Prevention of tracheal aspiration in a patient with a high risk of regurgitation using a new double-lumen gastric laryngeal mask airway.
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Biomedical subjects
Publications and source records attributed to P Pellegrino.
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OBJECTIVE: To evaluate the antiretroviral effect of a combination of zidovudine (ZDV) and didanosine (ddl) on plasma, peripheral blood mononuclear cells (PBMC) and lymph nodes after 24 weeks. METHODS: Eight patients naive of antiretroviral therapy were followed by monthly blood samples and two surgical lymph-node biopsies taken at baseline and after 24 weeks. CD4+ T cells were counted monthly by flow cytometry. Plasma HIV-1 RNA was measured monthly by polymerase chain reaction (PCR). Infectious cellular viraemia was measured monthly by a culture technique. Proviral DNA titres in PBMC were measured by endpoint dilution PCR at baseline and 24 weeks. Infectious HIV-1 and proviral DNA titres were measured in the lymph-node mononuclear cells (LNMC). The total HIV-1 RNA content of lymph nodes was measured by PCR. In some cases, phenotypic resistance to ZDV was measured, and codon 215 and 74 mutations in PBMC and LNMC were analysed. RESULTS: A mean increase in CD4 cell count of 122 x 10(6)/l, a mean decrease in HIV-1 RNA of 1.47 log10 in plasma and a mean decrease in HIV-1 DNA titre of 0.63 log10 were found after 24 weeks of therapy. Nevertheless, there were no statistically significant changes in the mean infectious HIV-1 titre in PBMC and LNMC, in the HIV-1 DNA titre in LNMC or in the total lymph-node HIV-1 RNA burden at week 24. Phenotypic or genotypic markers of drug resistance were rarely found in PBMC at week 24, although they were detected in LNMC from some patients. CONCLUSION: A discrepancy in the therapeutic effect can be observed between lymphoid organs and blood after 24 weeks of therapy with ZDV and ddl. This difference could be explained by the insufficient antiretroviral potency of this combination facing the significant viral burden present in lymph nodes. Development of drug resistance in this compartment prior to blood can be demonstrated in some cases, although other mechanisms remain to be investigated in future studies to explain this difference.
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OBJECTIVE: To compare the viral burden and the biological phenotype of HIV-1 isolates obtained from lymphoid node mononuclear cells (LNMC) and peripheral blood mononuclear cells (PBMC) in 11 HIV-infected patients. METHODS: Viral burden was quantified by cocultivating LNMC and PBMC from HIV-infected patients with PBMC from seronegative donors. For each patient, LNMC and PBMC isolates were characterized in terms of susceptibility to neutralizing antibodies, syncytium-inducing capacity and sensitivity to zidovudine. RESULTS: Our data show that: (1) viral burden was 1.73 log higher in LNMC than PBMC in patients with persistent generalized lymphadenopathy and only 0.37 log higher in patients with AIDS-related complex; (2) five out of 11 LNMC bulk isolates were phenotypically distinct from autologous PBMC isolates; (3) in three patients, the autologous serum neutralized the PBMC isolates but not the LNMC isolates. CONCLUSIONS: These results suggest that the relatively high level of HIV-1 replication in lymph nodes may favour the emergence of viruses exhibiting specific phenotypes, including neutralization escape variants. The existence of viral variants in lymphoid tissue at all stages of HIV infection may elucidate certain aspects of the pathogenesis of HIV-1 infection.
Surrogate markers generally used for observation of patients infected with human immunodeficiency virus (HIV) and their plasma and cellular viral load were assayed in a series of 40 patients before initiation of zidovudine therapy. Plasma viremia was positive in 62.5% of patients and was statistically correlated with clinical stage, CD4+ T cell count, CD8+ T cell count, beta 2-microglobulin level, neopterin level, and immunoglobulin A level. Cellular viremia was positive in 95% of patients and was correlated with clinical stage, CD4+ T cell count, beta 2-microglobulin, neopterin levels, and disease progression during the following months. A discordance was found between p24 antigenemia, even after acid dissociation of immune complexes, and plasma viremia. In fact, p24 antigenemia was correlated with only biological markers of immune activation as beta 2-microglobulin and neopterin levels. The measurement of anti-p24 antibodies did not appear discriminative in our staging. Plasma viremia, like CD4+ T cell count, reflects the patient's status at the time of assessment. Cellular viremia could be more informative for the prediction of future clinical progression.
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Frequency of mucosal damage to the esophagus, stomach, and duodenum was investigated in 176 children with coeliac disease (CD) during 230 upper GI endoscopies performed to obtain duodenal biopsy specimens and was compared with findings in 230 age-matched children who underwent endoscopy for upper GI complaints without CD (non-CD patients). To evaluate a possible association with gluten ingestion, we then compared frequency of mucosal damage in patients on a gluten-containing diet and those on a gluten-free Diet (GFD). In children with CD, frequency of esophageal damage seen at endoscopy and of peptic esophagitis shown by histology were significantly lower than in non-CD patients (p < 0.01) due to the very low frequency of mucosal damage in CD children on GFD; however, frequency of columnar metaplasia was significantly higher (p < 0.05). At endoscopy, CD children had a significantly lower frequency of gastric abnormalities, but histology showed a higher prevalence of superficial chronic gastritis (SCG; p < 0.01). SCG was associated with gluten ingestion, since its frequency in CD children on GFD was similar to the frequency in non-CD patients. At endoscopy, frequency of duodenal mucosal damage was similar in CD and non-CD patients. In addition to villous atrophy, histology showed a significantly higher frequency of duodenitis in CD children on a gluten-containing diet (p < 0.001 vs. non-CD patients; p < 0.05 vs. CD children on GFD). Our findings show that the mucosa of the whole upper GI tract can be damaged in CD patients and that the prevalence of some changes is higher with a gluten-containing diet.
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