Impaired distensibility of ascending aorta in patients with HIV infection.

BACKGROUND: Our aim was to investigate the aortic distensibility (AD) of the ascending aorta and carotid artery intima-media thickness (c-IMT) in HIV-infected patients compared to healthy controls. METHODS: One hundred and five HIV-infected patients (86 males [82%], mean age 41 ± 0.92 years), and 124 age and sex matched HIV-1 uninfected controls (104 males [84%], mean age 39.2 ± 1.03 years) were evaluated by high-resolution ultrasonography to determine AD and c-IMT. For all patients and controls clinical and laboratory factors associated with atherosclerosis were recorded. RESULTS: HIV- infected patients had reduced AD compared to controls: 2.2 ± 0.01 vs. 2.62 ± 0.01 10(-6) cm(2) dyn(-1), respectively (p < 0.001). No difference was found in c-IMT between the two groups. In multiadjusted analysis, HIV infection was independently associated with decreased distensibility (beta -0.45, p < 0.001). Analysis among HIV-infected patients showed that patients exposed to HAART had decreased AD compared to HAART-naïve patients [mean (SD): 2.18(0.02) vs. 2.28(0.03) 10(-6) cm(2) dyn(-1), p = 0.01]. In multiadjusted analysis, increasing age and exposure to HAART were independently associated with decreased AD. CONCLUSION: HIV infection is independently associated with decreased distensibility of the ascending aorta, a marker of subclinical atherosclerosis. Increasing age and duration of exposure to HAART are factors further contributing to decreased AD.

Human herpesvirus-8 seropositivity and clinical correlations in HIV-1-positive and highly exposed, persistently HIV-seronegative individuals in Greece.

The prevalence of anti-human herpesvirus 8 (HHV-8) antibodies was retrospectively assessed in a cohort of 248 consecutive HIV-1-positive patients followed up in an academic unit in Greece during a 14-year period and in 46 highly exposed, persistently HIV-seronegative (HEPS) individuals. The impact of the initial anti-HHV-8 status on tumorgenesis and mortality was studied. The first available serum sample from the department's pool was tested. Demographics and data regarding history of sexually transmitted diseases, Hepatitis B surface antigen (HbsAg) and hepatitis C (HCV) status were collected. Patients who developed either HHV-8-related or non-HHV-8-related neoplasms during long-term follow-up were also identified. Forty-eight percent of the HIV-1-positive patients and 56% of the HEPS subjects were found anti-HHV-8-positive. No difference was observed regarding the development of HHV-8-related or non-HHV-8-related neoplasia and mortality on grounds of initial anti- HHV-8 status. Mortality was positively associated with the presence of HBsAg. HCV infection showed a trend to be more common in anti-HHV-8-positive patients. In summary, the seroprevalence of HHV-8 among HIV-1-positive patients is higher than the one reported in the Western world. The initial anti-HHV-8 status is not a prognostic factor in HIV-1-positive individuals. The high seroprevalence in HEPS individuals possibly reflects their risk-prone lifestyle. HbsAg-positive status is a long-term negative prognostic factor in HIV infection.

Successful salvage therapy of refractory HIV-related cryptococcal meningitis with the combination of liposomal amphotericin B, voriconazole, and recombinant interferon-γ.

We present 2 cases of HIV-related cryptococcal meningitis, persisting after 3 and 9 months, respectively, of standard treatment. Both patients were treated successfully with a salvage regimen consisting of the combination of liposomal amphotericin B (3 mg/kg), intravenous voriconazole, and subcutaneous recombinant interferon γ-1b (200 µg thrice weekly). Voriconazole was administered at an increased dose (5 mg/kg, twice daily) to overcome interactions with co-administered ritonavir. In both patients, resolution of clinical signs and symptoms, as well as sterilization of cerebrospinal fluid cultures occurred after 10 weeks of salvage therapy. No major side effects were encountered. At the end of treatment, both patients were placed on maintenance therapy with oral fluconazole; no recurrence has been observed after 4 years of follow-up.

Circulating antibodies to endogenous erythropoietin and risk for HIV-1-related anemia.

OBJECTIVES: In a previous retrospective study we have shown that circulating antibodies to endogenous erythropoietin (anti-EPO) are associated with HIV-1-related anemia. The present longitudinal cohort study was conducted to examine the effect of anti-EPO on the risk of developing anemia over time. METHODS: The study population consisted of 113 HIV-1 seropositive patients, who were screened for the presence of anti-EPO, with a mean+/-SD follow up of 105+/-40 months, for a total of 2190 visits. Anti-EPO were detected with an ELISA assay. RESULTS: Anti-EPO were detected in 41% (46/113) at enrollment and 29% (320/1094) for all visits, and were associated with higher EPO levels for all visits (45.7+/-60.4 vs. 31.8+/-31.7 IU/ml, p<0.001). After adjusting for other significant confounders, anti-EPO has been associated with increased risk of anemia both at enrollment (odds ratio [OR], 5.07; 95% confidence interval [CI], 1.25-20.49) as well as for all visits ([OR], 2.15; 95% [CI]: 1.29-3.56). During follow up, a decline in prevalence of both anti-EPO and anemia was observed as the percentage of patients receiving HAART was increasing. CONCLUSIONS: Anti-EPO are an independent risk factor for anemia in HIV-1-infected patients. HAART seems to reduce both anti-EPO and anemia prevalence.