Explore the vast range of titles available.

Background. This prospective study verified the effect of adherence on the risk of virologic failure. Methods. At enrollment in the study, a total of 543 patients who were following a steady (duration, ⩾6 months) and effective (viral load, <50 human immunodeficiency virus [HIV] RNA copies/mL) regimen of highly active antiretroviral therapy (HAART) completed a self-reported questionnaire derived from the Adult AIDS Clinical Trials Group Adherence Follow-up Questionnaire. Patients were followed up for the subsequent 6 months to document virologic failure, which was defined as 2 consecutive viral load measurements of >500 HIV RNA copies/mL. Results. Only the type of treatment and the adherence rate at baseline were significantly associated with the virologic end point. Among patients who reported an adherence rate of ⩽75%, the rate of virologic failure was 17.4%; this rate decreased to 12.2% for patients whose adherence rate was 76%–85%, to 4.3% for patients whose adherence rate was 86%–95%, and to 2.4% for patients whose adherence rate was >95%. When analysis was adjusted according to the type of regimen received, patients who were receiving protease inhibitor (PI)—based HAART and who had an adherence rate of up to 85% had a virologic failure rate of >20%, whereas, only for patients who were receiving nonnucleoside reverse-transcriptase inhibitor (NNRTI)—based HAART and who had an adherence rate of ⩽75%, the virologic failure rate was >10%. For the comparison of NNRTI-treated patients and PI-treated patients with an adherence rate of 75%–95%, the odds ratio was 0.157 (95% confidence interval, 0.029–0.852). The number of pills and daily doses received correlated with the reported adherence rate. Conclusions. Patients receiving NNRTIs report a higher rate of adherence than do patients receiving PIs. Adherence is significantly influenced by the number of pills and daily doses received. Low adherence is a major determinant of virologic failure; however, different therapies have different cutoff values for adherence that determine a significant increment of risk.

In a prospective, open-label, 104-week study, patients who were infected with human immunodeficiency virus type 1 (virus load, <50 copies/mL) and who were receiving protease inhibitor-based therapy were randomly assigned to continue treatment with a protease inhibitor or to replace it with abacavir or efavirenz. Treatment failure, defined as virological failure (virus load, >500 copies/µL) or any clinical or biochemical adverse event with a grade of ⩾3 (on the basis of the World Health Organization [WHO] or American Heart Association [AHA] scales), was the primary outcome measurement. Failure rates were more frequent in the group treated with protease inhibitors (P <.01), and there were no significant differences in the rate of treatment failure between the group treated with efavirenz and the group treated with abacavir. Tolerability was better in the groups treated with abacavir or with efavirenz versus those treated with protease inhibitors. Fewer patients who received efavirenz experienced viral rebound. Among all groups, the mean increase in the CD4 cell count was 131 cells/µL (P <.001), with no significant difference between groups. This switching strategy maintains optimal levels of virological suppression and may improve lipid profiles in most patients.

Background. The tuberculosis epidemic is still a global emergency, and its spread in the past 20 years has been fueled by the acquired immune deficiency syndrome pandemic and increasing drug resistance. International travel and migration may increase the incidence of tuberculosis in industrialized countries. Methods. We reviewed the clinical charts of patients admitted to the infectious diseases unit of Ospedali Riuniti (Bergamo, Italy) to identify patients with intracranial mass lesions caused by Mycobacterium tuberculosis. Results. During the past 6.5 years, 5 of 30 patients with a mass of infectious origin in the brain had tuberculous brain lesions diagnosed. All 5 were human immunodeficiency virus (HIV)-negative adults and African immigrants. No patient had concomitant meningitis, 1 had a concomitant pulmonary disease, and 3 subjects reported a past history of tuberculosis. At presentation, no patient had fever and 3 had seizures. Examination of cerebrospinal fluid revealed normal findings for 4 of 4 subjects, and neuroimaging showed multiple intracranial mass lesions in 4 of 5 patients. The diagnosis was definite for 2 subjects (based on analysis of brain specimens) and presumptive for 3 subjects (1 had concomitant pulmonary tuberculosis, and 2 had clinical response to therapy). Results of susceptibility tests for M. tuberculosis were available for 2 patients: both isolates were resistant to isoniazid, and 1 was also resistant to streptomycin. Duration of medical treatment ranged from 11 to 23 months, and 2 subjects underwent surgical procedures at the time of diagnosis. All 5 patients recovered. Conclusions. Clinicians in western countries should consider the possible role of tuberculosis in causing mass lesions in the brain, particularly in immigrants from regions where tuberculosis is endemic.