OBJECTIVE: The aim of this study is to explore the correlation among serum hepcidin, ferritin, and q-Dioxn MRI with upgrading, upstaging and biochemical recurrence in prostate cancer (PCa) patients. METHODS: A total of 103 PCa patients diagnosed by biopsy were selected for this study. All patients underwent q-Dixon MRI prior to biopsy for T2* value measurement. Then serum hepcidin and ferritin were measured before receiving radical prostatectomy. Pathological grading and staging were conducted both preoperatively and postoperatively. The correlations among hepcidin, ferritin, T2* values, and postoperative upgrading, upstaging, biochemical recurrence were subsequently analyzed. RESULTS: The hepcidin level of PCa patients was measured at (123.51 ± 23.03) ng/mL, while the ferritin level was recorded at (239.80 ± 79.59) ng/mL, and the T2* value was (41.07 ± 6.37) ms. A total of 49 and 36 cases were observed with upgrading and upstaging in postoperative pathology, respectively. The median follow-up duration was 28.0 months (6.0－38.0 months), during which biochemical recurrence was observed in 12 cases. For upgrading, hepcidin and ferritin demonstrated the predictive efficacy, with areas under the ROC curve of 0.777 and 0.642, respectively, whereas T2* values did not show sufficient predictive power. For upstaging, hepcidin, ferritin, and T2* exhibited predictive efficacy, with areas under the ROC curve of 0.806, 0.696, and 0.655, respectively. Multivariate Logistic regression analysis indicated that hepcidin served as an independent risk factor for both upgrading (OR 1.055, 95%CI 1.027－1.085, P<0.001) and upstaging (OR 1.094, 95%CI 1.040－1.152, P<0.001). Cox regression analysis showed that hepcidin (95%CI 1.000－1.052, P = 0.049) was a significant risk factor for predicting biochemical recurrence. CONCLUSION Hepcidin could serve as a predictor for pathological upgrading, upstaging and biochemical recurrence after radical prostatectomy, which provides a novel potential index for risk stratification and prognostic evaluation of PCa patients.
Humans ; Male ; Prostatic Neoplasms/diagnosis* ; Hepcidins/blood* ; Ferritins/blood* ; Middle Aged ; Magnetic Resonance Imaging/methods* ; Aged ; Neoplasm Recurrence, Local ; Neoplasm Staging

OBJECTIVE: This study was designed to evaluate hematological disorders and the orchestrating roles of hepcidin and IL-6 in rat models of thioacetamide (TAA) and carbon tetrachloride (CCl4) hepatotoxicity. METHODS: Rats were intraperitoneally injected with TAA (10 mg/100 g rat weight dissolved in isosaline) or CCl4 (100 μL/100 g rat weight diluted as 1:4 in corn oil) twice weekly for eight consecutive weeks to induce subchronic liver fibrosis. Blood and tissue samples were collected and analyzed. RESULTS: CCl4 but not TAA significantly decreased the RBCs, Hb, PCV, and MCV values with minimal alterations in other erythrocytic indices. Both hepatotoxins showed leukocytosis, granulocytosis, and thrombocytopenia. By the end of the experiment, the erythropoietin level increased in the CCl4 model. The serum iron, UIBC, TIBC, transferrin saturation%, and serum transferrin concentration values significantly decreased, whereas that of ferritin increased in the CCl4 model. TAA increased the iron parameters toward iron overload. RT-PCR analysis revealed increased expression of hepatic hepcidin and IL-6 mRNAs in the CCl4 model and suppressed hepcidin expression without significant effect on IL-6 in the TAA model. CONCLUSION These data suggest differences driven by hepcidin and IL-6 expression between CCl4 and TAA liver fibrosis models and are of clinical importance for diagnosis and therapeutics of liver diseases.
Animals ; Blood Chemical Analysis ; Carbon Tetrachloride ; toxicity ; Hepcidins ; pharmacology ; Injections, Intraperitoneal ; Interleukin-6 ; pharmacology ; Iron ; blood ; metabolism ; Leukocytosis ; chemically induced ; therapy ; Liver Cirrhosis ; chemically induced ; therapy ; Male ; Rats ; Thioacetamide ; toxicity ; Thrombocytopenia ; chemically induced ; therapy ; Transferrin ; metabolism

BACKGROUNDObesity has an adverse effect on iron status. Hepcidin-mediated inhibition of iron absorption in the duodenum is a potential mechanism. Iron-deficient obese patients have diminished response to oral iron therapy. This study was designed to assess whether acupuncture could promote the efficacy of oral iron supplementation for the treatment of obesity-related iron deficiency (ID).

METHODSSixty ID or ID anemia (IDA) patients with obesity were screened at Beijing Hospital of Traditional Chinese Medicine and were randomly allocated to receive either oral iron replacement allied with acupuncture weight loss treatment (acupuncture group, n = 30) or oral iron combined with sham-acupuncture treatment (control group, n = 30). Anthropometric parameters were measured and blood samples were tested pre- and post-treatment. Differences in the treatment outcomes of ID/IDA were compared between the two groups.

RESULTSAfter 8 weeks of acupuncture treatment, there was a significant decrease in body weight, body mass index, waist circumference, and waist/hip circumference ratio of patients in the acupuncture group, while no significant changes were observed in the control group. Oral iron supplementation brought more obvious improvements of iron status indicators including absolute increases in serum iron (11.08 ± 2.19 μmol/L vs. 4.43 ± 0.47 μmol/L), transferrin saturation (11.26 ± 1.65% vs. 1.01 ± 0.23%), and hemoglobin (31.47 ± 1.19 g/L vs. 21.00 ± 2.69 g/L) in the acupuncture group than control group (all P < 0.05). Meanwhile, serum leptin (2.26 ± 0.45 ng/ml vs. 8.13 ± 0.55 ng/ml, P < 0.05) and hepcidin (3.52 ± 1.23 ng/ml vs. 6.77 ± 0.84 ng/ml, P < 0.05) concentrations declined significantly in the acupuncture group than those in the control group.

CONCLUSIONAcupuncture-based weight loss can enhance the therapeutic effects of iron replacement therapy for obesity-related ID/IDA through improving intestinal iron absorption, probably by downregulating the systemic leptin-hepcidin levels.

Acupuncture Therapy ; Adult ; Female ; Hepcidins ; blood ; Humans ; Intestinal Absorption ; physiology ; Iron ; deficiency ; metabolism ; Leptin ; blood ; Male ; Middle Aged ; Obesity ; blood ; metabolism ; therapy ; Young Adult

BACKGROUND: Anemia of chronic disease (ACD) and iron deficiency anemia (IDA) are the two most prevalent forms of anemia having interrelated characteristics. Hepcidin, a newly introduced biomarker for assessment of iron status, is a homeostatic regulator of iron metabolism. We investigated the role of hepcidin and other conventional iron parameters to assess iron status among children with ACD and IDA. We also identified children with ACD who developed iron deficiency (ID). METHODS: The study was undertaken in anemic children with 30 cases each of ACD and IDA along with 30 age and sex-matched controls. The ACD cases were subdivided into pure ACD and ACD with coexistent ID. All cases were subjected to following tests: complete blood count with peripheral smear, serum C-reactive protein, serum interleukin-6, iron studies, serum soluble transferrin receptor (sTfR), and serum hepcidin. RESULTS: The mean serum hepcidin concentration was significantly increased in pure ACD patients (143.85±42.76 ng/mL) as compared to those in IDA patients (6.01±2.83 ng/mL, P < 0.001) and controls (24.96±9.09 ng/mL, P <0.001). Also, compared to pure ACD patients [normal sTfR levels (<3 µg/mL)], the serum hepcidin concentration was reduced significantly in ACD patients with ID [high sTfR levels (≥3 µg/mL)] with a mean of 10.0±2.97 ng/mL. CONCLUSION: Hepcidin measurement can provide a useful tool for differentiating ACD from IDA and also help to identify an iron deficiency in ACD patients. This might aid in the appropriate selection of therapy for these patients.
Anemia* ; Anemia, Iron-Deficiency* ; Blood Cell Count ; C-Reactive Protein ; Child* ; Chronic Disease* ; Hepcidins* ; Humans ; Interleukin-6 ; Iron* ; Metabolism ; Receptors, Transferrin

OBJECTIVE: The purpose of this study is to evaluate the clinical and hematological effects of tocilizumab in active rheumatoid arthritis (RA) patients. METHODS: Fourteen patients with active RA were enrolled in this study. The patients received tocilizumab 8 mg/kg intravenously every four weeks for 6 months. Disease activity, anemia-related factors including serum hepcidin-25, and hematological parameters were monitored at baseline and at 1, 3, and 6 months after the initiation of treatment. RESULTS: Significant reductions in tender joint count, swollen joint count, visual analogue scale, erythrocyte sedimentation rate (ESR), and C-reactive (CRP) protein plus reductions in a 28-joint disease activity score were observed within one month after the first tocilizumab treatment. These effects lasted throughout the six-month study period. In addition, significant improvements in anemia-related factors such as hepcidin-25, ferritin, iron, hemoglobin, red blood cell counts and mean corpuscular volume were observed during the treatment period. Hematological parameters were improved with reductions in counts for leukocytes, monocytes, neutrophils, and platelets. The lymphocyte counts and their subset numbers were unchanged. Changes in hepcidin levels showed significant correlation with changes in CRP, ESR, ferritin, hemoglobin and counts for red blood cells, leukocytes, and neutrophils during the treatment period. CONCLUSION: This study demonstrates that tocilizumab significantly and meaningfully reduces disease burden in patients with active RA. In addition, tocilizumab diminishes the levels of inflammatory anemia by inhibiting hepcidin production. These clinical data provide evidence of a favorable outcome from tocilizumab in RA.
Anemia* ; Arthritis, Rheumatoid* ; Blood Sedimentation ; Erythrocyte Count ; Erythrocyte Indices ; Erythrocytes ; Ferritins ; Hepcidins* ; Humans ; Iron ; Joints ; Leukocytes ; Lymphocyte Count ; Monocytes ; Neutrophils

OBJECTIVETo explore the clinical diagnostic value and significance of hepciden level by detecting the expression of serum hepcidin before and after treatment of infant iron deficiency anemia (IDA) with or without vitamin D deficiency.

METHODSA total of 60 cases of infamt IDA were divided into A and B groups, the group A consisted of 20 IDA infants with vitamin D deficiency, group B consisted of 48 IDA infants without vitamin D deficiency and the control group included 26 healthy infants. Blood examination including HGB, MCV, MCH and MCHC was performed by hematological analyzer, the level of serum ferritin was assayed by chemiluminescence immunoassay, the levels of hepcidin and 25- (OH) D were assayed by ELISA.

RESULTSThe levels of serum hepcidin in group A, B and control group before treatment were (29.16 ± 7.50), (27.11 ± 7.10) and (29.25 ± 8.39) ng/ml, respectively (P > 0.05). The level of serum hepcidin in group A and B after treatments was significantly higher than that in control group [ (36.21 ± 5.68) ng/ml vs (29.25 ± 8.39) ng/ml, P < 0.01; (34.16 ± 4.54) ng/ml vs (29.25 ± 8.39) ng/ml, P < 0.01]; but there were no significantly difference between group A and B (P > 0.05). The serum ferritin positively correlated with hepcidin in group B both before and after treatments (r = 0.352 and 0.367, P < 0.05, P < 0.05).

CONCLUSIONThe level of serum hepcidin has an important significance in poccess of evaluatng for therapeutic effect in infant iron deficiency anemia, but the interference effect of vitamin D deficience should be eliminated when the expression level of hepcidin is applicated for diagnosis and differential diagnosis.

Anemia, Iron-Deficiency ; diagnosis ; Case-Control Studies ; Diagnosis, Differential ; Enzyme-Linked Immunosorbent Assay ; Hepcidins ; blood ; Humans ; Infant ; Vitamin D Deficiency ; blood

BACKGROUNDHepcidin, as a regulator of body iron stores, has been recently discovered to play a critical role in the pathogenesis of anemia of chronic disease. Atherosclerotic cardiovascular disease is the most common complication and the leading cause of death in chronic hemodialysis (CHD) patients. In the current study, we aimed to explore the relationship between serum hepcidin and uremic accelerated atherosclerosis (UAAS) in CHD patients with diabetic nephropathy (CHD/DN).

METHODSA total of 78 CHD/DN and 86 chronic hemodialyzed nondiabetic patients with chronic glomerulonephritis (CHD/non-DN) were recruited in this study. The level of serum hepcidin-25 was specifically measured by liquid chromatography-tandem mass spectrometry. Serum levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured by enzyme-linked immunosorbent assay.

RESULTSHigh serum level of hepcidin-25 was seen in CHD patients. Serum hepcidin-25 in CHD/DN was significantly higher than that in CHD/non-DN patients. Serum hepcidin-25 was positively correlated with ferritin, high-sensitivity C-reactive protein (hs-CRP), TNF-α, and IL-6 in CHD/DN patients. CHD/DN patients exhibited higher common carotid artery intima media thickness (CCA-IMT), hs-CRP, and hepcidin-25 levels than that in CHD/non-DN patients. Moreover, in CHD/DN patients, CCA-IMT was positively correlated with serum hepcidin, hs-CRP, and low-density lipoprotein-cholesterol. On multiple regression analysis, serum hepcidin and hs-CRP level exhibited independent association with IMT in CHD/DN patients.

CONCLUSIONSThese findings suggest possible linkage between iron metabolism and hepcidin modulation abnormalities that may contribute to the development of UAAS in CHD/DN patients.

Adult ; Aged ; Atherosclerosis ; blood ; Diabetic Nephropathies ; blood ; therapy ; Female ; Hepcidins ; blood ; Humans ; Male ; Middle Aged ; Renal Dialysis ; Young Adult

OBJECTIVETo detect the concentration of serum hepcidin and the mRNA expression level of ferroportin1 (FPN1) in the placenta membrane from full term pregnant women with different degree of iron deficiency, and explore their roles for iron transport in placental.

METHODSThe concentration of HGB, serum iron (SI) and serum ferritin (SF) of mothers and infants were detected in 55 full term pregnant women and neonates. The expression level of FPN1 mRNA in placental was detected by the RT-PCR technique. The concentration of serum hepcidin was detected by double antibody sandwich biotin avidin enzyme-linked immunosorbent assay. The serum hepcidin level and the FPN1 mRNA expression in the full term placenta from different maternal iron status were compared in three groups.

RESULTSThere were no significant differences in the cord blood HGB, SI and SF of newborns from pregnant women with different iron status (P>0.05). The concentration of serum hepcidin of pregnant women among normal, iron deficiency and mild iron deficiency anemia were (193.637±52.219), (176.523±43.875), and (147.623±37.768) μg/L respectively, with statistical significance (F=3.872, P=0.027). The expression levels of FPN1 mRNA among three groups were 0.462±0.077, 0.507±0.074 and 0.551±0.104 respectively, with statistical significance (F=4.767, P=0.013). A negative correlation between maternal serum hepcidin and placental FPN1 mRNA (r=-0.383, P=0.004) was identified.

CONCLUSIONThere were no significant differences in the iron status of corresponding newborns from pregnant women with different iron status. With the severity of maternal iron deficiency, the concentration of serum hepcidin was down-regulated, while the expression of FPN1 mRNA in placenta was up-regulated.

Anemia, Iron-Deficiency ; Cation Transport Proteins ; Enzyme-Linked Immunosorbent Assay ; Female ; Fetal Blood ; Hepcidins ; Humans ; Infant, Newborn ; Iron ; Mothers ; Placenta ; Pregnancy ; RNA, Messenger

OBJECTIVETo report the clinical data of a case of iron-refractory iron deficiency anemia (IRIDA), so as to improve the understanding of IRIDA.

METHODSThe IRIDA patient's hematological characteristics were summarized and analyzed. The hepcidin levels were tested by ELISA kit. The TMPRSS6 gene was amplified by PCR reaction and its mutation was analyzed by sequencing. The effect of TMPRSS6 gene mutation on TMPRSS6 protein tertiary structure was predicted by Swiss-Model.

RESULTSThe patient was characterized by typical microcytic hypochromic anemia, low transferrin saturation, more reduction of intracellular iron than exocellular iron. The plasma hepcidin level was 213.77 μg/L which was significantly higher than that of IDA patients [5.19(3.31-12.02) μg/L]. The patient also carried a homozygous missense mutation of K253E in exon 7 of TMPRSS6.

CONCLUSIONIn children and younger IDA patients with no reason for iron deficiency but unresponsiveness to routine iron treatment, the diagnosis of IRIDA needs to be considered. Serum hepcidin level and TMPRSS6 gene mutation should be detected.

Anemia, Iron-Deficiency ; blood ; genetics ; Female ; Hepcidins ; blood ; Humans ; Membrane Proteins ; genetics ; Mutation ; Protein Structure, Tertiary ; Serine Endopeptidases ; genetics ; Young Adult

Disorders of iron utilization caused by abnormal elevation of hepcidin levels are the main mechanism of anemia of chronic disease. Hepcidin is mainly produced by the liver. Recently it has been found that monocytes are another source of hepcidin. The increased hepcidin in serum and urine of multiple myeloma patients may be one cause of anemia of chronic disease (ACD). However it is unclear whether the peripheral blood monocyte hepcidin is involved in the pathogenesis of anemia of chronic disease. This study was purposed to investigate the role of monocyte hepcidin in multiple myeloma patients with anemia of chronic disease. The clinical data and peripheral venous blood of multiple myeloma patients were collected.Serum concentration of IL-6 and TNF-α was detected by ELISA. Peripheral blood monocytes were isolated by CD14(+) magnetic beads. Hepcidin, IL-6 and TNF-α mRNA of monocytes were detected by real time quantitative PCR. The results showed that the expression level of monocyte hepcidin mRNA in myeloma patients was higher than that in normal controls. In untreated patients, the expression level of monocyte hepcidin mRNA was negatively correlated with hemoglobin, and positively correlated with serum ferritin and IL-6 levels, but unrelated with TNF-α levels.It is concluded that the increased monocyte hepcidin levels in multiple myeloma patients may play an etiologic role in ACD.
Adult ; Aged ; Anemia ; etiology ; Case-Control Studies ; Chronic Disease ; Female ; Ferritins ; blood ; Hepcidins ; blood ; Humans ; Interleukin-6 ; blood ; Leukocytes, Mononuclear ; metabolism ; Male ; Middle Aged ; Monocytes ; metabolism ; Multiple Myeloma ; blood ; complications ; Tumor Necrosis Factor-alpha ; blood