| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1998: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1997: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1996: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Research Abstract |
The aim of this study was to explore, in patients with complex regional pain syndrome and patients with postherpetic neuralgia, whether this polymorphism (DD and II bomozygotes, and ID heterozygotes) associates heart rate and blood pressure variabilities, and the genetic risk factor for neuropathic pain. The distribution of the DD, ID and II genotypes in the study group is 33%, 33% and 33%, respectively. ACE activity was significantly higher in subjects with the ACE DD genotype than subjects with the ID and II genotypes. No significant difference in heart rate and blood pressure variabilities, plasma renin activity, angiotensin I and II was detected among the ACE genotypes. The frequency of the ACE DD genotype in the present population (33%) was higher than those previously described in other normal populations of the same race (2O%).^3 In addition, the frequency of the ACE DD genotype in CRPS type I was higher than those in CRPS type II.
It is possible that the DD genotype favors the development of neuropathic pain as well as cardiovascular disease, perhaps through the presence of higher ACE concentrations. Elevated ACE activity in these subjects may result in increased angiotensin II levels in the effector site, and this might be a mechanism underlying the association between the ACE deletion polymorphism and the increased genetic risk for susceptibility to neuropathic pain. Typing for ACE I/D gene poly-morphism, thus, might be a useful predictor of neuropathic pain.
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