Medial arterial calcification in diabetes and its relationship to neuropathy

被引:86
作者
Jeffcoate, W. J. [1 ]
Rasmussen, L. M. [2 ]
Hofbauer, L. C. [3 ]
Game, F. L. [1 ]
机构
[1] Nottingham Univ Hosp Trust, Dept Endocrinol & Diabet, Nottingham NG5 1PB, England
[2] Odense Univ Hosp, Dept Biochem Pharmacol & Genet, DK-5000 Odense, Denmark
[3] Tech Univ, Dept Med 3, Div Endocrinol Diabet & Bone Dis, Dresden, Germany
关键词
Cardiovascular disease; Diabetes; Medial artery calcification; Neuropathy; Osteoporosis; Osteoprotegerin; RANKL; Renal disease; Review; GENE-RELATED PEPTIDE; SMOOTH-MUSCLE-CELLS; PLASMA OSTEOPROTEGERIN LEVELS; NECROSIS-FACTOR-ALPHA; KAPPA-B LIGAND; VASCULAR CALCIFICATION; MORPHOGENETIC PROTEIN-2; MONCKEBERGS SCLEROSIS; RECEPTOR ACTIVATOR; KIDNEY-FUNCTION;
D O I
10.1007/s00125-009-1521-6
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Calcification of the media of arterial walls is common in diabetes and is particularly associated with distal symmetrical neuropathy. Arterial calcification also complicates chronic kidney disease and is an independent risk factor for cardiovascular and all-cause mortality. The term calcification is not strictly accurate because the morphological changes incorporate those of new bone formation, i.e. ossification. The processes are complex, but are closely related to those involved in bone homeostasis, and it is relevant that calcification of the arterial wall and osteopenia often co-exist. One particular factor linked to the development of arterial calcification is distal symmetrical neuropathy; indeed, it has been suggested that neuropathy explains the distal distribution of arterial calcification in diabetes. It has also been suggested that the link with neuropathy results from loss of neuropeptides, such as calcitonin gene-related peptide, which are inherently protective. The association between distal symmetrical neuropathy and calcification of the arterial wall highlights the fact that neuropathy may be an independent risk factor for cardiovascular mortality.
引用
收藏
页码:2478 / 2488
页数:11
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