| Project/Area Number |
10670431
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
内科学一般
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
TERAI Chihiro Tokyo Women's Medical University, Institute of Rheumatology, Associate Profesor, 医学部, 助教授 (40188660)
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| Co-Investigator(Kenkyū-buntansha) |
KOSEKI Yumi Tokyo Women's Medical University, Institute of Rheumatoloy, 医学部, 助手
UESATO Masashi Tokyo Women's Medical University, Institute of Rheumatoloy, 医学部, 助手
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1999: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1998: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | amyloidosis / SAA / SAA1 / SAA2 / amyloid / rheumatoid arthritis / gene / gene polymorphism / SAAI |
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| Research Abstract |
To examine whether polymorphism at the SAA loci is associated with the development of AA-amyloidosis, we determined the genotypes at the SAA1 and SAA2 loci in 43 AA-amyloidosis patients (amyloidosis population) and 77 patients with rheumatoid arthritis who had been ill for less than 5 years (early RA population). We also compared the frequencies of the genotypes at the SAA1 locus among 90 Korean, 95 Taiwanese and 103 Japanese healthy subjects. The frequencies of the γ/γ genotype and γ alleles at the SAA1 locus were significantly higher in the amyloidosis population than in the early RA population (34.9% versus 7.8% and 58.1% versus 33.8%, c2 test p=0.0001). The frequencies of the γ allele at the SAA1 locus in Koreans, Taiwanese and Japanese were 41.6%, 35.6% and 37.4%, respectively. The length of the latent period of AA-amyloidosis was significantly longer in the patients with smaller numbers of the γ allele at SAA1 locus (Spearman's correlation coefficient : -0.42 ; p<0.05). On the other hand, the mean CRP level during 2 years prior to the diagnosis of AA-amyloidosis was significantly higher in the patiesnts with larger numbers of the γ allele at the SAA1 locus (Spearman's correlation coefficient : 0.34 ; p<0.05). No significant association was found between amyloidosis and polymorphism at the SAA2 locus. We postulate that the allele SAA1 γ renders an RA patient susceptible to amyloidosis, possibly by affecting the severity of inflammation in RA.
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