Inflammation can increase hepcidin in HFE-hereditary hemochromatosis

W. Moris; P.L.M. Verhaegh; A.A.M. Masclee; D.W. Swinkels; C.M. Laarakkers; G.H. Koek; C.T.B.M. van Deursen

doi:10.1002/ccr3.4114

Inflammation can increase hepcidin in HFE-hereditary hemochromatosis

W. Moris
, P.L.M. Verhaegh
, A.A.M. Masclee
, D.W. Swinkels
, C.M. Laarakkers
, G.H. Koek
, C.T.B.M. van Deursen^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

We present a p.C282Y homozygous patient with high hepcidin levels and normal iron parameters during systemic inflammation. This suggests that in the absence of a proper functioning HFE, resulting in blockage of the BMP/SMAD pathway, the innate low hepcidin concentration can he upregulated by inflammation, probably via the JAK/STAT3 pathway.

Original language	English
Article number	e04114
Number of pages	4
Journal	Clinical Case Reports
Volume	9
Issue number	5
DOIs	https://doi.org/10.1002/ccr3.4114
Publication status	Published - 1 May 2021

Keywords

hemochromatosis
hepcidin
inflammation
iron overload
IRON
EXPRESSION
PATHWAY

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10.1002/ccr3.4114Licence: CC BY-NC-ND

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title = "Inflammation can increase hepcidin in HFE-hereditary hemochromatosis",

abstract = "We present a p.C282Y homozygous patient with high hepcidin levels and normal iron parameters during systemic inflammation. This suggests that in the absence of a proper functioning HFE, resulting in blockage of the BMP/SMAD pathway, the innate low hepcidin concentration can he upregulated by inflammation, probably via the JAK/STAT3 pathway.",

keywords = "hemochromatosis, hepcidin, inflammation, iron overload, IRON, EXPRESSION, PATHWAY",

author = "W. Moris and P.L.M. Verhaegh and A.A.M. Masclee and D.W. Swinkels and C.M. Laarakkers and G.H. Koek and \{van Deursen\}, C.T.B.M.",

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AU - Moris, W.

AU - Verhaegh, P.L.M.

AU - Masclee, A.A.M.

AU - Swinkels, D.W.

AU - Laarakkers, C.M.

AU - Koek, G.H.

AU - van Deursen, C.T.B.M.

PY - 2021/5/1

Y1 - 2021/5/1

N2 - We present a p.C282Y homozygous patient with high hepcidin levels and normal iron parameters during systemic inflammation. This suggests that in the absence of a proper functioning HFE, resulting in blockage of the BMP/SMAD pathway, the innate low hepcidin concentration can he upregulated by inflammation, probably via the JAK/STAT3 pathway.

AB - We present a p.C282Y homozygous patient with high hepcidin levels and normal iron parameters during systemic inflammation. This suggests that in the absence of a proper functioning HFE, resulting in blockage of the BMP/SMAD pathway, the innate low hepcidin concentration can he upregulated by inflammation, probably via the JAK/STAT3 pathway.

KW - hemochromatosis

KW - hepcidin

KW - inflammation

KW - iron overload

KW - IRON

KW - EXPRESSION

KW - PATHWAY

U2 - 10.1002/ccr3.4114

DO - 10.1002/ccr3.4114

M3 - Article

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SN - 2050-0904

VL - 9

JO - Clinical Case Reports

JF - Clinical Case Reports

IS - 5

M1 - e04114

ER -

Inflammation can increase hepcidin in HFE-hereditary hemochromatosis

Abstract

Keywords

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