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Biomedical subjects

V Le Moing

Publications and source records attributed to V Le Moing.

At least 19 recordsLinked to original sources

The dynamic of adherence to highly active antiretroviral therapy: results from the French National APROCO cohort.

OBJECTIVES: Our objective was to describe the evolution of adherence to highly active antiretroviral therapy (HAART) over a 20-month period and its relationship with virologic success. METHODS: Self-reported adherence, clinical, and virologic data were collected 4 (M4), 12 (M12), and 20 (M20) months after initiation of a protease inhibitor-containing regimen in the French APROCO cohort. At each visit, patients were classified as nonadherent, moderately, or highly adherent, and HIV plasma RNA was determined. RESULTS: Among the 762 patients who were regularly followed until M20, the 436 patients who answered to all questionnaires, including adherence measurement, were selected for the analysis. The proportion of highly adherent patients was 55.7%, 62.2%, and 60.3% at M4, M12, and M20, respectively. A total of 137 patients (31.4%) was "always," 225 (51.6%) "sometimes," and 74 (17.0%) "never" "highly adherent" during follow-up. After multiple adjustment for known baseline predictors, virologic success after 20 months of HAART was more likely achieved in patients who were always (odds ratio [OR] 95% confidence interval [CI], 3.02 [1.64-5.58]) or sometimes (OR [95% CI], 2.15 [1.24-3.74]) "highly adherent." CONCLUSION: Adherence behavior is a dynamic process. Continued adherence was associated with better response to therapy and should be encouraged to reduce the risk of virologic failure.

Adult↗

Clinical, biologic, and behavioral predictors of early immunologic and virologic response in HIV-infected patients initiating protease inhibitors.

Predictors of virologic (plasma HIV RNA viral load [VL] < 500 copies/ml) and immunologic (rise in CD4+ cell count > 50 cells/mm3) response after 4 months of therapy (M4) were studied in 750 HIV-1-infected patients prospectively enrolled at the initiation of a protease inhibitor (PI)-containing regimen. A virologic response was observed in 80% of patients, and an immunologic response was observed in 64%. Sixty-two percent of patients self-reported full adherence to therapy at 1 month of therapy (M1) and M4. In multivariate analysis, a virologic response was more frequent in fully adherent patients (odds ratio [OR] = 2.0; p =.001). An immunologic response was associated with age < 36 years (OR =1.4; p =.03), baseline VL (OR = 1.5 per 1 log10 copies/ml higher; p <.01), decrease in VL at M1 (OR = 1.5 per 1 log10 copies/ml decrease; p <.01), baseline total lymphocyte count (OR = 1.7 per 50% lower; p <.001), and baseline CD4+ cell percentage > or = 20% (OR =1.9; p <.001) but not with adherence to therapy. Full adherence seems to be a major predictor of a virologic response to PI-containing triple therapy. An immunologic response may be possible despite incomplete adherence, at least early in therapy.

Adult↗

[Paradoxical aggravation of tuberculosis after antiretroviral therapy in HIV-infected patients].

BACKGROUND: Restoration of immunocompetence in HIV-infected patients after antiretroviral treatment can have unexpected effects. CASE REPORTS: An unusual course of treated tuberculosis was observed in four HIV-infected patients soon after initiation of antiretroviral therapy. These patients developed fever and enlarged necrotic adenopathies despite an efficacious antituberculous therapy. They were in the initial stage of their antituberculous therapy that had been initiated a mean 12 days prior to initiation of antiretroviral therapy. The antiretroviral therapy led to an undetectable HIV load within 2 months. DISCUSSION: These unusual features, which also occurred with an increase in CD4 cell counts, could be related to the immunological restoration and to the reappearance of delayed type hypersensitivity. The onset of antiretroviral therapy could thus be delayed by several weeks in HIV-infected patients treated for active tuberculosis and who have never received antiretroviral therapy.

Antitubercular Agents↗

Pneumocystis carinii pneumonia recurrence in HIV patients on highly active antiretroviral therapy: secondary prophylaxis.

The incidence and risk factors for Pneumocystis carinii pneumonia (PCP) recurrence were evaluated in 451 HIV-infected patients enrolled in the French Hospital Database on HIV who started highly active antiretroviral therapy (HAART) while receiving secondary PCP prophylaxis after a first episode occurring between January 1995 and December 1998. There were 18 episodes of recurrent PCP. On HAART, the CD4+ cell count increased to above 200 x 106/L in 274 patients, 51 of whom stopped PCP prophylaxis. None of these patients had PCP recurrences during 363 person-years (PY) of follow-up after the CD4+ cell count had reached 200 x 106/L (incidence rate [IR], 0.00 cases/100 PY; 95% confidence interval [CI], 0.00-0.82), and 37 PY of follow-up after the CD4+ cell count had reached 200 x 106/L and PCP prophylaxis had been discontinued (IR, 0.00 cases/100 PY; 95% CI, 0.00-7.84). The CD4+ cell count remained < 200 x 106/L in 177 patients; 9 patients stopped PCP prophylaxis, and 6 of these had a disease recurrence. Multivariate Cox analysis (time censored when CD4+ cell count > 200 x 106/L) showed that discontinuation of secondary prophylaxis (relative hazard [RH], 25.95; p <.0001) was associated with recurrence, whereas higher CD4+ cell counts during follow-up (RH, 0.39/50 x 106/L increment; p <.002) were protective.

AIDS-Related Opportunistic Infections↗

The influence of human immunodeficiency virus coinfection on chronic hepatitis C in injection drug users: a long-term retrospective cohort study.

In this study we analyzed the influence of human immunodeficiency virus (HIV) infection on the course of chronic hepatitis C through multivariate analysis including age, alcohol consumption, immune status, and hepatitis C virus (HCV)-related virologic factors. Eighty HIV-positive and 80 HIV-negative injection drug users included between 1980 and 1995 were matched according to age, gender, and duration of HCV infection and followed-up during 52 months. The progression to cirrhosis was the primary outcome measure. The impact of HIV on HCV-RNA load, histologic activity index, response to interferon therapy, and liver-related death was also considered. In HIV-positive patients, chronic hepatitis C was characterized by higher serum HCV-RNA levels (P =.012), higher total Knodell score (P =.011), and poorer sustained response to interferon therapy (P =.009). High serum HCV-RNA level was associated with low CD4-lymphocyte count (P =.001). Necroinflamatory score was higher in HIV-positive patients (P =.023) independently of the CD4-lymphocyte count, whereas increased fibrosis was related to decreased CD4-lymphocyte count (P =.011). The progression to cirrhosis was accelerated in HIV-positive patients with low CD4 cell count (RR = 4.06, P =.024) and in interferon-untreated patients (RR = 4.76, P =.001), independently of age at HCV infection (P =.001). Cirrhosis caused death in 5 HIV-positive patients. The risk of death related to cirrhosis was increased in heavy drinkers (RR = 10.8, P =.001) and in HIV-positive patients with CD4 cell count less than 200/mm(3) (RR = 11.9, P =.007). In this retrospective cohort study, HIV coinfection worsened the outcome of chronic hepatitis C, increasing both serum HCV-RNA level and liver damage and decreasing sustained response to interferon therapy. Age and alcohol were cofactors associated with cirrhosis and mortality. Interferon therapy had a protective effect against HCV-related cirrhosis no matter what the patient's HIV status was.

Adult↗

[Long-term immunologic response in HIV-infected patients with CD4 cell counts </= 50/mm3 when initiating protease inhibitor therapy].

From March to July 1996, 61 patients with CD4<50/mm(3)began a therapy with protease inhibitors. Increase and maintenance of CD4>100/mm(3) was observed in 39/61 patients with a protective effect for occurrence of AIDS or death. This immunological response was correlated with the duration of the virological response. However, 38% of patients with long-term immunological response never had a undetectable viral load.

CD4 Lymphocyte Count↗

Clinical outcome of patients with HIV-1 infection according to immunologic and virologic response after 6 months of highly active antiretroviral therapy.

BACKGROUND: The prognostic value of discordant immunologic (CD4 cell increase) and virologic (plasma HIV RNA level decrease) responses to antiretroviral treatment is not known. OBJECTIVE: To study the relation between clinical outcome of HIV-infected patients receiving highly active antiretroviral therapy (HAART) and early immunologic and virologic responses to such therapy. DESIGN: Prospective cohort study. SETTING: 68 hospitals in France. PATIENTS: 2236 protease inhibitor-naive patients. INTERVENTION: Initiation of HAART with one protease inhibitor and two nucleoside analogues between July 1996 and March 1997. MEASUREMENTS: Immunologic and virologic response at 6 months. Multivariate Cox models were used to assess the relation between these responses and progression to a new AIDS-defining event or death. RESULTS: On the basis of 6-month immunologic and virologic responses, patients were classified into four groups: complete response (47.5%), complete nonresponse (16.2%), immunologic response only (19.0%), and virologic response only (17.3%). After month 6 and within a median of 18 months, 69 patients died and 123 experienced a new AIDS-defining event. After adjustment, complete nonresponders and those with only a virologic response had significantly higher risks for clinical progression at 6 months (relative risk, 3.38 [95% CI, 2.28 to 5.02] and 1.98 [CI, 1.26 to 3.10], respectively) than complete responders. The difference between complete responders and those with only an immunologic response at 6 months was weaker and nonsignificant (relative risk, 1.55 [CI, 0.96 to 2.50]). CONCLUSIONS: Immunologic response after 6 months of HAART indicates a favorable clinical outcome in HIV-infected patients regardless of virologic response. This suggests that both immunologic and virologic markers should be used in clinical practice to evaluate treatment response.

Adult↗

Hepatitis B or hepatitis C virus infection is a risk factor for severe hepatic cytolysis after initiation of a protease inhibitor-containing antiretroviral regimen in human immunodeficiency virus-infected patients. The APROCO Study Group.

In a cohort of 1,047 human immunodeficiency virus type 1-infected patients started on protease inhibitors (PIs), the incidence of severe hepatic cytolysis (alanine aminotransferase concentration five times or more above the upper limit of the normal level >/= 5N) was 5% patient-years after a mean follow-up of 5 months. Only positivity for hepatitis C virus antibodies (hazard ratio [HR], 7. 95; P < 10(-3)) or hepatitis B virus surface antigen (HR, 6.67; P < 10(-3)) was associated with severe cytolysis. Before starting patients on PIs, assessment of liver enzyme levels and viral coinfections is necessary.

AIDS-Related Opportunistic Infections↗

[New antivirals for respiratory tract viruses].

NEURAMINIDASE INHIBITORS: Zanamivir, the leading neuraminidase inhibitor has been awarded marketing approval in France for curative treatment of flu. It has been demonstrated that zanamivir reduces the duration of symptoms and the frequency of recourse to antibiotics. INDICATIONS FOR ZANAMIVIR: Besides early prescription for curative treatment of flu, as soon as the first symptoms occur, particularly in vaccinated elderly patients (vaccination is effective in only 70 to 80% of cases), zanamivir could also be used as a preventive treatment in subjects exposed to an index case. EARLY TRIALS WITH PLECONARIL: Pleconaril is active against picomaviruses and appears to have interesting efficacy against exceptionally severe enterovirus infections. Conversely, trials conducted in cases of upper respiratory tract infections and meningitis caused by enteroviruses have shown modest results.

Antiviral Agents↗

Use of corticosteroids in glomerulonephritis related to infective endocarditis: three cases and review.

We report the cases of three patients treated for infective endocarditis (IE) for whom corticosteroids were added to the antibiotic treatment. They all had clinical and biological evidence of immune-mediated glomerulonephritis. The microorganisms responsible for IE were Coxiella burnetii, Streptococcus bovis, and Cardiobacterium hominis. Median duration of IE before antimicrobial therapy was 7 months. In all patients, renal function deteriorated despite appropriate antimicrobial treatment for a mean duration of 16 days, but it improved after addition of corticosteroid therapy. All patients were cured of IE. A literature review revealed four additional cases of IE-related glomerulonephritis in which adjunctive immunosuppressive therapy was considered to be effective. Although corticosteroid therapy is generally not recommended for IE, it should be considered for patients whose renal dysfunction secondary to glomerulonephritis does not improve with appropriate antimicrobial treatment, especially if the duration of the illness is long.

Aged↗

[Infections and lupus].

Infections are one of the major causes of morbidity and mortality during the course of systemic lupus erythematosus, and are promoted by various dysfunctions of the immune system, some of which are poorly understood. Other predisposing factors have been also identified such as the presence of glomerulonephritis and a treatment with high-dose corticosteroids or immunosuppressors. These factors have been particularly associated with the occurrence of opportunistic infections such as systemic candidiasis or Pneumocystis carinii pneumonia, whose frequency has increased with the intensity of therapeutic strategies. The most frequent infections encountered are induced by community-acquired microorganisms. Thus, initiating an empirical antibiotic treatment is justified in febrile patients with lupus erythematosus. In case of marked lymphopenia, it is recommended to start cotrimoxazole as primary prophylaxis against P. carinii pneumonia.

Adrenal Cortex Hormones↗