Evaluating Disability Insurance Assistance as a Specific Intervention by Physiatrists at a Cancer Center.

Because of their expertise, physiatrists provide disability insurance assistance for cancer survivors. In this brief report, we perform a descriptive retrospective analysis of all new (354) outpatient physiatry consultations from January 1, 2009, to December 31, 2013, at a National Cancer Institute Comprehensive Cancer Center. Disability and/or work accommodations were brought up at some point with the physiatrist during the duration of their care for 131 (37%) of 354 patients. More than 90% of the discussions took place during the first visit. Of those patients who had a documented disability/employment discussion, 58 (44.3%) of 131 patients were originally referred for disability assistance specifically, and 58 (44.3%) of 131 also had disability insurance paperwork completed by the physiatrist. Outcomes of initial physiatry disability insurance assistance were 45 (77.6%) of 58 approved/renewed, 5 (8.6%) of 58 denied, and 8 (13.8%) of 58 unknown/died during the disability application process. The median form size was 33 (SD, 25.95) items. This study is the first of its kind and provides an initial look at work-related discussions and support with disability insurance paperwork as a specific intervention provided by physiatrists at a cancer center. The results are compelling and demonstrate that physiatrists frequently provide these interventions. These interventions take considerable time and effort but are generally successful.

The short-term effects of antioxidant and zinc supplements on oxidative stress biomarker levels in plasma: a pilot investigation.

PURPOSE: To determine if short-term Age-Related Eye Disease Study (AREDS) antioxidant and zinc supplementation affects biomarkers of oxidative stress, possibly serving as a predictor of their efficacy. DESIGN: Prospective interventional case series. METHODS: Nineteen subjects, 12 with intermediate or advanced age-related macular degeneration (AMD) (AREDS categories 3 or 4) and 7 non-AMD controls, were admitted to the Vanderbilt General Clinical Research Center and placed on a controlled diet for 7 days. Antioxidant and zinc supplements were stopped 2 weeks prior to study enrollment. Dietary supplementation with 500 mg vitamin C, 400 IU vitamin E, 15 mg ß-carotene, 80 mg zinc oxide, and 2 mg cupric oxide per day was instituted on study day 2. Blood was drawn on study days 2 and 7, and plasma concentrations of cysteine (Cys), cystine (CySS), glutathione (GSH), isoprostane (IsoP), and isofuran (IsoF) were determined. RESULTS: Short-term AREDS supplementation significantly lowered mean plasma levels of CySS in participants on a regulated diet (P = .034). No significant differences were observed for Cys, GSH, IsoP, or IsoF. There were no significant differences between AMD patients and controls. CONCLUSIONS: This pilot interventional study shows that a 5-day course of antioxidant and zinc supplements can modify plasma levels of CySS, suggesting that this oxidative stress biomarker could help predict how likely an individual is to benefit from AREDS supplementation. Further, CySS may be useful for the evaluation of new AMD therapies, particularly those hypothesized to affect redox status.

Plasma biomarkers of oxidative stress and genetic variants in age-related macular degeneration.

PURPOSE: To compare plasma levels of oxidative stress biomarkers in patients with age-related macular degeneration (AMD) and controls and to evaluate a potential relationship between biochemical markers of oxidative stress and AMD susceptibility genotypes. DESIGN: Prospective case-control study. METHODS: Plasma levels of oxidative stress biomarkers were determined in 77 AMD patients and 75 controls recruited from a clinical practice. Cysteine, cystine (CySS), glutathione, isoprostane, and isofuran were measured, and participants were genotyped for polymorphisms in the complement factor H (CFH) and age-related maculopathy susceptibility 2 (ARMS2) genes. RESULTS: CySS was elevated in cases compared with controls (P = .013). After adjustment for age, sex, and smoking, this association was not significant. In all participants, CySS levels were associated with the CFH polymorphism rs3753394 (P = .028) as well as an 8-allele CFH haplotype (P = .029) after correction for age, gender, and smoking. None of the other plasma markers was related to AMD status in our cohort. CONCLUSIONS: Our investigation of the gene-environment interaction involved in AMD revealed a relationship between a plasma biomarker of oxidative stress, CySS, and CFH genotype. These data suggest a potential association between inflammatory regulators and redox status in AMD pathogenesis.

Polymorphisms in the VEGFA and VEGFR-2 genes and neovascular age-related macular degeneration.

PURPOSE: Genetic factors influence an individual's risk for developing neovascular age-related macular degeneration (AMD), a leading cause of irreversible blindness. Previous studies on the potential genetic link between AMD and vascular endothelial growth factor (VEGF), a key regulator of angiogenesis and vascular permeability, have yielded conflicting results. In the present case-control association study, we aimed to determine whether VEGF or its main receptor tyrosine kinase VEGFR-2 is genetically associated with neovascular AMD. METHODS: A total of 515 Caucasian patients with neovascular AMD and 253 ethically-matched controls were genotyped for polymorphisms in the VEGFA and VEGFR-2 genes. A tagging single nucleotide polymorphism (tSNP) approach was employed to cover each gene plus two kilobases on each side, spanning the promoter and 3' untranslated regions. SNPs with a minimum allele frequency of 10% were covered by seven tSNPs in VEGFA and 20 tSNPs in VEGFR-2. Two VEGFA SNPs previously linked with AMD, rs1413711 and rs3025039, were also analyzed. RESULTS: The 29 VEGFA and VEGFR-2 SNPs analyzed in our cohort demonstrated no significant association with neovascular AMD. A single rare haplotype in the VEGFR-2 gene was associated with the presence of neovascular AMD (p=0.034). CONCLUSIONS: This study is the first to investigate the association of VEGFR-2 polymorphisms with AMD and evaluates VEGFA genetic variants in the largest neovascular AMD cohort to date. Despite the angiogenic and permeability-enhancing effects of VEGF/VEGFR-2 signaling, we found minimal evidence of a significant link between polymorphisms in the VEGFA and VEGFR-2 genes and neovascular AMD.