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High dioxins exposure triggers gout: NCKU research

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Tainan, Taiwan, October 22, 2013

A study conducted by a Tainan-based National Cheng Kung University (NCKU) research team reveals that men with higher Polychlorinated Dioxins and Furans (PCDD/F) exposure would have a significantly higher hyperuricemia risk than men with lower PCDD/F exposure.

Dr. Jung-Wei Chang, an assistant researcher, together with his colleagues from Research Center for Environmental Trace Toxic Substances, NCKU, had conducted a study involving 1531 residents near the abandoned sodium-pentachlorophenol factory from July 2005 through May 2010.

The study had been published in Epidemiogy. Chang had also received an Excellent Article Award on Public Health, the 19th Professor Kung-Pei Chen Memorial Award of Taiwan Public Health Association, October 19, for his outstanding performance.

Chang said, the aim of the study was to investigate the relationship among exposure to PCDD/Fs, serum uric acid levels, and glomerular filtration rate. The 80-mL samples of venous blood were drawn for analysis for biochemistry examination and PCDD/Fs.

The gout, a common metabolic disorder in Taiwan, results from the abnormality of purine degradation in humans, Chang revealed.

“The underlying cause of gout is hyperuricemia, which means that serum uric acid level is above 7 mg/dL in men and 6 mg/dL in women as recommended, and easily being formed crystals in articular cavity and become swollen.”

He also added, hyperuricemia has been linked to many of the most dangerous diseases such as hypertriglyceridemia, diabetes mellitus, hypertension, and atherosclerosis and which is also a risk factor for coronary artery disease.

Animal studies have also provided evidence that the dioxins would cause renal toxicity and elevate uric acid.

Chang’s findings support efforts to reduce potential sources of environmental exposure to PCDD/Fs and may offer possibilities for decreasing the risk of hyperuricemia in populations even moderately exposed to PCDD/Fs.

Chang found that both serum PCDD/F levels and estimated Glomerular Filtration Rate (eGFR) were independently associated factors of serum uric acid levels in the study participants after adjusting for confounding factors.

In addition to reducing eGFR, PCDD/Fs may directly elevate serum uric acid, according to Chang who added, “Men had higher serum PCDD/F levels and percentage of hyperuricemia than did women, and serum PCDD/F levels were associated with higher uric acid levels and reduced eGFR in men but not in women.”

The results shown that men with higher serum PCDD/F levels would have a 3 fold increased risk of hyperuricemia than men with lower levels.

The possible mechanism remains unclear and may be attributable to the lack of estrogen protection from the detrimental effect of dioxin on renal proximal tubule function.

The underlying biological mechanism causing women to have lower serum uric acid levels might be the effect of estrogens on the renal tubular handling of uric acid, one that increases the excretion of uric acid.

People pay more attention to the disease accompanied by the symptoms of high blood pressure, diabetes and high cholesterol.

However, there is also increasing evidence to show that hyperuricemia may have a pathogenetic role in the progression of renal diseases, and has been associated with hypertriglyceridemia and diabetes mellitus, and is also a risk factor for coronary artery disease.
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