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.

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A total of 351 determinations of sexual hormones were carried out in 189 HIV-infected men in stable clinical condition. Highly active antiretroviral therapy (HAART) was associated with increased levels of both testosterone and 17beta-estradiol, but not with luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Protease inhibitors were more associated with testosterone, and non-nucleoside reverse transcriptase inhibitors with 17beta-estradiol. The values of both hormones, but not those of LH and FSH, increased with respect to pre-treatment levels in those patients who initiated HAART.

Although clinical manifestations of adrenal dysfunction are uncommon in patients infected with human immunodeficiency virus (HIV), subclinical functional abnormalities of the hypothalamic-pituitary-adrenal axis are frequent. Patients infected with HIV usually have higher basal serum cortisol and lower serum dehydroepiandrosterone concentrations than HIV-seronegative individuals. This imbalance has been related to progression of the infection by inducing a shift from T(H)1 to T(H)2 immunologic responses. Although, adrenal reserve may be marginal in HIV-infected patients, clinically evident adrenal insufficiency is uncommon and, when present, it is observed in advanced stages of the infection. Hypocortisolemia should be treated regardless of the existence of associated symptoms. On the contrary, hypercortisolemia in the absence of features of Cushing syndrome is common and should not promote treatment nor specific studies. The possible influence that alterations of the adrenal function could have on the patients' immune status and the eventual effect of antiretrovirals on these alterations merit further investigation.

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We describe a patient with salmonella pyomyositis and review 30 other cases reported during the past 4 decades. Men outnumbered women by 2.9 to 1, and the median age of the patients was 51 years. Approximately one-half the cases were caused by Salmonella enteritidis. Infected vascular aneurysms were observed in seven patients. Prior salmonella infections and local trauma or lesions were common. Diverse underlying conditions, mainly diabetes and human immunodeficiency virus infection, were present in 81% of the patients, and the psoas muscle was involved in 55% of the cases. One-third of the patients died, and relapses were common after a median time of 5 weeks (range, 4.5-27 weeks) in those who survived. Most patients had anemia, and pathogens were recovered from blood samples from two-thirds of the patients. Salmonella should be considered as a causative agent of muscle infections in the appropriate clinical setting, particularly in patients with underlying diseases or preexisting vascular aneurysms.

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HIV/HCV-coinfected patients with previous SVR may develop HCC in the mid term and long term. These cases account for a significant proportion of the total cases of HCC in this setting. Our findings reinforce the need to continue surveillance of HCC with ultrasound examinations in patients with cirrhosis who respond to anti-HCV therapy.