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Biomedical subjects

B Charpentier

Publications and source records attributed to B Charpentier.

300 records · Page 17Linked to original sources
PubMedDate not supplied

Post-transplantation polyomavirus infections.

Increasing attention has been recently accorded to BK and JC viruses (BKV and JCV). Both these human polyomavirus (HPV) are members of the papovavirus family which includes the simian virus SV 40. BKV and JCV infect more than 60% of the population worldwide. After primary infection, they remain harboured in the kidneys and may become reactivated in situations of immune impairment. HPV were first described in 1971. BKV was isolated in a renal transplant patient with ureteral stricture and JCV in a patient with progressive multifocal leukoencephalopathy (PML). BKV was known to be involved in post-bone marrow transplantation (BMT) hemorrhagic cystitis. In renal transplantation, BKV and JCV were initially found in the post-transplant ureteric stricture and PML. They are now recognised as a possible cause of transplant interstitial nephritis, mimicking rejection (satisfying the Banff criteria for acute rejection) or drug toxicity. In HPV nephritis there is a mixed interstitial inflammatory infiltrate with focal tubular injury; the tubular epithelium shows marked anisonucleosis, nuclear atypia and basophilic or amphophilic intranuclear inclusions. Tubulitis is frequent. DNA hybridisation or gene amplification by polymerase chain reaction usually demonstrate HPV. Although histology with viral nucleic acid detection may be helpful in differentiating viral infection and rejection, confusion between these complications may lead to either anti-rejection therapy, with the risk of over-immunosuppression, or reduction of immunosuppression, with the risk of graft loss. Confusion may also arise with inclusions of other viruses, such as cytomegalovirus, herpes virus and adenovirus. Reactivation of BKV and JCV infection was demonstrated in respectively 22.2% and 10.9% of renal transplant recipients and 55% and 6.7% of BMT patients. Unfortunately, no routine screening is available for these viruses, so this complication is probably underestimated. No specific therapy of HPV infection is currently available.

Bone Marrow Transplantation↗
PubMedDate not supplied

[Rejection reaction. Elements of diagnosis, monitoring, therapeutic attitude in the case of kidney].

Allograft rejection reaction must be integrated in the broader sense of alloreactivity, i.e. involving a huge T cell repertoire with a high number of alloreactive precursors. This reaction is modulated by the particular immunological state induced by chronic renal insufficiency, by haemodialysis and by the primary kidney disease. The imperfect effect of current immunosuppressive drugs is illustrated by a sizeable proportion of grafts undergoing a chronic rejection process where many growth factors are involved. It has to be noted that allostimulating cells are different from target cells. At present, the therapeutical rejection involves corticosteroids and serotherapy, but it is hoped that new immunosuppressive drugs will increase the efficacy of the rejection crisis treatment.

Acute Kidney Injury↗
PubMedDate not supplied

IL-2-R beta expression and function within resting CD8+ T cells preferentially segregate with the CD45R0+ subset.

Human peripheral blood CD8+ T cells constitutively express a low level of IL-2-R beta chains which were shown in this study to be preferentially carried by the CD45R0+ subset. Such receptors can transduce signals for in vitro IL-2-induced cytolytic function and for the initiation of soluble anti-CD3 and IL-2-induced cell proliferation. Using these stimulation models, a comparison was made between the responsiveness of resting, small CD45R0+ and CD45RA+ subpopulations of CD8+ T cells, both of them being isolated by negative selection and rigorously depleted of monocytes and of IL-2-inducible non-MHC-restricted CTL. Strong proliferation was induced in CD8+/CD45R0+ cells in response to IL-2 and soluble anti-CD3 (each of these stimuli being by itself ineffective), while in contrast, CD8+/CD45RA+ cells manifested, in this system, little reactivity. Accordingly, no conversion to the CD45R0 phenotype occurred in single stained CD45RA+ T cells following their incubation with the stimuli. A similar restriction of reactivity to CD8+/CD45R0+ T cells was observed with respect to IL-2-induced targetable T cell cytotoxicity. The CTL activity induced by IL-2 alone occurred without cell division. In contrast, the additional increase in CTL activity occurring upon the synergistic actions of anti-CD3 mAb and IL-2 coincided with intense cell proliferation, with no generation of LAK activity. The inhibition exerted by anti-IL-2-R beta mAb in the cytolytic and the proliferative activities induced by these stimuli in resting CD8+/CD45R0+ T cells emphasizes the importance of constitutive IL-2-R beta chains in the biology of these cells.

Antigens, CD↗
PubMedDate not supplied

[Urological complications in renal transplantation].

1,224 renal transplant patients were studied. 50 kidneys were obtained from living related donors. The mean age of the recipients was 34.6 years (16.8 to 67.6 years) Ureteric reimplantation was initially performed by uretero-ureteric anastomosis (19%), then into the bladder according to the Leadbetter-Politano technique (69%) and subsequently according to the Lich-Gregoire extra-vesical technique (10%). A cutaneous ileostomy or reimplantation into the renal pelvis was performed in the remaining 2% of cases. The risk of one or more urological complications was 11.2% (137/1,224) and 7.9% when only those patients requiring surgical intervention were taken into account. These complications were classified into 3 categories: strictures (60.6%), fistulae (35.8%) and stones (6.6%). The frequency of urological complications was lower with the Lich-Gregoire technique (4.1%) which we have currently adopted. The renal transplant was lost in 6.1% of cases directly related to a urological complication. The presence of urinary tract fistulae had an unfavourable influence on graft survival due to detransplantations. Whenever possible, our preferred approach consists of percutaneous and/or endourological techniques as first-line treatment followed by second-line surgical treatment in the event of failure of the percutaneous approach.

Adolescent↗
PubMedDate not supplied

[Gastrointestinal complications of renal transplantation].

Out of a series of 614 renal transplantation performed over a 4-year period, using cyclosporin and cimetidine, 100 patients developed a gastrointestinal complication: 9.6% of gastroduodenal ulcers, 4.4% of intestinal complications, 1.3% of pancreatic complications. 7 patients died: 5 from stress haemorrhages, 2 from peritonitis secondary to intestinal perforation. 32% of patients who developed an ulcer had a history of ulcer, but none of them developed a serious complication of their ulcer under cimetidine treatment. 18% of patients with colonic diverticula developed a diverticular complication after transplantation. The patients who died died from stress haemorrhage generally in a context of sepsis or from peritonitis secondary to intestinal perforation diagnosed after a delay of 24 hours.

Adult↗
PubMedDate not supplied

[Cyclosporin, toxicity and efficacy in rejection of liver allografts in the rat].

52 orthotopic liver transplants were performed in DA to lewis rat strain combination, in order to appreciate cyclosporine toxicity, and efficacy at doses of 10 mg/kg day (G II) and 20 mg/kg/day (GIII) compared to liver allografts in DA/lewis rats. The first signs of cyclosporine hepatotoxicity are biological (increased plasma level of bilirubine and transaminase) that were noticed at the dose of 20 mg/kg/day. Histological signs (cells inclusion, hepatocytic necrosis) appeared late and were less constant as well as difficult to assert creatinine plasma level was the best reflect of cyclosporine nephrotoxicity. Renal toxicity was practically constant at the dose of 20 mg/kg/day. In spite of renal and hepatic toxicity, cyclosporin by itself, allows the abolition of the acute rejection of liver allografts in the rat.

Animals↗
PubMedDate not supplied

[The treatment of urinary fistula in renal transplantation].

61 renal transplant patients developed a urinary fistula (4%). The diagnosis was established rapidly (after an average of 12 days) by the presence of urine in the drains and a urine collection on ultrasonography. The exact topographical diagnosis, the nature of the fistula, necrosis or dehiscence, is more difficult, even with modern imaging techniques. The incidence of fistula was decreased by the use of a short ureter, a Lich-Grégoir ureterovesical anastomosis and the prophylactic insertion of a ureterovesical stent. The first 36 ureteric fistulae were treated by open surgery and the last 7 were treated by antegrade stent insertion. 87% of patients were cured of their fistula and retained their transplant: 31 of the 36 patients undergoing open surgery and all 7 patients treated percutaneously. Percutaneous treatment should be proposed as first-line treatment in the case of ureteric fistula after renal transplantation.

Anastomosis, Surgical↗
PubMedDate not supplied

[Surgical treatment of hyperparathyroidism in renal transplant patients].

The authors present their experience of surgery for persistent hyperparathyroidism in renal transplant recipients, based on a series of 944 patients transplanted between 1983 and 1992. 56 patients underwent subtotal parathyroidectomy for persistent secondary hyperparathyroidism. Control of serum calcium was excellent in 83% of patients: 2 patients retained a well controlled hypocalcaemia, 2 are still hypercalcaemic and 3 others have developed recurrent hyperparathyroidism. The postoperative course was marked by one death not related to parathyroidectomy and one recurrent laryngeal nerve palsy. Subtotal parathyroidectomy combined with removal of the thyrothymic tissue is an effective operation to control phosphorus and calcium metabolism in patients with persistent hyperparathyroidism after renal transplantation.

Adult↗
PubMedDate not supplied

Incidence and consequences of post-transplantation lymphoproliferative disorders.

Post-transplant lymphoproliferative disorder (PTLD) is a recognized severe complication arising in allograft recipients treated with immunosuppressive drugs. Although not common, PTLD is one of the most frequent tumours among graft recipients, comprising 15-25% of neoplasms, compared with 5% in the general population. The introduction of cyclosporin A (CyA) in the early 1980's and the very potent new immunosuppressants such as anti-CD3 monoclonal OKT3 and FK506 have been associated with a significant rise in the incidence of PTLD and with their earlier presentation. The incidence of this malignancy varies with the organ transplanted (1-2% of renal transplant recipients) and with the nature and severity of the accompanying immunosuppressive regimen. While the precise etiology of PTLD is still unclear, significant advances have been made recently in the understanding of its pathogenesis. Most PTLD tumour cells present an activated B-cell phenotype and an unrestricted pattern of latent EBV gene products. It is generally accepted that Epstein-Barr virus (EBV) infection or reactivation and intensive anti-T lymphocyte regimens play a major role in the genesis of PTLD. They include a spectrum of EBV-related disorders ranging from lymphoid hyperplasia to frank malignant non-Hodgkin's lymphoma. Although different therapeutic attempts have been proposed, optimal treatment remains elusive. The mortality rate for monoclonal lymphomas was reported to be as high as 80%. Infusion of anti-B monoclonal antibodies seems to be a promising modality. Different preventive approaches have been proposed, including EBV sero-negative donor/recipient matching and careful monitoring of EBV infection. Cautious use of anti-rejection treatment in combination with prophylactic antiviral therapy is recommended.

Humans↗