Health inequities and socioeconomic factors predicting the access to treatment for unruptured intracranial aneurysms in the USA in the last 20 years: interaction effect of race, gender, and insurance.

BACKGROUND: The literature suggests that minority racial and ethnic groups have lower treatment rates for unruptured intracranial aneurysms (UIA). It is uncertain how these disparities have changed over time. METHODS: A cross-sectional study using the National Inpatient Sample database covering 97% of the USA population was carried out. RESULTS: A total of 213 350 treated patients with UIA were included in the final analysis and compared with 173 375 treated patients with aneurysmal subarachnoid hemorrhage (aSAH) over the years 2000-2019. The mean (SD) age of the UIA and aSAH groups was 56.8 (12.6) years and 54.3 (14.1) years, respectively. In the UIA group, 60.7% were white patients, 10.2% were black patients, 8.6% were Hispanic, 2% were Asian or Pacific Islander, 0.5% were Native Americans, and 2.8% were others. The aSAH group comprised 48.5% white patients, 13.6% black patients, 11.2% Hispanics, 3.6% Asian or Pacific Islanders, 0.4% Native Americans, and 3.7% others. After adjusting for covariates, black patients (OR 0.637, 95% CI 0.625 to 0.648) and Hispanic patients (OR 0.654, 95% CI 0.641 to 0.667) had lower odds of treatment compared with white patients. Medicare patients had higher odds of treatment than private patients, while Medicaid and uninsured patients had lower odds. Interaction analysis showed that non-white/Hispanic patients with any insurance/no insurance had lower treatment odds than white patients. Multivariable regression analysis showed that the treatment odds of black patients has improved slightly over time, while the odds for Hispanic patients and other minorities have remained the same over time. CONCLUSION: This study from 2000 to 2019 shows that disparities in the treatment of UIA have persisted but have slightly improved over time for black patients while remaining constant for Hispanic patients and other minority groups.

Paliperidone to Treat Psychotic Disorders.

PURPOSE OF REVIEW: This is a comprehensive review of the literature regarding the use of paliperidone in the treatment of schizophrenia and schizoaffective disorder. It covers the background and presentation of schizophrenia and schizoaffective disorder, as well as the mechanism of action and drug information for paliperidone. It covers the existing evidence of the use of paliperidone for the treatment of schizophrenia and schizoaffective disorder. RECENT FINDINGS: Schizophrenia and schizoaffective disorder lead to significant cognitive impairment. It is thought that dopamine dysregulation is the culprit for the positive symptoms of schizophrenia and schizoaffective disorder. Similar to other second-generation antipsychotics, paliperidone has affinity for dopamine D2 and serotonin 5-HT2A receptors. Paliperidone was granted approval in the United States in 2006 to be used in the treatment of schizophrenia and in 2009 for schizoaffective disorder. SUMMARY: Schizophrenia and schizoaffective disorder have a large impact on cognitive impairment, positive symptoms and negative symptoms. Patients with either of these mental illnesses suffer from impairments in everyday life. Paliperidone has been shown to reduce symptoms of schizophrenia and schizoaffective disorder.

Dual biologic therapy in a patient with severe asthma and other allergic disorders.

Severe asthma is very difficult to manage in many individuals, and systemic corticosteroids are often used to prevent or manage acute exacerbations. Furthermore, comorbid allergic conditions may render standard therapies inadequate. A 51-year-old man presented with severe eosinophilic asthma requiring nearly constant oral corticosteroid usage despite using high-dose inhaled corticosteroids and secondary asthma controllers. His condition was complicated by aspirin-exacerbated respiratory disease, including severe nasal polyposis, chronic rhinosinusitis, as well as chronic idiopathic urticaria. Mepolizumab was initiated and led to dramatic improvement of asthma over 6 months. However, he continued to experience exacerbations of chronic idiopathic urticaria not responsive to H1-antihistamines. Omalizumab was added, and the patient's urticaria attained marked improvement with only an occasional breakthrough rash. Dual biologic therapies can be a unique and useful steroid-sparing treatment option for patients with uncontrolled severe asthma and chronic idiopathic urticaria.

Human Cytomegalovirus Promotes Survival of Infected Monocytes via a Distinct Temporal Regulation of Cellular Bcl-2 Family Proteins.

UNLABELLED: Monocytes play a key role in the hematogenous dissemination of human cytomegalovirus (HCMV) to target organ systems. To infect monocytes and reprogram them to deliver infectious virus, HCMV must overcome biological obstacles, including the short life span of monocytes and their antiviral proapoptotic response to infection. We have shown that virally induced upregulation of cellular Mcl-1 promotes early survival of HCMV-infected monocytes, allowing cells to overcome an early apoptotic checkpoint at around 48 h postinfection (hpi). Here, we demonstrate an HCMV-dependent shift from Mcl-1 as the primary antiapoptotic player to the related protein, Bcl-2, later during infection. Bcl-2 was upregulated in HCMV-infected monocytes beginning at 48 hpi. Treatment with the Bcl-2 antagonist ABT-199 only reduced the prosurvival effects of HCMV in target monocytes beginning at 48 hpi, suggesting that Mcl-1 controls survival prior to 48 hpi, while Bcl-2 promotes survival after 48 hpi. Although Bcl-2 was upregulated following viral binding/signaling through cellular integrins (compared to Mcl-1, which is upregulated through binding/activation of epidermal growth factor receptor [EGFR]), it functioned similarly to Mcl-1, adopting the early role of Mcl-1 in preventing caspase-3 cleavage/activation. This distinct, HCMV-induced shift from Mcl-1 to Bcl-2 occurs in response to a cellular upregulation of proapoptotic Bax, as small interfering RNA (siRNA)-mediated knockdown of Bax reduced the upregulation of Bcl-2 in infected monocytes and rescued the cells from the apoptotic effects of Bcl-2 inhibition. Our data demonstrate a distinct survival strategy whereby HCMV induces a biphasic regulation of cellular Bcl-2 proteins to promote host cell survival, leading to viral dissemination and the establishment of persistent HCMV infection. IMPORTANCE: Hematogenous dissemination of HCMV via infected monocytes is a crucial component of the viral survival strategy and is required for the establishment of persistent infection and for viral spread to additional hosts. Our system of infected primary human blood monocytes provides us with an opportunity to answer specific questions about viral spread and persistence in in vivo-relevant myeloid cells that cannot be addressed with the more traditionally used replication-permissive cells. Our goal in examining the mechanisms whereby HCMV reprograms infected monocytes to promote viral dissemination is to uncover new targets for therapeutic intervention that would disrupt key viral survival and persistence strategies. Because of this important role in maintaining survival of HCMV-infected monocytes, our new data on the role of Bcl-2 regulation during viral infection represents a promising molecular target for mitigating viral spread and persistence.