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Serum prohepcidin concentrations in rheumatoid arthritis.
Pathology. 2009 Feb; 41(2):178-82.P

Abstract

AIM

Hepcidin, a recently identified peptide, acts as a central regulator of iron metabolism. It is regarded as a factor regulating the uptake of dietary iron and its mobilisation from macrophages and hepatic stores. It is considered as a mediator of anaemia of inflammation. The aim of this study was to assess whether serum prohepcidin concentration is able to distinguish iron deficiency from anaemia of inflammation in patients with rheumatoid arthritis (RA).

METHOD

Blood samples were obtained from 20 healthy blood donors, 30 RA patients who presented with anaemia and 30 patients who had pure iron deficiency anaemia (IDA). The samples were analysed for full blood count, iron, ferritin, transferrin, soluble transferrin receptor and prohepcidin.

RESULTS

The mean prohepcidin level in the control subjects was 256 microg/L. The prohepcidin level was significantly lower in IDA patients (100 microg/L; p < 0.0001) but not significantly different from that of control in RA patients (250 microg/L; p > 0.05). Higher serum soluble transferrin receptor (sTfR) levels were observed in IDA (p < 0.0001) but not in RA compared with that of control (p > 0.05). RA patients were divided into iron depleted and iron repleted subgroups based on the ferritin level. Prohepcidin in the iron depleted group was significantly lower than the iron repleted group and the control (p < 0.0001) and higher levels were observed in the iron repleted group (p < 0.01). sTfR levels in the iron depleted group were significantly higher than the control and the iron repleted patients (p < 0.001). In the iron repleted group, sTfR level was not statistically different from that of control (p > 0.05).

CONCLUSION

Serum prohepcidin is clearly reduced in uncomplicated iron deficiency anaemia. The reduced prohepcidin levels in the iron depleted RA patients suggests that there may be conflicting signals regulating hepcidin production in RA patients. In RA patients who have reduced hepcidin in the iron depleted group (ferritin <60 microg/L) where sTfR levels are increased suggests that these patients are iron deficient. Further studies with a larger cohort of patients are required to substantiate this point.

Authors+Show Affiliations

Department of Pathology, Faculty of Medicine, University of Malaya, Lembah Pantai, Kuala Lumpur, Malaysia. jayaranee@um.edu.myNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18972320

Citation

Jayaranee, S, et al. "Serum Prohepcidin Concentrations in Rheumatoid Arthritis." Pathology, vol. 41, no. 2, 2009, pp. 178-82.
Jayaranee S, Sthaneshwar P, Sokkalingam S. Serum prohepcidin concentrations in rheumatoid arthritis. Pathology. 2009;41(2):178-82.
Jayaranee, S., Sthaneshwar, P., & Sokkalingam, S. (2009). Serum prohepcidin concentrations in rheumatoid arthritis. Pathology, 41(2), 178-82. https://doi.org/10.1080/00313020802436840
Jayaranee S, Sthaneshwar P, Sokkalingam S. Serum Prohepcidin Concentrations in Rheumatoid Arthritis. Pathology. 2009;41(2):178-82. PubMed PMID: 18972320.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Serum prohepcidin concentrations in rheumatoid arthritis. AU - Jayaranee,S, AU - Sthaneshwar,Pavai, AU - Sokkalingam,Sargunan, PY - 2008/10/31/pubmed PY - 2009/5/1/medline PY - 2008/10/31/entrez SP - 178 EP - 82 JF - Pathology JO - Pathology VL - 41 IS - 2 N2 - AIM: Hepcidin, a recently identified peptide, acts as a central regulator of iron metabolism. It is regarded as a factor regulating the uptake of dietary iron and its mobilisation from macrophages and hepatic stores. It is considered as a mediator of anaemia of inflammation. The aim of this study was to assess whether serum prohepcidin concentration is able to distinguish iron deficiency from anaemia of inflammation in patients with rheumatoid arthritis (RA). METHOD: Blood samples were obtained from 20 healthy blood donors, 30 RA patients who presented with anaemia and 30 patients who had pure iron deficiency anaemia (IDA). The samples were analysed for full blood count, iron, ferritin, transferrin, soluble transferrin receptor and prohepcidin. RESULTS: The mean prohepcidin level in the control subjects was 256 microg/L. The prohepcidin level was significantly lower in IDA patients (100 microg/L; p < 0.0001) but not significantly different from that of control in RA patients (250 microg/L; p > 0.05). Higher serum soluble transferrin receptor (sTfR) levels were observed in IDA (p < 0.0001) but not in RA compared with that of control (p > 0.05). RA patients were divided into iron depleted and iron repleted subgroups based on the ferritin level. Prohepcidin in the iron depleted group was significantly lower than the iron repleted group and the control (p < 0.0001) and higher levels were observed in the iron repleted group (p < 0.01). sTfR levels in the iron depleted group were significantly higher than the control and the iron repleted patients (p < 0.001). In the iron repleted group, sTfR level was not statistically different from that of control (p > 0.05). CONCLUSION: Serum prohepcidin is clearly reduced in uncomplicated iron deficiency anaemia. The reduced prohepcidin levels in the iron depleted RA patients suggests that there may be conflicting signals regulating hepcidin production in RA patients. In RA patients who have reduced hepcidin in the iron depleted group (ferritin <60 microg/L) where sTfR levels are increased suggests that these patients are iron deficient. Further studies with a larger cohort of patients are required to substantiate this point. SN - 0031-3025 UR - https://www.unboundmedicine.com/medline/citation/18972320/Serum_prohepcidin_concentrations_in_rheumatoid_arthritis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/904908884 DB - PRIME DP - Unbound Medicine ER -