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Objectives
Professional athletes undergo annual pre-season laboratory screening, although clinical evidence supporting the practice is limited and no uniform set of guidelines on pre-season laboratory screening exists. The aim of this study was to assess the clinical value of annual pre-season laboratory screening tests for a major professional sports team over multiple years.Design
Retrospective chart review.Methods
A retrospective analysis was performed of all laboratory results as well as screening ECGs for a single major professional sports team over a 9-year timeframe (2009–2017).Results
The data show that 10.01% of initial screening test results were abnormal and 40.32% of abnormal tests resulted in additional testing. Overall, only 0.35% of initial tests resulted in a clinically significant outcome. Non-US born players showed a significantly higher average rate of abnormal tests/year compared to US-born players (p-value 0.006), but there was no difference in clinically significant outcomes. There was no relationship between athlete age and laboratory screening outcomes.Conclusions
In our study population, yearly pre-season laboratory screening of professional athletes did not yield substantial clinically significant outcomes and would not be warranted under normal clinical standards. Future best practice guidelines should combine research concerning effects of family medical history, race, gender, country of origin, and type of sport on athlete health when creating recommendations for which pre-season laboratory screenings may be pertinent even with evidence of little utility. 相似文献The co-occurrence of HIV and alcohol use disorder (AUD) amplifies risk for neural injury and neurocognitive deficits. However, the substantial neurocognitive heterogeneity across HIV+/AUD+ individuals suggests inter-individual differences in vulnerability to the neurotoxicity of comorbid HIV/AUD. Genetic variation in alcohol dehydrogenase (ADH), which metabolizes ethanol, may contribute to inter-individual neurocognitive variability. We evaluated associations between five ADH single-nucleotide polymorphisms (SNPs) and neurocognition in men stratified by HIV and lifetime AUD status. Neurobehavioral assessments were administered to 153 men. Three-way ANOVAs examined the interaction of HIV, AUD, and ADH SNPs on global and domain-specific demographically corrected T scores. Follow-up ANCOVAs adjusted for age, estimated verbal IQ, depression, and remote non-alcohol substance use disorders. HIV/AUD groups differed globally and for verbal fluency, working memory, executive function, and processing speed T scores specifically, with HIV+/AUD+ exhibiting the poorest performance. ADH4 (rs1126671) was associated with large effects on working memory (d?=???1.16, p?=?.001) and executive function (d?=???0.77, p?=?.028) selectively in HIV+/AUD+, which remained significant in ANCOVA models. ADH1A (rs3819197) moderated the deleterious effects of HIV+/AUD+ on processing speed such that HIV+/AUD+ related to slower information processing in A allele carriers but not GG homozygotes (ps?<?0.03). Preliminary findings suggest genetic variation in the ADH pathway moderates the deleterious neurocognitive effects of comorbid HIV/AUD. Differential metabolism of heavy ethanol exposure may compromise neurocognition under conditions of neurobiological stress, such as in HIV infection. The functional effects on ethanol metabolism of ADH SNPs examined in this study remain poorly understood, warranting further examination of pharmacokinetic mechanisms mediating ADH gene-neurobehavior relationships in HIV.
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