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D Sicard

Publications and source records attributed to D Sicard.

At least 73 records · Page 4Linked to original sources
PubMed1997

Haemophagocytic syndrome in patients infected with the human immunodeficiency virus: nine cases and a review.

We report nine cases of haemophagocytic syndrome (HS) in patients with human immunodeficiency virus infection, and review the 17 cases described to date in the literature. In 21 of 26 cases, HS developed during an advanced stage of immunodeficiency. Clinical and haematological signs are not specific in this setting, and the diagnosis relies on histological features, mainly bone marrow examination. An opportunistic infection was associated in three cases and a lymphoid malignancy in two of our nine cases. The role of the human immunodeficiency virus in the occurrence of the HS remains to be defined. The overall prognosis is poor as six of our nine patients died within 12 months of presentation.

Adult↗
PubMed1997

Exacerbations of clinical symptoms in human immunodeficiency virus type 1-infected patients with multicentric Castleman's disease are associated with a high increase in Kaposi's sarcoma herpesvirus DNA load in peripheral blood mononuclear cells.

The epidemiologic link between multicentric Castleman's disease (MCD) and Kaposi's sarcoma (KS) and the high frequency of KS herpesvirus (KSHV) detection in both diseases raise the question of a role of this new virus in the pathogenesis of MCD. To explore this hypothesis, the KSHV DNA load was investigated in peripheral blood mononuclear cells of 3 human immunodeficiency virus (HIV)-infected patients with MCD at different points during the clinical course. Clinical parameters, such as fever and the presence of lymphadenopathy, were systematically assessed. Hemogram and C-reactive protein level determinations were performed as standard procedures. KSHV DNA load was investigated by means of semiquantitative polymerase chain reaction assay using peripheral blood mononuclear cells of the patients. A correlation between the variation in clinical and biologic parameters related to MCD and KSHV DNA load was found, suggesting a close relationship between KSHV and MCD in HIV-1-infected patients.

Castleman Disease↗
PubMed1997

[Characteristics of rapid progressors in HIV infection].

Approximately 10% of HIV-infected patients, the rapid progressors, progress to AIDS within the first 2 to 3 years of HIV infection. Their biological characteristics are not clearly known. They have a particular phenotype (DR) of major histocompatibility complex class-II. Anti-HIV antibodies are not neutralizing and may even be facilitators in vitro. Progressors CTL responses are also defective and the production of the cytokines, specially the chemokines RANTES, MIP-1 alpha et MIP-1 beta which may have a role in inhibition of cellular infection by HIV, is impaired. In addition, the rapid progressors have high levels of inflammatory markers which suppose a chronic activation of the immune system. The virological findings are more inconsistent. A uniform finding is a high viral load that does not fall dramatically after primary HIV infection. Some rapid progressors may be infected with more rapidly replicating, virulent HIV strains. However, the question regarding the homogeneity or the other characteristics of viral load remains to be resolved.

Antibody Formation↗
PubMed1996

Delayed virus-specific CD8+ cytotoxic T lymphocyte activity in an HIV-infected individual with high CD4+ cell counts: correlations with various parameters of disease progression.

This 4-year longitudinal study monitored the temporal association between the HIV-specific cytotoxic T lymphocyte (CTL) response and the control viremia in an individual infected with human immunodeficiency virus type (HIV-1). At the beginning of the study, this asymptomatic individual with a high CD4+ cell count showed no HIV-specific cytotoxic activity after polyclonal in vitro restimulation with autologous PHA-blasts, unlike most HIV-seropositive individuals. Anti-HIV CTLs were detected only in the last year of the study, both after in vitro restimulation and directly ex vivo. This was correlated with the inversion of the CD4+/CD8+ ratio, essentially due to increased numbers of CD8+CD28- T lymphocytes. The HIV-specific cytolytic activity was mediated by this CD28+CD28- subpopulation. The amount of HIV-1 provirus in peripheral blood mononuclear cells (PBMCs) did not change during the study, but the HIV RNA in plasma increased and virus was isolated from PBMCs only at the time when HIV-specific CTL activity was detected. This suggests overall that the HIV-1 replication was low in this individual, with a transient increase that could have reached the threshold for CTL reactivation, and was perhaps controlled thereby.

CD28 Antigens↗
PubMed1996

[Retrospective evaluation of the detection of Toxoplasma gondii by polymerase chain reaction in AIDS patients].

OBJECTIVES: We retrospectively evaluated routine detection of Toxoplasma gondii by polymerase chain reaction (PCR) amplification of the B1 gene and the TGR 1E sequence in blood and CSF samples from patients with acquired immune deficiency syndrome (AIDS) and suspected toxoplasmosis. METHODS: From January 1993 to February 1994, 93 blood, 33 cerebrospinal fluid (CSF) and 1 aqueous humor samples were obtained from 83 HIV-positive patients with CD4 counts under 200/mm3 and suspected toxoplasmosis. RESULTS: Authentic cerebral toxoplasmosis was confirmed by response to specific treatment in 18/29 patients with typical focal brain lesions. Blood samples were available in 17/18 and CSF in 6. PCR was positive for both B1 and TGR (23.5% sensitivity, 100% specificity) in 4/17 blood samples and for either B1 or TGF (58.9% sensitivity, 72.7% specificity) in 10/18. PCR of CSF was positive in only 1/6 patients with cerebral toxoplasmosis. PCR (TGR 1E only) was positive in 3/11 blood samples and in one CSF sample from patients without cerebral toxoplasmosis. Five out of 21 patients with diffuse neurologic symptoms and presumed HIV encephalitis had positive Toxoplasma detection in blood or CSF. However, no clinical improvement was obtained after specific antitoxoplasmic therapy. Two out of 38 patients with unexplained fever with or without pneumonia had a proven disseminated toxoplasmosis. These two patients had PCR-positive blood samples. One of them was cured by a specific anti-toxoplasmic treatment and the other died two days later. Seven other patients had a positive PCR result in blood or CSF. Three of them improved with specific treatment and 2 died before treatment could be initiated. The one patient with toxoplasmic retinitis was PCR-positive both in blood and aqueous humor. CONCLUSION: PCR detection of Toxoplasma gondii appears to add little to the diagnosis of cerebral toxoplasmosis but could be helpful in the diagnosis of cerebral toxoplasmosis associated with extracerebral reactivation and in disseminated toxoplasmosis.

AIDS-Related Opportunistic Infections↗
PubMed1996

[Left vocal cord paralysis in cytomegalovirus multifocal neuropathy in a patient with HIV infection].

Cytomegalovirus multifocal neuropathies (CMV-MN) in patients with AIDS are much less frequent than meningoradiculitis. We report here the case of a patient with AIDS hospitalized because of severe motor weakness and paralyzed left true vocal cord (PVC), related to a multifocal neuropathy. CSF analysis was normal with a negative PCR for CMV, but neuromuscular biopsy showed typical CMV inclusions. The patient's condition improved with high dose foscarnet therapy, followed by a combination of ganciclovir plus foscarnet, during a five-month follow-up period. Twenty three case reports of CMV-MN have been published in the literature, only 2 of them presenting with a PVC. Extraneurological CMV involvement was usually documented. PCR for CMV in CSF was most often positive. However CMV inclusions were not frequently observed. The patients were usually improved under therapy with usually ganciclovir but relapse was observed in fifty percent within 3 to 6 months despite secondary prophylaxis.

AIDS-Related Opportunistic Infections↗