidin concentration of patients with liver congestion was higher than those without liver congestion (p = 0.0316). Moreover, in heart failure patients with liver congestion (n = 19), the anemia was associated with the higher serum hepcidin concentrations, which is a type of anemia characterized by induction of hepcidin. Subsequently, we produced a rat model of heart failure with liver congestion by injecting monocrotaline that causes pulmonary hypertension. The monocrotaline-treated rats displayed liver congestion with increase of hepcidin expression at 4 weeks after monocrotaline injection, followed by anemia and functional iron deficiency observed at 5 weeks. We conclude that liver congestion induces hepcidin production, which may result in anemia and functional iron deficiency in some patients with heart failure.

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Effect of Oral Iron Repletion on Exercise Capacity in Patients With Heart Failure With Reduced Ejection Fraction and Iron Deficiency

Lewis

Malhotra

Hernandez

et al. 2017

JAMA

392

298

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Importance Iron deficiency is present in approximately 50% of patients with heart failure with reduced left ventricular ejection fraction (HFrEF) and is an independent predictor of reduced functional capacity and mortality. However, the efficacy of inexpensive, readily available oral iron supplementation in heart failure is unknown. Objective To test whether therapy with oral iron improves peak exercise capacity in patients with HFrEF and iron deficiency. Design, Setting, and Participants Phase 2, double-blind, placebo-controlled randomized clinical trial of patients with HFrEF (<40%) and iron deficiency, defined as serum ferritin level between 15–100 ng/ml or serum ferritin 101-299 ng/ml with transferrin saturation (Tsat) <20%. Patients were enrolled between September 2014 and November 2015 at 23 US sites. Interventions Oral iron polysaccharide (n = 111) or placebo (n = 114), 150 mg twice daily for 16 weeks. Main Outcomes and Measures The primary endpoint was a change in peak oxygen uptake (VO2), from baseline to 16 weeks. Secondary endpoints included changes in six minute walk distance; plasma NT-pro BNP levels; and health status as assessed by Kansas City Cardiomyopathy Questionnaire (KCCQ, range 0-100, higher scores reflect better quality of life). Results Among 225 randomized patients (median age 63 years, 36% women) 203 completed the study. The median baseline peak VO2 was 1196 ml/min (887, 1448 ml/min) in the oral iron group and 1167 ml/min (887, 1449 ml/min) in the placebo group. The primary endpoint, change in peak VO2, did not significantly differ between the oral iron and placebo groups (+23 ml/min vs −2 ml/min; difference, 21 ml/min [95% CI, −34 to +76]; P=.46). Similarly, at 16 weeks there were no significant differences between treatment groups in changes in 6-minute walk distance (−13, −32 to 6m), NT-pro BNP levels (159, −280 to 599 pg/ml), KCCQ Score (1, −2.4 to 4.4) or time to first adverse event (hazard ratio 0.85, 0.56 to 1.31), all p>0.05. Conclusion Among patients with HFrEF with iron deficiency, high-dose oral iron did not improve exercise capacity over 16 weeks. These results do not support use of oral iron supplementation in patients with HFrEF.

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Serum hepcidin levels and iron parameters in children with iron deficiency

Cited by 63 publications

References 30 publications

Serum hepcidin, iron metabolism and infection parameters in children with anemia of inflammation and with iron deficiency anemia

Serum hepcidin, iron metabolism and infection parameters in children with anemia of inflammation and with iron deficiency anemia

Liver Congestion in Heart Failure Contributes to Inappropriately Increased Serum Hepcidin despite Anemia

Effect of Oral Iron Repletion on Exercise Capacity in Patients With Heart Failure With Reduced Ejection Fraction and Iron Deficiency

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