The SMAQ appears to be an adequate instrument with which to assess adherence in HIV-infected patients, and may be applied in most clinical settings.

Women have more favourable clinical and viroimmunological patterns than men both at baseline and during antiretroviral treatment. Sex has a small but significant influence on the clinical and laboratory outcomes of HIV infection.

Many of the adverse events induced by rifampin have been considered allergic in origin. The flu-like syndrome and other hypersensitivity reactions seem to be caused by immune complexes, although their pathogenetic mechanisms are not fully elucidated. Many cases have been reported of the flu-like syndrome, thrombocytopenia, hemolytic anemia, and renal failure caused by rifampin. In almost all of the patients in whom they were sought, nonreaginic antirifampin antibodies were detected. On the other hand, anaphylactic reactions seem to be IgE-mediated. We have analyzed the 18 reported cases of anaphylactic reactions severe enough to cause marked hypotension. The interval between the onset of treatment and the anaphylactic reaction was highly variable. Most patients presented with prodromes, mainly rash, before the development of anaphylactic symptoms, and, in most cases, the reaction occurred after reexposure to rifampin. Clinical findings include a variety of symptoms, such as fever, exanthem, dyspnea, abdominal pain, and vomiting. Seven of the 9 patients in whom HIV status was known were seropositive, including the only 2 patients who died. We believe that, in case of a non-life-threatening adverse reaction caused by immune complexes, rifampin could be readministered, if necessary, at a more frequent and reduced dose, perhaps with the addition of corticosteroids. In case of anaphylactic reactions the drug should be avoided, although desensitization procedures may be useful. Certain laboratory findings may serve as a clue to predict anaphylactic reactions in patients who have experienced minor adverse events to rifampin. However, the diagnostic value of such findings is not well established and, therefore, patients with previous adverse reactions should be carefully monitored if reexposure to rifampin is essential.

Sexual disturbances develop in some patients treated with highly active antiretroviral therapy (HAART). To evaluate sexual dysfunction and the influence that different antiretrovirals could have on those parameters, we conducted a prospective study in patients with stable clinical condition attending an HIV outpatient clinic. A total of 351 evaluations were performed in 189 HIV-infected men, who were interviewed about symptoms of sexual dysfunction. Sexual hormones as well as other clinical and laboratory parameters were also measured at the time of each evaluation. The mean CD4 count was 451.1 x 10(6) cells/L, and viral load was undetectable in two thirds of the determinations. The prevalence of sexual dysfunction was 19.5% overall, but it was influenced by treatment, particularly (although not exclusively) by protease inhibitors (PIs) (27.1% vs. 3.8% for untreated patients). Sexual dysfunction was not related to hypophyseal or gonadal hormonal values. Although several parameters were associated with sexual dysfunction in the univariate analysis, only antiretroviral treatment was significantly predictive of this disorder in a logistic regression analysis. Sexual dysfunction is common in HIV-infected patients in stable clinical condition receiving HAART, and all antiretroviral drugs, particularly PIs, seem to be related to it. Sexual dysfunction in these patients is not related to hormonal causes.

The CNS is the second most commonly affected organ in patients with AIDS. Many opportunistic infections may involve the brain, but the four most frequent conditions are toxoplasmosis, progressive multifocal leukoencephalopathy (PML), cryptococcosis and cytomegalovirus infection. Although the incidence of these infections among patients with AIDS has decreased in the past years as a consequence of the introduction of highly active antiretroviral therapy (HAART), they remain a major cause of morbidity and mortality in this patient group. This article summarises the clinical manifestations, diagnostic procedures and management strategies for these four conditions. The clinical manifestations are nonspecific and depend on the type and location of the lesions. In clinical practice, the diagnosis of these entities is made with noninvasive methods. Imaging studies, especially magnetic resonance imaging, are very useful for the diagnosis of toxoplasmic encephalitis and PML, although their usefulness for the diagnosis of cryptococcal meningitis and cytomegalovirus infections is lower. The presence of multiple ring-enhancing lesions with surrounding oedema and mass effect is characteristic of toxoplasmosis. The response to antitoxoplasmic therapy, which is usually observed within the first 2 weeks, is also used for diagnostic purposes. Molecular methods applied to the CSF are essential for the diagnosis of PML and cytomegalovirus infections. In addition, the quantification of viral DNA of both JC virus (the causative agent of PML) and cytomegalovirus has prognostic implications and may serve to evaluate the response to therapy. Cryptococcosis may be easily diagnosed by CSF stains and cultures, as well as by the detection of the cryptococcal capsular polysaccharide antigen in the blood and, especially, the CSF. Effective treatments are available for toxoplasmosis and cryptococcosis, although adverse effects are common and some patients may not respond to therapy. In contrast, there is no specific treatment for PML, and the efficacy of anticytomegalovirus therapy is poor and the toxicity significant. HAART has improved the outcome of patients with AIDS who have infections of the CNS, and the initiation of this therapy is mandatory for all patients with such infections, particularly in those conditions for which effective therapy is not available. Lifelong secondary prophylaxis with agents for the opportunistic infections was necessary before the HAART era because the risk of recurrence was very high if only induction therapy was administered. However, today, the discontinuation of secondary prophylaxis in patients treated with HAART who have stably reached a certain immune reconstitution is possible.