Grade 3–4 neutropenia was seen in 75% of patients,

with six episodes of grade 3–4 infection. Of note, only two patients received HAART during chemotherapy, three patients received zidovudine monotherapy and G-CSF was optional, given in only 54% of the cycles; all these factors most selleck kinase inhibitor likely contributing to the very significant toxicity reported in this study [44]. In contrast, in the above-mentioned stage-adapted study, 94% of patients received HAART during chemotherapy and G-CSF was recommended in all those receiving BEACOPP. Patients with early unfavourable HL (13% of the study population) received BEACOPP x4 or ABVD x4 + 30 Gy IF-RT, whereas those with advanced stage received BEACOPP x6–8. The CR/CRu rate was 100% and 86% for the early-unfavourable and the advanced-stage groups, respectively, and the 2-year PFS was 88% for both groups. Treatment-related mortality was 0% in the early-unfavourable group and 6% in the advanced-stage group [36]. We recommend for early-favourable HL: ABVD x2–4 + IFRT 20–30 Gy (level of evidence 1B). We recommend

for early-unfavourable HL: ABVD x4 + IFRT 30 Gy (level of evidence 1B). We recommend for advanced-stage HL: ABVD x6–8 +/− RT (level of evidence 1B). Prior to HAART, the prognosis selleck chemical of HIV-HL was significantly worse than that of the HIV-negative population with reduced CR rates ranging from 44 to 65% [45–47] and median OS of about 18 months. Since HAART, the outcomes for patients with HIV-HL have dramatically improved with CR rates Megestrol Acetate of 70–80% and EFS that are similar to the HIV-negative population [17,19]. Moreover, in recent studies, 5-year OS rates approach that of the HIV-negative population [17–19]. Higher CD4 cell counts, HL stage appropriate therapy and HAART are key factors that correlate with these improved outcomes [48]. Although HAART and ABVD can be safely co-administered [17–19], patients remain at increased risk for treatment-related toxicities [19]. Similarly, drug–drug interactions

between chemotherapy and specific types of HAART may drive adverse outcomes [19,49–52]. Clinically important adverse events such as additive vinblastine-mediated neurotoxicity and neutropenia in the presence of ritonavir have been described [49,50]. Some of these adverse events, such as increased neutropenia, can cause delays in the chemotherapy schedule thereby compromising CR rates [50]. We recommend patients should receive HAART during chemotherapy (level of evidence 1A). We recommend to avoid PI/ritonavir-boosted regimens (level of evidence 1D). Once again the addition of rituximab to ABVD chemotherapy has been explored mostly in the setting of immunocompetent patients, with no studies in people living with HIV. Rituximab has demonstrated single-agent activity in HL, in spite of the fact that only 20–30% of classical HL expresses CD20.