RESUMO
OBJECTIVE: Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly prescribed for pain and inflammation. NSAIDs are associated with serious adverse effects and cardiovascular (CV) risks that include myocardial infarction, stroke and heart failure. In the period of time immediately after a CV event, modification to the drug therapy regimen and lifestyle habits should be instituted to decrease morbidity and mortality. The objective of this study is to measure the prevalence of NSAIDs prescribing in the immediate 90 days after a CV-related hospitalization in Medicaid beneficiaries in Puerto Rico. METHODS: Hospitalization claims were used to identify beneficiaries with a CVrelated hospitalization during the study period, and pharmacy claims were used to evaluate the occurrence of NSAIDs prescribing post-discharge. RESULTS: A total of 4,195 beneficiaries with at least one CV-related hospitalization were identified. Out of these beneficiaries, 774 (18.5%) had at least one pharmacy claim for an NSAID post discharge, and 401 (9.6%) had at least one pharmacy claim for an NSAID within 90 days post-discharge. The average time span between the discharge date and the first NSAID claim was 135 days. CONCLUSION: Almost 20% of all beneficiaries who were hospitalized for a CV event received an NSAID during the study period, with 10% of patients receiving it during the immediate 90 days post-discharge. It represents a major challenge for our healthcare system, as it may reflect unawareness on the impact of proved evidence in clinical decision making.
Assuntos
Anti-Inflamatórios não Esteroides/uso terapêutico , Doenças Cardiovasculares , Hospitalização , Medicaid , Doenças Cardiovasculares/terapia , Prescrições de Medicamentos/estatística & dados numéricos , Insuficiência Cardíaca/terapia , Humanos , Estudos Longitudinais , Infarto do Miocárdio/terapia , Porto Rico , Acidente Vascular Cerebral/terapia , Estados UnidosRESUMO
Approximately 30-50% of the >30 million HIV-infected subjects develop neurological complications ranging from mild symptoms to dementia. HIV does not infect neurons, and the molecular mechanisms behind HIV-associated neurocognitive decline are not understood. There are several hypotheses to explain the development of dementia in HIV(+) individuals, including neuroinflammation mediated by infected microglia and neuronal toxicity by HIV proteins. A key protein associated with the neurological complications of HIV, gp120, forms part of the viral envelope and can be found in the CSF of infected individuals. HIV-1-gp120 interacts with several receptors including CD4, CCR5, CXCR4, and nicotinic acetylcholine receptors (nAChRs). However, the role of nAChRs in HIV-associated neurocognitive disorder has not been investigated. We studied the effects of gp120(IIIB) on the expression and function of the nicotinic receptor α7 (α7-nAChR). Our results show that gp120, through activation of the CXCR4 chemokine receptor, induces a functional up-regulation of α7-nAChRs. Because α7-nAChRs have a high permeability to Ca(2+), we performed TUNEL staining to investigate the effects of receptor up-regulation on cell viability. Our data revealed an increase in cell death, which was blocked by the selective antagonist α-bungarotoxin. The in vitro data are supported by RT-PCR and Western blot analysis, confirming a remarkable up-regulation of the α7-nAChR in gp120-transgenic mice brains. Specifically, α7-nAChR up-regulation is observed in mouse striatum, a region severely affected in HIV(+) patients. In summary, CXCR4 activation induces up-regulation of α7-nAChR, causing cell death, suggesting that α7-nAChR is a previously unrecognized contributor to the neurotoxicity associated with HIV infection.