Assessment of laboratory measurements and -308 TNFα gene promoter polymorphisms in normal bone mineral density

被引:12
作者
Canhao, Helena [1 ,2 ,3 ,4 ]
Fonseca, Joao Eurico [2 ,3 ]
Caetano-Lopes, Joana [2 ]
Saldanha, Carlota [4 ]
Queiroz, Mario Viana [3 ]
机构
[1] Hosp Santa Maria, Serv Reumatol, P-1649035 Lisbon, Portugal
[2] Univ Lisbon, Fac Med, Inst Mol Med, Rheumatol Res Unit, P-1649028 Lisbon, Portugal
[3] Hosp Santa Maria, Dept Rheumatol, P-1649035 Lisbon, Portugal
[4] Univ Lisbon, Fac Med, Inst Mol Med, Unidade Biopatol Vasc,Inst Biopatol Quim, P-1649028 Lisbon, Portugal
关键词
-308 TNF alpha gene promoter polymorphisms; laboratory measurements; normal bone mineral density; osteoporosis; risk factors;
D O I
10.1007/s10067-007-0706-y
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
The aim of this study was to identify and evaluate laboratory parameters associated with normal bone mineral density (BMD) and to test if -308 tumour necrosis factor (TNF) alpha gene promoter polymorphisms could influence BMD. We performed a comparative cross-sectional study of four main groups: young healthy individuals (20-30 years); subjects aged 50 years or over with normal BMD; osteoporotic subjects aged 50 years or over; osteoporotic women with active rheumatoid arthritis. Variables assessed included anthropometric features, diet intake, lifestyle, calcium-phosphorus balance, markers of bone turnover, sexual hormones, hormones related with body mass and growth, cytokines involved in inflammation and bone turnover, and -308 TNF alpha gene promoter polymorphisms. One hundred fifty-nine subjects were evaluated. Across the four groups, zinc serum levels were higher in men as compared to women. In addition, zinc serum levels were also higher in individuals with normal BMD as compared to osteoporotic subjects. Serum calcium levels were higher in normal BMD group. On the other hand, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels were significantly higher in normal bone mass postmenopausal women and men as compared to age-matched osteoporotic groups. Finally, leptin was significantly lower in men, after correcting these results for body mass index values. The remaining variables assessed had a similar distribution among the different studied groups. In our population, low serum levels of leptin and high serum levels of zinc, calcium, FSH, and LH were associated with a higher BMD.
引用
收藏
页码:301 / 307
页数:7
相关论文
共 42 条
[1]
THE AMERICAN-RHEUMATISM-ASSOCIATION 1987 REVISED CRITERIA FOR THE CLASSIFICATION OF RHEUMATOID-ARTHRITIS [J].
ARNETT, FC ;
EDWORTHY, SM ;
BLOCH, DA ;
MCSHANE, DJ ;
FRIES, JF ;
COOPER, NS ;
HEALEY, LA ;
KAPLAN, SR ;
LIANG, MH ;
LUTHRA, HS ;
MEDSGER, TA ;
MITCHELL, DM ;
NEUSTADT, DH ;
PINALS, RS ;
SCHALLER, JG ;
SHARP, JT ;
WILDER, RL ;
HUNDER, GG .
ARTHRITIS AND RHEUMATISM, 1988, 31 (03) :315-324
[2]
CANHAO H, 2004, ACTA REUMATOL PORT, V29, P63
[3]
Canhao Helena, 2006, Acta Reumatol Port, V31, P331
[4]
CHEN BH, 1999, J MED SCI, V15, P464
[5]
Tumor necrosis factor α, CYP 17, urokinase, and interleukin 10 gene polymorphisms in postmenopausal women:: correlation to bone mineral density and susceptibility to osteoporosis [J].
Chen, HY ;
Chen, WC ;
Hsu, CM ;
Tsai, FJ ;
Tsai, CH .
EUROPEAN JOURNAL OF OBSTETRICS & GYNECOLOGY AND REPRODUCTIVE BIOLOGY, 2005, 122 (01) :73-78
[6]
Compston J., 1999, Osteoporosis, V2nd
[7]
Leptin inhibits bone formation through a hypothalamic relay: A central control of bone mass [J].
Ducy, P ;
Amling, M ;
Takeda, S ;
Priemel, M ;
Schilling, AF ;
Beil, FT ;
Shen, JH ;
Vinson, C ;
Rueger, JM ;
Karsenty, G .
CELL, 2000, 100 (02) :197-207
[8]
Serum leptin level is a regulator of bone mass [J].
Elefteriou, F ;
Takeda, S ;
Ebihara, K ;
Magre, J ;
Patano, N ;
Kim, CA ;
Ogawa, Y ;
Liu, X ;
Ware, SM ;
Craigen, WJ ;
Robert, JJ ;
Vinson, C ;
Nakao, K ;
Capeau, J ;
Karsenty, G .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (09) :3258-3263
[9]
Favier A, 1990, Rev Fr Gynecol Obstet, V85, P13
[10]
Polymorphism at position-308 of the tumour necrosis factor α gene and rheumatoid arthritis pharmacogenetics [J].
Fonseca, JE ;
Carvalho, T ;
Cruz, M ;
Nero, P ;
Sobral, M ;
Mourao, AF ;
Cavaleiro, J ;
Ligeiro, D ;
Abreu, I ;
Carmo-Fonseca, M ;
Branco, JC .
ANNALS OF THE RHEUMATIC DISEASES, 2005, 64 (05) :793-794