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Biomedical subjects

Alessandro Cozzi-Lepri

Publications and source records attributed to Alessandro Cozzi-Lepri.

28 records · Page 2Linked to original sources
PubMed2004

The management of hepatitis B virus/HIV-1 co-infected patients starting their first HAART regimen. Treating two infections for the price of one drug?

We examined the impact of a lamivudine-containing highly active antiretroviral therapy (HAART) regimen on 164 hepatitis B virus/HIV co-infected individuals starting their first HAART. Lamivudine-treated patients (accounting for 73% of the study population) showed a significantly lower level of alanine aminotransferase over follow-up [-81.1 mU/ml mean difference; 95% confidence intervals (95% CI): -30.3; -131.7, P=0.003] and a significantly reduced risk of liver-related morbidity/mortality [Relative hazard (RH)=0.07; 95% CI: 0.01-0.38, P=0.002] than those starting a lamivudine sparing-regimen.

Adult↗
PubMed2003

Adherence to highly active antiretroviral therapy is better in patients receiving non-nucleoside reverse transcriptase inhibitor-containing regimens than in those receiving protease inhibitor-containing regimens.

The difference between adherence to non- nucleoside reverse transcriptase inhibitor (NNRTI) and protease inhibitor (PI)-based regimens was investigated. Better adherence was found in NNRTI-treated patients, especially when efavirenz was included in the regimen, compared with single PI-treated patients and in those with CD4 cell counts less than 200 x 10(6)/l. By contrast, younger age, self-report of active drug use, fatigue or vomiting negatively affected adherence. Self-reported sexual dysfunction was significantly associated with non-adherence only in PI-treated individuals.

Adult↗
PubMed2003

Changes in viral load in people with virological failure who remain on the same HAART regimen.

OBJECTIVES: To assess the rate of change in viral load and CD4 count over time in HIV-infected patients experiencing virological failure on a HAART regimen. DESIGN: Study population included patients from EuroSIDA, a large, multicentre, observational study enrolling HIV-infected patients across Europe. METHODS: Median change in viral load and CD4 count per month were estimated using the viral load and CD4 measurements obtained over a 12-month period after confirmed virological failure between 3 and 4 log10 copies/ml in a population of 488 HIV-infected patients who were left on a failing HAART regimen. RESULTS: The estimated median viral load change in our study population was 0.024 log10 copies/ml per month, statistically different from 0 (P=0.0001). In 20.9% of the patients studied viral load showed a tendency to decrease, in 47.8% showed a tendency to increase by a positive rate no higher than 0.04 log10 copies/ml per month and in the remaining 31.3% showed a tendency to increase by a rate greater than 0.04 log10 copies/ml per month. On average, CD4 counts were estimated to remain stable (decrease at a slow rate of about -0.53 cells/microl per month). CONCLUSIONS: In patients that remained on a stable, but virologically failing HAART regimen (with viral load ranging 1000-10000 copies/ml), the viral load over the ensuing 12-month period increased at a relatively slow rate. In contrast, the CD4 count remained stable, possibly because of partial but sustained viral suppression below the viral load natural set-point. The time-course of selecting more replication-competent virus in patients with virological failure remains to be fully clarified.

Adult↗
PubMed2002

Virologic correlates of adherence to antiretroviral medications and therapeutic failure.

Adherence to antiretroviral therapy affects the pharmacokinetics of antiviral drugs and activates a cascade of events ultimately leading to therapeutic success or failure. An optimal adherence usually affords minimal rounds of virus replication and rare spontaneous mutations, which are unable to be fixed in the genome because of the competition of wild-type (more fit) strains. Therefore, adherence-based therapeutic success is mostly accompanied by the prevalence of wild-type strains. In case of poor adherence, virus replication is substantial, and mutations randomly occurring tend to be fixed within the genome. Under these conditions, mutated-resistant strains will outgrow wild-type virus (sensitive to antivirals and thereby unable to compete enough with resistant strains for cellular targets): thus, therapeutic failure occurs, and mutated resistant strains are predominant. In the case of very low or absent adherence, virologic failure occurs, although wild-type virus (whose replication is not significantly affected by antivirals) is not outgrown by mutated strains randomly produced but unable to be fixed within the genome. Taken together, these events and their consequences strongly support the relevance of a tight and continuous monitoring of adherence to antiretroviral drugs to prevent the risk of development of mutated strains often cross-resistant to the majority of antiretroviral drugs currently available.

Anti-HIV Agents↗
PubMed2002

Relationship between HAART adherence and adipose tissue alterations.

Adipose tissue alterations (ATA), which are common among persons treated with highly active antiretroviral therapy (HAART), can have substantial psychologic repercussions, with a subsequent negative impact on the patient's quality of life and on HAART adherence. However, the cross-sectional nature of the studies precludes establishing the direction and causality of the relationship. The authors evaluated the longitudinal relationship between ATA and adherence to HAART. The analysis included all participants in the AdICoNA and the LipolCoNA substudies of the Italian Cohort Naive Antiretrovirals (ICoNA). Adherence was assessed using a 16-item self-administered questionnaire, which also included a question on self-perceived fat accumulation experienced during the past 4 weeks. ATA was diagnosed by physicians at enrollment and evaluated every 6 months thereafter. There were 207 patients, with a median age of 35 years; 73% were men; and 34% acquired HIV through injection drug use. At baseline, nonadherence was reported by 63% of participants, and ATA was self-perceived by 15% and clinically diagnosed in 25%. Using Cox regression analysis, patients with good adherence at baseline were more likely to develop ATA (RH = 2.58; 95% CI, 1.09-6.11) and developed it sooner. Self-perceived ATA at baseline was independently related to subsequent nonadherence (OR, 4.67; 95% CI, 1.01-22.4), but clinically diagnosed ATA was not (OR, 0.77; 95% CI, 0.37-1.61). Patients' adherence to HAART is a dynamic process that interacts with ATA. Better adherence is associated with a higher risk of subsequent occurrence of ATA, while patient-perceived onset of morphologic alterations can reduce adherence to antiretroviral therapy.

Adipose Tissue↗
PubMed2002

Virologic and immunologic response to regimens containing nevirapine or efavirenz in combination with 2 nucleoside analogues in the Italian Cohort Naive Antiretrovirals (I.Co.N.A.) study.

This nonrandomized study compared the virologic and immunologic responses to potent regimens containing either efavirenz or nevirapine after considering potential systematic differences between patients receiving these drugs. Virologic failure was defined as the first of 2 consecutive measurements of virus load >500 human immunodeficiency virus RNA copies/mL. Of the 694 patients included in the analysis, 460 (66.3%) started nevirapine and 234 (33.7%) started efavirenz. The adjusted relative hazard of virologic failure for patients who started nevirapine, compared with those who started efavirenz, was 2.08 (95% confidence interval, 1.37-3.15; P=.0006). In addition, patients receiving efavirenz tended to recover 5 CD4 cells/microL more per quarter (P=.05). Although comparisons of drug efficacy in nonrandomized studies should be viewed with caution, no results from randomized controlled comparisons of these drugs are thought to be available. The findings of this study are in agreement with those of other observational studies.

Acquired Immunodeficiency Syndrome↗
PubMed2002

Raised viral load in patients with viral suppression on highly active antiretroviral therapy: transient increase or treatment failure?

OBJECTIVE: To assess the occurrence of viral load greater than 50 copies/ml in patients on highly active antiretroviral therapy (HAART) having achieved less than 50 copies/ml and the chance of whether a viral load greater than 50 copies/ml would lead to a sustained and increasing viral load. DESIGN: A cohort of 553 patients on HAART with viral loads of less than 50 copies/ml were followed. RESULTS: Over a median of 56 weeks 35% of patients experienced a transient increase and 8% virological failure (two consecutive viral loads of > 400 copies/ml). Transient increases and virological failure were more common in those with greater drug experience, and those with initial raised viral load values of more than 400 copies/ml were more likely to have a sustained increase and become virological failures. CONCLUSION: Transient increases in viral load are common, mainly in the 50-400 copies/ml range, and the majority of subsequent viral load estimations show a return to less than 50 copies/ml. A single raised viral load should lead to adherence support and intensified monitoring. Subsequent treatment decisions can then be based on evidence of true virological rebound and failure.

Antiretroviral Therapy, Highly Active↗
PubMed2002

Low prevalence of primary mutations associated with drug resistance in antiviral-naive patients at therapy initiation.

OBJECTIVE: To assess the prevalence of mutations in the reverse-transcriptase (RT) and protease (PR) region in a cohort of chronically-infected HIV-positive patients requiring highly active antiretroviral therapy (HAART). METHODS: The study included 347 patients enrolled in the Italian Cohort of Antiretroviral Naive patients (I.CO.NA) who had to initiate HAART. The whole PR-region, and amino acids 1-320 of RT-region were sequenced from plasma samples at baseline. RESULTS: Median CD4-lymphocytes and HIV-RNA at baseline were 231 x 10(6) cells/l and 4.89 log(10) copies/ml; 307 of 347 (88.5%) patients carried no mutations in the RT region, whereas 40 (11.5%) carried one or more mutations associated with resistance to nucleoside-RT inhibitor (NRTI) (7.8%), or non-nucleoside-RTI (NNRTI) (4.9%), with four patients carrying mutations to both classes. Among mutations associated with high-level resistance to RTI, T215Y was found in only two patients, M184V in two cases, T69D and T215C in other two cases (one each), and K103N in only one patient, for a total of six patients (one carrying both T215Y and M184V) (1.7%). Seventy-six patients (21.9%) carried no mutations in the PR region, whereas 271 (78.1%) had one or more mutations. Primary mutations associated with substantial resistance to protease inhibitors were found in only five of 347 patients (1.4%) (M46V/L, I54V, V82A/I); all the other patients carried only secondary mutations (L10F/I/V, M36I, L63P, A71T/V, V77I). CONCLUSIONS: Prevalence of mutations associated with high-level resistance to antiretroviral drugs is low in HIV-infected patients with long-term infection. This suggests no preclusion in principle to any antiretroviral drug at the time of decision of the first therapeutic regimen.

Adult↗
PubMedDate not supplied

Incidence of adipose tissue alterations in first-line antiretroviral therapy: the LipoICoNa Study.

BACKGROUND: Adipose tissue alterations (ATAs) are a frequent untoward effect of antiretroviral therapy, the causes of which remain incompletely explained. OBJECTIVES: To assess the incidence of ATAs and to identify the associated risk factors in patients infected with human immunodeficiency virus type 1 starting their first-line antiretroviral treatment. METHODS: In a multicenter investigation designed to study issues related to the treatment of patients starting antiretroviral therapy, physicians were requested to assess the presence of ATAs at enrollment and every 6 months thereafter. The ATAs were considered altogether and grouped as fat loss (lipoatrophy), adipose tissue accumulation (lipohypertrophy), and combined forms. RESULTS: A total of 655 patients were followed up for a median of 86 weeks; 128 patients (19.6%) were diagnosed as having at least 1 morphologic alteration during the study. Female gender and positivity for hepatitis C virus were independently linked to an increased risk of developing morphologic alterations. Age was another independent correlate of risk of developing ATAs. To have been infected through drug injection was a correlate of reduced risk of ATAs. Stavudine exposure was predictive at borderline statistical significance of lipoatrophy (but not of the other forms), and indinavir exposure was associated with a significantly higher risk of developing combined forms. Patients who started therapy with 2 nucleoside reverse transcriptase inhibitors and subsequently added a protease inhibitor during the follow-up had a significantly higher risk of having ATAs compared with patients who continued taking 2 nucleoside reverse transcriptase inhibitors up to the end of follow-up. CONCLUSIONS: Different types of ATAs might derive from distinct pathways and multifactorial causes. Adipose tissue alterations are a frequent and relatively early finding during first-line antiretroviral therapy.

Adipose Tissue↗