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Biomedical subjects

F Bouscarat

Publications and source records attributed to F Bouscarat.

At least 37 records · Page 2Linked to original sources
PubMed1997

Human herpesvirus 6 infection associated with anticonvulsant hypersensitivity syndrome and reactive haemophagocytic syndrome.

Viral infections are thought to play a part in some cutaneous drug reactions. Human herpesvirus 6 (HHV6), which is the agent of exanthema subitum (sixth disease), has never been implicated in a drug reaction. We report a patient with severe phenobarbital-induced anticonvulsant hypersensitivity syndrome in whom a fulminant haemophagocytic syndrome was associated with HHV6 infection. We discuss the possible role of HHV6 in this reactive condition.

Adult↗
PubMed1997

Polyarthritis with cutaneous mucinosis and intrasynovial mucin deposits.

We report the first case of cutaneous and articular mucinosis with presence of mucin deposits within the synovium in an HIV-positive patients. Presentation was asymmetric polyarthritis, and subcutaneous nodules developed two months later. Treatment was with hydroxychloroquine. The outcome of both the skin and joint lesions was favourable.

Adult↗
PubMed1996

[Characteristics of mucocutaneous infections in immunocompromised patients].

Among the different targets affected by immunodeficiency, skin is at the first line. Infections are the most frequent causes of cutaneous manifestations in immunocompromised subjects. They are primitive or secondary cutaneous infections occurring during disseminated disease. Skin manifestations may reveal the systemic disease. Primary or secondary bacterial, viral, fungic, and parasitic mucocutaneous diseases are often atypical, extensive and frequently follow chronical course. These peculiar presentations makes diagnosis difficult. The knowledge of the clinical pleomorphism of skin infections in immunocompromised subjects is essential. All doubtfull lesions must lead to histological and microbiological study. Diagnosis delay may increase the risk of dissemination resulting in morbidity and mortality.

AIDS-Related Opportunistic Infections↗
PubMed1996

Correlation of CD8 lymphocyte activation with cellular viremia and plasma HIV RNA levels in asymptomatic patients infected by human immunodeficiency virus type 1.

The relationship between CD8 lymphocyte phenotypic alterations and virological parameters was studied in 47 asymptomatic subjects with human immunodeficiency virus type 1 (HIV-1) infection and CD4 T cell counts above 400/microliters. CD8 subsets were examined by means of three-color flow cytometry, using an extensive panel of monoclonal antibody combinations. Virological parameters were measured by both end-point dilution culture of peripheral blood mononuclear cells (PBMCs) and plasma and branched-DNA (bDNA) signal amplification of plasma HIV RNA. Whereas HIV-infected patients had a near-normal CD4 cell count (mean, 782 cells/microliter), several subsets of activated CD8 cells were markedly expanded relative to values in 23 HIV-seronegative controls. The PBMC cultures were positive in 38 cases and plasma HIV RNA was detected in 31. The percentage of CD4 cells correlated negatively with both cellular viremia and plasma HIV RNA levels. Conversely, a positive correlation was observed between viral load and the percentage of CD8 cells. Among CD8 lymphocytes, the CD38+CD8 and HLA-DR+CD8 subsets correlated best with viral load. Three-color analysis showed that the subpopulations involved in this relationship were CD38+HLA-DR+, CD38+CD28-, HLA-DR+CD28+, HLA-DR+CD57-, CD38+CD57-, CD38+CD45RO+, and HLA-DR+CD45RO+. Our data provide the first evidence that viral load correlates with subsets of activated CD8 lymphocytes in asymptomatic HIV-infected subjects who have near-normal numbers of CD4 lymphocytes.

Adult↗
PubMed1996

[Paraneoplastic pemphigus in chronic lymphocytic leukemia].

INTRODUCTION: Paraneoplastic pemphigus is an autoimmune bullous disease described by precise clinical, histological and immunological features presented by Anhalt in 1990. Prognosis is very severe and depends on the associated neoplasia and the gravity of the mucosal damage. CASE REPORT: Paraneoplastic pemphigus was diagnosed in a 62-year-old man with chronic lymphoid leukemia. The course was favorable up to one-year follow-up after general corticosteroid therapy. DISCUSSION: This case illustrates that paraneoplastic pemphigus can be controlled by general corticosteroids and would suggest the severe prognosis may be improved.

Glucocorticoids↗
PubMed1995

Impairment of polymorphonuclear neutrophil function in HIV-infected patients.

Impaired polymorphonuclear neutrophil (PMN) function may contribute to the onset of certain bacterial and fungal infections and to tissue damage in human immunodeficiency virus (HIV)-infected patients. Published data on PMN function in HIV infection are controversial, possibly because most studies have involved PMNs isolated from the normal blood environment by various procedures that may modify PMN responses. We therefore used flow cytometry to study the expression of adhesion molecules at the PMN surface, actin polymerization, and the oxidative burst of whole-blood PMNs in 42 HIV-infected patients at different stages of the disease. These PMNs were activated in vivo, as shown by increased expression of the adhesion molecule CD11b/CD18, reduced L-selectin antigen expression, increased actin polymerization, and increased H2O2 production. The alterations were present in asymptomatic patients with CD4+ cell counts above 500/microliters and did not increase with progression of the disease. This PMN activation could contribute to the oxidative stress described in HIV infection. Stimulation by bacterial N-formyl peptides showed dysregulation of L-selectin shedding and decreased H2O2 production after cx vivo priming with tumor necrosis factor-alpha or interleukin-8. These latter impairments, which correlated with the decrease in CD4+ lymphocyte numbers, could contribute to the increased susceptibility of HIV-infected patients to bacterial infections.

Actins↗
PubMed1994

Polymorphonuclear neutrophils from human immunodeficiency virus-infected patients show enhanced activation, diminished fMLP-induced L-selectin shedding, and an impaired oxidative burst after cytokine priming.

Impaired polymorphonuclear neutrophil (PMN) function may contribute to the onset of certain life-threatening bacterial and fungal infections in human immunodeficiency virus (HIV)-infected patients. Published data on PMN functional activity in HIV infection are controversial, possibly because most studies have involved PMNs isolated from their blood environment by means of various procedures that may differently affect surface receptor expression and thereby alter cellular responses. We therefore used flow cytometry to study the expression of adhesion molecules at the PMN surface, actin polymerization, and the oxidative burst of whole-blood polymorphonuclear neutrophils in 42 HIV-infected patients at different stages of the disease. These PMNs were activated in vivo, as demonstrated by increased expression of the adhesion molecule CD11b/CD18, reduced L-selectin antigen expression, increased actin polymerization, and increased H2O2 production. The alterations were present in asymptomatic patients with CD4+ cell counts greater than 500/microL and did not increase with the progression of the disease. Stimulation by bacterial N-formyl peptides showed dysregulation of L-selectin shedding and decreased H2O2 production after ex vivo priming with tumor necrosis factor alpha or interleukin-8 (IL-8). These latter impairments, which correlated with the decrease in CD4+ lymphocyte numbers and with IL-8 and IL-6 plasma levels, could contribute to the increased susceptibility of HIV-infected patients to bacterial infections.

Acquired Immunodeficiency Syndrome↗
PubMed1994

An observational study of 11 French liver transplant recipients infected with human immunodeficiency virus type 1.

We report the clinical and biological course of infection with human immunodeficiency virus (HIV) type 1 in 11 liver transplant recipients who acquired this infection between 1985 and 1987. Eight patients were infected by blood or blood products from graft-related transfusions and one by the graft itself; the remaining two patients were infected after transplantation and had independent risk factors. All patients received a triple-drug immunosuppressive regimen including cyclosporine. The mean duration of follow-up after liver transplantation was 52 months (standard error, +/- 32 months). Chronic graft rejection was documented in four cases. The cumulative incidences of HIV-related complications and HIV-related deaths were 82% and 27%, respectively. Three patients died rapidly of HIV disease. The survival rate 7 years after transplantation was 36% among the 11 HIV-infected patients, whereas it was approximately 70% among HIV-negative liver transplant recipients during the same period. The course of HIV infection in the four survivors did not appear to differ from that in other patients infected by blood transfusion.

Acquired Immunodeficiency Syndrome↗