Review article: iron and inflammatory bowel disease.

被引:83
作者
Oldenburg, B
Koningsberger, JC
Henegouwen, GPV
Van Asbeck, BS
Marx, JJM
机构
[1] Univ Utrecht, Med Ctr, Dept Gastroenterol, NL-3584 CX Utrecht, Netherlands
[2] Univ Utrecht, Med Ctr, Dept Internal Med, NL-3584 CX Utrecht, Netherlands
[3] Univ Utrecht, Med Ctr, Eijkman Winkler Inst Microbiol, NL-3584 CX Utrecht, Netherlands
关键词
D O I
10.1046/j.1365-2036.2001.00930.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Both anaemia of iron deficiency and anaemia of chronic disease are frequently encountered in inflammatory bowel disease. Anaemia of iron deficiency is mostly due to inadequate intake or loss of iron. Anaemia of chronic disease probably results from decreased erythropoiesis, secondary to increased levels of proinflammatory cytokines, reactive oxygen metabolites and nitric oxide. Assessment of the iron status in a condition associated with inflammation, such as inflammatory bowel disease, is difficult. The combination of serum transferrin receptor with ferritin concentrations, however, allows a reliable assessment of the iron deficit. The best treatment for anaemia of chronic disease is the cure of the underlying disease. Erythropoietin reportedly may increase haemoglobin levels in some of these patients. The anaemia of iron deficiency is usually treated with oral iron supplements. Iron supplementation may lead to an increased inflammatory activity through the generation of reactive oxygen species. To date, data from studies in animal models of inflammatory bowel disease support the theoretical disadvantage of iron supplementation in this respect. The results, however, cannot easily be extrapolated to the human situation, because the amount of supplemented iron in these experiments was much higher than the dose used in patients with iron deficiency.
引用
收藏
页码:429 / 438
页数:10
相关论文
共 97 条
[51]   Iron, infections, and anemia of inflammation [J].
Jurado, RL .
CLINICAL INFECTIOUS DISEASES, 1997, 25 (04) :888-895
[52]   IRON SUPPLEMENTATION GENERATES HYDROXYL RADICAL IN-VIVO - AN ESR SPIN-TRAPPING INVESTIGATION [J].
KADIISKA, MB ;
BURKITT, MJ ;
XIANG, QH ;
MASON, RP .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 96 (03) :1653-1657
[53]   THE ETIOLOGY OF THE ANEMIA OF CHRONIC DISEASE AND INFECTION [J].
KENT, S ;
WEINBERG, ED ;
STUARTMACADAM, P .
JOURNAL OF CLINICAL EPIDEMIOLOGY, 1994, 47 (01) :23-33
[54]   REPERFUSION INJURY AFTER MYOCARDIAL-INFARCTION - THE ROLE OF FREE-RADICALS AND THE INFLAMMATORY RESPONSE [J].
KILGORE, KS ;
LUCCHESI, BR .
CLINICAL BIOCHEMISTRY, 1993, 26 (05) :359-370
[55]   REGULATING THE FATE OF MESSENGER-RNA - THE CONTROL OF CELLULAR IRON-METABOLISM [J].
KLAUSNER, RD ;
ROUAULT, TA ;
HARFORD, JB .
CELL, 1993, 72 (01) :19-28
[56]  
KOPP EB, 1995, ADV IMMUNOL, V58, P1, DOI 10.1016/S0065-2776(08)60618-5
[57]  
Linder M.C, 1991, NUTR BIOCH METABOLIS, P215
[58]   CLINICAL EVALUATION OF SERUM FERRITIN AS AN INDEX OF IRON STORES [J].
LIPSCHITZ, DA ;
COOK, JD ;
FINCH, CA .
NEW ENGLAND JOURNAL OF MEDICINE, 1974, 290 (22) :1213-1216
[59]   LONG-TERM DEVELOPMENTAL OUTCOME OF INFANTS WITH IRON-DEFICIENCY [J].
LOZOFF, B ;
JIMENEZ, E ;
WOLF, AW .
NEW ENGLAND JOURNAL OF MEDICINE, 1991, 325 (10) :687-694
[60]  
MACDERMO.RP, 1969, GASTROENTEROLOGY, V57, P117