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Biomedical subjects

Renato Maserati

Publications and source records attributed to Renato Maserati.

25 records · Page 2Linked to original sources
PubMed2002

Modulation of human immunodeficiency virus (HIV)-specific immune response by using efavirenz, nelfinavir, and stavudine in a rescue therapy regimen for HIV-infected, drug-experienced patients.

Analysis of the virologic and immunomodulatory effects of an association of efavirenz (EFV), nelfinavir (NFV), and stavudine (d4T) was performed in 18 human immunodeficiency virus (HIV)-infected and highly active antiretroviral therapy (HAART)-experienced patients who failed multiple therapeutic protocols. Patients (<500 CD4(+) cells/ micro l; >10,000 HIV copies/ml) were nonnucleoside reverse transcriptase inhibitor (NNRTI)-naive and were treated for 10 months with EFV (600 mg/day) in association with NFV (750 mg three times daily) and d4T (30 or 40 mg twice daily). Measurement of HIV peptide- and mitogen-stimulated production of interleukin-2 (IL-2), gamma interferon (IFN-gamma), IL-4, and IL-10 as well as quantitation of mRNA for the same cytokines in unstimulated peripheral blood mononuclear cells were performed at baseline and 2 weeks (t1), 2 months (t2), and 10 months (t3) into therapy. The results showed that HIV-specific (but not mitogen-stimulated) IL-2 and IFN-gamma production was augmented and IL-10 production was reduced in patients who received EFV, NFV, and d4T. Therapy was also associated with a reduction in HIV RNA in plasma and an increase in CD4(+) cell count. These changes occurred in the first year of therapy (t2 and t3) and were confirmed by quantitation of cytokine-specific mRNA. Therapy with EFV, NFV, and d4T increases HIV-specific type 1 cytokine production as well as CD4 counts and reduces plasma viremia. This therapeutic regimen may be considered for use in cases of advanced HIV infection.

Adult↗
PubMed2002

Evaluation of the risk factors associated with lipodystrophy development in a cohort of HIV-positive patients.

The prevalence of lipodystrophy in an HIV-infected population and the risk factors associated with body shape changes were analysed in this study. Five hundred and four subjects were included. Among these, 201 (39.9%) had features of lipodystrophy syndrome (cases); 303 (60.1%) constituted the control group. Compared with the control group, the lipodystrophy subjects were different in age (P = 0.01); duration of antiretroviral therapy (P < 0.001); length of exposure to nucleoside reverse transcriptase inhibitors (NRTIs) (P < 0.001) and to protease inhibitors (P < 0.001); nadir of CD4 cell count (P < 0.001); and value of plasma HIV-RNA before antiretroviral therapy (P = 0.008). In a multivariate analysis, length of therapy and a nadir CD4 cell count below 250 cell/microl were associated with an increased risk of lipodystrophy. Among patients with lipodystrophy, isolated fat loss was observed in 46 (23%); isolated fat accumulation in 40 (20%); mixed (loss and accumulation) syndrome in 50 (25%); and isolated metabolic changes in 65 (32%). Subjects with morphological alterations displayed a greater cumulative time of exposure to NRTIs and to protease inhibitors than patients with isolated metabolic alterations. Patients with lipoatrophy had had a greater exposure to stavudine.

Adolescent↗
PubMedDate not supplied

Control of HIV during a structured treatment interruption in chronically infected individuals with vigorous T cell responses.

PURPOSE: To study whether and under what circumstances HIV can be controlled in chronically infected patients. METHOD: Nine patients treated with hydroxyurea and didanosine (PANDAs) were compared with 7 patients on highly active antiretroviral therapy (HAART) during an 8-week treatment interruption. Both groups had similar baseline viral load, CD4 count, and length of treatment. Treatment was resumed if viral rebound >10,000 copies/mL (virological failure) or CD4 count decrease below 200 cells/mm(3) (immunological failure) occurred in two consecutive measurements. RESULTS: None of the PANDAs failed. Viral rebound was spontaneously contained, and CD4 count remained stable. Four out of 7 patients in the HAART group failed to control HIV by week 6 and had to restart therapy due to either viremia rebound or CD4 decrease. Before therapy interruption, the PANDAs had a vigorous HIV-specific T cell immune response (median CD4VIR 1.2%), while the HAART-treated patients did not (median CD4VIR 0.2%) (CD4VIR represents the percentage of HIV-specific CD4 subpopulation expressing IFN-gamma within the total CD4 population [CD3+, CD4+, IFN-gamma+]). This difference was statistically significant (p =.002). CONCLUSION: This study shows that HIV can be controlled during therapy interruption in patients with established infection, and that control of viral replication correlates with vigorous anti-HIV specific immune responses.

Anti-HIV Agents↗
PubMedDate not supplied

Evaluation of infectious complications and immune recovery following high-dose chemotherapy (HDC) and autologous peripheral blood progenitor cell transplantation (PBPC-T) in 148 breast cancer patients.

BACKGROUND AND OBJECTIVES: High-dose chemotherapy (HDC) with autologous PBPC-T has been reported to be effective in hematological and in selected solid malignancies. In this setting, infectious complications represent a relevant cause of morbidity. PATIENTS AND METHODS: To ascertain the incidence, types and factors influencing the development of early and late infections, we retrospectively analyzed 148 consecutive breast cancer (BC) patients receiving HDC and PBPC-T, both for primary high-risk BC (pBC) and metastatic disease (mBC). RESULTS: Early infection strongly associated with the occurrence of grade 4 mucositis (p < 0.001), was documented in 28 patients (19%). Late re-activation of varicella zoster virus (VZV) occurred in 14 patients (9%); an inverse correlation between the VZV re-activation and the total amount of T-cells transferred with the graft was observed. Evaluation of immune reconstitution, carried out in 10 out of 148 patients, showed a long-lasting CD+ T-cells depression (> 2 year), mainly involving the naive CD4+ T-cell subset. Conversely, the analysis of the frequency of proliferating T-lymphocyte precursors, specific for antigens expressed by 3 different widespread pathogens, demonstrated that, notwithstanding the delayed recovery of CD4+ cells, many T-lymphocyte functions were within normal range 1 year after PBPC-T. CONCLUSION: Altogether these results show that severe mucositis is associated with early bacterial infections and the infusion of large numbers of T-cells plays a role in controlling late VZV reactivation.

Adult↗
PubMedDate not supplied

Antiretroviral therapy in chronic liver disease: focus on HIV/HCV coinfection--statements of the First Italian Consensus Workshop.

Hepatitis C virus common transmission routes and HCV coinfection is frequent in persons living with HIV. Liver enzyme elevation following the initiation of antiretroviral therapy is frequently seen in HIV-infected patients with chronic liver disease, particularly those with chronic hepatitis C. This complication may lead to treatment discontinuation, complicating HIV therapeutic management. Multiple factors influence the risk of liver toxicity under antiretroviral therapy, including the specific drug in use (e.g. use of full doses of ritonavir), and environmental factors (e.g. alcohol abuse). However a beneficial effect of antiretroviral therapy on liver disease has been supported by some studies. Despite increasing knowledge of HCV/HIV coinfection, there is no clear consensus on how to treat HIV in HCV-coinfected patients An Italian group of experts were invited to discuss in detail the current risks and implications of antiretroviral treatment in HIV-infected persons with chronic hepatitis C, and their main conclusions are summarized in this consensus document.

Anti-HIV Agents↗
PubMedDate not supplied

Atherosclerosis in HIV patients: a new face for an old disease?

As we have become more familiar with the pathogenesis of atheroma, it has become recognized atherogenesis is mainly an inflammatory disease. Therefore, it is not surprising that a body of evidence demonstrates that endothelium injury is associated with the progression and severity of HIV infection. Another important question is: do antiretroviral drugs increase or reduce endothelial injury? Various studies support the hypothesis that HAART does induce activation of endothelial function. Thus, HIV virus as well as immune reconstitution and HAART itself promote premature endothelial activation. Such a prominent role played by inflammatory events could affect the structure of the arterial lesions in HIV patients that could present different characteristics with respect to the classical atheroma. In fact, in two HIV patients with severe stenosis of the carotid, histology revealed extensive inflammatory infiltration of the vascular wall. The characteristics of these lesions were similar to those of arteritis. Another study evidenced that the ultrasonographic structure of the lesions in HIV patients substantially differ from those found in atherosclerosis, sharing similar characteristics with arteritis. We hypothesize that the atherosclerotic lesions in HIV patients develop in two distinct phases: the first one characterized by an inflammation of the vascular wall, and subsequently, the lesions could evolve towards the classic feature of the atheroma. The lesions in the first phase are probably determined by immunodeficiency, immune reconstitution, and the same effect of HAART. In the second phase they could be maintained by the classic risk factors.

Animals↗