Etanercept may play an important role in modulating the inflammatory activity and progression of human immunodeficiency virus (HIV)-associated psoriasis and psoriatic arthritis. We report the case of a 45-year-old homosexual man with a CD4 cell count of less than 0.05 x 10(9)/L and an HIV viral load of 4200 copies/mL (while receiving highly active antiretroviral therapy) who developed extensive psoriatic plaques, 4.5-kg weight loss, onychodystrophy, and psoriatic arthropathy with severe periarticular bone demineralization. The arthritis progressed despite the use of several disease-modifying medications, including corticosteroids, hydroxychloroquine, and minocycline. Because of uncontrolled, progressive, and disabling arthritis and resulting profound disability, he was treated with etanercept. Within 3 weeks, his psoriasis had improved dramatically and his joint inflammation had stabilized. For the next 4 months, immunologic and viral parameters remained stable, but his clinical course was complicated by frequent polymicrobial infections. Etanercept was thus discontinued despite continued improvements in his psoriasis, psoriatic arthritis, and functional status. While both cutaneous and joint manifestations of psoriasis improved dramatically, the experience with this patient dictates that caution and careful follow-up must be exercised when prescribing etanercept in the setting of HIV infection.

Combined therapy with interferon-alpha and zidovudine can be safely administered to patients with AIDS and Kaposi sarcoma. The observed effects on tumor growth, HIV replication, and immune function support further studies of the combination in patients at various stages of HIV infection.

No abstract

Highly active antiretroviral therapy (HAART) consisting of multiple combinations of antiretroviral agents that inhibit HIV (HIV) replication has been associated with improvements in CD4+ T-lymphocyte cell counts, suppression of HIV replication, and regression of HIV-associated Kaposi's sarcoma (KS). Several of these agents have complex drug-drug interactions and have the potential to aggravate paclitaxel-associated toxicities. Herein two patients with KS are described who received paclitaxel while on HAART and who developed life-threatening toxicities. These cases are presented to alert clinicians to potentially serious drug interactions that can occur between various components of HAART and paclitaxel. Clinicians contemplating taxane-based chemotherapy for HIV-associated KS should carefully monitor patients for adverse events and, depending on their patient's HAART regimen, consider reducing the taxane dose.

Objective: To evaluate the safety, dose tolerance, and anti-tumor effects of 9-cis-retinoic acid in the treatment of Kaposi sarcoma (KS) related to acquired immunodeficiency syndrome (AIDS). Design: Phase 2, open-label clinical trial of oral doses of 9-cis-retinoic acid increasing in 40-mg increments every 2 weeks from 60 mg/m 2 per day to a maximum of 140 mg/m 2 per day. Setting: Five hospital or health maintenance organization outpatient clinics. Patients: Fifty-seven adult male patients with human immunodeficiency virus and biopsy-proven KS. Main Outcomes Measures: Safety was evaluated by adverse events, physical examination, laboratory test abnormalities, treatment-limiting toxic effects, and reasons for early withdrawal. Response (Ն50% improvement) was evaluated by an overall KS response and by the area and height from 6 index lesions selected at baseline. Results: Patients tolerated 60 and 100 mg/m 2 per day. Most patients found 140 mg/m 2 per day intolerable owing to headache. Common treatment-related adverse events were headache, xerosis, rash, alopecia, and hyperlipemia. The patient response rate for the overall KS disease was 19% (11/57), including 1 patient with clinically complete response. The response rate assessed by measuring 6 index lesions during treatment was 39% (22/57). Sixteen responding patients (73%) were refractory to at least 1 previous anti-KS therapy. Patients with CD4 + counts of 150 cells/µL or lower were as likely to respond as patients with counts of higher than 150 cells/ µL. The median time to response was 8.5 weeks (range, 4.0-21.1 weeks). The median duration of treatment was 15.1 weeks (range, 0.14 to Ն62 weeks). Conclusion: 9-cis-retinoic acid capsules have moderate activity and provide durable responses, but substantial toxic effects at higher doses limit its suitability as an anti-KS therapy.