Because effects of cigarette smoking on health-related quality of life (HRQL) have not been well described, we carried out a cross-sectional assessment of HRQL using the Medical Outcomes Survey Scale adapted for patients with human immunodeficiency virus (MOS-HIV questionnaire) in 585 HIV-infected homosexual/bisexual men, injection drug users, and female partners enrolled in a multicenter, prospective study of the pulmonary complications of HIV infection. Mean scores for the following dimensions of HRQL were calculated: general health perception, quality of life, physical functioning, bodily pain, social functioning, role functioning, energy, cognitive functioning, and depression. A multivariate model was used to determine the impact on HRQL of the following factors: smoking, CD4 loss, acquired immune deficiency syndrome (AIDS) diagnoses, number of symptoms, study site, education, injection drug use, gender, and age. Current smoking was independently associated with lower scores for general health perception, physical functioning, bodily pain, energy, role functioning, and cognitive functioning (all with p < 0.05). We conclude that patients with HIV infection who smoke have poorer HRQL than nonsmokers. These results support the use of smoking cessation strategies for HIV-infected persons who smoke cigarettes.
"There are few reports showing the cognitive impairment in heavy smokers [68-71]. Effects of cigarette smoking on cognitive disorders in HIV infected patients are scanty [23,72]. This is the first study in analyzing the molecular mechanisms behind the increased risk of HAND in HIV infected nicotine users. "
[Show abstract][Hide abstract] ABSTRACT: Background:
HIV-associated neurocognitive disorder (HAND) is characterized by development of cognitive, behavioral and motor abnormalities, and occurs in approximately 50% of HIV infected individuals. In the United States, the prevalence of cigarette smoking ranges from 35-70% in HIV-infected individuals compared to 20% in general population. Cognitive impairment in heavy cigarette smokers has been well reported. However, the synergistic effects of nicotine and HIV infection and the underlying mechanisms in the development of HAND are unknown.
In this study, we explored the role of nicotine in the progression of HAND using SK-N-MC, a neuronal cell line. SKNMC cells were infected with HIV-1 in the presence or absence of nicotine for 7 days. We observed significant increase in HIV infectivity in SK-N-MC treated with nicotine compared to untreated HIV-infected neuronal cells. HIV and nicotine synergize to significantly dysregulate the expression of synaptic plasticity genes and spine density; with a concomitant increase of HDAC2 levels in SK-N-MC cells. In addition, inhibition of HDAC2 up-regulation with the use of vorinostat resulted in HIV latency breakdown and recovery of synaptic plasticity genes expression and spine density in nicotine/HIV alone and in co-treated SK-N-MC cells. Furthermore, increased eIF2 alpha phosphorylation, which negatively regulates eukaryotic translational process, was observed in HIV alone and in co-treatment compared to untreated control and nicotine alone treated SK-N-MC cells.
These results suggest that nicotine and HIV synergize to negatively regulate the synaptic plasticity gene expression and spine density and this may contribute to the increased risk of HAND in HIV infected smokers. Apart from disrupting latency, vorinostat may be a useful therapeutic to inhibit the negative regulatory effects on synaptic plasticity in HIV infected nicotine abusers.
"; Pines, Koutsky, & Buskin, 2011; Rahmanian et al., 2011). Similarly, continued smoking among PLHIV has been linked to lower quality of life (Crothers et al., 2005; Ingersoll, Cropsey, & Heckman, 2009), increased pain (Turner et al., 2001), and diminished cognitive functioning (Turner et al., 2001). Moreover, both uncontrolled HIV infection and antiretroviral therapy may confer an elevated risk for cardiovascular disease that is further exacerbated by cigarette use (Elzi et al., 2006; Lifson et al., 2010). "
[Show abstract][Hide abstract] ABSTRACT: PLHIV have higher rates of smoking and lower motivation to quit smoking; thus to impact smoking rates, cessation interventions need to be acceptable to a wider range of PLHIV smokers as well as feasible to implement in a busy clinical setting. The purpose of this study was to evaluate the acceptability, feasibility, and effects of a Screening, Brief Intervention, and Referral for Treatment (SBIRT) model in an HIV/AIDS clinic among a sample of PLHIV.
PLHIV smokers (N=40) were randomized at baseline, irrespective of their self-reported discrete smoking cessation motivation status, to receive either 8-weeks of combination nicotine replacement therapy (NRT) in conjunction with brief counseling (SBIRT framework) (n=23) or usual care (n=17). Smoking outcome measures included cigarettes smoked per day, nicotine dependence, smoking urge, and smoking withdrawal symptoms.
The SBIRT intervention appeared to be acceptable and feasible, and produced medium to large reductions in cigarettes smoked per day, physical nicotine dependence, smoking urge, and smoking withdrawal symptoms, even for smokers not ready to quit within 6months.
Findings provide preliminary support for the integration of an SBIRT model in an HIV/AIDS clinic setting to screen and provide active treatment to all smokers, regardless of readiness to quit smoking. Given the high prevalence and incredible health burden of continued smoking in this population, identifying brief and effective interventions that are easily translated into clinical practice represents an enormous challenge that if met, will yield significant improvements to overall patient outcomes.
[Show abstract][Hide abstract] ABSTRACT: Tobacco addiction and chronic pain represent 2 highly prevalent and comorbid conditions that engender substantial burdens upon individuals and systems. Interrelations between pain and smoking have been of clinical and empirical interest for decades, and research in this area has increased dramatically over the past 5 years. We conceptualize the interaction of pain and smoking as a prototypical example of the biopsychosocial model. Accordingly, we extrapolated from behavioral, cognitive, affective, biomedical, and social perspectives to propose causal mechanisms that may contribute to the observed comorbidity between these 2 conditions. The extant literature was 1st dichotomized into investigations of either effects of smoking on pain or effects of pain on smoking. We then integrated these findings to present a reciprocal model of pain and smoking that is hypothesized to interact in the manner of a positive feedback loop, resulting in greater pain and increased smoking. Finally, we proposed directions for future research and discussed clinical implications for smokers with comorbid pain disorders. We observed modest evidence that smoking may be a risk factor in the multifactorial etiology of some chronically painful conditions and that pain may come to serve as a potent motivator of smoking. We also found that whereas animal studies yielded consistent support for direct pain-inhibitory effects of nicotine and tobacco, results from human studies were much less consistent. Future research in the emerging area of pain and smoking has the potential to inform theoretical and clinical applications with respect to tobacco smoking, chronic pain, and their comorbid presentation. (PsycINFO Database Record (c) 2011 APA, all rights reserved).
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.