Objective: To assess the epidemiologic evidence on melanoma in relation to Parkinson disease (PD) via systematic review and meta-analysis.Methods: Epidemiologic studies on melanoma and PD were searched using PubMed, Web of Science, Scoups, and Embase (1965 through June 2010). Eligible studies were those that reported risk estimates of melanoma among patients with PD or vice versa. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using random-effects models. Results:We identified 12 eligible publications on melanoma and PD: 8 had fewer than 10 cases with both PD and melanoma, and 7 provided gender-specific results. The pooled OR was 2.11 (95% CI 1.26-3.54) overall, 2.04 (1.55-2.69) for men, and 1.52 (0.85-2.75) for women. Analyses by temporal relationship found that melanoma occurrence was significantly higher after the diagnosis of PD (OR 3.61, 95% CI 1.49-8.77), but not before PD diagnosis (OR 1.07, 95% CI 0.62-1.84). Further analyses revealed that the lack of significance in the latter analysis was due to one study, which when excluded resulted in a significant association (OR 1.44, 95% CI 1.06-1.96). We also analyzed nonmelanoma skin cancers in relation to PD and found no significant relationship (OR 1.11, 95% CI 0.94-1.30). Conclusions:Collective epidemiologic evidence supports an association of PD with melanoma.Further research is needed to examine the nature and mechanisms of this relationship. Neurology Accumulating epidemiologic evidence suggests a low occurrence of most cancer types in patients with Parkinson disease (PD).1 Intriguingly, melanoma is among the few cancer types that are more likely to occur among patients with PD.2,3 A link between melanoma and PD was first suspected following a case report of recurrent malignant melanoma in a patient with PD treated with levodopa. 4 Since then, a number of case reports have suggested that levodopa therapy increased the risk of melanoma. Reviews of these case reports have concluded, however, that the relationship between levodopa therapy and melanoma was "coincidental rather than causal." 4 Although suspicions surrounding levodopa therapy and increased risk of melanoma were largely dismissed, findings from recent clinical and epidemiologic studies increasingly suggest that PD is associated with a higher risk of melanoma and vice versa. The evidence from these studies, however, is not conclusive. Both malignant melanoma and PD are rare, and most available studies had fewer than 10 cases with both diseases occurring in the same individual, thus reducing the statistical power to adequately analyze the relationship. In addition, variations in study design, disease identification, and other methodologic limitations further weaken the ability of individual studies to draw a solid conclusion. We therefore conducted a system-
BackgroundNonmotor symptoms are common among patients with Parkinson’s disease (PD) and some may precede disease diagnosis.MethodsWe conducted a meta-analysis on the prevalence of selected nonmotor symptoms before and after PD diagnosis, using random-effect models. We searched PubMed (1965 through October/November 2012) for the following symptoms: hyposmia, constipation, rapid eye movement sleep behavior disorder, excessive daytime sleepiness, depression, and anxiety. Eligible studies were publications in English with original data on one or more of these symptoms.ResultsThe search generated 2,373 non-duplicated publications and 332 met the inclusion criteria, mostly (n = 320) on symptoms after PD diagnosis. For all symptoms, the prevalence was substantially higher in PD cases than in controls, each affecting over a third of the patients. Hyposmia was the most prevalent (75.5% in cases vs. 19.1% in controls), followed by constipation (50% vs. 17.7%), anxiety (39.9% vs. 19.1%), rapid eye movement sleep behavior disorder (37.0% vs. 7.0%), depression (36.6% vs. 14.9%), and excessive daytime sleepiness (33.9% vs. 10.5%). We observed substantial heterogeneities across studies and meta-regression analyses suggested that several factors might have contributed to this. However, the prevalence estimates were fairly robust in several sensitivity analyses. Only 20 studies had data on any symptoms prior to PD diagnosis, but still the analyses revealed higher prevalence in future PD cases than in controls.ConclusionThese symptoms are common among PD patients both before and after diagnosis. Further studies are needed to understand the natural history of nonmotor symptoms in PD and their etiological and clinical implications.Electronic supplementary materialThe online version of this article (doi:10.1186/2047-9158-4-1) contains supplementary material, which is available to authorized users.
Catheter ablation of AF in patients with HCM is feasible, although more repeat procedures and AAD are needed to prevent AF recurrence.
BackgroundTo update and refine systematic literature review on the association between outpatient statins use and mortality in patients with infectious disease.Materials and MethodsWe searched articles published before September 31, 2012, on the association between statins and infectious disease-related mortality through electronic databases. Eligible articles were analyzed in Review Manager 5.1. We conducted stratification analysis by study design, infection types, clinical outcomes and study locations.ResultsThe pooled odds ratio (OR) for death (statins use vs. no use) across the 41 included studies was 0.71 (95% confidence interval: 0.64, 0.78). The corresponding pooled ORs were 0.58 (0.38, 0.90), 0.66 (0.57, 0.75), 0.71 (0.57, 0.89) and 0.83 (0.67, 1.04) for the case-control study, retrospective cohort studies, prospective cohort studies and RCTs; 0.40 (0.20, 0.78), 0.61 (0.41, 0.90), 0.69 (0.62, 0.78) and 0.86 (0.68, 1.09) for bacteremia, sepsis, pneumonia and other infections; 0.62 (0.534, 0.72), 0.68 (0.53, 0.89), 0.71 (0.61, 0.83) and 0.86 (0.70, 1.07) for 30-day, 90-day, in-hospital and long-term (>1 year) mortality, respectively.ConclusionsOutpatient statins use is associated with a lower risk of death in patients with infectious disease in observational studies, but in a less extent in clinical trials. This association also varies considerably by infection types and clinical outcomes.
The estrogenic and antiestrogenic potential of perfluorooctanoic acid (PFOA) was assessed using an immature mouse uterotrophic assay and by histologic evaluation of the uterus, cervix and vagina following treatment. Female offspring of CD-1 dams were weaned at 18 days old and assigned to groups of equal weight, and received 0, 0.01, 0.1, or 1 mg PFOA/kg BW/d by gavage with or without 17-β estradiol (E 2 , 500 μg/kg/d) from PND18-20 (n=8/treatment/block). At 24 hr after the third dose (PND 21), uteri were removed and weighed. Absolute and relative uterine weights were significantly increased in the 0.01 mg/kg PFOA only group. Characteristic estrogenic changes were present in all E 2 -treated mice; however, they were minimally visible in Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Conflict of interestAll authors declare there are no financial conflict of interest issues. DisclaimerThe information in this document has been subjected to review by the National Institute of Environmental Health Sciences, NIH and the U.S. EPA's National Health and Environmental Effects Laboratory and approved for publication. This article may be the work product of an employee or group of employees of the National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH), however, the statements, opinions or conclusions contained therein do not necessarily represent the statements, opinions or conclusions of NIEHS, NIH or the United States government. NIH Public Access
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