高尿酸血症與戴奧辛暴露之關係研究

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Research Express@NCKU Volume 25 Issue 3 - November 8, 2013

[ http://research.ncku.edu.tw/re/articles/e/20131108/2.html ]

Hyperuricemia after exposure to polychlorinated

dibenzo-p-dioxins and dibenzofurans near a highly

contaminated area

Jung-Wei Chang

a

, Horng-Yih Ou

b

, Hsiu-Ling Chen

c

, Huey-Jen Su

a,d

, Ching-Chang Lee

a,d,*

a_{Department of Environmental and Occupational Health, College of Medicine, National Cheng Kung} University, Tainan, Taiwan

b_{Division of Endocrinology and Metabolism, Department of Internal Medicine, National Cheng Kung} University Hospital, Tainan, Taiwan

c_{Department of Industrial Safety and Health, Hung Kuang University, Taichung, Taiwan} d_{Research Center for Environmental Trace Toxic Substances, National Cheng Kung University,} Tainan, Taiwan

cclee@mail.ncku.edu.tw

Epidemiology. 2013 Jul;24(4):582-9. doi:10.1097/EDE.0b013e318294ef68.

H

yperuricemia means too much uric acid in the blood. Uric acid is a metabolic product resulting from the metabolism of purines (found in many foods and in human tissue).1,2 Hyperuricemia is associated with hypertriglyceridemia, diabetes mellitus,3 and coronary artery disease.4 Polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) cause renal dysfunction and elevate uric acid.5,6 The aim of this work was to study the relationship between exposure to PCDD/Fs and serum uric acid levels, and to examine whether the risk of hyperuricemia is different between males and females.

This cross-sectional study recruited 1531 healthy participants living near a deserted pentachlorophenol factory. We measured seventeen 2,3,7,8-substituted PCDD/Fs, then examined associations between the main predictor variable, serum TEQ_DF-2005, and dependent variables, e.g., uric acid, estimated glomerular filtration rates (eGFR), and hyperuricemia risk.

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CI: 1.08-3.22]; ≥ 75th percentile, AOR = 3.00 [95% CI: 1.69-5.31]). These data show that serum PCDD/Fs affected the risk of hyperuricemia in apparently healthy men.

FIGURE 1. Adjusted regression coefficients (β [95% CI]) for change in eGFR in relation to serum TEQ_DF-2005 quartiles for (A) men and (B) women. Values are adjusted for smoking, drinking, bodyfat, and insulin resistance.

FIGURE 2. Adjusted regression coefficients (β [95% CI]) for change in uric acid in relation to serum TEQ

DF-2005 quartiles for (A) men and (B) women. Values are adjusted for age, smoking, drinking, bodyfat, eGFR, and

insulin resistance.

We conclude that in populations with moderate exposure to environmental PCDD/Fs, serum PCDD/F levels are an important independent determinant of serum uric acid levels. Men with higher PCDD/F exposure had a significantly higher hyperuricemia risk than did women with higher PCDD/F exposure. Our results support efforts to reduce potential sources of environmental exposure to PCDD/Fs and to offer possibilities for decreasing the risk of hyperuricemia in the general population.

References:

1. Wortmann RL. Gout and hyperuricemia. Curr Opin Rheumatol. 2002;14:281-286

2. Terkeltaub RA. Gout: Epidemiology, pathology and pathogenesis. In:Klippel JH, Crofford L, Stone JH, eds. Primer on the Rheumatic Disease. 12th ed. Atlanta: Arthritis Foundation; 2001:307–312.

3. Berkowitz D. Gout, hyperlipidemia, and diabetes interrelationships. JAMA. 1966;197:77–80.

4. A bbott RD, Brand FN, Kannel WB, Castelli WP. Gout and coronary heart disease: the Framingham Study. J Clin Epidemiol. 1988;41:237–242.

5. Han HJ, Lim MJ, Lee YJ, Kim EJ, Jeon YJ, Lee JH. Effects of TCDD and estradiol-17beta on the proliferation and Na+/glucose cotransporter in renal proximal tubule cells. Toxicol In Vitro. 2005;19:21– 30.

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