final program.qxd - Parallels Plesk Panel

PP 4.24
Early aplasia resulting from interaction between antiretroviral therapy and
vinblastine in a patient with HIV-associated Hodgkin's disease
1
A. Makinson, 2 N. Martelli, 2 H. Peyrière, 1 Ch Turriere, 1 J Reynes
1
Infectious Diseases Department, Gui de Chauliac Hospital, University Hospital of
Montpellier 2 Medical Pharmacology Department, Lapeyronie Hospital, University Hospital
of Montpellier, France.
Background
Pharmacokinetic interactions between anti-neoplastic drugs and highly active
antiretroviral therapy (HAART), especially protease inhibitors, have been recently
described. Data regarding drug to drug interactions and recommendations of dose
modifications or drug monitoring are scarce. Methods: We report a case of early severe
aplasia following anti-neoplastic drug administration with vinblastine for a HIV-associated
Hodgkin lymphoma in a patient treated by boosted protease inhibitor based salvage
HAART. Follow-up and management of this case are discussed.
Results
A 36-year-old HIV-infected man was treated with lamivudine, tenofovir, lopinavir-ritonavir
and enfuvirtide, with a viral load and T CD4 lymphocyte count in January 2006
respectively measured at 188 copies/ml and 164/mm 3 . Other daily treatments included
clindamycin (600mg), pyrimethamine (50mg) for secondary prevention of cerebral
toxoplasmosis, monthly pentamidine aerosols for prevention of pneumocystosis and
spironolactone (25mg), perindopril (2mg) for a HIV related cardiomyopathy. Stage IVB
Hodgkin lymphoma was diagnosed in februrary 2006 and treated according to the ABVD
protocol: vinblastine (6mg/m 2 ), doxorubicine (25mg/m 2 ), bleomycine (10mg/m 2 ),
dacarbazine (375mg/m 2 ) and prednisolone (40mg/m 2 ). Severe febrile aplasia was
diagnosed 6 days after administration with neutrophil nadir of 0/mm 3 . The following cure
was realised with reduced doses of vinblastine (4mg/m2) and administration of
dexrazoxane (500mg/m 2 ), but febrile aplasia also ensued with neutrophil nadir of 87/mm 3 .
POSTERS
Conclusion: In this case report, inhibition of cytochrome P4503A4 by ritonavir probably
contributed to severe aplasia, as this isoenzyme is the major metabolic pathway of
vinblastine. Inhibition of P-glycoprotein efflux pump by ritonavir may represent an
additional mechanism. Patients with HAART receiving anticancer drugs should be
closely monitored and dosage reductions should be considered, especially if treated with
boosted protease inhibitors and vinblastine. However, recommendations regarding
dosage modifications or drug monitoring are lacking and pharmacological studies should
be performed
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