ABSTRACT
In this multicenter study (ISS 902), 554 previously untreated patients with <500 CD4 cells/mm3 and mildly symptomatic human immunodeficiency virus disease were randomized to receive zidovudine or didanosine (ddI). After a mean follow-up of 20 months, 80 patients (40 zidovudine, 40 ddI) had died and 146 had at least one AIDS-defining event (73 zidovudine, 73 ddI). Overall, no difference was found between treatments with respect to progression to AIDS or death. The analysis of relative risk (RR) of progression over time, however, showed an initially minor risk for zidovudine patients and an inversion in the zidovudine-ddI RR in the second and third years of follow-up. Didanosine showed a greater effect on CD4 cell count response. The two drugs confirmed the toxicity patterns already reported in other trials, with a low occurrence of pancreatitis (ddI 1.3%, zidovudine 0.4%). The overall results suggest that, in this population, zidovudine and ddI monotherapies have comparable long-term clinical efficacy and that more powerful regimens should be preferred.
Subject(s)
Anti-HIV Agents/therapeutic use , Didanosine/therapeutic use , HIV Infections/drug therapy , Zidovudine/therapeutic use , Acquired Immunodeficiency Syndrome/diagnosis , Adult , Anti-HIV Agents/adverse effects , Body Weight , CD4 Lymphocyte Count , Didanosine/adverse effects , Disease Progression , Female , HIV Core Protein p24/analysis , HIV Core Protein p24/blood , HIV Infections/mortality , Humans , Male , Risk , Zidovudine/adverse effectsABSTRACT
Anti-HBc IgM were determined in 46 patients whose serum was positive for hepatitis B surface antigen (HBsAg). All sera were tested from 1:4000 up to 1:8128000 dilution with a radioimmunometric assay. Anti-HBc IgM persisted at detectable level for up 15 months from acute infection in more than 50% of the patients. High levels of anti-HBc IgM are seen only in the acute phase but it is difficult to establish a cut-off dilution displaying diagnostic value between current and remote infection. Anti-HBc IgM are always detectable in acute hepatitis B virus (HBV) so that the absence of HBc IgM in acute hepatitis with positive HBsAg allows to discard HBV as the causative agent and to suspect a non-B hepatitis (A, delta, NANB). On the contrary the presence of anti-HBc IgM in detectable amounts in patients with acute hepatitis and negative HBsAg makes possible the diagnosis of acute B virus hepatitis.