Bacterial Pneumonia among HIV-Infected Patients: Decreased Risk After Tobacco Smoking Cessation. ANRS CO3 Aquitaine Cohort, 2000–2007

BACKGROUND: Bacterial pneumonia is still a substantial cause of morbidity and mortality in HIV-infected patients in the era of combination Antiretroviral Therapy. The benefit of tobacco withdrawal on the risk of bacterial pneumonia has not been quantified in such populations, exposed to other important risk factors such as HIV-related immunodeficiency. Our objective was to estimate the effect of tobacco smoking withdrawal on the risk of bacterial pneumonia among HIV-infected individuals. METHODOLOGY/PRINCIPAL FINDINGS: Patients of the ANRS CO3 Aquitaine Cohort with >or= two visits during 2000-2007 and without bacterial pneumonia at the first visit were included. Former smokers were patients who stopped smoking since >or= one year. We used Cox proportional hazards models adjusted on CD4+ lymphocytes (CD4), gender, age, HIV transmission category, antiretroviral therapy, cotrimoxazole prophylaxis, statin treatment, viral load and previous AIDS diagnosis. 135 cases of bacterial pneumonia were reported in 3336 patients, yielding an incidence of 12 per thousand patient-years. The adjusted hazard of bacterial pneumonia was lower in former smokers (Hazard Ratio (HR): 0.48; P = 0.02) and never smokers (HR: 0.50; P = 0.01) compared to current smokers. It was higher in patients with <200 CD4 cells/microL and in those with 200 to 349 CD4 cells/microL (HR: 2.98 and 1.98, respectively; both P<0.01), but not in those with 350 to 499 CD4 cells/microL (HR: 0.93; P = 0.79), compared to those with >or=500 CD4 cells/microL. The interaction between CD4 cell count and tobacco smoking status was not statistically significant. CONCLUSIONS/SIGNIFICANCE: Smoking cessation dramatically reduces the risk of bacterial pneumonia, whatever the level of immunodeficiency. Smoking cessation interventions should become a key element of the clinical management of HIV-infected individuals

Rituximab Efficacy during a Refractory Polyarteritis Nodosa Flare

Polyarteritis nodosa (PAN) is a systemic vasculitis whose severe forms are treated with glucocorticoids and cyclophosphamide. Refractory patients are exposed to many complications, notably accelerated atherosclerosis. We report a case report of 71-year-old man followed for polyarteritis nodosa refractory to glucocorticoids and cyclosphosphamide. Systemic vasculitis relapses are followed to accelerated atherosclerosis: severe ischemic lesions led to amputation of lower limbs. Remission of refractory PAN is obtained with rituximab. Disappearance of biological inflammatory is allowed to regression of ischemic lesions in upper limbs. In this situation, we recommend a systematic vascular work-up for patients suffered from refractory vasculitis. On the other hand, therapeutic trials are needed to determine the real efficacy and place of rituximab in the treatment of polyarteritis nodosa

The role of lipopolysaccharide as a marker of immune activation in HIV-1 infected patients: a systematic literature review

Abstract Background Recent observational studies suggest a role for lipopolysaccharide (LPS) as a marker of immune activation in HIV-infected patients, with potential repercussions on the effectiveness of antiretroviral regimens. Object A systematic review of LPS as a marker of immune activation in HIV-1 infected patients. Data sources MEDLINE register of articles and international conference proceedings. Review methods Case–control studies comparing the role of plasma LPS as a marker of immune activation in HIV-infected patients versus HIV negative subjects. Data synthesis Two hundred and six articles were selected using MEDLINE, plus 51 studies presented at international conferences. Plasma LPS is a marker of immune activation in HIV-infected patients, determining the entry of central memory CD4+ T cells into the replication cycle and finally generating cell death. Plasma LPS probably results from immune-mediated alterations of the intestinal barrier, which can occur soon after HIV seroconversion. LPS is a likely marker of disease progression, as it drives chronic monocyte activation, and some studies suggest that hyperexpression of CCR5 receptors, related to LPS plasma levels, could be responsible for monocyte trafficking in the brain compartment and for the appearance of HIV-associated neurocognitive disorders. Long-term combination antiretroviral therapy (cART) generally reduces LPS concentrations, but rarely to the same levels as in the control group. This phenomenon probably depends on ongoing but incomplete repair of the mucosal barrier. Only in patients achieving maximal viral suppression (i.e. viral load  Conclusions LPS is a marker of microbial translocation, responsible for chronic immune activation in HIV-infected patients. Even in successfully treated patients, LPS values are rarely normal. Several studies suggest a role for LPS as a negative predictive marker of immune restoration in patients with blunted CD4 T cell gain.</p

The role of lipopolysaccharide as a marker of immune activation in HIV-1 infected patients: a systematic literature review

BACKGROUND: Recent observational studies suggest a role for lipopolysaccharide (LPS) as a marker of immune activation in HIV-infected patients, with potential repercussions on the effectiveness of antiretroviral regimens. OBJECT: A systematic review of LPS as a marker of immune activation in HIV-1 infected patients. DATA SOURCES: MEDLINE register of articles and international conference proceedings. REVIEW METHODS: Case–control studies comparing the role of plasma LPS as a marker of immune activation in HIV-infected patients versus HIV negative subjects. DATA SYNTHESIS: Two hundred and six articles were selected using MEDLINE, plus 51 studies presented at international conferences. Plasma LPS is a marker of immune activation in HIV-infected patients, determining the entry of central memory CD4+ T cells into the replication cycle and finally generating cell death. Plasma LPS probably results from immune-mediated alterations of the intestinal barrier, which can occur soon after HIV seroconversion. LPS is a likely marker of disease progression, as it drives chronic monocyte activation, and some studies suggest that hyperexpression of CCR5 receptors, related to LPS plasma levels, could be responsible for monocyte trafficking in the brain compartment and for the appearance of HIV-associated neurocognitive disorders. Long-term combination antiretroviral therapy (cART) generally reduces LPS concentrations, but rarely to the same levels as in the control group. This phenomenon probably depends on ongoing but incomplete repair of the mucosal barrier. Only in patients achieving maximal viral suppression (i.e. viral load < 2.5 cp/ml) are LPS levels comparable to healthy donors. In successfully treated patients who did not restore CD4+ T cells, one hypothesis is that the degree of residual microbial translocation, measured by LPS, alters the turnover of CD4+ T cells. CONCLUSIONS: LPS is a marker of microbial translocation, responsible for chronic immune activation in HIV-infected patients. Even in successfully treated patients, LPS values are rarely normal. Several studies suggest a role for LPS as a negative predictive marker of immune restoration in patients with blunted CD4 T cell gain

Cannabis Use and Plasma Human Immunodeficiency Virus (HIV) RNA Levels in Patients Coinfected With HIV and Hepatitis C Virus Receiving Antiretroviral Therapy: Data From the ANRS CO13 HEPAVIH Cohort

International audienceNo abstract availabl

Tobacco use in people living with HIV: The need for complementary descriptive data to see beyond the smoke screen

International audienceNo abstract availabl

Eur J Intern Med

Antisynthetase syndrome (ASyS) is a rare autoimmune disease. We aimed to determine clinical, biological, radiological, and evolutive profiles of ASyS patients with anti-PL7 or anti-PL12 autoantibodies. We performed a retrospective study that included adults with overt positivity for anti-PL7/anti-PL12 autoantibodies and at least one Connors' criterion. Among 72 patients, 69% were women, 29 had anti-PL7 and 43 anti-PL12 autoantibodies, median age was 60.3 years, and median follow-up period was 52.2 months. At diagnosis, 76% of patients had interstitial lung disease, 61% had arthritis, 39% myositis, 25% Raynaud's phenomenon, 18% mechanic's hands, and 17% had fever. The most frequent pattern on initial chest computed tomography was non-specific interstitial pneumonia and 67% had fibrosis at last follow-up. During follow-up, 12 patients had pericardial effusion (18%), 19 had pulmonary hypertension (29%), 9 (12.5%) had neoplasms, and 14 (19%) died. Sixty-seven patients (93%) received at least one steroid or immunosuppressive drug. Patients with anti-PL12 autoantibodies were younger (p=0.01) and more frequently exhibited anti-SSA autoantibodies (p=0.01); patients with anti-PL7 autoantibodies had more severe weakness and higher maximum creatine kinase levels (p=0.03 and 0.04, respectively). Initial severe dyspnoea was more common in patients from the West Indies (p=0.009), with lower predicted values of forced vital capacity, forced expiratory volume in 1s, and total lung capacity (p=0.01, p=0.02, p=0.01, respectively) contributing to a more severe 'respiratory' initial presentation. The high mortality and significant numbers of cardiovascular events, neoplasms and lung fibrosis in anti-PL7/12 patients justify close monitoring and question addition of antifibrotic drugs

Determinants of smoking cessation attempts among HIV-infected patients results from a hospital-based prospective cohort.

Non-acquired immune-deficiency syndrome (AIDS) defining malignancies (especially lung cancer) and bacterial infections as well as cardiovascular diseases now account for almost one third of deaths and morbid events in treated patients infected by the Human Immunodeficiency Virus (HIV). Tobacco smoking is a major modifiable risk factor of these emergent conditions and almost half of these patients are regular smokers in resource-rich countries. To estimate the effect of HIV infection characteristics on smoking cessation attempts among HIV-infected smokers. All smokers of the ANRS CO3 Aquitaine Cohort with at least two visits between 2000 and 2005 were included in this analysis. The probability of smoking cessation attempts was estimated using survival analyses for recurrent events (frailty model). Covariates were CD4 cell count, gender, age, HIV transmission categories, duration since HIV-diagnosis, AIDS stage, antiretroviral therapy, and cardiovascular history. Among 2223 smokers, 743 attempted to quit smoking at least once. The incidence of smoking cessation attempt was lower among patients infected through injection drug use (IDU) and was higher among patients aged 50 or older (HR=1.4), those with a known duration of HIV infection &gt;15 years (HR=1.5), and those who had already tried to quit smoking once (HR=4.2) or more (HR=5.8). Traditional characteristics associated with smoking cessation attempts are the most important to explain smoking cessation attempts in HIV-infected patients. These results indicate that strategies successfully implemented in other populations should be reinforced to fit the needs of HIV-infected patients