Intestinal Ferroportin Expression in Pediatric Crohn's Disease

被引:8
作者
Burpee, Tyler [1 ,2 ]
Mitchell, Paul [3 ]
Fishman, Douglas [1 ,2 ]
Islam, Shabana [1 ,2 ]
Nemeth, Elizabeta [4 ]
Westerman, Mark [5 ]
Wessling-Resnick, Marianne [6 ]
Grand, Richard J. [1 ,2 ]
机构
[1] Harvard Univ, Sch Med, Ctr Inflammatory Bowel Dis, Childrens Hosp Boston, Boston, MA USA
[2] Harvard Univ, Sch Med, Childrens Hosp Boston, Div Gastroenterol & Nutr, Boston, MA USA
[3] Childrens Hosp, Clin Res Program, Boston, MA 02115 USA
[4] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA
[5] Intrins Life Sci LLC, La Jolla, CA USA
[6] Harvard Univ, Sch Publ Hlth, Dept Genet & Complex Dis, Boston, MA 02115 USA
基金
美国国家卫生研究院;
关键词
Crohn's disease; anemia; ferroportin; iron; INFLAMMATORY-BOWEL-DISEASE; NECROSIS-FACTOR-ALPHA; ORAL FERROUS FUMARATE; IRON-DEFICIENCY; TRANSPORTER EXPRESSION; INTRAVENOUS IRON; HEPCIDIN; ANEMIA; EPIDEMIOLOGY; MACROPHAGES;
D O I
10.1002/ibd.21367
中图分类号
R57 [消化系及腹部疾病];
学科分类号
100201 [内科学];
摘要
Background: Anemia is a frequent complication of Crohn's disease (CD). The intestinal iron exporter ferroportin (FPN) is involved in both iron deficiency anemia and the anemia of chronic disease. To examine its role in CD, intestinal FPN expression was studied in subjects with and without CD. Methods: Duodenal mucosal biopsies from 29 pediatric subjects with CD (n = 19) and without CD (n = 10) were obtained. FPN protein was measured using Western blot analysis and mRNA was assessed using quantitative real-time polymerase chain reaction (PCR). Results: Intestinal FPN protein was higher in anemic CD subjects than in nonanemic CD subjects (P = 0.01), while FPN mRNA levels were not different (P = 0.66). In nonanemic CD subjects, erythrocyte sedimentation rate (ESR) (P = 0.04), C-reactive protein (CRP) (P = 0.03), and interleukin-6 (IL-6) (P = 0.01) levels were elevated compared to controls. Nonanemic CD subjects had a lower median FPN protein than nonanemic controls, although it did not reach statistical significance (P = 0.07). Median FPN mRNA was similar between groups (P = 0.71). Although no correlation between FPN protein and IL-6 was noted, there was a strong negative correlation between serum iron and IL-6, both in subjects with CD (r = -0.88, P < 0.0001) and those without anemia (r = -0.58, P = 0.02). Conclusions: Intestinal FPN protein is upregulated in anemic CD subjects, suggesting that iron deficiency or anemia is the driving force regulating FPN levels. A transporter distinct from FPN appears to be involved in the hypoferremia associated with the inflammatory process of CD.
引用
收藏
页码:524 / 531
页数:8
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