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BACKGROUND Patients with HIV infection tend to have poor intensive care unit (ICU) outcomes; however, survival in the modern combination antiretroviral therapy (cART) era has markedly improved, but Pneumocystis jirovecii pneumonia (PJP) still remains a preeminent cause of respiratory failure in AIDS patients. Extracorporeal membrane oxygenation (ECMO) is an adapted cardiopulmonary bypass circuit for temporary life support for patients not responding to conventional treatment. CASE REPORT A 43-year-old male HIV "late presenter" was admitted to our hospital for fever and dyspnea. A chest CT scan revealed bilateral ground-glass opacities. Empiric antibiotic treatment and cART were started. The emergence of ARDS due to PJP dictated urgent veno-venous (VV) ECMO placement. One week later, radiologic findings and respiratory function had improved and the patient was started on a weaning trial from ECMO and removed 12 days after placement. CONCLUSIONS Acute respiratory distress syndrome (ARDS) is a potentially reversible clinical syndrome with a high mortality rate. ECMO is a rescue therapy allowing lung recovery during acute processes and should be considered an adequate treatment option in HIV+ patients with respiratory failure. ECMO should be considered a useful and adequate treatment option in AIDS patients who have a high risk of dying from respiratory failure.

Kaposi's sarcoma (KS) is a multicentric angioproliferative cancer of endothelial origin typically occurring in the context of immunodeficiency, i.e. coinfection with Human Immonodeficiency Virus (HIV) or transplantation. The incidence of KS has dramatically decreased in both US and Europe in the Highly Active Antiretroviral Therapy (HAART) era. However, KS remains the second most frequent tumor in HIV-infected patients worldwide and it has become the most common cancer in Sub-Saharan Africa. In 1994, Yuan Chang et al discovered a novel γ-herpesvirus in biopsy specimens of human KS. Epidemiologic studies showed that KS-associated herpesvirus (KSHV) or human herpesvirus-8 (HHV-8) was the etiological agent associated with all subtypes of KS. KS has a variable clinical course ranging from very indolent forms to a rapidly progressive disease. HAART represents the first treatment step for slowly progressive disease. Chemotherapy (CT) plus HAART is indicated for visceral and/or rapidly progressive disease. The current understanding of KS as a convergence of immune evasion, oncogenesis, inflammation and angiogenesis has prompted investigators to develop target therapy, based on anti-angiogenic agents as well as metalloproteinase and cytokine signaling pathway inhibitors. These drugs may represent effective strategies for patients with AIDS-associated KS, which progress despite chemotherapy and/or HAART. In this review, we focus on the current state of knowledge on KSHV epidemiology, pathogenesis and therapeutic options.

Cases of visceral leishmaniasis (VL) in HIV-positive individuals have been reported from most areas of the world where the geographical distributions of the two infections overlap. The majority of the co-infected cases that have been recorded, however, live around the Mediterranean basin. In these subjects, the length of the incubation period of VL is presumably very short, particularly in those who have severe immunodepression. At diagnosis, almost all cases of VL/HIV co-infection have been found to have fewer than 200 CD4+ cells/microl blood, and about 50% meet the AIDS-defining criteria during their first episode of VL. The clinical manifestations of VL in HIV-infected individuals may be similar to those seen in HIV-negative cases; fever, pancytopenia and hepato-splenomegaly, for example, are found in 75% of all the HIV-positive cases. Following the dissemination of the parasites, however, the HIV-positive cases may develop unusual, multi-organ pathology. Almost all the cases of co-infection are very prone to VL relapses, even after carefully managed antileishmanial treatment. The opportunistic infections that are often seen in HIV-positives frequently develop during VL episodes, the signs and symptoms of the leishmaniasis then confusingly overlapping with those of the other infections.

Background: Clinical variability in the natural course of cryptosporidiosis in patients affected by acquired immunodeficiency syndrome has been correlated to the degree of T-cell immunosuppression; however, cryptosporidiosis can occur as a self-limiting disease even in patients with very low T-lymphocyte count., Aims: We tested the serum values of a panel of cytokines in AIDS patients with cryptosporidial enteritis in order to evaluate their role in predicting the clinical outcome of the disease., Patients and Methods: Thirty one HIV-positive patients with cryptosporidiosis and a CD4+ count of less than 100/mm3 were studied. Interleukin-2, Interleukin-4, Interleukin-10, Interferon-gamma, Interleukin-12, Tumor Necrosis Factor alpha values were measured in serum at diagnosis., Results: Interleukin-4 and Interleukin-10 concentration was significantly lower in patients with mild disease whereas serum Interleukin-2 and -12 was higher in this same group. The serum level of Interferon-gamma did not differ in relation to the severity of the disease. Patients with self-limiting diarrhoea showed significantly lower levels of Tumor Necrosis Factor-alpha than subjects who did not show any clinical improvement., Conclusions: In our study, it has been shown that cytokine levels in serum may represent early predictive markers both for the severity of symptoms and the clinical outcome of cryptosporidial enteritis in AIDS patients with a low CD4+ count.

It is supposed that Leishmania infection increases human immunodeficiency virus (HIV) replication in seropositive individuals. Two groups of 9 HIV-infected intravenous drug users each, one group with HIV-Leishmania coinfection (as determined by bone marrow microscopy, culture and an immunofluorescent assay, the other with HIV infection alone, but no evidence of Leishmania coinfection were matched for sex, age, time since first diagnosis of HIV infection, number of AIDS-defining diseases, proportion of patients treated with AZT and months of treatment, CD4/CD8 ratio, beta 2-microglobulin level and HIV p24 antigen positivity rate. IL-4, -6, -10 and -12 and IFN-gamma levels were determined by commercial enzyme immunoassays. The HIV-1 RNA copy number was quantified with the nucleic-acid-sequence-based amplification method (NASBA). The differences between the two groups were highly significant for all markers determined except for IL-12 and IFN-gamma. We found a higher viral load in the patients with HIV-Leishmania coinfection compared to the patients with HIV infection alone (p < 0.009). In 6 HIV-positive individuals without Leishmania coinfection, the HIV-1 RNA copy number was below the detection limit of NASBA (i. e. < 400 copies/100 microliters). Plasma levels of IL-4, -6, and -10 were significantly elevated in the coinfected group (p < 0.0001; p < 0.02, and p < 0.005). The results of our study show that the viral load is increased in patients with HIV-Leishmania coinfection in comparison to the controls. This might be partly due to Th2 immune activation, as demonstrated by higher plasma levels of IL-4, -6 and -10 in HIV-Leishmania-coinfected patients than in HIV-infected individuals.