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Mary Price

Publications and source records attributed to Mary Price.

6 recordsLinked to original sources

Unintended consequences of caps on Medicare drug benefits.

BACKGROUND: Little information exists about the consequences of limits on prescription-drug benefits for Medicare beneficiaries. METHODS: We compared the clinical and economic outcomes in 2003 among 157,275 Medicare+Choice beneficiaries whose annual drug benefits were capped at 1,000 dollars and 41,904 beneficiaries whose drug benefits were unlimited because of employer supplements. RESULTS: After adjusting for individual characteristics, we found that subjects whose benefits were capped had pharmacy costs for drugs applicable to the cap that were lower by 31 percent than subjects whose benefits were not capped (95 percent confidence interval, 29 to 33 percent) but had total medical costs that were only 1 percent lower (95 percent confidence interval, -4 to 6 percent). Subjects whose benefits were capped had higher relative rates of visits to the emergency department (relative rate, 1.09 [95 percent confidence interval, 1.04 to 1.14]), nonelective hospitalizations (relative rate, 1.13 [1.05 to 1.21]), and death (relative rate, 1.22 [1.07 to 1.38]; difference, 0.68 per 100 person-years [0.30 to 1.07]). Among subjects who used drugs for hypertension, hyperlipidemia, or diabetes in 2002, those whose benefits were capped were more likely to be nonadherent to long-term drug therapy in 2003; the respective odds ratios were 1.30 (95 percent confidence interval, 1.23 to 1.38), 1.27 (1.19 to 1.34), and 1.33 (1.18 to 1.48) for subjects using drugs for hypertension, hyperlipidemia, and diabetes. In each subgroup, the physiological outcomes were worse for subjects whose drug benefits were capped than for those whose benefits were not capped; the odds ratios were 1.05 (95 percent confidence interval, 1.00 to 1.09), 1.13 (1.03 to 1.25), and 1.23 (1.03 to 1.46), respectively, for subjects with a systolic blood pressure of 140 mm Hg or more, a serum low-density-lipoprotein cholesterol level of 130 mg per deciliter or more, and a glycated hemoglobin level of 8 percent or more. CONCLUSIONS: A cap on drug benefits was associated with lower drug consumption and unfavorable clinical outcomes. In patients with chronic disease, the cap was associated with poorer adherence to drug therapy and poorer control of blood pressure, lipid levels, and glucose levels. The savings in drug costs from the cap were offset by increases in the costs of hospitalization and emergency department care.

Antihypertensive Agents↗

Autoreactive T cells mediate NK cell degeneration in autoimmune disease.

Emerging evidence indicates that NK cells play an important and complex role in autoimmune disease. Humans with autoimmune diseases often have reduced NK cell numbers and compromised NK cell functions. Mechanisms underlying this NK cell degeneration and its biological significance are not known. In this study we show that, in an experimental model of human autoimmune myasthenia gravis induced by a self-Ag, the acetylcholine receptor, NK cells undergo proliferation during the initiation of autoimmunity, followed by significant degeneration associated with the establishment of the autoreactive T cell response. We show that NK cell degeneration was mediated by IL-21 derived from autoreactive CD4(+) T cells, and that acetylcholine receptor-immunized IL-21R-deficient mice, with competent NK cells, developed exacerbated autoimmunity. Thus, NK cell degeneration may serve as a means evolved by the immune system to control excessive autoimmunity.

Animals↗

Cost-sharing for emergency care and unfavorable clinical events: findings from the safety and financial ramifications of ED copayments study.

OBJECTIVE: To evaluate the effect of emergency department (ED) copayment levels on ED use and unfavorable clinical events. Data Source/Study Setting. Kaiser Permanente-Northern California (KPNC), a prepaid integrated delivery system. STUDY DESIGN: In a quasi-experimental longitudinal study with concurrent controls, we estimated rates of ED visits, hospitalizations, ICU admissions, and deaths associated with higher ED copayments relative to no copayment, using Poisson random effects and proportional hazard models, controlling for patient characteristics. The study period began in January 1999; more than half of the population experienced an employer-chosen increase in their ED copayment in January 2000. DATA COLLECTION/EXTRACTION METHODS: Using KPNC automated databases, the 2000 U.S. Census, and California state death certificates, we collected data on ED visits and unfavorable clinical events over a 36-month period (January 1999 through December 2001) among 2,257,445 commercially insured and 261,091 Medicare insured health system members. PRINCIPAL FINDINGS: Among commercially insured subjects, ED visits decreased 12 percent with the $20-35 copayment (95 percent confidence interval [CI]: 11-13 percent), and 23 percent with the $50-100 copayment (95 percent CI: 23-24 percent) compared with no copayment. Hospitalizations, ICU admissions, and deaths did not increase with copayments. Hospitalizations decreased 4 percent (95 percent CI: 2-6 percent) and 10 percent (95 percent CI: 7-13 percent) with ED copayments of $20-35 and $50-100, respectively, compared with no copayment. Among Medicare subjects, ED visits decreased by 4 percent (95 percent CI: 3-6 percent) with the $20-50 copayments compared with no copayment; unfavorable clinical events did not increase with copayments, e.g., hospitalizations were unchanged (95 percent CI: -3 percent to +2 percent) with $20-50 ED copayments compared with no copayment. CONCLUSIONS: Relatively modest levels of patient cost-sharing for ED care decreased ED visit rates without increasing the rate of unfavorable clinical events.

Cost Sharing↗

Cooperation of invariant NKT cells and CD4+CD25+ T regulatory cells in the prevention of autoimmune myasthenia.

CD1d-restricted NKT cells and CD4+CD25+ regulatory T (Treg) cells are thymus-derived subsets of regulatory T cells that have an important role in the maintenance of self-tolerance. Whether NKT cells and Treg cells cooperate functionally in the regulation of autoimmunity is not known. We have explored this possibility in experimental autoimmune myasthenia gravis (EAMG), an animal model of human myasthenia gravis, induced by immunization of C57BL/6 mice with the autoantigen acetylcholine receptor. We have demonstrated that activation of NKT cells by a synthetic glycolipid agonist of NKT cells, alpha-galactosylceramide (alpha-GalCer), inhibits the development of EAMG. alpha-GalCer administration in EAMG mice increased the size of the Treg cell compartment, and augmented the expression of foxp3 and the potency of CD4+CD25+ cells to inhibit proliferation of autoreactive T cells. Furthermore, alpha-GalCer promoted NKT cells to transcribe the IL-2 gene and produce IL-2 protein. Depletion of CD25+ cells or neutralization of IL-2 reduced the therapeutic effect of alpha-GalCer in this model. Thus, alpha-GalCer-activated NKT cells can induce expansion of CD4+CD25+ Treg cells, which in turn mediate the therapeutic effects of alpha-GalCer in EAMG. Induced cooperation of NKT cells and Treg cells may serve as a superior strategy to treat autoimmune disease.

Animals↗

Differential effects of IL-21 during initiation and progression of autoimmunity against neuroantigen.

The cytokine IL-21 is closely related to IL-2 and IL-15, a cytokine family that uses the common gamma-chain for signaling. IL-21 is expressed by activated CD4(+) T cells. We examined the role of IL-21 in the autoimmune disease experimental autoimmune encephalomyelitis (EAE), an animal model for human multiple sclerosis. IL-21 administration before induction of EAE with a neuroantigen, myelin oligodendrocyte glycoprotein peptide 35-55, and adjuvant enhanced the inflammatory influx into the CNS, as well as the severity of EAE. Autoreactive T cells purified from IL-21-treated mice transferred more severe EAE than did the control encephalitogenic T cells. No such effects were observed when IL-21 was administered after EAE progressed. Additional studies demonstrated that IL-21 given before the induction of EAE boosted NK cell function, including secretion of IFN-gamma. Depletion of NK cells abrogated the effect of IL-21. Therefore, IL-21, by affecting NK cells, has differential effects during the initiation and progression of autoimmune responses against neuroantigens.

Amino Acid Sequence↗