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Biomedical subjects

F Berthoux

Publications and source records attributed to F Berthoux.

At least 37 records · Page 2Linked to original sources
PubMed1998

Is there IgA from gut mucosal origin in the serum of children with Henoch-Schönlein purpura?

Thirty-two children with Henoch-Schönlein purpura with or without renal symptoms were studied to characterize the IgA hyperglobulinemia observed in the serum of most patients. It was shown that only the IgA1 subclass concentration was increased. Secretory IgA and IgA to gliadin levels were frequently increased in serum, with a good correlation between them. Circulating IgA immune complexes were detected often and contained high activity to gliadin. In contrast, IgA activity to tetanus toxoid did not change. We failed to show any differences in renal involvement. These data suggest that elevation of serum IgA in Henoch-Schönlein purpura is due in part to a disturbance of the gut mucosal immune system, and the presence of circulating IgA immune complexes with dietary antigens can be postulated but cannot explain the occurrence of urinary symptoms.

Adolescent↗
PubMed1998

A randomized prospective study comparing low-dose OKT3 to low-dose ATG for the treatment of acute steroid-resistant rejection episodes in kidney transplant recipients.

Acute steroid-resistant rejection episodes in kidney allograft recipients require treatment with antilymphocyte antibodies. Monoclonal anti-CD3 and polyclonal antilymphocyte antibodies have been widely used but seldom compared. Recent data have suggested that these antibodies could be used at reduced doses without jeopardizing their efficacy. In this study, we randomized renal transplant recipients who encountered a first acute steroid-resistant rejection episode to low-dose ATG or low-dose OKT3 treatment. Sixty patients were enrolled in the study. They received prophylactic immunosuppression with cyclosporin, azathioprine, and prednisolone. Treatment of biopsy-proven rejection consisted of a 10-day course of either ATG (n = 31) or OKT3 (n = 29). The total ATG dose was 484 +/- 110 mg, i.e., 0.75 mg/kg per day. The total OKT3 dose was 32 +/- 4 mg, i.e., 0.05 mg/kg per day. We compared reversion of rejection, side effects, immunodepression, and graft function. Reversion of rejection was similar in the two groups, although we noted a trend in favor of ATG. Results were 3% vs 10% early graft failures, 13% vs 23% overall graft failures, 28% vs 38% 3-month actuarial incidence of rebound rejection, and 89% vs 81% 1-year graft survival rate in the ATG and OKT3 groups, respectively. Tolerance was worse in the OKT3 group due to the first-dose syndrome. Infections and cancers occurred with the same frequency. ATG resulted in a deeper and longer decrease in peripheral lymphocyte subsets. Graft function was similar in the two groups. We conclude that low-dose ATG and low-dose OKT3 are equally effective in reversing steroid-resistant acute rejection. Tolerance was better with ATG, which also gave a more potent and longlasting immunodepression. The use of reduced doses of ATG and OKT3 did not appear to lessen their efficacy.

Adult↗
PubMed1998

High prevalence of hepatitis G virus (HGV) infection in renal transplantation.

INTRODUCTION: The newly discovered (1995) hepatitis G virus (HGV) is an RNA virus from the Flaviviridae family with 85% genomic homology to GB virus C (GBV-C). We studied the prevalence of HGV infection among a cohort of 398 renal transplant recipients (RTR), all of whom had previously received blood transfusions, been grafted between August 1984 and December 1991, and been treated by cyclosporin A (CsA) as the main immunosuppressant. SUBJECTS AND METHODS: According to hepatitis C virus (HCV) antibody status, and after exclusion of 28 HBs antigen-positive recipients, this cohort had previously been divided into an HCV +ve subgroup (106 RTR; 62 M vs 44 F; 29 French vs 77 non-French) and an HCV -ve subgroup (264 RTR; 181 M vs 83 F, 196 French vs 68 non-French). We randomly selected 27 RTR in the HCV+/HBV- subgroup (14 M vs 13 F, 10 French vs 17 Italians) and 27 RTR in the HCV-/HBV- subgroup (19 M vs 8 F, 18 French vs 9 Italians) for HGV screening. The detection of HGV RNA sequences in serum (viraemia) was done by double nested RT-PCR using specific primers chosen in the 5' non-coding genomic region. The serum detection of specific antibodies (anti E2) was done by ELISA test. All sera (at time of liver biopsy or at last follow-up) were tested in duplicate. RESULTS: The prevalence of HGV viraemia was 26% (14/54) in the whole group and in both HCV +ve and -ve subgroups (7/27). The prevalence of HGV infection (viraemia + and/or anti E2 antibodies +) was 44% (24/54) in the whole group and in both HCV +ve and -ve subgroups (12/27). In addition, the prevalence was similar in males vs females and in French vs foreigners recipients (mostly Italians). In the HCV +ve subgroup, the seven HGV viraemia-positive patients who previously had liver biopsies disclosed chronic active hepatitis in four (mean Knodell score 5.75) and normal livers in three, with only one case of elevated ALT (CAH 5). In the HCV- subgroup, none of the seven HGV+ viraemic patients had elevated ALT and liver biopsy was not performed. CONCLUSION: HGV infection prevalence is high (44%) in RTR, but clearly independent of HCV status and/or the geographical origin of the recipients. This data indicates a different epidemiology as compared to our HCVs previous experience.

Adult↗
PubMed1998

Advantage of antithymocyte globulin induction in sensitized kidney recipients: a randomized prospective study comparing induction with and without antithymocyte globulin.

BACKGROUND: Sensitized kidney allograft recipients require special management to improve their outcome. One strategy is heavy immunosuppression with antilymphocyte antibodies. Controversy continues about the actual advantage of induction protocols whilst infections and cancers are a constant risk. In addition, little is known about how to handle sensitized patients with low levels of sensitization. METHODS: In this study, we randomized sensitized renal transplant recipients, who received prophylactic treatment with or without antithymocyte globulin (ATG), in addition to a standard triple regimen consisting of cyclosporin, steroids and azathioprine at ATG discontinuation. The induction treatment consisted of a low-dose ATG course over 10 days. Randomization was stratified on the maximum PRA, according to the five following classes: 5% < PRA < or = 20%, 20% < PRA < or = 40%, 40% < PRA < or = 60%, 60% < PRA < or = 80% and 80% < PRA < or = 100%. RESULTS: Eighty nine patients were enrolled: 47 patients received ATG and 42 did not. ATG induction lowered the incidence of biopsy-proven acute rejection episodes from 64 to 38%, increased 1 year graft survival from 76 to 89% and was associated with a higher 1 year inulin clearance (37+/-15 vs 49+/-18 ml/min). ATG-associated side effects were restricted to leucopenia and thrombocytopenia, whereas bacterial and viral infections, gammopathies and cancers did not occur more frequently. ATG induction benefited all sensitized patients, and not only the hypersensitized patients. CONCLUSIONS: We conclude that ATG induction is beneficial for all sensitized patients, regardless of their level of sensitization, with regard to acute rejection episodes, graft survival and graft function. Low-dose ATG is sufficient and prevents additional complications.

Adult↗
PubMed1997

Lack of evidence for natural cytotoxicity deficiency against human ex vivo tumour cells in allograft recipients.

BACKGROUND: Allograft recipients, who have a high risk of developing malignancies, are deficient in natural killer cells which mediate natural cytotoxicity against tumour cells. We evaluated the relevance of NK deficiency in transplant patients with regard to the natural lysis of human tumour cells. METHODS: Target cells were ex vivo tumour cells, obtained from solid tumours from kidney transplant patients and non-immunocompromised patients. Peripheral blood was extracted from kidney recipients and from normal controls. Mononuclear cells were separated after anti-CD3 and anti-TCR immunostaining to obtain NK and T cell subsets. LAK cells were obtained by in vitro IL2-activation. For each tumour, natural cytotoxicity assays were performed to compare effector cells from a kidney recipient with those from a normal control. Twenty-seven solid tumours, either allogenic or syngenic, were analysed, mainly consisting of renal, colon, and skin carcinomas. RESULTS: Natural cytotoxicity assays on K562 targets confirmed the expected NK deficiency in the kidney recipients. However, the NK and LAK cells from the kidney recipients did not kill a smaller number of tumour target cells than the controls, whatever the tumour type, under both the syngenic and allogenic conditions. CONCLUSIONS: We conclude that natural cytotoxicity against human tumour cells cannot be extrapolated from the cytotoxicity assays with established cell lines, and that natural lysis of ex vivo human tumour cells is not impaired in transplant patients.

Case-Control Studies↗
PubMed1997

[Can one graft with a positive cross-match?].

Differential cross-matches have been proposed to allow immunised patients to be grafted, whereas the dogma of a global positive cross-match discarded them from renal transplantation. We report our one-center experience considering current T positive cross-match as the only contra-indication to grafting, as well as patients whose sera comprise specific anti-donor antibodies. A comprehensive characterization of the antibodies was achieved by identification of auto-antibodies and specification of IgM and IgG isotype, class I and class II specificities, as well as HLA specificities. The differential cross-match comprised an auto and an allo-cross-match, against T and B lymphocytes. Historical and current sera were analysed either untreated or after DTT-treatment, at +4 degrees C and +22 degrees C. We performed 79 renal transplantations across positive cross-matches, which were 20 historical T positive cross-matches, 26 historical B positive cross-matches and 33 current B positive cross-matches. Results and graft survival were strictly identical as those obtained in the transplantations achieved with negative cross-matches throughout the same period, especially in sensitized patients. Current positive B cell cross-matches due to IgG were associated with an increased risk for early graft failure. We conclude that differential cross-match is a safe strategy permitting immunised patients to be grafted.

Autoantibodies↗
PubMed1996

HCV liver disease in renal transplantation: a clinical and histological study.

The prevalence of HCV infection is high in renal transplantation (RT) patients: 29% in our cohort of 399 RT recipients. The consequences of that infection on the liver have to be carefully assessed. Clinical chronic hepatitis was detected from ALT concentrations (> x 1.5 N) in only 26 patients (22%) with constant (15%) or fluctuating (85%) ALT elevation. Only three of 117 cases developed cirrhosis (3%). No liver cancer was noted. Liver biopsy was performed (mean interval = 60.2 months) in 62 patients with HCV infection alone. We found 26 cases (42%) of chronic active hepatitis (CAH) with a mean Knodell score as low as 6.1 (range: 3-12), a mean activity grade of 4.9, and a fibrosis stage of 1.3. Twelve patients (19%) presented with normal liver pathology and met the criteria of healthy HCV carriers (positive viraemia, normal ALT and normal liver). The rest presented with portal lesions, either inflammation or fibrosis. In addition, patient and graft survival rates did not differ in HCV+ recipients. To conclude, HCV infection did not appear too deleterious for the liver in this cohort of patients. There is therefore no contraindication for HCV-positive recipients to undergo renal transplantation.

Adolescent↗
PubMed1996

Glomerular disease during HCV infection in renal transplantation.

In general nephrology, HCV infection has been associated with type I membranoproliferative glomerulonephritis (MPGN type I) associated with cryoglobulinaemia. In a cohort of 399 renal transplantation (RT) recipients, 117 of whom (29%) were HCV-positive, we selected all patients diagnosed as having membranous GN or type I MPGN by graft biopsy. The prevalence of MGN was 16/399 (4%) with three recurrences, and 13 de novo cases. Only 5/16 (31%) were HCV+, not different from the general RT population. Five patients had an outcome of graft failure after 43 months. Conversely, there were 15 cases of type I MPGN (two recurrences, 13 de novo) but with eight HCV+ recipients (53%, P = 0.02). Considering only the French patients, prevalence was 44% vs 12% in the French RT population (P = 0.006). Eight patients had graft rejection after 59 months (five HCV+). In this type I MPGN subgroup, there were two positive cryoglobulins, two rheumatoid factors and four hypocomplementaemias. In conclusion, there is a clear association between HCV infection and the occurrence of type I MPGN in the allograft in renal transplantation, with terminal renal failure as an outcome.

Adolescent↗
PubMed1995

High frequency of IL-10-secreting CD4+ graft-infiltrating T lymphocytes in promptly rejected kidney allografts.

IFN-gamma and IL-10 secretion by sorted T cell subsets of irreversibly rejected kidney graft-infiltrating cells (GIC) and normal PBMC was studied by ELISPOT. The low spontaneous frequency of IFN-gamma-producing cells (IFN-gamma-PC) was strongly increased by anti-CD3 activation within unsorted, CD3+CD4+, and CD3+CD4- subsets of GIC and PBMC. In contrast with PBMC, IL-10-PC from GIC were at higher frequency within CD4+ cells than among CD4- ones (P < 0.03). Four kidneys removed after 3.7 +/- 0.8 months showed acute vascular rejection, high frequency of activated CD4+ IL-10-PC (118 +/- 68 per 10(4) cells), and high percentage of anti-class II antibody reactivity (87.6 +/- 6.3%). In contrast, four patients with kidneys removed later (53.7 +/- 1.6 months, P = 0.02) displayed chronic rejection with superimposed acute cellular rejection, low frequency of CD4+ IL-10-PC (7.0 +/- 3.0 per 10(4) cells, P = 0.02), and low percentage of anti-class II antibody reactivity (12.9 +/- 6.1%, P = 0.02). Thus, accelerated vascular rejection appears to be associated with preferential production of IL-10 by activated CD4+ GIC, which may act by shifting the effector arms of alloreaction toward humoral responses.

Acute Disease↗
PubMed1995

IgA serology in recurrent and non-recurrent IgA nephropathy after renal transplantation.

BACKGROUND: This study investigated whether abnormal circulation of macromolecular IgA and IgA with altered glycosylation or electrical charge plays a role in the recurrence of IgA nephropathy (IgAN) after transplantation. STUDY DESIGN: A total of 92 renal transplant patients were enrolled; 52 IgAN patients and 40 with other non-IgAN. The IgAN group included 10 patients showing IgA mesangial deposits in the grafted kidneys (recurrent group) and 10 who did not (immunohistochemically proven non-recurrent group). In addition another 22 IgAN transplant patients were clinically free of recurrent disease. METHODS: The analyses included macromolecular IgA (IgAIC) detected by the conglutinin assay (K), heavy IgA precipitated in 2.5% polyethylene glycol (PEG), IgA-fibronectin aggregates (IgA/F Aggr), mixed IgA/IgGIC, IgA binding to mesangial matrix components (fibronectin, laminin, type IV collagen) or polycations (poly-L-lysine) and IgA with altered glycosylation (Jacalin-binding assay). RESULTS: After transplantation, IgAN patients displayed significantly higher mean levels for each variable measured than non-IgAN (ANOVA, P < 0.05). By stepwise regression analysis, the binding of IgA to fibronectin had the highest coefficient. By comparing data in recurrent and clinically non-recurrent IgAN, we observed that two groups could be distinguished by the results of the two assays for macromolecular IgA (conglutinin IgAIC and IgA-fibronectin aggregates) and IgA with increased affinity for type IV collagen (P < 0.05). When the selected group of immunohistochemically proven non-recurrent IgAN was compared to the recurrent one, a statistically significant difference was found only for the binding of IgA to type IV collagen (P < 0.05). Data from this test were significantly related with proteinuria (P < 0.05) and microscopic haematuria (P < 0.04). CONCLUSIONS: Even though the IgA serology of renal transplant IgAN patients shows peculiar features and recurrent and non-recurrent IgAN differ in many aspects, the prevalence of positive data in the two groups had no predictive value. This suggests that the recurrence of IgAN is modulated by factors affecting the interaction between circulating abnormal IgA and mesangial cells and/or matrix.

Analysis of Variance↗