Evidence for a metabolic shift of arginine metabolism in sickle cell disease

被引:62
作者
Schnog, JJB
Jager, EH
van der Dijs, FPL
Duits, AJ
Moshage, H
Muskiet, FD
Muskiet, FAJ
机构
[1] Slotervaart Hosp, Dept Internal Med 9B, NL-1066 EC Amsterdam, Netherlands
[2] Red Cross Blood Bank Fdn, Curacao, Neth Antilles
[3] Univ Groningen Hosp, Dept Pathol & Lab Med, Groningen, Netherlands
[4] Analyt Diagnost Ctr, Curacao, Neth Antilles
[5] Univ Groningen Hosp, Div Gastroenterol & Hepatol, Groningen, Netherlands
[6] St Elizabeth Hosp, Dept Pediat, Curacao, Neth Antilles
关键词
sickle cell disease; arginine; nitric oxide; hemolysis; endothelium;
D O I
10.1007/s00277-004-0856-9
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Over the last few years, a pivotal role has been ascribed to reduced nitric oxide (NO) availability as a contributing factor to the vaso-occlusive process of sickle cell disease. We investigated whether arginine metabolism in sickle cell patients is different from healthy controls. Blood samples were drawn by venipuncture in the fasting state from 8 clinically asymptomatic HbSS patients and 14 race-matched HbAA controls. HbSS patients had decreased plasma arginine (p=0.001) and increased proline (p=0.015) levels as compared to controls. Ratios of arginine to ornithine (p<0.001), proline (p<0.001), glutamate (p=0.003), and citrulline (p=0.026) were lower in HbSS patients. There were significant correlations of ornithine (r(s)=-0.71, p=0.047), citrulline (r(s)=-0.79, p=0.021), arginine/ornithine (r(s)=0.93, p=0.001), and arginine/citrulline (r(s)=0.81, p=0.015) to hemoglobin and of arginine/proline (r(s)=-0.76, p=0.028) and citrulline (r(s)=0.71, p=0.048) to leukocyte counts. These data indicate that in clinically asymptomatic sickle cell patients increased arginine metabolism is shifted to the arginase pathway and that this seems to be more profound in patients with higher hemolytic rates and leukocyte counts.
引用
收藏
页码:371 / 375
页数:5
相关论文
共 33 条
[1]   Endothelial dysfunction in patients with sickle cell disease is related to selective impairment of shear stress-mediated vasodilation [J].
Belhassen, L ;
Pelle, G ;
Sediame, S ;
Bachir, D ;
Carville, C ;
Bucherer, C ;
Lacombe, C ;
Galacteros, F ;
Adnot, S .
BLOOD, 2001, 97 (06) :1584-1589
[2]   Plasma amino acid levels with a note on membrane transport: Characteristics, regulation, and metabolic significance [J].
Cynober, LA .
NUTRITION, 2002, 18 (09) :761-766
[3]   NITROGEN-METABOLISM IN SICKLE-CELL-ANEMIA - FREE AMINO-ACIDS IN PLASMA AND URINE [J].
ENWONWU, CO ;
XU, XX ;
TURNER, E .
AMERICAN JOURNAL OF THE MEDICAL SCIENCES, 1990, 300 (06) :366-371
[4]   PLATELETS, COAGULATION, AND FIBRINOLYSIS IN SICKLE-CELL DISEASE - THEIR POSSIBLE ROLE IN VASCULAR OCCLUSION [J].
FRANCIS, RB .
BLOOD COAGULATION & FIBRINOLYSIS, 1991, 2 (02) :341-353
[5]   Sickle cell vaso-occlusion: multistep and multicellular paradigm [J].
Frenette, PS .
CURRENT OPINION IN HEMATOLOGY, 2002, 9 (02) :101-106
[6]   Divergent nitric oxide bioavailability in men and women with sickle cell disease [J].
Gladwin, MT ;
Schechter, AN ;
Ognibene, FP ;
Coles, WA ;
Reiter, CD ;
Schenke, WH ;
Csako, G ;
Waclawiw, MA ;
Panza, JA ;
Cannon, RO .
CIRCULATION, 2003, 107 (02) :271-278
[7]   Reduced arginine availability and nitric oxide production [J].
Hallemeesch, MM ;
Lamers, WH ;
Deutz, NEP .
CLINICAL NUTRITION, 2002, 21 (04) :273-279
[8]   Nitric oxide regulates vascular cell adhesion molecule 1 gene expression and redox-sensitive transcriptional events in human vascular endothelial cells [J].
Khan, BV ;
Harrison, DG ;
Olbrych, MT ;
Alexander, RW ;
Medford, RM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (17) :9114-9119
[9]   Neutrophil activation in sickle cell disease [J].
Lard, LR ;
Mul, FPJ ;
de Haas, M ;
Roos, D ;
Duits, AJ .
JOURNAL OF LEUKOCYTE BIOLOGY, 1999, 66 (03) :411-415
[10]   Regulatory role of arginase I and II in nitric oxide, polyamine, and proline syntheses in endothelial cells [J].
Li, H ;
Meininger, CJ ;
Hawker, JR ;
Haynes, TE ;
Kepka-Lenhart, D ;
Mistry, SK ;
Morris, SM ;
Wu, GY .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2001, 280 (01) :E75-E82