MONOCLONAL GAMMOPATHY IN ATOMIC-BOMB SURVIVORS

被引:9
作者
NERIISHI, K
YOSHIMOTO, Y
CARTER, RL
MATSUO, T
ICHIMARU, M
MIKAMI, M
ABE, T
FUJIMURA, K
KURAMOTO, A
机构
[1] FUNAIRI HIROSHIMA CITY HOSP,DEPT CLIN LABS,NAKA KU,HIROSHIMA 730,JAPAN
[2] HIROSHIMA UNIV,NUCL MED & BIOL RES INST,DEPT INTERNAL MED,MINAMI KU,HIROSHIMA 732,JAPAN
[3] RADIAT EFFECTS RES FDN,DEPT EPIDEMIOL,MINAMI KU,HIROSHIMA 732,JAPAN
[4] RADIAT EFFECTS RES FDN,DEPT STAT,MINAMI KU,HIROSHIMA 732,JAPAN
[5] NAGASAKI UNIV,SCH MED,INST ATOM DIS,DEPT HEMATOL,NAGASAKI 852,JAPAN
关键词
D O I
10.2307/3578221
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
An analysis of monoclonal gammopathy in relation to radiation exposure was conducted on atomic bomb survivors examined between October 1979 and September 1981 and between June 1985 and May 1987. There was no overall increase in the relative risk of monoclonal gammopathy and only a suggestive increase in benign monoclonal gammopathy in the second survey which did not achieve statistical significance (P = 0.17). Thirty-one cases were detected among 8796 individuals studied in the first survey, whereas 68 cases were found among 7350 people in the second survey. Among the 31 cases found in the first survey, 9 individuals (29%) died before the second survey: 4 of cancer, 4 of vascular disease, and 1 of infection. Among the 8 individuals with benign monoclonal gammopathy examined in both surveys, 4 developed suppression of residual immunoglobulin(s), suggesting the progression of monoclonal gammopathy. The overall relative risks of monoclonal gammopathy in atomic bomb survivors in the two surveys were not significantly increased with increasing radiation dose. Only benign monoclonal gammopathy in 1985- 1987 showed a suggestive increase with radiation exposure. The relative risk of benign monoclonal gammopathy in 1985-1987 was 2.64 in the group exposed to 0.01-0.49 Gy and 2.14 in the ≥0.50-Gy group (95% confidence intervals = 0.90-8.82 and 0.69-7.31, respectively).
引用
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页码:351 / 359
页数:9
相关论文
共 33 条
[1]  
AKU E, 1990, BIOCHIM BIOPHYS ACTA, V1052, P243
[2]   ACTION OF RECOMBINANT HUMAN INTERLEUKIN-6, INTERLEUKIN-1-BETA AND TUMOR NECROSIS FACTOR-ALPHA ON THE MESSENGER-RNA INDUCTION OF ACUTE-PHASE PROTEINS [J].
ANDUS, T ;
GEIGER, T ;
HIRANO, T ;
KISHIMOTO, T ;
HEINRICH, PC .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1988, 18 (05) :739-746
[3]   SERUM LEVELS OF INTERLEUKIN-6, A POTENT MYELOMA CELL-GROWTH FACTOR, AS A REFLECT OF DISEASE SEVERITY IN PLASMA-CELL DYSCRASIAS [J].
BATAILLE, R ;
JOURDAN, M ;
ZHANG, XG ;
KLEIN, B .
JOURNAL OF CLINICAL INVESTIGATION, 1989, 84 (06) :2008-2011
[4]  
BERKOW RL, 1987, J IMMUNOL, V139, P3783
[5]  
BRIERE RO, 1964, AM J CLIN PATHOL, V42, P547
[6]   RECOMBINANT HUMAN INTERLEUKIN-6 (IL-6/BSF-2/HSF) REGULATES THE SYNTHESIS OF ACUTE PHASE PROTEINS IN HUMAN HEPATOCYTES [J].
CASTELL, JV ;
GOMEZLECHON, MJ ;
DAVID, M ;
HIRANO, T ;
KISHIMOTO, T ;
HEINRICH, PC .
FEBS LETTERS, 1988, 232 (02) :347-350
[7]   RADIATION-INDUCED MYELOMATOSIS [J].
CUZICK, J .
NEW ENGLAND JOURNAL OF MEDICINE, 1981, 304 (04) :204-210
[8]  
DINARELLO CA, 1984, NEW ENGL J MED, V311, P1413
[9]  
DURIE BGM, 1985, NEOPLASTIC DISEASES, P513
[10]   MARKERS OF MULTIPLE HEMATOPOIETIC-CELL LINEAGES IN MULTIPLE-MYELOMA [J].
EPSTEIN, J ;
XIAO, HQ ;
HE, XY .
NEW ENGLAND JOURNAL OF MEDICINE, 1990, 322 (10) :664-668