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R Jardí

Publications and source records attributed to R Jardí.

35 records · Page 2Linked to original sources
PubMed1994

[Infection with hepatitis B and C viruses in the mentally retarded].

AIM: To study the prevalence of hepatitis C virus infection (HCV) and the associated risk factors in an institution for the mentally retarded, in addition to its relation with hepatitis B infection (HBV). METHODS: The presence of antibodies against the HCV (anti-HCV) and markers for the HBV was evaluated in 94 mentally retarded subjects admitted to a single institution. Information concerning the sex, age, length of admission, type and degree of mental retardation, history of sexual promiscuity, surgery and blood transfusions was collected in every individual. RESULTS: The prevalence of infection by HBV was 22.3%. Only one individual was detected as being positive for the HCV.

Adolescent↗
PubMed1991

[Long term follow-up of non-symptomatic HBsAg carriers].

232 asymptomatic HBsAg carriers were controlled between May/1986 and May/1990. The were detected in our blood bank between 1974 and 1976 or during pregnancy or delivery period after 1981. 23 of 232 (10%) became negative during the follow-up, this happening more frequently in carriers after 5 years of follow-up. Only 2 of 209 carriers with HBsAg were HBeAg positive and 1 of these was also DNA-VHB positive. None of the HBeAg negative carriers showed DNA-VHB; only 5 had increased transaminases. 7 were anti-VHC positive, these individuals experiencing more frequent increases in transaminases. The results of this study suggests that the determination of transaminases, viral activity markers, anti-HD, anti-VHC in HBsAg carriers are enough to identify those with hepatic disease.

Adolescent↗
PubMed1990

[A study of 158 cases of acute delta hepatitis].

We have prospectively studied 158 cases of acute hepatitis delta observed during the last 7 years in a general hospital. Among them 136 were male and 22 female. The mean age was 22.7 years with a range between 16 and 61 years. The epidemiologic factors were drug addiction by parenteral route in 145 cases (92%), sexual transmission in 5 (3%), post transfusional in 2 (1%) and unknown in 6 (4%). With respect to the delta type infection, 105 cases (66%) were coinfections with type B and delta, and 53 patients had a type delta superinfection (34%). The clinical course was a fulminant hepatitis in three cases (two cases of coinfection B and delta an one case of delta superinfection), and an acute benign hepatitis in 155 patients. The follow-up of 118 patients revealed that 96% of coinfections by type B and delta evolved to the chronicity showing findings of active chronic hepatitis or hepatic cirrhosis. It should be noted that in 4 cases of superinfection delta type (11%) the HBsAg was negative after several months of positivity. In these patients the level of transaminases normalized and the hepatic histology evidenced alterations of chronic active hepatitis (2 cases) and hepatic cirrhosis (2 cases) without identification of tissular delta antigen.

Acute Disease↗
PubMed1990

Hepatitis B virus and hepatitis D virus replication in HBsAg-positive fulminant hepatitis.

Hepatitis B virus DNA and hepatitis D virus RNA, the most sensitive markers of hepatitis B and hepatitis D virus replication, were sought by molecular hybridization with radioactive probes in serial serum samples from 29 consecutive patients with HBsAg-positive fulminant hepatitis. Nineteen patients had evidence of hepatitis D virus infection, as assessed by the presence in serum of delta antigen, anti-delta antibodies, or both. Hepatitis B virus DNA was found in only two patients: one was a chronic HBsAg carrier with hepatitis D virus superinfection and the other had fulminant hepatitis caused by hepatitis B and hepatitis D coinfection. Hepatitis D virus RNA was detected in three patients: two with hepatitis B and hepatitis D coinfection and also in the HBsAg carrier with positive hepatitis B virus DNA and hepatitis D virus superinfection. None of 10 patients with hepatitis B virus infection alone had detectable viral nucleic acids in serum. Overall, viral nucleic acids were detected in the sera of 4 of the 29 patients (14%). Hepatitis D virus antigenemia did not indicate hepatitis D virus replication because hepatitis D virus RNA was not detected in 9 of 12 patients with hepatitis D virus antigen in their sera. The low frequency of viral replication found in fulminant hepatitis B or D may explain the low recurrence rate of viral hepatitis in patients with fulminant hepatitis who have received liver transplantations.

Adolescent↗
PubMed1986

Serological diagnosis of acute delta hepatitis.

Sixty-three intravenous drug addicts with HBsAg positive hepatitis were studied to evaluate the diagnostic usefulness of hepatitis delta virus (HDV) markers for diagnosis of acute HDV infection. Patients were tested for HBsAg, anti-HBc-IgM, and anti-HD-IgM by radioimmunoassay (RIA), and for hepatitis delta antigen (HD-Ag) by a commercial enzyme-linked immunoassay (ELISA). At least two serum samples at a mean interval of 4 wk were examined from each patient. HDV markers were found in 41 cases. In the first serum sample (obtained within 1-5 wk after onset of illness) HD-Ag was found in 32 cases and was the only HDV marker in 22; in the remaining 10 cases, HD-Ag was found along with total anti-HD, and in 6 of them anti-HD-IgM was also detected. Five additional patients were only positive for total anti-HD, and anti-HD of the IgM class was the only marker in one patient. HD-Ag was found more often in the patients studied during the first 2 wk of illness. In the second serum sample, HD-Ag was never the only marker detected, seven patients were still positive, and in all of them anti-HD was also present. Thirty patients were only positive for anti-HD. Seroconversion from HD-Ag to anti-HD occurred in 20 of 22 (91%) patients. The results suggest that HD-Ag determination by ELISA in the initial serum sample, during the first 2 wk of illness, may be the most sensitive test for the diagnosis of acute delta infection, and that seroconversion to anti-HD usually occurs after the sixth week of illness.

Acute Disease↗
PubMed1986

Prolonged inhibition of hepatitis B virus replication with vidarabine monophosphate in chronic active type B hepatitis.

Eight patients with chronic (mean 52 months) type B hepatitis (chronic active hepatitis and active cirrhosis) and markers of active viral replication (presence of HBeAg and HBV-DNA in serum) were treated with Ara-AMP for 7-12 weeks. The mean follow-up time was 18.3 months. All but one patient responded to treatment. In seven patients, HBeAg and HBV-DNA became negative and developed anti-HBe. One patient lost HBsAg as well as HBeAg and HBV-DNA. HBcAg in liver tissue became undetectable or greatly reduced in the seven patients in whom it was strongly positive. Aminotransferase and immunoglobulin levels reverted to normal in the seven responders and remained normal through the entire follow-up period. A second liver biopsy, performed after completion of therapy, showed improvement in six of eight cases, with disappearance of lobular activity. Two patients treated for 12 weeks developed a severe polyneuropathy lasting for 6 months. A 7-week course of Ara-AMP seems to induce long-lasting inhibition of viral replication, along with an improvement in liver function tests and liver histology, without significant side effects. On the other hand, a 12-week course was associated with the development of a severe and prolonged polyneuropathy.

Adult↗
PubMedDate not supplied

[Clinical usefulness of oligoclonal bands].

The presence of oligoclonal bands (OCB) of immunoglobulin G (IgG) is in our days the most useful finding in the study of the CSF for the diagnosis of multiple sclerosis (MS). The most sensitive method for the detection of OCB is the isoelectric focusing followed by immunoblotting. The prevalence of OCB changes in different populations with a rank of results from 60 to 95 97%. We have determined the prevalence of OCB in our population and the sensitivity and the specificity of the technique used in our laboratory. We have included 391 patients in whom we analysed the presence of OCB, subdivided in; Group 0: Diagnosed of MS, group 1: First episode of demyelinating process, group 2: Neurological disorders considered noninflammatory or nonautoimmune (NINA),group 3: Neurological disorders considered inflammatory, infectious or autoimmune (IIA). The presence of OCB was searched in CSF and serum simultaneously using isoelectric focusing and immunoblotting. In order to standardize the technique we achieved and internal and external validation. Internal validation: sensitivity and specificity (using as a control group first the group NINA and after the group IA). External validation: we choose 10 pairs of CSF/serum from patients with different diagnostics and sent to a reference laboratory ( Karolinska Institute Medical School) that was blind of our results and of the diagnostics. The prevalence of OCB in each group has been: group 0 (MS): 87.7%, group 1: 54.8%, group 2 (NINA): 17.5%, group 3(IIA): 52.7%. Sensitivity: 97.7%, specificity using group NINA as control 82.5% and using group IIA 45.7%. Concordance with the reference laboratory in 9/10 determinations. We conclude that in our population the prevalence of OCB, in patients with MS, is lower than in Northern Europe. The OCB appear in may inflammatory, autoimmune diseases, their specificity for the diagnostic of MS is low.

Autoimmune Diseases↗
PubMedDate not supplied

[Quantitative determination of HBV-DNA in chronic hepatitis B: comparison of three methods].

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.

DNA, Viral↗