Human herpesvirus-6 reactivation in a longitudinal study of two HIV-1 infected patients.

After primary infection, human herpesvirus-6 (HHV-6) persists in latent form and can be reactivated in immunocompromised subjects. A longitudinal study of HHV-6 infection was carried out in two HIV-1 seropositive patients to provide in vivo evidence of HHV-6 reactivation. Concomitant with a significant rise of anti-HHV-6 IgG detected by IFA, a transient increase of HHV-6 viral load was shown in PBLs by PCR. During HHV-6 reactivation it was also identified either cell-free HHV-6 by PCR in plasma or IgM antibody titers. HHV-6 reactivation was followed by a temporary decrease in CD4+ count and by a progressive dramatic loss of CD4+ during the following 18 months. HHV-6 strain characterization by PCR demonstrated that first patient (MM) initially showed the B variant, followed by reactivation and persistence of the A variant, while in the second (SG) only the A variant was detected. The evidence of HHV-6 reactivation suggests its involvement in immunologic damage underlying the disease.

Quantitation of HCV viraemia by branched DNA signal amplification in patients treated with alpha-interferon--a longitudinal study.

Using bDNA, the plasma viral load trend of HCV-infected patients undergoing IFN therapy was analyzed. Nine patients were enrolled, each assigned to one of three groups, based on IFN response as determined by ALT and AST level trend. HCV was genotyped using DEIA. Each patient's clinical stage was determined by liver biopsy analysis. In nonresponding patients elevated viral loads and biochemical parameters were observed. These values were not influenced by IFN treatment. In relapsed patients the cessation of IFN treatment increased viral load; this was associated with a rise in ALT and AST values. In responders ALT and AST levels remained normal; viral load was low. Patients with elevated HCV viral load showed a worsening in their liver histology during the follow-up period. These results confirm that plasma viral load is a good marker of biochemical change and disease progression.

Prolonged bedtime treatment with H2-receptor antagonists (ranitidine and famotidine) does not affect blood alcohol levels after ethanol ingestion in male patients with duodenal ulcer.

OBJECTIVE: To verify whether a prolonged (therapeutic) treatment with ranitidine or famotidine may affect blood alcohol concentrations (BAC) in patients with duodenal ulcer (DU). METHODS: Sixteen male patients with DU were studied. Subjects with Helicobacter pylori-associated DU did not enter the study. Patients randomly received either 300 mg ranitidine (n = 8) or 40 mg famotidine (n = 8) at bedtime for 2 months. They had a standard lunch (1:00 PM), and 0.3 g/kg of alcohol was given 15 min after the meal. BAC were measured by head-space gas chromatography up to 150 min. RESULTS: The rate of GFPM was checked in all patients before they entered the study; we found it to be 53%, by comparing the area under the curve (AUC) of BAC after either intravenous or oral (po) administration of 0.3 g/kg ethanol. Ranitidine did not significantly modify either the mean AUCpo (5.8 +/- 1.8 vs. 6.2 +/- 1.4 mM/h, before vs. after treatment) or the peak BAC (4.6 +/- 1.1 vs. 5.3 +/- 1.7 mM) after 2 months of treatment. Famotidine failed to affect BAC in the second group of patients (AUCpo 5.0 +/- 1.4 vs. 5.6 +/- 1.7 mM/h, peak BAC 4.0 +/- 1.7 vs. 4.3 +/- 1.8 mM; before vs. after treatment). CONCLUSIONS: These findings suggest that, in males with DU, prolonged treatment with ranitidine or famotidine had no effect on BAC after administration of a small dose of postprandial alcohol.