Time filter

Source Type

Pescara, Italy

Schillaci G.,University of Perugia | Maggi P.,University of Bari | Madeddu G.,University of Sassari | Pucci G.,University of Perugia | And 10 more authors.
Journal of Hypertension | Year: 2013

Objective: HIV infection has been associated with increased cardiovascular risk. Twenty-four-hour ambulatory blood pressure (BP) is a more accurate and prognostically relevant measure of an individual's BP load than office BP, and the ambulatory BP-derived ambulatory arterial stiffness index (AASI) and symmetric AASI (s-AASI) are established cardiovascular risk factors. Methods: In the setting of the HIV and HYpertension (HIV-HY) study, an Italian nationwide survey on high BP in HIV infection, 100 HIV-infected patients with high-normal BP or untreated hypertension (72% men, age 48 ± 10 years, BP 142/91 ± 12/7 mmHg) and 325 HIV-negative individuals with comparable age, sex distribution, and office BP (68% men, age 48 ± 10 years, BP 141/90 ± 11/8mmHg) underwent 24-h ambulatory BP monitoring. Results: Despite having similar office BP, HIV-infected individuals had higher 24-h SBP (130.6 ± 14 vs. 126.4 ± 10 mmHg) and pulse pressure (49.1 ± 9 vs. 45.9 ± 7mmHg, both P < 0.001), and a lower day-night reduction of mean arterial pressure (14.3 ± 9 vs. 16.3 ± 7%, P = 0.025). Both s-AASI and AASI were significantly higher in HIV patients (s-AASI, 0.22 ± 0.18 vs. 0.11 ± 0.15; AASI, 0.46 ± 0.22 vs. 0.29 ± 0.17; both P <0.001). In a multivariate regression, s-AASI was independently predicted by HIV infection (β = 0.252, P <0.001), age, female sex, and 24-h SBP. In HIV patients, s-AASI had an inverse relation with CD4+ cell count (Spearman's ρ -0.24, P = 0.027). Conclusion: Individuals with HIV infection and borderline or definite hypertension have higher symmetric AASI and 24-h systolic and pulse pressures than HIV-uninfected controls matched by office BP. High ambulatory BP may play a role in the HIV-related increase in cardiovascular risk. © 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins. Source

De Socio G.V.,Azienda Ospedaliero Universitaria di Perugia | Parruti G.,Pescara Hospital | Ricci E.,Luigi Sacco Hospital | Maggi P.,University of Bari | And 8 more authors.
AIDS | Year: 2014

Cardiovascular risk profile was compared in 765 Italian HIV-infected outpatients enrolled in 2005 and in 765 individually age-matched and sex-matched patients enrolled in 2011. Median Framingham risk score was 8.6% in 2005 vs. 7.9% in 2011 (PS=S0.04); metabolic syndrome was present in 40.3% vs. 33.4% (PS=S0.006). Blood glucose, triglycerides, prevalence of smokers, and lipodystrophy were all significantly lower in 2011 (all PS0.0001). Cardiovascular risk improved over a 6-year period in Italian HIV-infected patients. © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins. Source

Kritas S.K.,Aristotelian University | Caraffa A.,University of Perugia | Antinolfi P.,University of Perugia | Saggini A.,University of Rome Tor Vergata | And 9 more authors.
European Journal of Inflammation | Year: 2014

IgE is an important marker for allergy and plays a central role in the induction of allergic diseases through its binding of the high affinity receptor on mast cells. Mast cells can influence B cell survival, proliferation and differentiation into CD138+ cells. Among TH2 cytokines, interleukin (IL)-4 and IL-13 are responsible for class-switching in B cells which resolves in production of allergen-specific IgE antibodies that bind to specific receptor on mast cells. IgE synthesis by B cells is regulated by CD40 ligand, IL-4 and interferon-gamma, therefore inhibition of B cell antigen-specific IgE may prevent the cleavage of CD23 from B cells, having a therapeutic impact which also includes the removal of circulating free IgE, omalizumab, corticosteroids, mast cell stabilizers, leukotriene receptor antagonist, and others. B cell differentiation into IgE-producing cells requires two signals provided by TH2 cells and IL-4, however IL-4, IL-1 and IL-10 as well as several hormones are critical for the development of TH2 cells, while cytokines, such as interferon (IFN)-alpha, IFN-gamma, IL-12 and transforming growth factor (TGF)-beta play a negative role. However, the exact mechanism of this process has not yet been defined. Copyright © by BIOLIFE, s.a.s. Source

Kritas S.K.,Aristotelian University | Caraffa A.,University of Perugia | Antinolfi P.,University of Perugia | Saggini A.,University of Rome Tor Vergata | And 8 more authors.
International Journal of Immunopathology and Pharmacology | Year: 2014

Neuropeptides are involved in neurogenic inflammation where there is vasodilation and plasma protein extravasion in response to this stimulus. Nerve growth factor (NGF), identified by Rita Levi Montalcini, is a neurotrophin family compound which is important for survival of nociceptive neurons during their development. Therefore, NGF is an important neuropeptide which mediates the development and functions of the central and peripheral nervous system. It also exerts its proinflammatory action, not only on mast cells but also in B and T cells, neutrophils and eosinophils. Human mast cells can be activated by neuropeptides to release potent mediators of inflammation, and they are found throughout the body, especially near blood vessels, epithelial tissue and nerves. Mast cells generate and release NGF after degranulation and they are involved in iperalgesia, neuroimmune interactions and tissue inflammation. NGF is also a potent degranulation factor for mast cells in vitro and in vivo, promoting differentiation and maturation of these cells and their precursor, acting as a co-factor with interleukin-3. In conclusion, these studies are focused on cross-talk between neuropeptide NGF and inflammatory mast cells. Copyright © by BIOLIFE, s.a.s. Source

Madeddu G.,University of Sassari | De Socio G.V.L.,Unit of Infectious Diseases | Ricci E.,Epi2004 | Quirino T.,Unit of Infectious Diseases | And 14 more authors.
International Journal of Antimicrobial Agents | Year: 2015

Muscle alterations ranging from asymptomatic creatine phosphokinase (CPK) increases to rhabdomyolysis and central nervous system (CNS) symptoms have been reported in patients receiving raltegravir. Muscle symptoms and CPK increases were investigated in a cohort of HIV-infected patients receiving raltegravir-based antiretroviral therapy, and possible associated predictors were evaluated. The SCOLTA Project is a prospective, observational, multicentre study created to assess the incidence of adverse events in patients receiving new antiretroviral drugs in clinical practice. In total, 496 HIV-infected patients were enrolled [333 (67.1%) male]. CDC stage was C in 196 patients (39.5%). Mean age at enrolment was 45.9 ± 9.3 years. Median follow-up was 21 months. Twenty-six patients (5.2%) reported muscle symptoms (16 muscle pain and 17 weakness; 7 had both). Of 342 patients with normal baseline CPK values, 72 (21.1%) had a CPK increase. Seven patients (1.4%) discontinued raltegravir because of muscular events (three for muscle pain/weakness and four CPK increases). No cases of rhabdomyolysis were observed. Patients with muscle symptoms were more frequently receiving in their regimen than those not receiving atazanavir (P = 0.04) and were more likely to also report CNS symptoms (P < 0.0001). Significant predictors of muscle symptoms were CNS symptoms and use of atazanavir. Female sex was associated with a reduced risk of CPK increase. In conclusion, muscle symptoms and CPK elevations occurred frequently and caused most discontinuations due to adverse events. Their monitoring in patients receiving raltegravir should be considered, especially when co-administered with atazanavir or when CNS symptoms are also present. © 2014 Elsevier B.V. and the International Society of Chemotherapy. All rights reserved. Source

Discover hidden collaborations