The previous therapy regimens included ABV in 52, liposomal daunorubicin in 49, and liposomal doxorubicin in 40 patients. Moreover, only 77% were receiving concomitant HAART (all protease inhibitor based) and 33% started this treatment at the same time as the taxane chemotherapy. The paclitaxel protocol BIBW2992 supplier used was 100 mg/m2 fortnightly. The overall response rate was 56% with no significant difference in response rate when comparing patients on or not on HAART. Less surprising was the finding that patients on HAART had a significantly improved survival. The main side effect reported in these studies was neutropenia that generally

resolved prior to the next chemotherapy cycle [101]. A second study enrolled 17 patients with anthracycline refractory AIDS-KS, defined as KS that had progressed during or within 6 months of completing liposomal anthracycline chemotherapy. All patients were Ku 0059436 receiving a stable HAART regimen to avoid confounding of results. The treatment schedule was again 100 mg/m2 fortnightly. The objective response rate to paclitaxel was 71% (95% CI: 60–81), with 8 of 17 partial responses and 4 of 17 complete responses. There were no significant changes in CD4, CD8, CD16/56 (natural killer cells) and CD19

(B cells) lymphocyte subset cell counts during and for up to 1 year following chemotherapy. Similarly, plasma HIV-1 viral loads did not change significantly during or after treatment suggesting that the combined use of paclitaxel and HAART reduces the risk of chemotherapy-related immunological decline and opportunistic infections [102]. In contrast, previous trials without concomitant HAART were worrying in this respect; Gill [100] reported 51 AIDS-defining opportunistic infections in the 56 patients treated with paclitaxel (10.5/100 patient months on paclitaxel), only 36% of whom received HAART, and Welles [99] reported 27 opportunistic infections (8.4/100 person months on paclitaxel) among

her cohort of 28, none of whom received HAART. Thus the concomitant use of HAART Tyrosine-protein kinase BLK and paclitaxel appears to be safe and not detrimental to immune function despite initial concerns over pharmacological interactions [104–106]. These findings suggest that standard opportunistic infection prophylaxis guidelines may be followed when treating patients with taxane chemotherapy for KS. The higher rates of toxicity and the need for a 3-hour infusion make paclitaxel a less attractive first-line option than PLD [103]. The clinical experience in KS with docetaxel, another taxane, is much more limited though two small studies suggest that this agent can produce meaningful responses when used weekly [107], and in anthracycline pretreated individuals [108]. However, severe toxicities, including one death, have been reported in patients prescribed docetaxel with ritonavir-boosted protease inhibitors [109,110].