Bone mineral density was similar between HIV-infected patients aged 20-30 years than in age- and gender-matched controls. However, lower femoral T-scores and higher rate of osteopenia and osteoporosis were seen in HIV-infected men. Therapy with protease inhibitors, nadir CD4 counts, and fat and lean mass were predictive factors of PBM. Given that these patients will be living with HIV infection for many years, every effort should be made to modify risk factors.
Changes in body fat distribution in virologically suppressed HIV-infected patients switching from lopinavir/ ritonavir (LPV/r) to atazanavir/ritonavir (ATV/r) were assessed. A prospective comparative study was conducted of 37 patients receiving LPV/r regimens switching to ATV/r with 46 patients continuing with LPV/r. Body composition was assessed with whole-body dual-energy x-ray absorptiometry (DXA). Abdominal CT scans were also performed in a subset of patients. Groups were comparable in baseline demographic, clinical, and anthropometric characteristics. After 12 months, peripheral fat did not change significantly, but an increase in trunk fat was observed only in the ATV/r group (0.87 kg, p ¼ 0.021). The percentage of patients with an increase !20% in total fat was 37.8% and 15.2% in the ATV/r and LPV/r groups, respectively ( p ¼ 0.018). In the ATV/r group, the increase in trunk fat (9.4%) was significantly higher than in peripheral fat (3.7%) ( p ¼ 0.007), leading to a significant increase in fat mass ratio (3.76%, p ¼ 0.028), whereas no significant differences were found among LPV/r patients. CT scans showed that abdominal fat increase corresponded to both visceral (28%, p ¼ 0.008) and subcutaneous fat (42%, p ¼ 0.008). These data suggest that switching from LPV/r to ATV/r is associated with increased trunk fat, both subcutaneous and visceral.
Our results highlight the importance of monitoring bone mineral density given the high probability of progression to osteopenia/osteoporosis, especially in women. In the future, changes in antiretrovirals other than tenofovir, such as PIs, should be recommended to reduce the risk of fracture.
Background:Some autoimmune diseases, including rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), are considered to be independent risk factors for vascular morbidity and mortality. These pathologies present accelerated atherosclerosis, partly because of a chronic sustained inflammation, greater prevalence of cardiovascular risk factors (CVRFs) and pharmacological therapy. However, regarding primary Sjögren’s syndrome (pSS), available data are heterogeneous and proceed from small case series. For this reason, the aim of this study was to provide further information on the identification of atherosclerosis in pSS and its possible association with clinical and analytical parameters of the disease.Objectives:To assess presence of subclinical atherosclerosis by means of carotid ultrasound in patients with pSS and to analyze clinical, analytical and CVRF along with their potential association with the presence of subclinical cardiovascular affectation.Methods:This is a cross-sectional study of 38 patients with pSS (all patients met ACR/EULAR1classification criteria for pSS) and 38 age and sex matched controls. Demographic variables and classical CVRFs were collected (Hypertension, Diabetes mellitus, dyslipemia, Body Mass Index and smoking habit) and the presence of subclinical atherosclerosis was assessed by carotid ultrasound with carotid intima-media thickness (CIMT) measurement and determination of the presence of atheromatous plaques2, both in pSS patients and controls. Disease features were also collected in pSS patients (disease duration, disease activity measured by ESSDAI, glandular vs extraglandular involvement, serological features and treatments received).Statistical analysis: To evaluate differences between patients and controls, T-test or Wilcoxon test with continuity correction, were used for quantitative features and Fisher test for categorical variables. In order to test the presence of pSS as an independent risk factor for subclinical atherosclerosis, from other features as classic CVRFs or analytical data, first we adjusted logistic binomial regression in a bivariate analysis, to select possible predictors to be included in a multivariate analysis. Statistical significance was p<0.05, and OR CI 95% vas calculated.R-Statistics v- 3.6Table 1.Comparison of clinical data of two case groups and healthy control group M (p25, p75)GroupsCase group ACase group BHealthy control groupH valueP valueHistory of thrombus (case)4a8a-13.7090.001History of adverse pregnancy (case)3a19a-34.596<0.001ESR20.00(12.25,111.00)a35.00(14.25,95.00)a9.00(6.00,13.00)34.381<0.001CRP15.00(4.03,37.83)ab7.33(1.76,21.13)ab2.10(1.28,2.31)35.263<0.001PLT228.00(189.50,573.25)ab197.00(66.00,260.50)ab258.50(228.25,272.25)33.482<0.001Note:aComparison with healthy control groupP< 0.05;bComparison with case groupP<0.05.Table 2.Comparison of lymphocyte subsets in peripheral blood of two case groups and healthy control group M (p25, p75)Results:All of the 76 patients included were women, with a mean age of 53.7 ± 11.7 years. For both groups, no differences between prevalence of classical CVRFs were found. Subclinical atherosclerosis presence was higher in patients with pSS than in controls [OR= 4.17, 95%CI (1.27- 16.54), p<0.001], as well as CIMT values (0.79± 0.43 mm vs. 0.66 ± 0.27 mm; p=0.02). An association of subclinical atherosclerosis with erythrocyte sedimentation rate [OR=1.18, 95%CI (1.05-1.37), p<0.05] and Rheumatoid Factor [OR=1.28, 95%CI (1.63-2.26), p<0.05].Conclusion:This cohort showed a greater prevalence of subclinical atherosclerosis in patients with pSS, indicating this disease as an independent risk factor for presence of early vascular damage.References:[1]Vitali C et al. Classification Criteria for Sjögren Syndrome: a revised version of the European criteria proposed by the American-European Consensous Group. Ann Rheum Dis. 2002; 61: 554-8[2]Touboul PJ et al. Mannheim carotid intima-media thickness and plaque consensus (2004-2006-2011). An update on behalf of the advisory board of the 3rd, 4th and 5th watching the risk symposia, at the 13th, 15th and 20th European Stroke Conferences, Mannheim, Germany, 2004, Brussels, Belgium, 2006, and Hamburg, Germany, 2011. Cerebrovasc Dis. 2012; 34: 290-6Disclosure of Interests:Marta Novella-Navarro: None declared, José Luis Cabrera-Alarcón: None declared, José Luis Rosales Grant/research support from: I have received financial support from Novartis, UCB, Pfizer, Abvie to meeting and symposia, Jorge Juan González Martin Grant/research support from: I have received finacial grants from Novartis, Lilly, Pfizer, Abvie for meetings and symposia assistance, Paloma García de la Peña Grant/research support from: I have received finacial grants from Novartis, Lilly, Pfizer, Abvie for meetings and symposia assistance, Ofelia Carrion: None declared
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