The first patient was a 40-year-old HIV-1-infected man who was admitted for a 40°C fever and inflammatory oedema of both legs. He had a long history of HIV infection and was treated for cutaneous Kaposi’s sarcoma (KS) with bleomycin, which had been stopped 2 months before presentation. Twenty days before admission, a new HAART regimen combining efavirenz, abacavir and lopinavir was started because of virological failure. Two weeks later, he began to complain of painful oedema of both legs. Cutaneous KS lesions were not noted on the legs. Laboratory results showed a white blood cell count of 3.9x10E9, a CD4 cell count of 4/mm³, a plasma HIV-RNA level of 305 209 copies/ml, and a C-reactive protein level of 200 mg/l. Blood cultures were negative. A punch cutaneous biopsy of the leg did not show any superficial cellulitis or KS. Lopinavir was discontinued and the oedema resolved in 5 days. Two months later lopinavir was started again. After 20 days, the patient was readmitted for the same symptoms. The oedema resolved fully despite the maintenance of lopinavir.

The second patient was a 51-year-old HIV-infected woman who had started didanosine, indinavir and lopinavir 3 weeks before admission. She complained of a painful inflammatory oedema of both feet, without fever. Physical examination showed severe bilateral oedema of the legs. There were no signs of erysipela on physical examination. Laboratory results showed a white blood cell count of 6.2x10E9/L, a CD4 cell count of 28/mm³, a plasma HIV-RNA level of 330,000 copies/ml, and a C-reactive protein level of 64 mg/l. Blood cultures were negative. She received presumptive antibiotic therapy with pristinamycin. The oedema fully resolved within 7 days despite the maintenance of lopinavir.

The identification of a single antiretroviral drug as the cause of an adverse effect is difficult in HIV-infected patients because the drug is rarely used in monotherapy. Our two patients had the same clinical features of severe bilateral inflammatory oedema soon after the introduction of lopinavir. Other causes of oedema frequently seen in HIV-infected patients (i.e. erysipela, KS, nephropathy or cardiopathy) were excluded in both cases. In the first case, lopinavir was the only drug that was stopped. The recurrence of oedema, a few days after the reintroduction of lopinavir, suggests that it was the drug responsible.

Among 700 HIV-infected patients followed in our hospital clinic, inflammatory oedema has been observed in two out of 16 patients who received lopinavir, suggesting that this side-effect might be common with this drug. Physicians should be aware of this potential new drug event.

*Department of Clinical Immunology, Hôpital Henri Mondor, Créteil, France.

Abstract submitted by Neal Bodsworth, MD, MM (Venereology), MB, BS, FACSHP