Hepcidin, haemoglobin and ferritin levels in sickle cell anaemia

Ezeh, C O; Ugochukwu, Cynthia C.; Weinstein, J.L.; Okpala, Iheanyi

doi:10.1111/j.1600-0609.2004.00337.x

Cited by 17 publications

(19 citation statements)

References 24 publications

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“…In contrast to the present findings, Kulaksiz et al (2004) reported that haemochromatosis patients had significantly lower serum prohepcidin concentrations than controls, whereas renal patients undergoing haemodialysis had significantly higher concentrations. However, in support of the present observations that serum prohepcidin is relatively consistent across different physiological states, Ezeh et al (2005) demonstrated that serum prohepcidin concentrations in patients with sickle cell anaemia with abnormally high serum ferritin concentration were no different to controls.…”

Section: Discussionsupporting

confidence: 87%

“…The mean serum prohepcidin concentration (214 ng/ml, range 56-902 ng/ml) found in the present study in healthy men aged 40 years and over was higher than that reported in twenty-six healthy male and female subjects (mean 106, range 52-153 ng/ml) (Kulaksiz et al 2004) and in thirty healthy male and female subjects (mean 84 (SD 40)) (Ezeh et al 2005). The present data show no significant correlation between serum prohepcidin and serum ferritin or serum iron.…”

Section: Discussioncontrasting

confidence: 82%

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Serum prohepcidin concentration: no association with iron absorption in healthy men; and no relationship with iron status in men carrying HFE mutations, hereditary haemochromatosis patients undergoing phlebotomy treatment, or pregnant women

et al. 2007

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Serum prohepcidin concentration: no association with iron absorption in healthy men; and no relationship with iron status in men carrying HFE mutations, hereditary haemochromatosis patients undergoing phlebotomy treatment, or pregnant women Hepcidin plays a major role in iron homeostasis, but understanding its role has been hampered by the absence of analytical methods for quantification in blood. A commercial ELISA has been developed for serum prohepcidin, a hepcidin precursor, and there is interest in its potential use in the clinical and research arena. We investigated the association between serum prohepcidin concentration and iron absorption in healthy men, and its relationship with iron status in men carrying HFE mutations, hereditary haemochromatosis patients, and pregnant women. Iron absorption was determined in thirty healthy men (fifteen wild-type, fifteen C282Y heterozygote) using the stable isotope red cell incorporation technique. Iron status was measured in 138 healthy men (ninety-one wild-type, forty-seven C282Y heterozygote), six hereditary haemochromatosis patients, and thirteen pregnant women. Mean serum prohepcidin concentrations were 214 (SD 118) ng/ml [208 (SD 122) ng/ml in wild-type and 225 (SD 109) ng/ml in C282Y heterozygotes] in healthy men, 177 (SD 36) ng/ml in haemochromatosis patients, and 159 (SD 59) ng/ml in pregnant women. There was no relationship between serum prohepcidin concentration and serum ferritin in any subject groups, nor was it associated with efficiency of iron absorption. Serum prohepcidin is not a useful biomarker for clinical or research purposes. Hepcidin plays a major role in iron homeostasis, but full characterisation of its role in healthy humans and patients has been hindered by the absence of analytical methods to quantify circulating levels in the blood. Quantification of mRNA in the liver has been undertaken using reverse transcription and the polymerase chain reaction (Bridle et al. 2003;Gehrke et al. 2003), and polyclonal antibodies to refolded synthetic hepcidin have been produced and used for quantification in urine (Nemeth et al. 2003). Attempts to produce correctly folded synthetic hepcidin have proved difficult because the sequence contains eight cysteine residues that constrain the hepcidin molecule in a hairpin structure (Hunter et al. 2002). Hepcidin in urine has also been quantified using mass spectrometry methods (Kemna et al. 2005;Liang et al. 2006;Tomosugi et al. 2006).Prohepcidin, the sixty-amino-acid product of cleavage of the signal peptide from the hepcidin precursor, is expressed at the basolateral membrane domain of hepatocytes and is found in blood (Kulaksiz et al. 2004). Serum prohepcidin concentrations are significantly lower in patients with hereditary haemochromatosis compared to healthy control subjects (Kulaksiz et al. 2004), increase with declining kidney function (Taes et al. 2004), and are correlated with haematocrit in chronic haemodialysis patients (Hsu et al. 2006), but it is currently unclear whether * Corresponding author: ...

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Section: Discussionsupporting

confidence: 87%

Section: Discussioncontrasting

confidence: 82%

Serum prohepcidin concentration: no association with iron absorption in healthy men; and no relationship with iron status in men carrying HFE mutations, hereditary haemochromatosis patients undergoing phlebotomy treatment, or pregnant women

et al. 2007

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“…0.0001). This is in line with a few findings from smaller studies which suggest that prohepcidin concentrations are age-and gender-dependent [12,13,[35][36][37] .…”

supporting

confidence: 76%

Prohepcidin, B-Type Natriuretic Peptide, and Iron Status in a Cohort of Elderly Women from the Rhine-Ruhr Area

Henry

Casjens²,

Schikowski³

et al. 2010

Acta Haematol

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“…It is not clear whether the serum prohepcidin level measures the active hepcidin or whether there is a functional precursor. Changes in the level of serum prohepcidin have been reported to fail to reflect the iron status exactly (11,19,20). Serum prohepcidin levels were not found to be statistically significant difference compared to the control group in patients with high ferritin levels with hereditary hemochromatosis and sickle cell anaemia (19,20).…”

Section: Discussionmentioning

confidence: 79%

“…Changes in the level of serum prohepcidin have been reported to fail to reflect the iron status exactly (11,19,20). Serum prohepcidin levels were not found to be statistically significant difference compared to the control group in patients with high ferritin levels with hereditary hemochromatosis and sickle cell anaemia (19,20). Similarly, Kulaksiz et al (11) did not find any relationship of serum prohepcidin levels with serum iron, transfer saturation, and serum ferritin levels.…”

Section: Discussionmentioning

confidence: 83%