Non-steroidal anti-inflammatory drugs interact with testosterone glucuronidation

Sten, Taina; Finel, Moshe; Ask, Birgitta; Rane, Anders; Ekström, Lena

doi:10.1016/j.steroids.2009.07.004

Cited by 37 publications

(35 citation statements)

References 24 publications

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“…For conjugation reactions, inhibition properties of NSAIDs have been demonstrated for steroid glucuronidation in an in vitro assay,94 but the observations were not confirmed by in vivo experiments 95. One particular therapeutic drug, ketoconazole, should be mentioned due to its unique property to inhibit T synthesis,96 97 as well as the binding of DHT to SHBG,98 and to exhibit inhibition of CYP3A4 system 99.…”

Section: Abp and The Steroidal Modulementioning

confidence: 99%

Confounding factors and genetic polymorphism in the evaluation of individual steroid profiling

2014

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In the fight against doping, steroid profiling is a powerful tool to detect drug misuse with endogenous anabolic androgenic steroids. To establish sensitive and reliable models, the factors influencing profiling should be recognised. We performed an extensive literature review of the multiple factors that could influence the quantitative levels and ratios of endogenous steroids in urine matrix. For a comprehensive and scientific evaluation of the urinary steroid profile, it is necessary to define the target analytes as well as testosterone metabolism. The two main confounding factors, that is, endogenous and exogenous factors, are detailed to show the complex process of quantifying the steroid profile within WADA-accredited laboratories. Technical aspects are also discussed as they could have a significant impact on the steroid profile, and thus the steroid module of the athlete biological passport (ABP). The different factors impacting the major components of the steroid profile must be understood to ensure scientifically sound interpretation through the Bayesian model of the ABP. Not only should the statistical data be considered but also the experts in the field must be consulted for successful implementation of the steroidal module.

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Section: Abp and The Steroidal Modulementioning

confidence: 99%

Confounding factors and genetic polymorphism in the evaluation of individual steroid profiling

2014

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“…Specifically, this study was designed to investigate the influence of diclofenac on the excretion of stanozolol and 3'-hydroxystanozolol via analyses in hair, blood and urine in vivo in a rat study. Diclofenac was selected as the inhibition profiles were fully characterised in in vitro against studies against UGT2B17 and UGT2B15 with diclofenac being the most potent of the NSAID inhibitors [13].…”

Section: Aims and Research Hypothesesmentioning

confidence: 99%

Inhibitory Effects of Diclofenac on Steroid Glucuronidation in Vivo Do not Affect Hair-Based Doping Tests for Stanozolol

Zachár

Deshmukh

Petróczi

et al. 2017

Preprint

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In vitro studies show that diclofenac inhibits enzymatic steroid glucuronidation. This study was designed to investigate the influence of diclofenac on the excretion of stanozolol and 3'-hydroxystanozolol via analyses in hair, blood and urine in vivo in a rat study. Brown Norway rats were administered with stanozolol (weeks 1-3) and diclofenac (weeks 1-6). Weekly assessment of steroid levels in hair was complemented with spot urine and serum tests. Levels of both stanozolol and 3'-hydroxystanozolol steadily increased in hair during stanozolol treatment and decreased post-treatment, but remained readily detectable for 6 weeks. In contrast, compared to control rats, diclofenac significantly reduced urinary excretion of 3’-hydroxystanozolol which was undetectable in most samples. This is the first report of diclofenac altering steroid metabolism in vivo, detrimentally affecting detection in urine, but not in hair which holds considerable advantages over urinalysis for anti-doping tests.

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“…135 -139 These catabolism pathways have been studied in the context of drug-drug interactions, 140 are polymorphic, 135,141 and are susceptible to epigenetic programming 142 by a variety of factors during early life. 142,143 Examination of the pathways suggests that many common items may affect estrogen and/or androgens via these pathways, such as cotinine, 144,145 painkillers, 138,146,147 and many dietary items, 148 including potentially vitamin A, 149, 150 cruciferous vegetables, 151,152 citrus fruit, 151 chili, 153 sesame, 154 ginseng, 155,156 and fatty acids (eg, linoleic acid). 157 Although associations of various similar risk factors with hormone levels have been reported from high-quality studies, 158 -160 they are open to all the weaknesses of observational dietary epidemiologic analyses.…”

Section: Physiologic Pathwaysmentioning

confidence: 99%

Potential Intervention Targets in Utero and Early Life for Prevention of Hormone Related Cancers

2016

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Dr Schooling conceptualized the study, drafted the initial manuscript, and approved the fi nal manuscript as submitted; and Drs Houghton and Terry made substantial contributions to the conceptualization, reviewed and revised the manuscript, and approved the fi nal manuscript as submitted. Strong associations between diethylstilbestrol exposure in utero and the subsequent risk of clear cell vaginal cancer offered the first epidemiologic evidence that a prenatal exposure, particularly a hormonal one, could lead to cancer later in life. 1 -3 Endogenous hormones have been implicated in many cancers, including some of the most common cancers globally (breast and prostate) as well as some of the rarer cancers (endometrium, ovary, testis, thyroid, osteosarcoma, Ewing's sarcoma, and rhabdomyosarcoma). 4 -7 Key to interpreting the evidence base concerning the hormonal environment and cancer risk are specific issues of hormonal measurements, including the type (eg, direct as opposed to proxy indicators) and the timing (eg, adulthood versus in utero, infancy, childhood, and puberty), so that their effects can be understood within the context of their Hormone-related cancers have long been thought to be sensitive to exposures during key periods of sexual development, as shown by the vulnerability to such cancers of women exposed to diethylstilbestrol in utero. In addition to evidence from human studies, animal studies using new techniques, such as gene knockout models, suggest that an increasing number of cancers may be hormonally related, including liver, lung, and bladder cancer. Greater understanding of sexual development has also revealed the "mini-puberty" of early infancy as a key period when some sex hormones reach levels similar to those at puberty. Factors driving sex hormones in utero and early infancy have not been systematically identified as potential targets of intervention for cancer prevention. On the basis of sex hormone pathways, we identify common potentially modifiable drivers of sex hormones, including but not limited to factors such as obesity, alcohol, and possibly nitric oxide. We review the evidence for effects of modifiable drivers of sex hormones during the prenatal period and early infancy, including measured hormones as well as proxies, such as the second-to-fourth digit length ratio. We summarize the gaps in the evidence needed to identify new potential targets of early life intervention for lifelong cancer prevention.

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Non-steroidal anti-inflammatory drugs interact with testosterone glucuronidation

Cited by 37 publications

References 24 publications

Confounding factors and genetic polymorphism in the evaluation of individual steroid profiling

Confounding factors and genetic polymorphism in the evaluation of individual steroid profiling

Inhibitory Effects of Diclofenac on Steroid Glucuronidation in Vivo Do not Affect Hair-Based Doping Tests for Stanozolol

Potential Intervention Targets in Utero and Early Life for Prevention of Hormone Related Cancers

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