Chronic delta infection in a patient without detectable HBsAg in serum.
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Biomedical subjects
Publications and source records attributed to J Guardia.
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To evaluate the profile of hepatitis D virus replication and the corresponding immunoresponse after acute hepatitis D virus infection, sera from 50 patients with acute hepatitis D (36 with acute hepatitis B virus-hepatitis D virus coinfection and 14 HBsAg carriers with hepatitis D virus superinfection) were investigated for the presence of hepatitis D virus RNA and other serological hepatitis D virus markers. During the first week after onset of symptoms, hepatitis D virus RNA was detected by spot hybridization with a similar frequency among patients with coinfection (64%) and those with superinfection (71%). The presence of hepatitis D virus RNA in the first serum sample correlated with that of circulating hepatitis D antigen in both groups of patients. The presence of hepatitis D virus RNA was transient and its clearance paralleled that of serum hepatitis D antigen among patients with coinfection, so that 1 month after the onset of symptoms serum hepatitis D virus RNA was no longer detectable in any of these patients. Conversely, serum hepatitis D virus RNA was still present in 78% of those with superinfection, all of whom developed chronic liver disease, thus suggesting that the persistence of hepatitis D virus RNA in the serum for more than 4 weeks might indicate progression to chronicity. In nine of the 14 patients (64%) with hepatitis D virus superinfection progressing to chronicity, hepatitis D virus RNA was persistently detected throughout the follow-up, whereas in five patients it was detected occasionally. In four superinfected patients hepatitis D virus RNA and hepatitis B virus DNA were detected simultaneously in serial samples, thus suggesting that, at least during early stages of chronic hepatitis D virus infection, both viruses may replicate at the same time.
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The present study investigated the relationship between genetic variation, MRI measurements and neuropsychological function in a sample of 58 elders exhibiting memory decline. In agreement with previous reports, we found that the epsilon4 allele of the apolipoprotein E (APOE) and the D allele of the angiotensin converting enzyme (ACE) polymorphisms negatively modulated the cognitive performance. Further, we found an association between the A allele of the apolipoprotein C1 (APOC1) polymorphism and poorer memory and frontal lobe function. No clear associations emerged between MRI measures of white matter lesions (WML) or hippocampal sulcal cavities (HSC) and the cognitive performance after controlling for age effects. Further, the degree of WML or HSC lesions was in general not predisposed genetically except for the presence of the A allele of the APOC1 polymorphism that was related to a higher severity of HSC scores. Our results suggest that WML or HSC do not represent important brain correlates of genetic influences on cognitive performance in memory impaired subjects.
HBeAg and Ab are investigated by simple radial immunodiffusion in dextrane following Magnius. 14 patients (28%) were HBeAg positive and 2 patients HBeAb positive (4%). HBsAg subtyping was ad in 6 cases and ay in further 5. No relation was found between both determinants and HBeAg. Six of the 10 patients with HBeAg in their sera developed chronic liver disease o fulminant hepatitis, while only 3 of the 21 HBeAg negative controls did so (p less than 0.05). HBeAg is a marker of the evolution of virus B hepatitis.
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The aim of this study was to evaluate a technique of quantitative determination of DNA-HBV in serum, bDNA Quantiplex, in a series of 90 patients with chronic HBV infection: 75 with chronic hepatitis B (24 HBeAg positive and 51 with anti-HBe) and 15 asymptomatic carriers of HBV (anti-HBe positive). The results were related to DNA-HBV determination by hydridation techniques in dot-blot and PCR. DNA-HBV was detected by the Quantiplex bDNA technique in 61 (81%) of the 75 patients with chronic hepatitis B, in 24 (100%) of the 24 HBeAg positive patients and in 37 (72%) of the 51 anti-HBe positive (p < 0.05) patients and in none of the asymptomatic HBV carriers. The median of DNA-HBV concentration was 4,000 pg/ml in the hepatitis HBeAg and 71 pg/ml in the ati-HBe positive (p < 0.05). A significant relation was observed between the ALT value and the DNA-HBV concentration (p < 0.05). DNA-HBV by dot-blot was positive in 22 (29%) of the chronic hepatitis B and in none of the asymptomatic HBV carriers. DNA-HBV was not observed by dot-blot in 39 patients positive for DNA-HBV by the Quantiplex bDNA technique. DNA-HBV by PCR was identified in 65 (87%) of the chronic hepatitis B and in one of the asymptomatic HBV carriers. The sensitivity of the Quantiplex bDNA technique (98% versus the PCR technique) is much greater than that observed with dot-blot. In conclusion, the determination of DNA-HBV by the Quantiplex bDNA technique may be considered a good method for evaluating the viremia and degree of viral replication in patients with chronic hepatitis B.