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Biomedical subjects

C Legendre

Publications and source records attributed to C Legendre.

At least 91 records · Page 5Linked to original sources
PubMed1997

Vascular rupture complicating transluminal angioplasty applied on a failed dialysis vascular access in a patient under chronic steroid therapy.

We report a case of venous rupture complicating percutaneous transluminal angioplasty (PTA) applied on a failed dialysis vascular access (VA) in a patient on chronic steroid therapy. This complication resulted in a rapidly growing hematoma which was successfully controlled by a prolonged reinflation of the balloon catheter at the angioplasty site. The absence of oversizing of the balloon catheter and the low inflation pressure at which the perforation occurred suggest a vessel fragility which was probably induced by a long-standing steroid therapy. In dialysis patients in whom steroid therapy does not represent an infrequent therapeutic modality, this potential risk of vascular rupture should be carefully weighted while treating VA stenoses with the use of PTA.

Angioplasty, Balloon↗
PubMed1997

Treatment and prognosis of post-transplant lymphoproliferative disease.

Post-transplant lymphoproliferative diseases (PTLDs) are a clinically and morphologically heterogeneous group of lymphoid proliferations. They represent a life-threatening complication of solid organ transplantation. The mechanisms of their pathogenesis are not yet fully understood. A combination of impaired immunity, oncogenic consequences of immunosuppressive therapy and EBV infection may play a role. Studies on incidence, treatment and prognosis are difficult because of the small number of cases occurring at each transplant center and the lack of reliable classification. Overall mortality remains high even though 25% of patients require no other measure than reduction in immunosuppression which must be the first step of treatment. Several treatments are currently used but more adequate classification as well as multicenter studies are urgently needed because many questions remain with regard to therapeutic strategy. Late-onset monoclonal tumors may be treated by conventional chemotherapy, while EBV-positive PTLDs may benefit from other approaches such as antiviral therapies or immunologic modulation of tumor functions.

Humans↗
PubMed1996

Effect of hydroxyethylstarch in brain-dead kidney donors on renal function in kidney-transplant recipients.

BACKGROUND: Hydroxyethylstarch used as a plasma-volume expander in brain-dead kidney donors has been suggested to induce osmotic-nephrosis-like lesions. We have studied its effect on kidney-transplant function. METHODS: 52 patients who had received hydroxyethylstarch of iodinated contrast-media before brain death were excluded. 69 other brain-dead patients were prospectively included over 18 months and randomised into two groups. In the hydroxyethylstarch-gelatin group, patients received hydroxyethylstarch up to 33 mL/kg for colloid plasma-volume expansion, and afterwards received modified fluid gelatin. In the gelatin-only group, patients received only modified fluid gelatin as colloid plasma-volume expander. Multiple organs were procured in 29 cases, which included the kidneys in 27 cases (hydroxyethylstarch-gelatin 15, gelatin-only 12). FINDINGS: There were no significant differences in the characteristics of patients between the two groups of kidney donors or of recipients (except for a small imbalance in sex in the recipients). During the first 8 days after transplantation, nine of 27 (33%) patients required extrarenal haemodialysis or haemodiafiltration in the hydroxyethylstarch-gelatin group compared with one of 20 (5%) in the gelatin-only group (p = 0.029). Serum creatinine concentrations were significantly lower in the gelatin-only group than in the other group (p = 0.009). 10 days after transplantation, mean (SD) serum creatinine was, respectively, 145 (70) and 312 (259) mumol/L. INTERPRETATION: These data suggest that hydroxyethylstarch used as a plasma-volume expander in brain-dead donors impairs immediate renal function in kidney-transplant recipients.

Adult↗
PubMed1996

The long-term virologic and pathologic impact of renal transplantation on chronic hepatitis B virus infection.

In an attempt to evaluate the long-term reciprocal impact of renal transplantation on hepatitis B virus infection, we analyzed the clinical, virologic, and pathologic features of 151 HBsAg-positive kidney transplant recipients. The spontaneous disappearance rates of HBsAg, HBeAg, and HBV DNA during a median follow-up of 125 months (range 1 to 320) were 3, 30.6, and 3%, respectively, figures lower than in the general population. A high rate of persistent viral replication (50%) and reactivation (30%) was noted. Noteworthy was the high frequency of histologic deterioration (85.3%), accompanied by cirrhosis in 28% and by hepatocellular carcinoma in 23% of the patients with cirrhosis. Co-infection by hepatitis C and B viruses was significantly associated with histologic worsening. Liver disease was the leading cause of death (36.6%), especially in patients with cirrhosis. Despite persistent viral replication, histopathologic deterioration, and liver-related overmortality, there were paradoxically no significant differences in the survival of these 151 HBsAg-positive compared with 1247 HBsAg-negative kidney recipients--however, allograft actuarial survival was better in the former than in the latter group (P=0.0006). Chronic hepatitis B infection is not a contraindication to renal transplantation in the absence of cirrhosis. The presence of cirrhosis should lead either to dialysis continuation or to a combined liver/kidney transplantation, in the absence of viral replication.

Adult↗
PubMed1996

Azathioprine hepatitis in kidney transplant recipients. A predisposing role of chronic viral hepatitis.

Influence of viral liver diseases on the occurrence of azathioprine hepatitis was evaluated in 21 kidney transplant recipients. Diagnosis of azathioprine hepatitis was always based on jaundice, which disappeared after azathioprine withdrawal in 18 patients and after azathioprine dose reduction in 3 patients. Histopathological diagnosis of azathioprine toxicity was ascertained in 14 patients. Rechallenge with azathioprine performed in 4 patients, within 2-4 months after the first jaundice episode, resulted in relapse of jaundice in all cases. Viral hepatitis B virus and hepatitis C markers were present in all 20 tested patients (serum hepatitis B surface antigen in 6 patients and anti-HCV antibodies in 17 patients). Biopsy-proven chronic hepatitis was observed in 18 patients, including 14 chronic active hepatitis, 3 chronic persistent hepatitis and cirrhosis in 1. In kidney transplant recipients, azathioprine hepatitis seems to be facilitated or induced by hepatitis B virus or hepatitis C virus chronic hepatitis. Azathioprine reduction or withdrawal should therefore be combined with the diagnostic evaluation and the treatment of viral liver diseases.

Adult↗
PubMed1996

CD40/CD40L interactions and cytokines regulate HIV replication in B cells in vitro.

Using our in vitro model of normal B cell infection, we investigated whether cellular interactions and/or cytokines directing the B cell response also regulate HIV replication. Phorbol esters and CD40 Ab plus IL4, added prior to infection, substantially increased subsequent viral replication. Postinfection, IL2 with or without IL4 and, to a lesser extent, CD40/CD40L interactions enhanced viral replication. In contrast, IL10 down-regulated HIV replication induced by cytokines, without affecting spontaneous or CD40 Ab-induced replication. Both enhancing and inhibitory effects of cytokines on viral replication were independent of their ability to modulate B cell proliferation. Thus, these two phenomena seem to be independently regulated in human B cells.

Animals↗
PubMed1996

Mechanisms of opsonized HIV entry in normal B lymphocytes.

Using our in vitro model of normal B cell infection that functions with low doses of HIV but requires virus opsonization by seropositive patient serum, and complement, we analyzed what receptors allowed virus entry. Here, we show that HIV infection of B cells occurs through 2 major receptors: the CD4 antigen and the CR1/CR2 complex. These 2 pathways work independently since a complete inhibition of virus entry requires both CD4 and CD21/CD35 blockade on CD4dim tonsillar B cells whereas only the latter is critical on CD4-negative B cells.

Antibodies, Monoclonal↗
PubMed1996

Glutamine metabolism and neuropathological disorders in experimental hepatic encephalopathy: effect of transplanted hepatocytes.

BACKGROUND: Physiopathology of hepatic encephalopathy remains unclear. Recent studies have suggested that ammonia would not act by itself but through an increase in glutamine in the brain. We have previously demonstrated that transplantation of syngeneic hepatocytes into the spleen was able to correct both behavioral deficits and plasma amino acid changes observed in portacaval shunted rats. The aim of the present work was to show a correlation between the correction of chronic hepatic encephalopathy by means of intrasplenic hepatocyte transplantation and two parameters, brain glutamine concentration and ultrastructural aspects of astrocytes. METHODS: Inbred male Wistar Furth rats were divided into three groups: sham-operated rats (n = 10), rats subjected to portacaval shunt (n = 10), and rats subjected to portacaval shunt and intrasplenic hepatocellular transplantation of 10(7) hepatocytes isolated from livers of syngeneic rats (n = 10). Chronic hepatic encephalopathy was quantified 30 and 60 days after operation by means of nose-poke exploration and spontaneous activity. Pathologic examination and measurement of glutamine concentrations in the corpus striatus and in the cerebral cortex were performed 60 days after operation. RESULTS: Portacaval shunt rats showed reduced spontaneous activity and nose-poke exploration scores. After portacaval shunt a significant glutamine increase occurred in the corpus striatus and in the cerebral cortex when compared with sham rats (p < 0.05). Ultrastructural examination showed modification of astrocytes named Alzheimer type II after portacaval shunt. Correction of behavioral abnormalities by means of intrasplenic hepatocyte transplantation was associated with partial correction of striatal glutamine increase and with decrease in astrocyte alterations. Cortex glutamine concentration in portacaval shunt-intrasplenic hepatocyte transplantation group and in portacaval shunt rats did not differ significantly. CONCLUSIONS: These data show that intrasplenic hepatocyte transplantation not only prevents neurologic disorders of hepatic encephalopathy but can also decrease glutamine and ultrastructural alterations in the corpus striatus in an experimental model of chronic liver failure. These data are in favor of the involvement of glutamine in chronic hepatic encephalopathy. These results suggest that intrasplenic hepatocyte transplantation might be of therapeutic interest in chronic liver failure.

Animals↗