Résumé
Hepatitis B virus (HBV) molecular profiles were determined for 44 patients who were infected with human immunodeficiency virus (HIV) type 1 and had antibodies to the hepatitis B core antigen (anti-HBc), with and without other HBV serological markers. In this population, 70 percent of the patients were under lamivudine treatment as a component of antiretroviral therapy. HBV DNA was detected in 14 (32 percent) patients. Eight out of 12 (67 percent) HBsAg positive samples, 3/10 (30 percent) anti-HBc only samples, and 3/22 (14 percent) anti-HBs positive samples were HBV DNA positive. HBV DNA loads, measured by real time polymerase chain reaction, were much higher in the HBsAg positive patients (mean, 2.5 Î 10(9) copies/ml) than in the negative ones (HBV occult infection; mean, 2.7 Î 10(5) copies/ml). Nine out of the 14 HBV DNA positive patients were under lamivudine treatment. Lamivudine resistant mutations in the polymerase gene were detected in only three patients, all of them belonging to the subgroup of five HBsAg positive, HBV DNA positive patients. A low mean HBV load (2.7 Î 10(5) copies/ml) and an absence of lamivudine resistant mutations were observed among the cases of HBV occult infection.
Sujets)
Adulte , Femelle , Humains , Mâle , Adulte d'âge moyen , Agents antiVIH/usage thérapeutique , Infections à VIH/complications , VIH-1 (Virus de l'Immunodéficience Humaine de type 1) , Virus de l'hépatite B/immunologie , Hépatite B/diagnostic , Lamivudine/usage thérapeutique , Brésil , ADN viral/analyse , Résistance virale aux médicaments/génétique , Test ELISA , Infections à VIH/traitement médicamenteux , Infections à VIH/virologie , Anticorps de l'hépatite B/sang , Antigènes de la nucléocapside du virus de l'hépatite virale B/sang , Antigènes de surface du virus de l'hépatite B/sang , Virus de l'hépatite B/génétique , Hépatite B/complications , Mutation/génétique , Réaction de polymérisation en chaîne , Facteurs de risque , Charge viraleRésumé
The development of paradoxical clinical worsening following initiation of tuberculosis treatment may complicate the clinical course of both HIV-infected and uninfected patients. We report a severe manifestation of the so called paradoxical reaction to the treatment of tuberculosis that unmasked previously silent meningeal disease in a 34-year-old HIV-infected male patient.