High rate of nickel allergy in women with endometriosis: a 3-year population-based study.

AIM: The aim of this study was to evaluate the prevalence rates of nickel allergy, contact dermatitis, drug allergy, allergic rhinitis and atopic dermatitis among women with and without endometriosis. MATERIAL AND METHODS: Data were obtained from the National Patient Sample of the Republic of Korea, which was provided by the Korean Health Insurance Review and Assessment Service. We evaluated women aged 20-40 years who visited a health care institution from 2009-2011. We estimated the prevalence of allergic diseases among women with and without endometriosis. RESULTS: We extracted a sample of 1 843 447 women from the total patient sample of approximately 3 million. We identified 7259 women with endometriosis and 535 818 women without endometriosis. After adjusting for age and data year, the women with endometriosis had higher rates of nickel allergy (odds ratio = 1.175; 95% confidence interval, 1.011-1.366; P = 0.04). Additionally, after adjusting for age, data year and other allergic diseases, the women with endometriosis had higher rates of nickel allergy (odds ratio = 1.167; 95% confidence interval, 1.004-1.357; P = 0.04). After adjusting for other covariates, we found that other allergic disorders, such as allergic rhinitis, atopic dermatitis and contact dermatitis, were not associated with endometriosis. CONCLUSION: Women with endometriosis had higher rates of nickel allergy. Further research is required to clarify the relation between nickel allergy and endometriosis.

Effects of estrogen receptor α and ß on the expression of visfatin and retinol-binding protein 4 in 3T3-L1 adipocytes.

The aim of this study was to investigate the effects of estrogen and estrogen receptor α (ERα) and ß (ERß) on the expression of visfatin and retinol-binding protein 4 (RBP4) by treating 3T3-L1 adipocytes with estradiol (E2), estrogen receptor agonists and antagonists. Mature adipocytes were exposed to E2, the ERα agonist, 4,4',4''-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol (PPT), the ERß agonist, 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN), E2 with the ERα antagonist, 1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-1H-pyrazole dihydrochloride (MPP), and E2 with the ERß antagonist, (5R, 11R)-5,11-diethyl-5,6,11,12-tetrahydro-2,8-chrysenediol [(R,R)-THC], at various concentrations. To determine the effects of ER subtypes on the expression of adipokines, quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) and western blot analyses were performed. E2 concentrations of 10-5 and 10-6 mol/l induced a statistically significant increase in the expression of RBP4 (P=0.012 and P=0.011, respectively). In the cells treated with 10-5 mol/l PPT, RBP4 expression significantly increased (P<0.05) in a dose-dependent manner. Treatment with the ERα antagonist, MPP (10-5 mol/l), and E2 suppressed the expression of RBP4 (P=0.032). However, the expression of RBP4 was not significantly altered when the cells were treated with the ERß agonist or antagonist. The expression of visfatin was not affected by different concentrations of E2 and ERs. 17ß-estradiol significantly increased the secretion of RBP4 and upregulated RBP4 expression via ERα but not ERß in 3T3-L1 adipocytes. RBP4 expression was regulated by estrogen in the 3T3-L1 adipocytes and this effect was selectively mediated by ERα.